SELECTED PHYSIOLOGICAL CHARACTERISTICS OF ELITE ROWERS MEASURED IN THE LABORATORY AND FIELD AND THEIR RELATIONSHIP WITH PERFORMANCE
by
GILES D. WARRINGTON
A thesis submitted to the University of Surrey for the degree of
DOCTOR OF PHILOSOPHY
Robens Institute University of Surrey Guildford Surrey GU2 5XH England
July 1998 ProQuest Number: 27750273
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ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106 - 1346 ABSTRACT
In the present study, a number of physiological variables were measured on members of the Great Britain heavyweight rowing squad in the laboratory, field and also during altitude training. The main purposes of the study were to determine which of these physiological variables were important determinants of success in rowing and to evaluate the effects of a specific phase of training on these variables. Additionally, the study sought to assess the effectiveness of different modes of training by monitoring the physiological responses and adaptations to a period of altitude training and evaluating their impact on aerobic work capacity on return to sea level.
Of the 22 descriptive and physiological variables measured to determine their relationship with rowing performance, maximal oxygen uptake (FO2 max) expressed in absolute terms (Imin^) was found to be the best single predictor of rowing performance for the 6 minute (DIST6) and 2500 metre (T2500) performance tests used. Although a number of other physiological variables were found to be significantly related to rowing performance, their inclusion added little to a predictor model of performance. Analysis of the physiological responses to a 3 month phase of training revealed significant improvements in rowing economy (P<0.01) and the exercise intensity attained at a fixed blood lactate concentration of 4 mmol l'^ (P<0.05). In contrast to these improvements in submaximal variables, no significant change was observed for FO2 max.
Changes in the mean daily values for 10 physiological variables measured over 19 days of altitude training and were compared to pre-altitude values. The increase in haemoglobin (Hb) in response to training in a hypobaric environment appears to reflect an increase in haemoconcentration due to a reduction in plasma volume (PV) and to a lesser degree erythropoiesis. Additionally, it appears that those subjects with lower initial Hb levels experienced the greatest increase during altitude training. A significant rise in serum creatine kinase (CK) (P<0.01) and urea (P<0.01) were observed afi;er the period of acclimatisation, which tends to indicate that any increases were associated with a progressive elevation in training load, after this phase, rather than the hypoxic stimulusper se. On return to sea level, there was no significant (P>0.05) improvement in aerobic work capacity, as determined by a fall in submaximal blood lactate concentrations during prolonged exercise. DECLARATION
The work presented in this thesis is entirely my own work and it has not been previously submitted to this or any other institute of higher education for this or any other academic award.
Where use has been made of the work of other people, it has been acknowledged and is hilly referenced.
Signed Date ACKNOWLEDGEMENTS
Throughout the production of this study the author has been indebted to a number of people. Special acknowledgement goes to Professor Craig Sharp for his expert input during the early stages of the study and his continued support and friendship. Sincere thanks is extended to my former colleagues at the British Olympic Medical Centre for their assistance in the collection of data. My greatest debt is owed to my supervisors Professor Colin Boreham, Professor David Stubbs and Dr Mike Tipton for their valuable guidance, advice and encouragement throughout. Gratitude goes to Dr Kevin Hayes for his expertise and patients in explaining some of the more complex statistical procedures and to Donal O'Gorman for his technical advice and comment.
This study would have remained an aspiration without the unwavering support of my friends and family over the last 6 years. Last and by no means least, I would like to extend my sincere thanks the coaches and members of the Great Britain rowing squad who participated as subjects in the study and who’s motivation, dedication and determination in the quest to achieve excellence in their chosen sport inspired my interest in rowing in the first place.
Ill *DediMtco*t
To love is human, to be loved is special
IV GLOSSARY OF TERMS
Critical Power A theoretical concept that presumes that there is a maximum power that an individual can maintain indefinitely. It is based on the observation that the duration for which high intensity exercise can be performed to the point of fatigue is inversely proportional to the power.
2,3-diphosphoglycerate (2,3-DPG) An inorganic phosphate compound which is produced within the red blood cells during glycolysis. It is bound to haemoglobin in the red blood cells and reduces the affinity of haemoglobin for oxygen, shifting the oxygen dissociation curve to the right thereby assisting the unloading of oxygen to the tissues.
Erythropoietin (EPO) A glycoprotein which stimulates erythropoiesis by enhancing the mitotic frequency of erythroide precursors in the bone marrow.
Fractional Utilisation
The percentage of VO2 max utilised at any given submaximal work intensity.
Haematocrit (Hct) The volume of red blood cells usually expressed as a percentage of total blood volume.
Haemoblobin (Hb) The oxygen-transporting component of red blood cells. It consists of a large conjugated protein consisting of four polypeptide chains, each with a prosthetic haem group which contains ferrous iron, able to combine reversibly with oxygen. Maximal Oxygen Uptake (FO2 max) The maximal ability of an individual to take up, transport and utilise oxygen by the working muscles.
Myoglobin An oxygen-binding protein in skeletal muscle.
Oxygen Debt The amount of oxygen consumed during recovery from exercise above that which would be consumed at rest in the same period.
Oxygen Deficit The difference between the total oxygen consumed during exercise and the total that would have been consumed had a steady rate of aerobic metabolism been reached at the start.
Partial Pressure The pressure exerted by a single gas in a mixture of gases. It can be calculated by multiplying the total pressure of the mixture of gases within which the particular gas occurs, by the percentage of the total volume the gas occupies.
Peak Power The peak work output that a rower can achieve during a maximal performance test on a rowing ergometer measured in watts.
Polycythemia An increase in the total number of red blood cells per mm'^ of blood.
Rowing Economy The steady state oxygen consumption for a standardised submaximal workload or fixed reference point.
VI TABLE OF CONTENTS
Page CHAPTER 1 INTRODUCTION
1. Background 1 2. Statement of the Problem 2 3. Purpose 2 4. Hypotheses 4 5. Delimitations 5 6. Limitations 6
CHAPTER 2 REVIEW OF LITERATURE
1. Introduction 7
2. Predictors of Performance 8 2.1. Maximal Oxygen Uptake 8 2.2. Blood Lactate Indices 11 2.3. Maximum Power 14 2.4. Critical Power 15 2.5. Submaximal Ventilatory Parameters 17 2.5.1. Economy 17 2.5.2. Fractional Utilisation 19 2.6. Anaerobic Capacity 22
3. Physiological Responses to Rowing Training 24 3.1. Maximal Aerobic Power 25 3.2. Blood Lactate 25 3.3. Other Submaximal Variables 26 3.4. Strength and Power 27
4. Altitude Training and Sea Level Performance 28 4.1. Haematological Changes 28 4.2. Oxygen Release and 2, 3-diphosphoglycerate (2,3-DPG) 31 4.3. Cardiac Output 34 4.4. Altitude Training and Skeletal Muscle Metabolism 35 4.4.1. Skeletal Muscle Capillaries 36 4.4.2. Skeletal Muscle Enzymes 37 4.4.3. Myoglobin 39 4.5. Substrate Utilisation 40 4.6. Muscle and Blood Buffering Capacity 41 4.7. Maximal Aerobic Power 42 4.8. Altitude Training and Sea Level Performance 43 4.9 Summary 46 CHAPTER 3 A Comparison of Selected Physiological Parameters as Predictors of Rowing Performance.
MATERIALS AND METHODS
1. Introduction 48
2. Ethical Considerations 49
3. Subjects 49
4. Anthropometric Measurements 49 4.1. Body Mass and Stature 50 4.2. Body Composition 50 4.3. Breadths 52 4.3.1. Biacromial Breadth 52 4.3.2. Biiliac Breadth 52 4.3.3. Wrist Breadth 52 4.4. Circumferences 53 4.4.1. Thigh Circumference 5 3 4.4.2. Upper Arm Circumference 53 4.4.3. Forearm Circumference 5 4
5. Cardiorespiratory Evaluation 54 5.1. Ambient Conditions 5 4 5.2. Submaximal Discontinuous Incremental Test 54 5.3. Respiratory Analysis 56 5.4. Maximal Oxygen Uptake 57 5.5. Rowing Economy 57 5.6. Fractional Utilisation 58 5.7. Heart Rate Measurement 58 5.8. Blood Lactate Analysis 58 5.9. Determination of Fixed Blood Lactate Concentrations 60
6. Rowing Performance Tests 61 6.1. 6 Minute “All-Out” Test 61 6.2 2500 metre Test 62
7. Statistical Analysis 63
RESULTS 64
DISCUSSION 76
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS 83 CHAPTER 4 An analysis of the variation in selected physiological parameters during a 3 month period of training.
MATERIALS AND METHODS
1. Introduction 85
2. Ethical Considerations 86
3. Subjects 86
4. Test Procedures 86
5. Anthropometry 87 5.1. Body Mass and Stature 87 5.2. Body Composition 87
6. Cardiorespiratory Evaluation 88 6.1. Ambient Conditions 88 6.2. Maximal Discontinuous Incremental Test 88
7. Training Programme 90
8. Statistical Analysis 91
RESULTS
1. Physical Characteristics 92 2. Training Data 92 3. Anthropometric and Physiological Measures 93
DISCUSSION 95
SUMMARY. CONCLUSIONS AND RECOMMENDATIONS 97 CHAPTER 5 An analysis of selected physiological adaptations in response to altitude training in preparation for competition at sea level.
MATERIAL AND METHODS
1. Introduction 99
2. Ethical Considerations 100
3. Physiological Monitoring at Altitude 100 3.1 Climate Conditions 101
4. General Measurements 101 4.1. Body Mass 101 4.2. Resting Heart Rate 101
5. Haematological Analysis 102 5.1. Blood Gas 102 5.2. Haemoglobin 103 5.3. Haematocrit 105
6. Monitoring of Training Intensity 106 6.1. Urea and Creatine Kinase 106 6.2. Blood Lactate and Heart Rate 108
7. Evaluation of Changes in Aerobic Conditioning in Response to Altitude Training 109
8. Statistical Analysis 110
RESULTS
1. Physical Characteristics 112
2. Climatic Conditions 112
3. Training Data 113 4. Physiological Responses and Adaptations to the Period of Altitude T raining 115 4.1. PaOz and PaC02 116 4.2. pH 118 4.3. Blood Bicarbonate 119 4.4. Urea and Creatine Kinase 119 4.5. Resting Heart Rate 121 4.6. Body Mass 122 4.7. Haemoglobin and Haematocrit 123
5. Summary of Results 127
6. Changes in Submaximal Blood Lactate Response to Exercise 128
DISCUSSION 129
SUMMARY. CONCLUSION AND RECOMMENDATIONS 139
OVERALL SUMMARY 141
FUTURE RESEARCH DIRECTIONS 143
REFERENCES 145
APPENDICES LIST OF FIGURES. TABLES AND ILLUSTRATIONS
Page FIGURES
1. Schematic illustration of a Clark PO2 Electrode 59
2. Individual values for DIST6 plotted against VO2 max (1 min including outlier 65 3. Studentised residuals (SR) plotted against predicted values for DIST6 65 -1 4a. Relationship between DIST6 and VO2 max (1 min ) 68 -1 4b. Relationship between DIST6 and VO2 max (ml kg min ). 68
4c. Relationship between DIST6 and VO2 max (ml kg ^ min \ 68 -1 5a. Relationship between T2500 and VO2 max (1 min ). 69 -1 5b. Relationship between T2500 and VO2 max (ml kg min ). 69
5c. Relationship between T2500 and VO2 max (ml kg min \ 69 6. Total training volume expressed as monthly trained hours (MTH) 93 7. Reflotron® test strip 107 8. Schematic Representation of Experimental Design 109 9. Climatic conditions during the altitude training camp 113 10. Analysis of the training schedule of the elite rowers during the 19 days of altitude training. 115 11. Changes in PaC02 during altitude training compared to sea level (SL) values. 116 12. Changes in PaO^ during altitude training compared to sea level (SL) values. 117 13. Changes in blood pH during altitude training compared to sea level (SL) values. 118 14. Changes in HCO3' during altitude training compared to sea level (SL) values. 119 15. Changes in serum urea during altitude training compared to sea level (SL) values. 120 16. Changes in serum CK during altitude training compared to sea level (SL) values. 120 17. Changes in resting heart rate during altitude training compared to sea level (SL) values. 121 18. Changes in body mass during altitude training compared to sea level values. 122 19. Relationship between daily changes in plasma volume (PV) and body mass during the period of altitude training. 123 20. Standardised changes in haemoglobin (Hb) during altitude training compared to sea level (SL) values. 123 21. Standardised changes in haematocrit (Hct) during altitude training compared to sea level (SL) values. 124 22. Relationship between initial Hb concentration and the change in Hb following altitude training for male and female rowers. 124 23. Relationship between initial Hb concentration and the change in Hb following altitude training for male rowers. 125 24. Relationship between changes in PV and Hb concentrations during the period of altitude training. 126 Page TABLES
1. Exercise intensities and stoke rates used in the incremental test 55 2. Means and standard errors for variables measured 64 -1 3. Output for regression of DIST6 on VO2 max (1 min ) 66
4. Output for regression of T2500 on VO2 max (1 min"^) 66 -1 5. Output for regression of DIST6 onVO 2 max (ml kg min ). 70
6. Output for regression of DIST6 onVO 2 max (ml kg min \ 70 -1 7. Output for regression of T2500 onVO 2 max (ml kgmin ). 71
8. Output for regression of T2500 on VO2 max (ml kg ^ m in"\ 71 9. Relationship between physiological variables and rowing performance 72 10. Prediction of Rowing Performance 73 11. Actual and predicted rowing performances as computed from the regression equations 75 12. Characteristics of study group 92 13. Changes in selected anthropometric and physiological variables measured pre- and post- the 3 month training period 93 14. Characteristics of study group 112 15. General classification of training intensity 113 16. Rowing-specific and non-rowing specific classification of training intensity 114 17. Changes in physiological variables pre- and during-altitude training 127 18. Changes in physiological variables pre-and post- altitude training 128
ILLUSTRATIONS
1. Body composition measurement using skinfold callipers 51 2. Blood lactate sampling during the discontinuous incremental test 56 3. Cardiorespiratory evaluation on the Concept II rowing ergometer 62 4. Members of the great Britain women’s squad during training 91 5. Squad members undergoing training whilst at altitude 101 6. Squad members undergoing blood lactate testing and heart rate monitoring during a training session at altitude. 109 CHAPTER 1
INTRODUCTION
1. BACKGROUND
The origins of rowing can be traced back to ancient times, where early civilisations such as the Egyptians and Vikings were reliant on rowing for transportation. Rowing as a competitive sport originates from eighteenth century England, with a race for professional watermen being held on the Thames in 1715. The amateur code of the sport followed later in 1829, with the establishment of the annual Oxford and Cambridge boat race and the Henley Royal Regatta in 1839.
The qualities required for a successfiil performance in rowing include a high endurance capacity, muscular strength and power and the technical skills to transfer this power onto the water (Hagerman et al., 1978; Mahler et al., 1985). Additionally, Hay (1968), has suggested that a strong relationship exists between technical skills in rowing and anthropometric measures. Rowing has long been considered one of the most demanding endurance sports, with exceedingly high demands being placed on the aerobic and anaerobic energy systems during a 2000 metre race (Hagerman, 1984; Jackson and Secher, 1976; McKenzie and Rhodes, 1982). It has been estimated that the aerobic energy system contributes about 70% of total energy release with the remainder being derived from anaerobic sources (Hagerman et al., 1978). During competition, rowers have been found to exercise at what may be called “severe steady state”, with the majority of work performed at between 95 and 98% of maximal aerobic capacity (Hagerman et al., 1978; McKenzie and Rhodes, 1982). In addition rowers require very high muscular strength and power in order to sustain maximal effort during a race which typically lasts between 6 to 8 minutes (Secher, 1992). 2. STATEMENT OF THE PROBLEM
Rowing is a highly competitive and well established international sport. However, there is a lack of physiological data in the literature to assist the improvement of performance and monitor training adaptations in different environments. The present study, has sought to assess which physiological variables are important to performance in elite rowers. Additionally, the study has endeavored to evaluate changes in these variables in response to training. The final part of the study has attempted to monitor the rate and process of adaptation to altitude training and to determine what effect, if any, hypoxic exposure has on aerobic work capacity on return to sea level.
3. PURPOSE
The purpose of this study was to obtain a comprehensive physiological profile of elite rowers in the Great Britain national squad and to investigate the relationship between selected physiological characteristics, measured in the laboratory and field, with performance. The project was also designed to assess longitudinally responses and adaptations to the training undertaken. It was intended that the tests and protocols utilised in the present study would be sensitive enough to reflect changes in physical conditioning and subsequent performance. '
Between 1991 and 1993 studies were conducted on members of the Great Britain men’s and women’s heavy weight rowing squads. During this 3 year period, extensive physiological data was collected by the author in the human performance laboratories at the British Olympic Medical Centre. Experimentation was also carried out in the field during 3 altitude training camps in the Austrian Alps in preparation for subsequent World Championships and the 1992 Olympic Games. In this context the aims of this study were to investigate the following issues:
• To provide a complete description of the anthropometric size, proportionality and body composition characteristics of elite rowers in Great Britain.
• To determine the relationship between indicators of rowing performance and selected descriptive and laboratory physiological measures.
• To establish the variation in selected physiological parameters during a specific phase of training.
• To monitor the physiological responses and adaptations to altitude training and analyse the effects on performance on return to sea level. 4. HYPOTHESES
For the physiological variables examined, the null hypotheses were as follows:
Experiment 1. A comparison of selected physiological parameters as predictors of rowing performance.
1) Of the physiological parameters measured, VOi max is not the single best predictor of rowing performance.
2) VO2 max expressed in absolute terms (fmin ^), is not a better predictor of rowing performance than when expressed in relative to body mass (mlkgmin^) or an
exponent of body mass (ml kg -min).
Experiment 2. An analysis of the variation in selected physiological parameters during a 3 month period of training.
1) Following the 3 month training period there is no significant difference in any of the physiological variables measured.
Experiment 3. An analysis of selected physiological adaptations in response to altitude training in preparation for competition at sea level.
1) Compared to pre-altitude values, there is no significant difference in any of the physiological variables measured in response to the period of altitude training. 2) There is no significant change in aerobic work capacity as determined by a fall in submaximal blood lactate concentration as a result of the measured physiological adaptations that occur in response to altitude training. 5. DELIMITATIONS
• All tests were administered by the author in order to avoid inter-tester error.
• The subjects selected for the study were restricted to those members of the Great Britain National Rowing squad who were selected to compete in the subsequent World Championships or Olympic Games.
• The study was restricted to elite heavyweight rowers and excluded their lightweight counterparts.
• The study focused exclusively on physiological characteristics of rowing. Psychological and biomechanical factors, which have previously been shown to be important during training and competition, were not considered.
• Analysis concentrated solely on descriptive, anthropometric and aerobic characteristics of rowing performance during training and competition. No attempt was made to evaluate strength or anaerobic capacity measurements.
• The performance tests were restricted to ergometer rowing in order that conditions were controlled and standardised and so that individual rather than crew performance could be evaluated. 6. LIMITATIONS
• Due to the limited number of subjects who fulfilled the necessary selection criteria for the study, it was not possible to include in the experiment design a group of matched controls. Therefore the subjects acted as their own controls in all studies.
• Despite the fact that rowing ergometers have previously been shown to replicate the rowing task and physiological demands of actual rowing, evaluation of rowers in the laboratory setting does not allow a direct prediction of performance during on-water rowing.
• Following the period of altitude training, performance analysis was restricted to submaximal tests. CHAPTER!
REVIEW OF LITERATURE
1. INTRODUCTION
Despite the physiological attributes of rowers being among the highest recorded for any sport (Hagerman et al., 1979), rowing has comparatively rarely been studied. In contrast to other modes of endurance activity, such as running and cycling, which are frequently investigated, there is a scarcity of descriptive data on the physiological characteristics of elite rowers. This may in part be explained by the fact that rowing differs from other types of endurance sports more commonly studied due to a number of factors. During the rowing action, almost every muscle group contributes to the development of propulsive force, in each stroke. In contrast to other forms of human locomotion, the legs work simultaneously rather than alternatively and as a consequence of the relatively low stroke cadence characteristic of the rowing action, there is a potential to generate large forces during each stroke. The situation is Anther compounded by the unique pacing strategy used in rowing competitions. It is therefore not possible to draw direct comparisons from the more established and extensive body of research available for other endurance sports. Additionally, the water-based nature of rowing makes the accurate assessment of the physiological and metabolic demands of rowing relatively difficult.
Over the last number of years the availability of information concerning the physiological effects of exercise on trained athletes has increased. Physiological and metabolic data has been shown to be usefiil for evaluating training and competition results (Steinacker, 1993). Nevertheless, few studies have analysed the physiological effects of specific training programmes in elite athletes. Furthermore, in rowing there is a dearth of information evaluating the physiological responses and adaptations to training undertaken by elite rowers or which physiological characteristics are critical to success at the highest level.
2. PREDICTORS OF PERFORMANCE
2.1. Maximal Oxygen Uptake
Maximal Oxygen Uptake (VO2 max) is the maximal ability of an individual to take up,
transport and utilise oxygen by the working muscle (Âstrand and Rodahl, 1986). As is
evident from this definition, it is the product of the maximal cadiac output (Q max
Imin^) and the maximal difference between the oxygen content of arterial and mixed
venous blood ( a - VO2 max ml f^).
Where VO2 max I min ^ = Q max I min'^ x a - 1 ^ 2 max ml l'^
Traditionally, VO2 max has been considered the “gold standard” laboratory measure of
endurance fitness and performance (Âstrand, 1955; Costill, 1967; Co still and Winrow,
1970; Costill et al., 1973; Mitchell et al., 1958; Robinson et al., 1937; Saltin and
Astrand, 1967; Taylor et al., 1955; Wyndham et al., 1969). However, more recent
evidence has brought this concept into question. Following training, changes in the
FO2 max of highly conditioned athletes have been found to be small, in spite of
significant improvements in performance (Daniels et al., 1978; Ingjer, 1991; Jacobs,
1986; Sjodin et al., 1982a; Sjogaard, 1984; Tanaka et al., 1984). As FO2 max primarily
measures central adaptations to endurance training, such as cardiac output and stroke
volume, (Saltin, 1985; 1988; Weltman, 1995), it has been postulated that ÛO 2 max is not sensitive to peripheral adaptations (Denis et al., 1984; Farrell et al., 1979;
Weltman, 1989; Williams et al., 1967). Furthermore, as competitive endurance exercise
is performed at the highest sustainable percentage of FDz max possible, Weltman
(1995) has suggested that a measure of peripheral muscle function might be a better
predictor of endurance performance than VOi max.
The degree of association between VOi max and endurance performance appears to be
dictated by the composition of the subject group being studied (Noakes, 1988;
Unnithan et al., 1995). Although FD: max has been shown to be a good predictor of
performance in heterogeneous groups, in terms of their performance abilities (Burke,
1976; Costill et al., 1973; Noakes, 1988), considerable differences have been found in
the values of athletes with similar performance times (Daniels, 1974; Noakes, 1986;
Pollock, 1977). Conversely, athletes homogeneous in VOimax values may achieve
different performance levels (Conley and Krahenbuhl, 1980; Costill et al, 1973; Costill
and Winrow, 1970; Noakes, 1988; Scrimgeour et al, 1986), indicating that other
factors must contribute to success in endurance events.
Of the numerous studies which have correlated VO2 max with endurance performance,
few investigations have dealt with rowing (Bloomfield and Roberts, 1972; Doherty et
al, 1994; Kinch et al, 1994; Klusiewicz et al, 1991; Kramer et al, 1994; Secher et al,
1982b; Williams, 1978; Womack et al, 1992). Despite the limited data available,
maximal aerobic capacity has been cited as a major factor influencing rowing
performance (Clark et al, 1983; Hagerman et al, 1978; Hagerman et al, 1979;
Jackson and Secher, 1973; Saltin and Astrand, 1967; Secher, 1983; 1990). However,
few studies have examined the relationship between ÛO 2 max and actual rowing
performance in competition (Nevill et al, 1992a; Secher et al, 1982b; Secher et al,
1983). Although VO2 max has been found to be an important factor predicting success in rowing, the issue as to which unit of VO2 max best predicts rowing performance has been brought into question. Nevill et al. (1992b) have suggested that the most appropriate method of scaling VO2 max data is to be independent of body size, which required the variable to be divided by a reduced proportion of body mass (ml kg"^^^ min-i). Data reported by Nevill et al. (1992a) revealed that the FD 2 max (1 min-i) of varsity oarsmen conformed very closely to this relationship and was proportional to body mass (kg^^es) indicating that the two variables are directly related. However, when both VO2 max (I min-i) and body mass (kg) were used, only absolute VO2 max
was necessary to predict rowing performance in a 7 minute ergometer test (r=0.86).
This confirmed the earlier work of Secher et al. (1982b), who found that there was a
strong relationship between VO2 max (I min-i) and placing in an international regatta
(r=0.87). When FO 2 max was expressed relative to body mass (ml kg min-i) no
significant relationship was found (r=0.38). In contrast to the findings of Secher et al.
(1982b), Klusiewicz et al. (1991) reported that VO2 max was only significantly related
to rowing performance (r=0.70) when expressed relative to body mass (ml kg min-i).
This may reflect the heterogeneous nature of the group in terms of training experience
and also their smaller body mass. Secher et al. (1983) subsequently observed that
medal winning heavyweight oarsmen had a mean VO2 max of 5.9 Imim^ compared to
5.6 1' min-i for those less successful. When the data was expressed in dimentionless
terms (ml kg"^^^ mim^) no significant difference was observed between the 2 groups
which suggested that the greater VO2 max values found in more successful oarsmen
mainly reflect their larger body dimensions (Astrand and Rodahl, 1986; Hagerman,
1984; Secher et al., 1983).
The contention that absolute ŸO2 max (1 min-i) may be more appropriate than other
units of measurement for the assessment of maximum aerobic capacity, and its
relationship to rowing performance, are supported by a number of other studies
(Doherty et al., 1994; Kinch et al, 1994; Nevill et al, 1992a; Secher et al, 1983;).
10 This may reflect the fact that the rower's body mass is supported by the boat in the water (Hagerman, 1984; Secher, 1990; Secher et al, 1982b). Whilst agreeing with this view, the modest correlation between absolute FDz max and ergometer rowing performance (r=0.51) reported by Tumilty et al. (1987) led the authors to suggest, that at least in rowing, there are other important factors in addition to VO2 max which can affect performance. Rowing ergometers have been shown to accurately replicate the rowing task and physiological demands of on-water rowing (Chenier and Leger, 1991;
Hagerman, 1984; Hagerman et al, 1979; Henry et al, 1995; Lamb, 1989; McKenzie
and Rhodes, 1982; Smith and Spinks, 1995; Steinacker et al, 1987; 1991; Tumilty et
al, 1987; Urhausen et al, 1993).
Based on the current evidence available, it appears that at least in rowing exercise, that
VO2 max is an important determinant in predicting success. This may well reflect the
typical duration of a 2000 metre rowing event, which requires a sustained maximal
effort lasting between 6 to 8 minutes, depending on the boat size and calibre of the
rowers (Secher, 1992). In contrast to other endurance activities, the data available
relating VO2 max to rowing performance is scarce and warrants further investigation,
particularly in relation to the elite performer.
2.2. Blood Lactate Indices
It has been suggested that the blood lactate response to incremental exercise, and in
particular the highest sustainable exercise intensity, without a gradual increase in blood
lactate levels, may predict endurance performance more accurately than FD 2 max
(Farrell et al, 1979; Kindermann et al, 1979; Lafontaine et al, 1981; Weltman, 1995).
There are a myriad of terms which have been adopted to describe the blood lactate
response during exercise, including lactate threshold (Ivy et al, 1980), onset of blood
lactate accumulation (OBLA) [Sjodin and Jacobs, 1981], individual anaerobic
11 threshold (Stegmann et al., 1981), fixed blood lactate concentration (Weltman et al.,
1987) and more latterly, the lactate minimum point (Tegtbur et al, 1993). For a detailed review of blood lactate terminology see Jacobs, 1986. During exercise lactate is produced predominantly by the active muscle cell, and is released into the blood. The rate of blood lactate accumulation primarily refers to the balance between the production and disappearance of this metabolite, predominantly by either uptake in the liver, heart and skeletal muscle (Jacobs, 1986). These "threshold" levels, in theory, represent the metabolic rate where the elimination of lactate from the blood is equal to the rate of diffusion from the exercising muscles (Stegman and Kinderman, 1982;
Stegman et al, 1981). At these exercise intensities maximum blood lactate steady state
is deemed to have occurred (Heck et al, 1985), with the inherent assumption that
above this workload blood lactate will accumulate exponentially and fatigue will
ultimately result (Farrell et al, 1979; Kumagai et al, 1982; Orok et al, 1989; Stegman
and Kinderman, 1982).
The blood lactate concentration at this maximum steady state has been shown to have
a high inter-subject variability, ranging from 2 to 7 mmol 1 . Those with a lower
aerobic capacity demonstrate a more accelerated net lactate accumulation, due to a
lower clearance capacity (Stegman and Kinderman, 1982; Stegman et al, 1981). In
rowing the blood lactate level at which a steady state is attained has been shown to be
variable and may be dependent on, among other factors, the intensity of habitual
training (Howald, 1988). Due to this individual variation in lactate response to
exercise, it has been proposed by Urhausen et al. (1986) that each rowers individual
lactate threshold should be determined.
Several studies have found that indices of blood lactate during submaximal exercise are
highly correlated with endurance performance in runners (Allen et al, 1985; Duggan
and Tebbutt, 1990; Farrell et al, 1979; Fay et al, 1989; Fohrenbach et al, 1987;
Kumagai et al, 1982; La Fontaine et al, 1981; Lehmann et al, 1983; Sjodin and
12 Jacobs, 1981; Tanaka and Matsuura, 1984; Williams et al., 1983; Yoshida et al.,
1987), cyclists (Barlow et al., 1985; Coyle et al., 1988; 1991; Jacobs et al., 1983; Orok
et al., 1989) and swimmers (Wakayoshi et al., 1992; 1993). The amount of information relating blood lactate data to performance in rowing is limited (Faff et al., 1993;
Klusiewicz, 1993; Klusiewicz et al., 1991; Steinacker et al., 1991; Wolf and Roth,
1987; Womack et al., 1992; 1996). In a number of studies (Faff et al., 1993;
Klusiewicz, 1993; Klusiewicz et al., 1991; Womack et al., 1992; 1996), the velocity -1 attained at a blood lactate reference level of 4 mmol 1 (vLT4mM) has been shown to
be closely related to ergometer rowing performance. Faff et al. (1993), reported a
strong correlation between mean power output achieved during a 2000 metre
ergometer time trial (T2000) and vLT4mM (r=-0.89) in junior rowers. Similar
observations were reported by Klusiewicz et al. (1991) and Womack et al. (1992),
who found vLT4mM to be the best predictor of T2000 ergometer performance (r=-
0.90 and r=-0.91, respectively). In addition, Womack et al. (1992) observed an almost -1 identical relationship for velocity attained at a blood lactate reference of 2.5 mmol l
(vLT2.5mM) and T2000 (r=-0.90). A later study by Womack et al. (1996) suggests
that lactate-related variables may be more sensitive indicators of adaptations to training
and performance than VGi max. Prior to training, vLT4mM was found to be closely
correlated to T2000 (r=-0.90) whilst a weaker relationship was reported between
T2000 and ÛO 2 max (r=-0.84). After 12 weeks of training, a higher correlation was
reported between vLT4mM and T2000 (r=-0.93) whilst a weaker correlation was
observed between VOiinax and T2000 (R=-0.82). The contention that lactate-related
variables may be more sensitive indicators of adaptations to training than VO2 max
were also support by other studies (Favier et al., 1986; Hurley et al., 1984; Williams et
al., 1967).
The rationale for using blood lactate measurement as a diagnostic tool for predicting
success in endurance activities has gained increasing support over recent years. It has
been suggested, in a number of studies, that indices of blood lactate response to
13 endurance exercise may account for a larger proportion of the variation in endurance exercise performance than other physiological variables such as VO2 max. This may in part be explained by the fact that blood lactate and VO2 max responses to exercise are determined by different mechanisms (Jacobs, 1986; Weltman, 1995). In rowing, whilst there is evidence of the predictive power of various blood lactate indices in relation to performance, the amount of data to support this contention is limited and merits further research.
2.3. Maximum Power
More recently, a number of investigations have indicated the importance of maximal
muscle power as a predictor of performance (Hawley and Williams, 1991; Noakes,
1988; Noakes et al, 1990). Several studies have suggested that the primary variable
predicting performance, at least in running (Daniels et al, 1986; Kolbe et al, 1995;
Morgan et al, 1986; Morgan et al, 1989; Noakes, 1988; Noakes et al, 1990;
Scrimgeour et al, 1986) and cycling (Hawley and Noakes, 1992) is the maximum
velocity or, a derivative, peak velocity that an athlete can achieve during a VO2 max
test. Similar findings have been documented in swimming studies where peak arm
power has been used to predict performance in middle distance and sprint swimmers
(Hawley and Williams, 1991; Sharp et al, 1982).
Daniels et al. (1986) reported that the velocity at ÛO 2 max (VÛO2 max), which
combines VO2 max and economy into one variable (Daniels, 1985; di Prampero, 1986),
may be important in explaining performance in runners of mixed ability. Velocity at
ÛO2 max appears to be a more appropriate predictor of performance than when
VO2 max or economy are independently assessed, since VVO2 max provides a reflection
as to what intensity an individual can work at when operating at ÛO 2 max or a
percentage of that FD 2 max (Daniels and Daniels 1992). Morgan et al. (1989), have
14 reported that vÛO: max was a better predictor of 10 km running performance than
VO2 max or running economy in a group of well-trained male runners. In accordance with this observation, Noakes et al. (1990) reported that, of a series of physiological parameters measured in a heterogeneous group of male marathon and ultramarathon runners, peak treadmill velocity at VO2 max accounted for at least as much variance in distance running performance from 10-90 km as the lactate turnpoint. By using peak running velocity rather than vFDz max, Noakes and co-workers (1990) avoided the necessity to calculate velocity associated with VO2 max and the energy cost of running and eliminated the subsequent inherent errors in these calculations (Billat and
Koralsztein, 1996). The greater importance played by peak power output in predicting
endurance performance than VO2 max, observed by Noakes et al. (1990) has led them
to question the necessity to measure VO2 max in the first place, particularly as changes
in performance with training often occur without equivalent changes in ÛO 2 max
(Noakes, 1988).
2.4. Critical Power
The critical power concept is based on the theoretical assumption that there is a work-
rate that can be maintained for a very long time without exhaustion (Monod and
Scherrer, 1965). The basis of the critical power principle, based on local muscular
exercise, is that there is a hyperbolic function between the power output and the time
to exhaustion at that particular power output. The asymptote of this relationship is
used to represent the critical power and is equivalent to the slope of the regression of
total work and the time to exhaustion. The concept of critical power was later applied
to cycling ergometry by Moritani et al. (1981) and has since been extended to running
(Hopkins et al., 1989; Hughson et al., 1984; Pepper et al., 1992), swimming
(Wakayoshi et al., 1992), kayaking (Clingeleffer et al., 1994) and rowing (Faff et al.,
1993).
15 In theory, the critical power represents the power output that could be maintained indefinitely (Monod and Sherrer, 1965; Moritani et al., 1981) and expresses an inherent characteristic of the aerobic energy system (Gaesser and Wilson, 1988), without a considerable contribution from anaerobic energy sources (Monod and
Sherrer, 1965; Moritani et al., 1981). In this regard, critical power has been related to fatigue thresholds, as estimated from integrated electromyograms (de Vries et al.,
1982), VO2 max (Kolbe et al., 1995; Moritani et al., 1981), ventilatory and lactate thresholds (Moritani et al., 1981; Nagata et al., 1983; Wakayoshi et al, 1992) and
endurance training status (Jenkins and Quigley, 1992; Hill, 1993). In practice,
however, it is not possible to sustain exercise at critical power without fatigue and
exhaustion, which usually occurs within about 30 minutes (Faff et al, 1993; Housh et
al, 1989; Jenkins and Quigley, 1990; McLellan and Cheung, 1992).
In a number of studies, critical power has been shown to overestimate the metabolic
rate associated with maximum steady state blood lactate (Clingeleffer et al, 1994;
Housh et al, 1991; Jenkins and Quigley, 1990; McLellan and Cheung, 1992) and
ventilatory response to exercise (Poole et al, 1988; Talbert et al, 1991). This has led
Clingeleffer et al. (1994) to suggest that critical power and anaerobic threshold
parameters are two different physiological events. The validity of critical power as a
sustainable power, or as an index of endurance, therefore remains inconclusive (Hill,
1993).
Although attempts have been made to relate the critical power concept to endurance
fitness (Jenkins and Quigley, 1992) and training status (Gaesser and Wilson, 1988;
Jenkins and Quigley, 1992; 1993; Poole et al, 1990), little is known about the
relationship between critical power and performance. Wakayoshi et al, (1992)
reported that critical velocity, based upon critical power and defined as the speed
which could theoretically be maintained without exhaustion, significantly correlated
16 with mean swimming velocity for 400 m freestyle (r= 0.86). Similarly, Kolbe et al.
(1995), observed a significant relationship between critical power and running times over 1 km (r= -0.75), 10 km (r=-0.85) and 21.1 km (r=-0.79) in a group of male long distance runners. Despite the significance of their findings, Kolbe and co-workers
(1995) concluded that the "rather low predictive value is unlikely to be useful for predicting running performance accurately or for monitoring small changes in performance as a result of training or other interventions".
Only one study in the literature was found to relate the critical power concept to rowing exercise. In this study Faff et al., (1993) reported that the maximal power that
could be maintained throughout 6 minutes of rowing, as predicted from critical power
values, was very strongly correlated with the time to row 2000 m (r=0.96) and the
mean power output during 6 minutes of maximal ergometer rowing (r=0.98). A
weaker, though nevertheless significant, relationship was observed for critical power
and the two performance tests (r=-0.74 and r=-0.71, respectively). The authors
concluded that indices of critical power are of a high diagnostic value when assessing
maximal work capacity in rowing.
2.5. Submaximal Ventilatory Parameters
2.5.1. Economy
It has been suggested that success in endurance activities is dependent on the
economical utilisation of a high aerobic capacity and the ability to employ a large
fraction of that capacity during competition (Costill et al., 1973). Economy, defined as
the steady state oxygen consumption for a standardised submaximal velocity (Farrell et
al., 1979), has been associated with success in distance running (Conley and
Krahenbuhl, 1980; Costill and Winrow, 1970; Daniels, 1974; Fay et al., 1989; Sjodin
17 and Scheie, 1982), particularly where differences in VO2 max values between subjects are small (Conley and Krahenbuhl, 1980; Morgan et al., 1989).
The possible importance of economy among a group of runners homogeneous in terms of ability was illustrated by Conley and Krahenbuhl (1980), who found that the mean
for 3 submaximal running speeds accounted for 65% of the variation in 10 km race performance in highly trained runners. This was supported by a later study by Morgan et al. (1989), who reported a significant relationship between running economy and 10 km running time (r= 0.64) in a group of runners of similar ability.
In contrast. Costill et al. (1973) suggested that the running economy at a standardised
speed bore no apparent relationship to running performance. The large intraindividual
variations in VO2 at standardised running speeds in the subjects tested suggested that
differences in economy were incidental, insignificant and of little value in differentiating
distance running ability. Additionally, Apor et al. (1980) have cast doubt on the
diagnostic merits of routine determination of aerobic economy. In comparison to the
findings of Costill et al. (1973), Farrell et al. (1979) reported a larger variation in VO2
for the same running speed (268m min ^), although the mean VO2 values were similar.
In both studies the subjects were heterogeneous in terms of distance running ability.
The failure of the majority of studies to show a significant relationship between running
economy and endurance performance (Conley et al., 1981; Davies and Thompson,
1979; Deason et al., 1991; Farrell et al., 1979; Kumagai et al., 1982; Powers et al.,
1983; Sjodin and Svedenhag, 1985) has led Noakes (1988) to suggest that economy
cannot be the principal factor predicting athletic ability. The relationships reported
between running economy and performance, have been shown to vary widely (Costill
et al, 1973; Conley and Krahenbuhl, 1980; Farrell et al., 1979). It appears that the
importance of economy to endurance performance, at least in running, may only be
expressed when the subjects are of a comparable ability and homogeneous in VO2 max
18 (Conley and Krahenbuhl, 1980; Morgan et al., 1989; Sparling, 1984). This contention was supported in a review by Daniels (1985), in which it was stated that within a group of runners of similar ability, economy has the potential of being the most important characteristic in the determination of success.
Current research investigating economy and endurance performance has almost exclusively focused on distance running. There is a dearth of information relating economy to other endurance activities. In rowing, no data is currently available investigating the importance of economy to performance. One longitudinal study by
Warrington et al. (1992) reported a significant improvement in rowing economy following 3 months training in elite female rowers. No similar improvement in
VO2 max was observed, which led the authors to suggest that rowing economy was
possibly a more sensitive measure of changes in endurance conditioning in elite rowers.
This was supported in an earlier study by Scrimgeour et al. (1986), who found that the
main effect of training more than 100 km per week may be an increase in running
economy. The faster running speed of the higher trained runners running at the same
fractional utilisation was due to superior running economy.
2.5.2. Fractional Utilisation
Endurance capability has been broadly defined as “the capacity to sustain a high
percentage of VO2 max for a prolonged period of time” (Lacour and Flandrois, 1977).
Fractional utilisation, or the percentage of peak aerobic power (VoV02 max) utilised at
a given submaximal work intensity (Unnithan et al., 1995), has been shown to be an
important measure in predicting running performance (Allen et al., 1985; Conley,
1981; Conley and Krahenbuhl, 1980; Conley et al., 1981; Costill et al., 1971; 1973;
Davies and Thompson, 1979; Fink et al., 1977; Leger et al., 1984; Maron et al., 1976,
Maughan and Leiper, 1983; Mayhew and Andrew, 1975; Peronnet et al., 1987;
19 Pollock, 1977; Sparling, 1984; Unnithan et al., 1995). This may reflect that %FÛ2 max indicates differences in both running economy and FO2 max (Sparling, 1984).
Although Costill et al. (1973) observed no significant relationship between running economy and performance, when the data was expressed as a percentage of maximal aerobic capacity (%FÛ2 max), it was found to be highly related to 10 mile running time
(r=0.94), as was FD 2 max (r=-0.91), across a group of subjects of a wide range of ability and ÛO 2 max readings. The authors concluded that performance could be reliably predicted from %FÛ2 max and was thus based on the variability of FO2 max rather than any differences in running economy. The significant correlation between
%PD2 max and blood lactate accumulation reported in the study led Costill and co workers (1973) to suggest that the ability to exercise for prolonged periods at a high
fractional utilisation appears to be related to the blood lactate concentration during
submaximal exercise. In accordance with this study, Allen et al. (1985) reported that in
a group of masters and junior runners with similar performance levels, the masters
runners were able to maintain a higher % ÛO 2 max during a 10 km race and also
possessed higher lactate thresholds. Farrell et al. (1979), suggested that race pace is
determined by the highest possible %F0 2 max immediately prior to an exponential rise
in plasma lactate. Once lactate accumulation is elevated above a certain work threshold
it appears to be a fimction of %Û02 max (Bransford and Howley, 1977; Farrell et al.,
1979).
The fraction of FO2 max that could be maintained throughout a race has been found to
be significantly related to marathon performance (Maughan and Leiper, 1983; Peronnet
et al., 1987). Costill and Fox (1969), have previously demonstrated that experienced
marathon runners utilise about 75% of their FO2 max during competition. Davies and
Thompson (1979) reported a higher figure of 82% of FO2 max could be sustained at
marathon running pace. The high correlation coefficients reported by Maughan and
Leiper (1983), highlighted the importance of both %U02 max and ÛO 2 max across a
20 broad range of performances. Peronnet et al. (1987), reported a wide variation in
VoVOimax at marathon race pace (67-87%) in the group of runners studied. They concluded that runners who were heterogeneous in terms of VOimax but similar economies may achieve similar performance times due to differences in endurance capability. Peronnet et al. (1987), went on to suggest that VOi max was the mediating factor in endurance performance. In support of this contention, Unnithan et al. (1995) maintained that any association between fractional utilisation and performance is merely a reflection of the effect of a heterogeneous sample in relation to peak VO2 .
In rowing, the importance of a high fractional utilisation to success was reported by
Hagerman et al. (1978) and McKenzie and Rhodes (1982) who observed extreme values of the fractional utilisation of VO2 max during simulated rowing (93-98%). This
has been referred to as “severe steady state” and has lead Hagerman et al. (1978) to
suggest that this was the most critical factor in maintaining such a high mean workload
during a 6 minute performance test. In contrast to this observation, Peronnet et al.
(1987) have suggested that in shorter duration running events (< 7 minutes), endurance
capability may not have a significant role to play since %V0 2 max may be close to or
greater than 100%. Davies and Thompson (1979) and Scrimgeour et al. (1986) have
previously reported that the % VO2 max that can be sustained during competition is
dependent on the duration rather than the distance of the activity. Accordingly,
%P0 2 max sustained decreases with increasing racing duration, and accounts for the
relatively high figure in rowing, which is typically performed over 2000 metres and
lasting approximately 5.8-7.4 minutes (Secher, 1992; Steinacker, 1993).
21 2.6. Anaerobic Capacity
The use of oxygen uptake to assess the contribution of aerobic metabolism during rowing has shown to be highly reliable. However, the role of anaerobic metabolism has proved to be much harder to identify (Hagerman et al., 1978). Lormes et al., (1991) reported that current tests of anaerobic capacity in rowing have not proved to be specific or sensitive enough to reflect changes in training status.
The assessment of the relative contribution of anaerobic metabolism to rowing performance has been traditionally evaluated by the measurement of blood lactate after maximal exercise (Secher, 1990). Peak post-exercise blood lactate concentrations in rowers have been shown to range between 14-18 mmoll following 6 minutes
simulated rowing (Hagerman et al, 1979); 11 mmoll'^ following maximal treadmill
running; 15 mmoll'^ after a national regatta and 17 mmol l^ after an international
regatta (Vaage, 1977). There is, however, considerable debate over the merits of using
blood lactate measurements to evaluate the overall anaerobic energy contribution to
specific exercise, since determination of the distribution volume of blood lactate and
the associated energy equivalent may be inaccurate (Hagerman, 1984; Hagerman et al,
1978; Klausen et al, 1974; Secher, 1983).
The contribution of anaerobic metabolism to total energy expenditure during maximal
rowing, based on oxygen debt and oxygen deficit analysis, has been estimated to be
between 20 and 30% (Grujic et al, 1987; Hagerman et al, 1978; 1979; Roth et al,
1983; Steinacker, 1988; Szogy and Cherebetiu, 1974). Nevertheless, anaerobic
capacity has been shown to explain only about 10-20% of the performance of well
trained rowers in competition (Howald, 1988; Steinacker, 1993; Wolf and Roth,
1987). It has been reported that oxygen debt is usually larger than oxygen deficit with
the differential being proportional to the intensity of exercise (Hagerman et al, 1979;
McMiken, 1976; Martin, 1974). In one study, Hagerman et al. (1979) reported that
22 oxygen debt was about 40% higher than oxygen deficit values following ergometer rowing. One theory for this disparity is that an appreciable part of oxygen debt is utilised for functions unrelated to skeletal muscle metabolism (Hagerman et al 1978;
Welch et al, 1970). Medbo et al. (1988), proposed that in exhaustive exercise greater than 2 minutes in duration, anaerobic capacity may be expressed quantitatively by determining maximal accumulated oxygen deficit (MACD). Consequently, although oxygen debt has been measured to reflect the anaerobic energy contribution it has been
suggested that, due to the nature of rowing and the duration of a race, that the use of
oxygen deficit might be more accurate (Hagerman et al, 1979; Secher, 1990).
However, methodological difficulties in the accurate calculation of oxygen deficit, due
to measurements being based on calculations rather than direct measurements, have
discouraged its widespread usage (Hagerman, 1984; Secher, 1983). Of the limited data
available oxygen deficits of 87-98 mlkg'^ have been reported for male and female
rowers (Hagerman, 1979), which are higher than those recorded for runners (Medbo et
al, 1988; Scott et al, 1991) and cyclists (Graham and McLellan, 1989) and may
reflect the “whole body” nature of rowing activity (Koutedakis and Sharp, 1985).
Hagerman et al. (1978), reported that during 6 minutes of maximal work on a rowing
ergometer, the high anaerobic and aerobic capacities of oarsmen enabled them to work
at the upper limits of anaerobic metabolism, normally associated with shorter maximal
efforts. Klusiewicz et al. (1992), observed a significantly higher peak lactate
concentration following a simulated race in senior rowers compared to juniors. This
finding was further supported by Secher et al. (1982a), who suggested that blood
lactate accumulation was volume dependent, and should increase to the third power of
a characteristic linear dimension of the subject. Thus larger rowers should have an
advantage over their smaller counterpart due to their higher anaerobic potential.
Several studies have reported that a high anaerobic capacity is of limited value, is not
among the most essential factors determining rowing work capacity (Klusiewicz, 1993;
23 Klusiewicz et al., 1991; Lormes et al. 1991; Steinacker et al., 1991) and, therefore, need not be developed above a certain level (Howald, 1988; Secher, 1983; Wolf and
Roth, 1987). Consequently, the merits of excessive high intensity training for success in rowing have been brought into question (Mader et al., 1986; Steinacker, 1993). The lack of importance placed on anaerobic metabolism may be reflective of the high aerobic capacity and also large muscle mass, with a large proportion of slow twitch muscle fibres, which has been shown to be characteristic of highly trained rowers
(Hagerman and Staron, 1983; Larsson and Forsberg, 1980).
3. PHYSIOLOGICAL RESPONSES TO ROWING TRAINING
Intensity, duration and frequency of training have been established as critical components in providing an adaptive response to training (Steinacker 1993; Tanaka et al., 1986; Vermulst et al., 1991). The availability of information concerning the physiological effects of exercise in highly trained athletes has grown in recent years. Such data has been used to establish physiological profiles of elite rowers. However, physiological testing may provide a greater benefit in evaluating training, since the different seasonal emphasis on rowing training highlights the potential value of serial testing and monitoring at specific phases (Mahler et al., 1984b; 1985). Despite this, few studies have reported the effects of training on rowers, even though the high volume of training of oarspersons is increasingly dependent on physiological monitoring for evaluation of exercise performance (Koutedakis, 1989; Koutedakis and Sharp, 1989; Mahler et al, 1984b; Steinacker, 1988; 1993; Strydom et al, 1967). This in part may be explained by the lack of controlled studies on such athletes and the complexity of training, making it impossible to draw any direct conclusions (Steinacker, 1993). Bell et al. (1993) have suggested that the physiological factors involved in rowing performance are complex and multi-faceted and may not follow the same time course for training induced adaptations as other components of fitness.
24 3.1. Maximal Aerobic Power (VO 2 max)
In rowing, maximal aerobic capacity (FD 2 max) has been cited as a major factor influencing rowing performance (Clark et al., 1983; Hagerman et al., 1978; 1979; Jackson and Secher, 1973; Saltin and Âstrand, 1967; Secher, 1983; 1990). Increases in
VO2 max in response training have been reported in rowers of different abilities (Fry et al., 1993; Hagerman and Staron, 1984; Korner and Schwanitz, 1985; Mahler et al, 1984b; 1985; Michalsky et al, 1988; Roth, 1979; Sheng and Xing, 1987; Steinacker,
1988). Comparison of values for FD 2 max between Winter training and the competitive season have been shown to increase by 22% (Hagerman and Staron, 1984) and 14% (Mahler et al, 1985), respectively. However changes have been found to be much smaller in elite rowers (Mahler et al, 1985; Secher et al, 1982a), with differences most likely reflecting variations in the initial training status of the respective
subjects. Secher et al. (1982a), observed a more modest increase in VO2 max of 4% in national level oarsmen following 6 month training, in preparation for Summer
competition. It has been suggested that increases in VO2 max observed in rowers are proportional to the level of training performed (Korner and Schwanitz, 1985), but plateaus at training volumes of approximately 5000-6000 km per annum (Roth, 1979). With more prolonged training, it has proven to be increasingly difficult to elicit further
improvements in VO2 max levels (Korner and Schwamtz, 1985).
3.2. Blood Lactate
Several studies have used the power output attained at fixed blood lactate concentrations to evaluate the performance of rowers in training (Klusiewicz, 1993; Roth, 1979; Tumulty et al, 1985; Vermulst et al, 1991; Vervoon et al, 1992; Warrington, 1992; Womack et al, 1996). As a consequence of annual planning, the velocity associated with a blood lactate level of 4.0 mmol l ^ (vLT4mM) may increase to higher values in response to seasonal training (Hagerman and Staron, 1983; Klusiewicz, 1993; Mahler et al, 1985; Michelson and Hagerman, 1982; Secher et al, 1982b; Steinacker et al, 1991; Womack et al, 1996). Roth et al. (1979) observed that
25 specific endurance training increased work output per stroke for a fixed lactate level. Similarly, Womack et al. (1996), reported a significant increase in vLT4mM in response to training in a group of collegiate oarsmen, while no improvement was observed for VOimax. Klusiewicz (1993), reported an increase of 7.6% in vLT4mM in a 3 month preparatory training phase in a group of elite rowers. This was comparable to the 5% increase following a 1 month aerobic training period reported by Steinacker et al. (1991). In one training study using elite female rowers, Vermulst et al. (1991) observed that vLT4mM increased to 81% of maximal power output due to the training performed. The vLT4mM has been shown to be closely related to ergometer rowing performance in a number of studies (Faff et al., 1993; Klusiewicz, 1993; Klusiewicz et al., 1991; Womack et al., 1992; 1996). Mickelson and Hagerman (1982), have suggested that the high anaerobic thresholds and aerobic capacities for rowers recorded are partly the result of the specific nature of the training regimens undertaken. Compared to maximal variables, such as VO2 max and peak power output, it has been argued that the blood lactate-power relationship and the anaerobic threshold offer a higher degree of sensitivity for controlling training (Mahler et al., 1984b; Michalsky et al., 1988; Urhausen et al, 1986; Wolf and R oth, 1987).
3.3. Other Submaximal Variables
A number of investigations have used submaximal variables such as fractional utilisation (Mahler et al, 1984b; 1985; Mickelson and Hagerman, 1982; Sheng and Xing, 1987, Steinacker, 1993), rowing economy (Secher et al, 1982a; Warrington et al, 1992; Womack et al, 1996) to evaluate the performance of rowers in training. In a recent study which investigated the effects of training on various physiological parameters and their relationship to rowing performance, Womack et al. (1996) suggested that the observed improvement in rowing economy at a fixed velocity
implied that a greater velocity could be reached for a given VO2 , up to and including
VO2 max. Womack et al. (1996), concluded that the training induced improvement in rowing economy, was associated with the observed increase in rowing performance.
26 In contrast, Bell et al. (1993) reported no improvement in fractional utilisation at ventilatory threshold, despite a significant improvement in VOimax following 16 weeks training in a group of female rowers. Although fractional utilisation did not improve in response to training, the power output attained at ventilatory threshold exhibited a significant increase. Contrary to these findings, in parallel with an improvement in ÊD 2 max, Mahler et al. (1984b) reported an increase in fractional utilisation from 78 to 89%, at the anaerobic threshold, over a 6 month training period, in a group of national level rowers. Similarly Mickelson and Hagerman (1982), observed a high fractional utilisation at ventilatory threshold of 83.5% in a group of elite oarsmen. It was suggested that this was a function of the rigorous training regimen undertaken. This is comparable to the value reported by Steinacker (1993), who found that the fractional ultilisation of highly trained rowers at vLT4mM equated to about 85% of VO2 max. This attests to the very high aerobic capacities of elite rowers and can be attributed in part to the specific training programmes undertaken (Hagerman, 1984).
3.4. Strength and Power
Enhancing force and power generation through improved technique and strength training is considered to be essential to optimising rowing performance (Bell et al, 1993; Hagerman, 1984; Larsson and Forsberg, 1980; Mahler et al, 1985; Secher, 1983). Vermulst et al. (1991), have suggested that changes in strength and power output may vary with training volume and intensity. This has been substantiated in a number of other rowing studies (Hagerman and Staron, 1983; Klusiewicz, 1993; Kramer et al, 1983; Mahler et al, 1985; Mason et al, 1988; Secher et al, 1982a). Mahler et al. (1985), observed an 18% increase in peak power output in female rowers following a 4 month training period. A similar increase of 14% was reported by Hagerman and Staron (1983), in the transition from off-season to in-season training in elite oarsmen. Secher et al. (1982a), observed a smaller increase of 4% following 6 months of specific rowing training in oarsmen. In one study. Mason et al. (1988) indicated a rise in the total work output and an increase in work output per stroke
27 following a period of training. Bell et al. (1993), suggested that increases in strength in response to training, may contribute to the higher mean power output achieved during a maximal rowing performance test. This reiterates the importance of strength training in improving rowing performance (Larsson and Forsberg, 1980; Secher, 1983). However anaerobic tests, which are currently used, may not be specific or sensitive enough to detect real changes with training (Lormes et al., 1991).
4. ALTITUDE TRAINING AND SEA LEVEL PERFORMANCE
It is commonly accepted that training at altitude enhances endurance performance when competing at altitude (Adams et al., 1975; Daniels and Oldridge, 1970; Faulkner et al, 1967; 1968; Terrados et al, 1988). Although many coaches, athletes and some sports scientists accept the benefits of altitude training for enhancing performance on return to sea level, much of the evidence to support this contention is purely anecdotal. H, The rationale for training at a higher altitude, in order to enhance athletic performance
at lower elevations, is based on the body’s adaptive responses to the decreased PO 2 at higher altitudes (Burns, 1996). The additional impact of hypoxic exposure in conjunction with the training stress will, in theory, compound training adaptations which in turn will further enhance sea level performance in elite athletes (Wolski et al, 1996). The purpose of this review, therefore, is to identify some of the possible physiological mechanisms which could provide a competitive advantage and how they might influence performance on return to sea level.
4.1. Haematological Changes
Hansen et al. (1967), have proposed that the most important physiological adaptation in response to altitude exposure, that may lead to an improvement in sea level endurance performance, is an enhanced oxygen carrying capacity of the blood due to an increase in haematocrit and haemoglobin levels. Increases in red cell volume and haemoglobin in addition to augmenting the oxygen content of arterial blood, provide the additional adaptation of enhancing blood buffering capacity, which may partly
28 compensate for renal bicarbonate excretion caused by hyperventilation (Boning et al, 1994; Mairbaurl, 1994).
During early altitude exposure, haemoglobin and haematocrit have been shown to increase. However, this initial increase is primarily due to a decrease in plasma volume leading to greater haemoconcentration (Berglund, 1992; Buskirk et al, 1967; Myhre et al, 1970; Wolski et al, 1996). At moderate altitude, once plasma volume has returned to normal levels, haemoglobin and haematocrit have been shown to be unchanged during the first 2 weeks of hypoxic exposure (Humpeler et al, 1979; Mairbaurl et al, 1986a). Dill et al. (1974), have reported that the plasma volume of athletes training at 2300 metres is still decreased after 3 weeks and appeared to normalised within 6 days of return to sea level.
Polycythaemia, the increase in red blood cells per unit volume of blood, with normalisation of plasma volume and acclimatisation, is mediated by the hormone erythropoietin (EPO) which promotes increased erythrocyte production (Milledge and Cotes, 1985). EPO is a glycoprotein which stimulates erythropoiesis by enhancing the mitotic frequency of erythroide precursors in the bone marrow (Erslev, 1991; Mairbaurl, 1994). Hypoxia, and the consequent decrease in tissue oxygen pressure, has been shown to stimulate a rise in circulating EPO levels (Berglund, 1992; Milledge and Cotes, 1985; Eckardt et al, 1989; Siri et al, 1966; Wichmann, 1983). Increased erythropoiesis has been observed within one to two hours of acute hypoxic exposure, with the maximal rate of increase and the time to reach this peak being influenced by the degree of hypoxia (Eckardt et al, 1989). Although increased erythropoiesis starts almost immediately upon arrival at altitude, it appears that the stimulation for the release and maturation of reticulocytes and the subsequent increase in haemoglobin levels only occurs after 4 to 7 days at altitude (Klausen et al, 1991). Hartmann et al. (1990a), observed that maximal reticulocytosis at a moderate altitude occurred after about 8 to 10 days and remained in an elevated state during 3 weeks of altitude training in a group of elite athletes. Furthermore, it has been suggested that a combination of hypoxia and exercise stimulates greater erythropoiesis than hypoxic exposure alone (Harper et al, 1995; Mairbaurl et al, 1986a). In a detailed review of the haematological adaptations to altitude training, Berglund (1992) suggested that for
29 athletes training at moderate elevations, a true increase in haemoglobin of 1% per week seemed realistic. Berglund (1992) also suggested that complete haematological adaptation is only deemed to have occurred when sea level residents had similar haemoglobin levels as their moderate altitude counterparts. Based on an estimated differential of 12% between sea level and moderate altitude (~ 2500m) haemoglobin levels, Berglund (1992) proposed a necessary adaptation time of about 12 weeks, well beyond the duration of the conventional altitude training camp of 2 to 3 weeks.
Increases in red cell volume (RCV) during hypoxic exposure appears to be dependent on the altitude level (Hahn, 1992). Terrados et al. (1988) and Weil et al. (1968) have shown that red cell mass does not increase until PaOi falls below a critical level of 65mm Hg, which equates to an altitude in the region of 2200 to 2500 metres. It is therefore unlikely that physiological adaptations which might enhance performance on return to sea level would occur at lower elevations (Levine and Stray-Gundersen, 1992a; Wolski et al., 1996). For residents at varying altitudes, greater values for haematocrit or haemoglobin have been reported at higher elevations (Reynafarje et al., 1959; Ward et al, 1989; Winslow et al, 1987). Similar findings have been reported in altitude training studies. Warrington et al. (1996) observed no improvement in haemoglobin levels in a group of elite female rowers during 17 days altitude training below 2000 metres (1850-2000 metres). The haemoglobin concentration actually fell below pre-altitude training levels 7 days after returning to sea level. In contrast Stray- Gundersen et al. (1992), observed a significant increase in red cell volume in a group of 10 runners training for 4 weeks at an altitude of 2500 metres. Interestingly, the study revealed that in a similar group of 9 runners training at the same altitude but who had low ferritin levels no such improvement in red cell volume was observed. This led the authors to emphasise the importance of ensuring adequate iron stores in order to optimise any potential benefits from hypoxic exposure.
Systemic acidosis in conditions of hypoxia has been shown to inhibit EPO release in human (Miller et al, 1973) and animal studies (Eckardt et al, 1990). This blunted EPO response has implications for athletes training at altitude in terms of training intensity. Training sessions which promote metabolic acidosis may have a detrimental effect in terms of increasing red cell volume, particularly during the initial days, when
30 erythropoiesis is at its highest (Hahn, 1992). Stressful endurance training has previously been shown to induce iron deficiency and low haemoglobin values (Hunding et al., 1981). Although intensive training may constitute a risk to early haematological adaptation, Berglund (1992) has suggested that it is necessary to optimise long term adaptation by securing the synergistic effect of the combination of exercise and hypoxia on the erothropoietic response, as previously reported (Harper et al., 1995; Mairbaurl et al., 1986a).
4.2. Oxygen Release and 2,3-diphosphogIycerate (2,3-DPG)
Oxygen transportation by Hb is regulated by the concentration of Hb per unit volume of blood and Hb oxygen affinity (Hb-Oz-affinity). The slope and position of the oxygen dissociation curve (GDC) is readily changeable and may shift to the left or right and vary in gradient (Imai, 1982). A shift to the left of the GDC indicates a high Hb-Gz- affinity which facilitates arterial oxygen loading even when PAGi is lowered (Eaton, 1974; Hebbel et al., 1978; West, 1969). In contrast, when the GDC is shifted to the right, Hb-Gz-afFinity is reduced, which in turn enhances oxygen release from Hb to the tissues (Boning et al., 1997; Humpeler et al., 1979; Mairbaurl et al., 1986; Samaja et al., 1986; Turek et al., 1973). The release of oxygen from the red blood cells is influenced by the relationship between haemoglobin oxygen affinity (Hb-Gz-affinity) and its affect on the oxygen dissociation curve. The relationship between Hb-Gi- afifmity and peripheral oxygen release is mediated by a number of factors including pH, carbon dioxide, body temperature and the concentration of 2,3-diphosphoglycerate (2,3-DPG) within the red blood cells (Mairbaurl, 1994). Evidence has shown that prolonged endurance training (Mairbaurl et al., 1983) and adaptation to altitude exposure (Mairbaurl et al., 1986b), both induce a right shift in the GDC at rest. This has been associated with an elevation in 2,3-DPG and a subsequent decrease in Hb-Gz- affinity (Boning et al., 1975; Rand et al., 1973; Remes et al., 1979; Rorth et al., 1972).
2,3-DPG is an inorganic phosphate compound which is produced within the red blood cell during glycolysis (Rapoport and Lubering, 1950). There is a lack of clear understanding as to the mechanism by which 2,3-DPG increases and the mode of
31 action by which it affects the affinity of haemoglobin for oxygen (Lenfant et al., 1971). Several authors have suggested that alkalosis and the reduction in oxygen saturation (SaOi) associated with hypoxia may be the primary cause for the increase in 2,3-DPG (Duhm and Gerlach, 1971; Lenfant et al., 1971; Oski et al., 1970). Conditions of alkalosis have been shown to increase 2,3-DPG, whereas acidosis leads to a reduction (Rapoport et al., 1977). Other studies have reported 2,3-DPG to be elevated in reticulocytes and young red blood cells (Haidas et al., 1971; Schmidt et al., 1987). Consequently a reduction in the average red blood cell age caused by increases in EPO, which stimulates erthropoiesis, has been observed under conditions of hypoxia (Berglund, 1992; Milledge and Cotes, 1985; Eckardt et al., 1989; Siri et al., 1966; Wichmann, 1983), and seems to contribute to the high levels of 2,3-DPG in the newly formed cells (Mairbaurl, 1994). During more prolonged exposure to altitude it appears that the latter may be the predominant mechanism, due to arterial desaturation being minor and pH reaching an equilibrium (Boning et al , 1980; Mairbaurl et al., 1990). Despite the importance of low oxygen saturation on erythropoiesis and 2,3-DPG formation, endocrine influences may have a role to play in 2,3-DPG regulation. Studies have indicated that aldosterone (Boning et al., 1976) and thryoid hormones (Snyder and Reddy, 1970) may stimulate the synthesis of 2,3-DPG. It has also been revealed that plasma concentrations of these hormones are elevated during hypoxia exposure (Humpeler and Skrabal, 1978; Surks et al., 1967).
Physical training induces a rise in 2,3-DPG concentrations (Boning et al., 1975; Braumann et al., 1979; Mairbaurl et al., 1983; Remes et al., 1979; Schmidt et al , 1988), reducing haemoglobin affinity for oxygen and resulting in a shift to the right in the GDC which leads to an increase in the delivery of oxygen to the tissues (Boning et al., 1975; Braumann et al., 1979; Rand et al., 1973). Decreases in 2,3-DPG only occur during exercise when acidosis is sufficiently accentuated. These changes appear to be unrelated to the duration of exercise (Mairbaurl et al., 1986b).
Elevations in 2,3-DPG have been reported for both natives of high altitude (Lenfant et al., 1968; Torrance et al., 1970) and sea level residents during sojourns to altitude (Astrup et al., 1970; Baumann et al., 1971; Duhm and Gerlach, 1971; Eaton et al., 1969; Lenfant et al, 1968; 1971; Mairbaurl et al, 1986a). Rorth et al. (1972),
32 postulated that exercise during acute adaptation to altitude may increase the impact of hypoxia on 2,3-DPG response and Hb- 0 2 -affinity. The authors went on to stress that muscular activity was critical for altitude increases in 2,3-DPG. Mairbaurl et al.,
(1986a) observed that the PO 2 at which haemoglobin was saturated by 50% (P 50) was higher in subjects performing training during a 13 day stay at 2300 metres compared to controls. In the majority of studies, 2,3-DPG concentrations have been reported to increase at altitude within a few hours of ascent, with levels beginning to stabilise after several days exposure and the magnitude of the increase being directly related to the degree of hypoxia (Torrance et al., 1970). The corresponding decrease in the Hb-02- affinity observed during acclimatisation to moderate altitude (Humpeler et al., 1979; Mairbaurl et al., 1986a) enhances tissue oxygen supply (Alexander et al., 1967; Grover
et al., 1976) and may in part compensate for the reduced PO 2 and oxygen saturation experienced at moderate and high altitudes.
Despite its effect of enhancing oxygen release at the tissue level, increases in 2,3-DPG observed at altitude may create disadvantages. The right shift in the ODC will lead to a relatively low oxygen tension in the lungs reducing the diffusion gradient between the alveoli and blood, limiting the oxygen loading of haemoglobin. This should be avoided in order to maintain a high Sa02 (West, 1969). While arterial blood at rest is normally
98% saturated with oxygen at sea level, reduced Pa 0 2 at altitude, coupled with a reduction in Hb-02-affmity, means that Sa02 is reduced to about 91% at 2500 metres (Levine et al., 1992). This diffusion limitation may be a determining factor in exercise tolerance at altitude (Bencowitz et al., 1982). Additionally, increases in 2,3-DPG and the consequent increase of oxygen delivery to the tissue may contribute to the early decline in EPO production thereby inducing a lower haemoglobin concentration (Berglund, 1992). At higher elevations, although 2,3-DPG concentration is greater, there is also an increase in respiratory alkalosis which counteracts the effect of 2,3-
DPG on P50 (Mairbaurl, 1994) and helps maintain Hb-02-affinity and Sa02 at a relatively high level (West, 1988). It appears, therefore, that the interaction of alterations of 2,3-DPG and acid-base status is essential for the effective regulation of oxygen transportation under conditions of hypoxia (Mairbaurl, 1994).
33 4.3. Cardiac Output
Following arrival at altitude, there is conflicting evidence as to whether, as an immediate response to the lowered oxygen saturation during submaximal exercise with reduced PO 2, cardiac output is elevated or remains unchanged. Some studies have reported an acute increase in cardiac output (Hannon and Vogel, 1977; Hartley et al., 1973; Klausen, 1966; Stenberg et al., 1966; Vogel et al., 1967), while others have observed no change (Horstman et al., 1980; Pugh, 1964). Cruz et al. (1976) have proposed that under conditions of reduced PaC 0 2 cardiac output may be preserved by venoconstriction which in turn increases central venous volume and cardiac filling pressure.
Cardiac output at rest and during submaximal and maximal exercise has been shown to be reduced both during and after acclimatisation (Alexander et al, 1967; Grover et al, 1976; Hartley et al, 1967; Saltin et al, 1968; Stenberg et al, 1966) and appears not to increase with more prolonged exposure (Alexander et al, 1967; Hartley et al, 1967; Klausen, 1969; Pugh, 1964). This reduction is due primarily to a decrease in stroke volume which has been documented at rest (Grover et al, 1976; Klausen, 1966), and during both submaximal (Alexander et al, 1967; Klausen, 1966; Stenberg et al, 1966; Vogel et al, 1967) and maximal exercise (Saltin et al, 1968; Pugh, 1964; Vogel et al, 1974). The time course of the reduction in stroke volume, which has been shown to be as rapid as 2 days at 4350 metres (Vogel et al, 1974), is thought to be partly due to a decrease in plasma and blood volume (Alexander and Grover, 1983; Merino, 1950) and an increased total peripheral resistance (Vogel et al, 1974).
Although any decrease in stroke volume has been shown to be partly offset by an initial increase in submaximal heart rate at altitude (Reeves et al, 1967; Vogel et al, 1974), prolonged exposure generally leads to a reduction in maximal heart rate (Klausen, 1970; Saltin, 1968). It appears that the magnitude of the decrease in maximal heart rate is greatest during longer sojourns at higher altitudes (Saltin et al, 1968; Vogel et al, 1967; 1974). Any reduction in maximal heart rate experienced at altitude may be influenced by an augmented parasympathetic tone induced by chronic hypoxic exposure (Hartley et al, 1974).
34 Pugh (1964), reported that during acclimatisation and more prolonged exposure to altitude, cardiac output at rest and during submaximal exercise remained the same as at sea level, but there was a marked reduction in maximal cardiac output which fell from an average of 23 I'min'^ to 16 lmin'\ This reduction in maximal cardiac output was ascribed to a lowered stroke volume and reduced maximal heart rate. A similar finding was reported by Saltin et al. (1968), who reported that after 2 weeks exposure at 4300 metres, that at a given submaximal oxygen uptake a similar cardiac output was observed, but heart rate was elevated compared to sea level. This would indicate a reduction in stroke volume, which was found to be 17 ml less at rest than at sea level. During maximal exercise cardiac output was reduced by 20% and maximal stroke volume was 19-23 ml (15-20%) less than at sea level. The heart rate response to maximal exercise was found to be non uniform. Two of the four subjects experienced a significant reduction (20-25 beatsmin^) while the maximal heart rate for the other two subjects remained essentially unchanged fi-om sea level values. It appears, as with other physiological adaptations, that there is a marked individual variability in maximal heart rate response to altitude exposure. The decline in maximal cardiac output usually experienced at altitude, has been shown to be a function of reduced stroke volume and a variable decrease in maximal heart rate (Pugh, 1964; Saltin et al., 1968; Vogel et al., 1974).
4.4. Altitude Training and Skeletal Muscle Metabolism
Despite a considerable body of research identifying several physiological responses to chronic hypoxia, there is a dearth of information relating to the structural and functional adaptations of skeletal muscle. Consequently, there is still considerable controversy as to skeletal muscle metabolic adaptations, which is primarily due to methodological problems such as lack of human biopsy studies, little use of control groups, different altitudes utilised and varying training intensities adopted (Terrados, 1992).
35 Following acclimatisation to altitude, despite minimal changes in VO2 max (Adams et al., 1975; Saltin et al., 1968), there is a disproportionate increase in submaximal work capacity (Wolfel et al., 1991;Wolski et al., 1996; Maher et al., 1974) and reduced blood lactate levels (Bender et al., 1989; Brooks et al., 1991; Green et al., 1989b; Kayser et al., 1993; West, 1986; Young et al., 1982; 1991), which would suggest a local muscular adaptation as opposed to enhanced oxygen transportation. The current literature would suggest that prolonged exposure to altitude leads to an improvement in the availability of oxygen to skeletal muscle (Banchero, 1987; Hoppeler and Desplanches, 1992) but also decreases the oxidative capacity of skeletal muscle (Hoppeler et al., 1990; Howald et al., 1990). Some of the potential mechanisms for adaptations to muscle tissue in response to hypoxia are discussed below.
4.4.1. Skeletal Muscle Capillaries
A number of studies have reported an increase in capillary density, defined as the capillary number per mm^ of muscle tissue or fibre, in response to prolonged altitude exposure (Cassin et al., 1971; Green et al., 1989a; Hoppeler and Desplanches, 1992; Hoppeler et al., 1990). In animal studies, skeletal muscle capillary density has been reported to be more concentrated in animals native to high altitude compared to their sea level counter-parts (Valdivia, 1958), while chronic exposure to hypoxia has been shown to lead to no change (Sillau et al., 1980), or even enhanced skeletal muscle capillarisation (Hudlicka, 1982). It appears however, at least in human studies, that any increase in capillary density is the result of a loss in muscle fibre cross-sectional area and not due to capillary proliferation (Hoppeler and Desplanches, 1992; Hoppeler et al., 1990; MacDougall et al., 1991). These structural changes lead to an improvement in muscle oxidative capacity at altitude due to an improvement in the diffiision of oxygen from capillaries to the muscle fibres (Banchero, 1987; Hoppeler and Desplanches, 1992). Decreased muscle mass has been observed following altitude acclimatisation (Bradwell et al., 1986; Hoppeler et al., 1990; Rose et al., 1988), and is characterised by a reduction in the diameter of muscle fibres, which appears to be mainly due to a loss of myofibrillar proteins as a result of an enhanced catabolism
36 (Hoppeler et al., 1990). Capillary to fibre ratio may actually be unchanged (Green et al., 1989a) or even reduced (Hoppeler et al., 1990). Hoppeler et al. (1990), reported that following two different expeditions to the Himalayas for 8 weeks mean fibre cross-sectional area was reduced by 20%. Although there was a resultant increase in capillary density per mean fibre cross sectional area, the capillary to fibre ratio was actually reduced by 10%.
Appell (1980), suggested that any morphological changes in skeletal muscle capillary structure are derived from altered capillary pattern and not capillary proliferation. Similarly, Hoppeler et al. (1990) has hypothesised that if their subjects experienced an increased capillary tortuosity, and subsequent increased capillary length, observed previously (Mathieu-Costello, 1986), then it would be reasonable to expect an increase in the absolute size of the capillary network after return from high altitude exposure. This potential increase in capillary length would subsequently increase the availability of oxygen to the reduced skeletal muscle mitochondria. This theory, however, has yet to be substantiated in human studies due to current limitations in human biopsy technology which prevents the accurate measurement of capillary tortuosity (Zumstein et al., 1983), but certainly merits further investigation.
4.4.2. Skeletal Muscle Enzymes
Information on the effects of exercise at altitude on enzyme activity in skeletal muscle are sparse (Howald et al., 1990). Endurance training has been shown to increase oxidative enzymes in exercising muscles (Holloszy, 1973; Varnauskas et al., 1970). Similar adaptations in muscle metabolism have been reported during prolonged exposure to altitude (Bigard et al., 1991; Young et al., 1982). Reynafaije (1962), reported that enzymatic and subsequently respiratory capacity of muscle was enhanced in altitude natives compared to sea level residents. In contrast, other studies have shown that altitude training has no potentiating effect on oxidative enzyme activity in muscle (Rahkila and Rusko, 1982; Young et al., 1984), furthermore exposure to extreme altitudes (> 5000 metres) may actually lead to a reduction (Green et al., 1989a; Howald et al., 1990).
37 In order to investigate the impact of hypoxia on oxidative enzymes Terrados et al. (1990) trained one leg of 10 healthy subjects under conditions of normoxia and the other under hypobaric conditions. There was a greater increase in citrate synthase (CS) activity (which is used together with cytochrome oxidase as a marker of oxidative capacity) in the leg trained under hypoxia, which led the authors to suggest that hypoxia is a stimulus for enzyme synthesis and enhanced local muscular oxidative potential. This has been supported in other studies (Kaijser et al., 1990; Melissa et al., 1997) which found a greater increase in CS activity in muscles trained under hypoxia rather than normoxia. In contrast, prolonged exposure to hypoxia appears to have no effect on skeletal muscle enzyme activity (Green et al., 1989a; MacDougall et al, 1991; Young et al, 1984) and may lead to a reduction is skeletal muscle mitochondria (Hoppeler et al, 1990). The loss of mitochondria is manifested by a reduction in oxidative muscle enzyme activity (Howald et al, 1990). It appears, therefore, that a limited daily period of hypoxia, in conjunction with endurance training, has a different effect on muscle tissue than continuous prolonged exposure to altitude. The findings of a recent study by Melissa et al. (1997) suggest that endurance training in combination with moderate hypoxia provides an enhanced stimulus for muscular adaptation and not hypoxia per se. Based on these findings and the earlier work of Terrados et al. (1990), Melissa et al. (1997) proposed that a training regimen which only exposed subjects to hypoxia during exercise bouts may be superior to actual altitude training in terms of skeletal muscle adaptation.
Despite an improvement in the availability of oxygen to skeletal muscle, prolonged exposure to hypoxia appears to lead to a decrease in muscle respiratory capacity. The primary medium for this adaptation is a reduction in the volume of muscle mitochondria which has been consistently observed in altitude training studies (Howald et al, 1990; Hoppeler and Desplanches, 1992; Hoppeler et al, 1990). This decrease has been shown to be the result of a decrease in both interfibrillar and subsarcolemmal mitochondria in response to enhanced muscle tissue catabolism (Hoppeler and Desplanches, 1992; Hoppeler et al, 1990), and consequently led to a reduction in mitochondrial enzyme activity (Boutellier et al, 1983; Green et al, 1989a). This is in direct contrast with sea level studies where increases in mitochondrial enzymes have been observed in response to training (Pette and Staron, 1990; Saltin and Gollnick,
38 1983; Svedenhag et al., 1983) and might be a reflection of different activity patterns which may influence the impact of hypoxia (Green et al., 1992).
4.4.3. Myoglobin
Myoglobin is a compound similar to haemoglobin that aids in the storage and transport of oxygen within the muscle cell as well as maintaining low intracellular oxygen pressure. In addition to storing oxygen, even at low oxygen tensions, myoglobin promotes oxygen diffusion within skeletal muscle at approximately double the level reported when the protein is not stimulated (Âstrand and Rodahl, 1986). Endurance training has been shown to result in an increase in myoglobin concentrations in trained skeletal muscle (Gollnick et al., 1973; Hickson, 1981; Holloszy, 1973). It appears however, that training intensity may be an important determinant of the myoglobin response (Hahn, 1992; Terrados et al., 1990), as other training studies under normobaric conditions have shown no such effect (Svedenhag et al., 1983; Terrados et
al., 1986; 1990).
Higher myoglobin concentrations in skeletal muscle have been reported in high altitude natives when compared to sea level residents (Bigard and Monod, 1989; Reynafarje, 1962; Tappan and Reynafarje, 1957). This possible evolutionary response would favour the kinetics of oxygen utilisation during the adaptation to a lower oxygen tension (Reynafarje, 1962). In one study in which one leg was trained under conditions of hypoxia and the other under normoxia, Terrados et al. (1990) reported that the myoglobin content increased in the leg trained under hypobaric conditions but decreased in the normobaric trained leg. Both legs were trained at the same intensity which led the authors to conclude that the stimulus for increased myoglobin concentration seemed to be related to the blood oxygen content. This is supported by other studies (Hoppeler and Desplanches, 1992; Terrados, 1992), which reported that intermittent exposure to hypoxia during bouts of endurance training led to an increase in myoglobin concentration in muscle tissue. This augmented myoglobin level would enhance oxygen diffusion within the muscle cell and, therefore, increase oxygen
39 availability to the mitochondria of the exercising muscles (Wittenberg and Wittenberg, 1989).
4.5. Substrate Utilisation
During acute altitude exposure blood lactate levels during exercise at a given intensity have been shown to be higher than at sea level (Brooks et al., 1991; Friedman et al., 1945; Young, 1991). This response could result from the effects of acute hypoxia on P-adrenergic stimulation (Young et al., 1991). Studies have demonstrated that following acclimatisation to moderate altitude, lactate concentrations during submaximal (Bender et al., 1989; Brooks et al., 1991; Young et al., 1982; 1991) and maximal (Green et al., 1989b; Kayser et al., 1993; West, 1986) exercise have been blunted. The precise mechanism for this adaptation, however, is not known. Short term acclimatisation to altitude is not associated with improvements in skeletal muscle mitochondrial enzyme activities (Young et al., 1984), or capillarisation (Green et al., 1992), which would indicate that a change in the availability of oxygen to the contracting muscle is not a factor in attenuated blood lactate levels (Bender et al., 1989). Young et al. (1982), observed that during exercise under conditions of chronic altitude exposure (18 days), there was a muscle glycogen sparing effect at the expense of increased mobilisation and utilisation of free fatty acids (FFA). Young et al. (1982), reported that muscle glycogen utilisation and the respiratory exchange ratio decreased by 41% and 15% respectively, compared to sea level values for the same relative exercise intensity. It has been postulated that this reduced glycogenolysis is due to a decrease in circulating adrenaline during exercise following altitude acclimatisation (Brooks et al., 1991; Green, 1992; Masseo et al., 1991). Therefore, sympathetic- adrenergic responses appear to be important in regulating metabolic reaction to altitude exposure (Brooks et al., 1991).
Post exercise plasma ammonia concentrations have been shown to decrease with acclimatisation to altitude compared to levels observed at sea level when exercising at the same relative exercise intensity (Young et al., 1987). Plasma ammonia and lactate
40 accumulation have been shown to be closely related during exercise at sea level (Wilkerson et al, 1977). Subsequently, it might be expected that any reduction in ammonia accumulation at altitude would shift substrate utilisation away from glycogenolysis and may contribute to enhanced endurance performance due to lower lactate levels (Young et al, 1987).
It has been suggested that the interrelationship between the hormonal response and the subsequent energy substrate utilisation are altered during exercise in hypoxic conditions, leading to increased gluconeogenesis and fat mobilisation (Âstrand and Rodahl, 1977). Sutton (1977) reported that the concentrations of FF A, lactate, plasma glucose and serum growth hormone all increased more during exercise in hypoxia. In contrast, serum insulin concentrations decreased by 50%.
4.6. Muscle and Blood Buffering Capacity
The effects of altitude training on enhanced buffering capacity has not been studied extensively. Svedenhag et al. (1991) have suggested that altitude training may influence anaerobic rather than aerobic metabolism. While 7 elite middle distance runners trained at altitude (2000 metres) for 14 days, a group matched for ability carried out similar training at sea level. On return to sea level no change was observed for VOi max, maximal treadmill running time and running economy for both groups. However, anaerobic capacity, as measured by maximum oxygen deficit, and 800 and 1500 metre performance times for the altitude group improved where as the sea level group did not. This is in keeping with the enhanced muscle buffering capacity observed within the altitude group at that time (Saltin et al, 1995). These findings are supported by Mizuno et al. (1990), who showed a mean increase in maximal oxygen deficit of 29% and muscle buffering capacity of 6% in 10 cross-country skiers following 2 weeks residence at 2100 metres and training at 2700 metres. A positive correlation was observed between improved short term running time (17%) and the relative change in buffering capacity (r=0.83), which led the authors to suggest that any improvements in performance observed in the study may be the result of an increase in buffering
41 capacity. Further evidence for the potentially beneficial effects that a hypoxic stimulus may have on buffering capacity was provided by Boning et al. (1980), who found that in vitro blood buffering (HCO 3') improved dramatically by 14 mmol l'^ following 14 days at 2200 metres.
In contrast to these findings, Kayser et al. (1993) reported a decrease in blood buffering capacity during supramaximal exercise in a group of 6 male subjects following one month sojourn at 5050 metres. The authors concluded that the decreased buffering capacity accompanying high-altitude acclimatisation was not responsible for the observed reduction in maximal lactate accumulation compared to sea level, despite times to exhaustion being similar. Similarly, Cerretelli et al. (1985), reported a decline in blood bicarbonate concentration (HCO3 ), which induced an appreciable reduction in blood buffering capacity. It has been postulated that any potential fall in HCO3' might be partially compensated for by an increase in haemoglobin concentration which has been shown to increase the buffering capacity of the blood (Mairbaurl J|p4).
It appears that hypojpa may be the stimulus for enhanced buffering capacity, as endurance training pèr se, does not seem to lead to any improvement (Parkhouse et al., 1985; Sahkin and Hei^riksson, 1984). This may be due to the greater anaerobic energy yield during training.'^ altitude (Mizuno et al., 1990). However, research into the effects of altitude acclimatisation and training on muscle buffering capacity is very limited and warrants f&fher investigation.
' 4'
4.7. Maximal Aerobic Power {VO2 max)
Whilst it is universally accepted that VO2 max declines with increasing altitude, the critical elevation at which a significant change occurs has not been definitively
established. Buskirk et al. (1966), have suggested that there is a loss in FD 2 max of 3.2% for every 305 metres of ascent above 1600 metres. More recently Squires and Buskirk (1982) have suggested that this impairment in maximum aerobic capacity may
42 commence at altitudes as low as 1200 metres. This was confirmed by Terrados et al.
(1985), who found that TD 2 max was reduced at 1200 metres in well-trained individuals and that ^additionally, a significant fall in VOi max could be observed at only 900 metres in elite athletes.
Based on the data from a number of studies (Buskirk et al., 1966; Pugh, 1964; Squires and Buskirk, 1982; Terrados, 1992), it appears that there is a somewhat linear relationship between decreases in TD 2 max and increases in altitude. This would indicate that any decrease in TD 2 max is proportional to the reduction in PO 2 in inspired air (Fulco et al., 1988).
Despite the possible beneficial adaptation to altitude training of an increased red blood cell density, unlike conventional endurance training, blood volume may be reduced due to decreased plasma volume. This may in turn negate any potential benefits such as an
increase in VO2 max on return to sea level (Wolski et al., 1996). Furthermore, due to
the reduction in FO 2 max at altitude it may not be possible to maintain the same absolute training intensity as at sea level and the ability to work maximally is impaired (Buskirk et al., 1966; Jackson and Sharkey, 1988; Kollias and Buskirk, 1974; Levine et al., 1991; Terrados, 1992). Consequently, there is a danger that as a result of the reduced absolute training intensity at altitude, athletes may exhibit a de-training effect which manifests itself as a decrease in aerobic conditioning on return to sea level (Jackson and Sharkey, 1988; Wolski et al., 1996). Additionally, this reduction in training intensity may also lead to a loss of specific neuromuscular adaptations which may have a negative impact on sea level performance (Hahn, 1991).
4.8. Altitude Training and Sea Level Performance
Some early studies have demonstrated an improvement in FD 2 max at sea level following a period of training at altitude (Balke et al., 1967; Daniels and Oldridge, 1970; Faulkner et al., 1967; 1968; Fellmann et al., 1986; Horstman et al., 1980; Klausen et al., 1966; 1970; Roskamm et al., 1969), while others have shown no benefit
43 (Buskirk et al., 1967; Grover and Reeves, 1967; Hansen et al., 1967; Mizuno et al., 1990; Rahkila, 1982) and even a possible decrement (Saltin, 1966). Of the scientific data available, much has been shown to be inconclusive and ambiguous (Berglund, 1992). This is primarily due to varying experimental design and other methodological problems such as the calibre of the athletes (Balke et al., 1965; Faulkner et al., 1967); insufficient subject numbers; different training altitudes; lack of controls; mode and. duration of training and exposure time to altitude and methods used to evaluate changes in performance. All these factors have contributed to making the interpretation of the results of studies problematical (Hahn, 1991).
The effects of altitude training on sea level performance in elite athletes still remains unresolved, due primarily to the fact that in the majority of studies, no appropriate control groups have been utilised (Buskirk et al., 1967; Daniels and Oldridge, 1970, Dill and Adams 1971; Faulkner et al., 1967; Grover and Reeves, 1967; Mizuno et al., 1990; Saltin, 1967). Of the few controlled studies using highly trained subjects, it has been shown that 3-4 weeks training at an altitude of 2300-3000 metres failed to provide any change in VOi max or performance beyond levels attained at sea level (Adams et al., 1975; Levine and Stray-Gundersen, 1992b). It appears that under these conditions the adaptations of training per se far exceed any additional benefit bestowed by exposure to altitude (Levine and Stray-Gundersen, 1992a). This may in part be due to the difficulty in trying to elicit any further training response from highly trained subjects. The situation is further compounded by the virtue that whilst training at altitude, most athletes are compelled to reduce training load as maximal aerobic power is depressed, due to the additional hypoxic stress, which impairs the ability to work maximally (Jackson and Sharkey, 1988; Levine et al., 1991) As a result elite athletes may not be able to maintain sufficiently high enough workloads at altitude to maintain competitive fitness (Saltin, 1970). This, in turn, may minimise any potential benefits of altitude training (Saltin, 1967). Levine et al. (1991), have proposed the optimal strategy for performance at sea level might be to live at altitude and train at sea level. Any potential detraining effect due to prolonged exposure to hypoxia would, therefore, be mitigated. In order to investigate this theory, Levine et al. (1991) had one group of competitive runners live and train near sea level (1,280 metres), while the other lived at
44 altitude (2,500 metres) but conducted their training with the first group at 1,280 metres. Despite performing identical training, the group living at 2,500 metres improved VO2 max by 5% and 5 km running time by 30 seconds, whereas the group living and training at 1,280 metres showed no change in either of these variables. A possible limitation of this study is that 1,280 metres was used as the “sea level” altitude. However VO2 max may already be impaired at this elevation (Squires and Buskirk, 1982; Terrados et al., 1985). Wolski et al. (1996) have, therefore, recommended further research using elite athletes and a true sea level altitude in order to determine the merits of this type of altitude acclimatisation and training regimen.
In a critical review of the literature. Smith and Sharkey (1984) cast doubt on the value of altitude training, highlighting that it is not possible to predict who will benefit from the experience. This contention is supported by Rahkila and Rusko (1982), who studied a group of 6 cross-country skiers during a 2 week altitude training camp. In terms of performance, while some skiers improved, others did not. Smith and Sharkey (1984) go further to recommend that future studies and experiments should attempt to document individual responses and correlates of the response to altitude training.
Despite the absence of any conclusive evidence to support the benefits on sea level performance, altitude training remains a popular training tool prior to major competition among elite athletes, including rowers (Hagerman et al., 1975; Hartmann 1987; Jensen et al., 1993; Nowacki et al., 1971). Jurgen Grobler, Director of Coaching to the Great Britain rowing team, reported that about 50% of rowing nations used altitude training in preparation of the 1993 World Championships (personal communication). Although considerable work has been published concerning altitude training little relates to rowing (Altenburg, 1992; Fischer et al., 1992; Hagerman et al., 1975; Hahn et al., 1992; Jensen et al., 1993; Jensen and Secher, 1986; Secher, 1990;
Secher et al., 1992). Of the data available, no effect on VO2 max or work capacity has been reported in oarsmen following altitude training (Hahn et al, 1992; Jensen et al, 1993; Jensen and Secher, 1986; Secher et al, 1992). In contrast, Jensen et al. (1993), Jensen and Secher (1986) and Secher et al. (1992) have all reported an improvement in both variables in groups of matched controls following similar training at sea level. On
45 the basis of their results, Jensen et al. (1993) have proposed that the ability of rowers to gain significant performance and physiological benefits depends on the ability to increase the volume of training, and is independent of any hypoxic stimulus.
4.9 Summary
Following acclimatisation, during prolonged altitude exposure, oxygen carrying capacity of blood may be enhanced due to a potential increase in red cell volume which helps optimise arterial oxygen loading. However, this is offset by a reduction in cardiac output. As a consequence oxygen transport to the tissues during rest and submaximal exercise is relatively constant. Adaptation to altitude results in a decrease in Hb-Oz- affinity, which may be explained by a small increase in 2,3-DPG due to respiratory alkalosis, therefore facilitating peripheral oxygen release to the tissues even under conditions of reduced PO 2 . Capillary density per cross sectional area of muscle tissue have been shown to increase during prolonged altitude exposure. However, it appears that this is due to a loss in muscle fibre cross-sectional area as opposed to capillary proliferation. Nevertheless, despite an improvement in the availability of oxygen to skeletal muscle, under conditions of prolonged exposure to hypoxia, it appears that there is a decrease in muscle respiratory capacity, possibly due a reduction in the volume of muscle mitochondria. This may be partly offset by an augmented myoglobin level which enhances oxygen diffusion within the muscle cell and therefore, increases oxygen availability to the mitochondria of the exercising muscles. Another potential benefit of altitude training is that hypoxia appears to offer a stimulus for enhanced buffering capacity. However, the research in this area is limited and requires further
analysis.
To date, of the different training strategies reported in the scientific literature, none have been successful in providing conclusive and unequivocal evidence to support the contention that altitude training elicits any advantage over conventional sea level training in terms of enhancing sea level performance in rowing. Further research using highly trained subjects and controls is therefore required. These studies should incorporate submaximal evaluation as well as the use of performance tests as means of
46 determining the effectiveness of altitude training in enhancing the sea level performance of elite rowers.
In light of the above review, it is clear that certain gaps remain in our knowledge of the physiology of rowing and how this may impact on training and performance. It was decided, therefore, to conduct a series of experiments to address some of these issues.
47 CHAPTERS
Experiment 1. A comparison of selected physiological parameters as predictors of rowing performance.
MATERIALS AND METHODS
1. INTRODUCTION
For many endurance sports, maximum oxygen uptake (VO2 max) has traditionally been regarded as the criterion determinant of performance. More recent research, particularly in running and cycling, has suggested that various blood lactate indices determined during submaximal exercise may serve as better predictors of endurance performance than ÛO 2 max. In contrast to the multitude of studies which have evaluated the relationship between various physiological parameters and performance in a number of endurance activities, few investigations have dealt with rowing. Due to the nature of rowing competition, being performed over 2000 metres, and typically lasting between 5.8-V.4 minutes (Secher, 1992; Steinacker, 1993), the majority of work is performed at between 95% and 98% of maximal aerobic capacity (Hagerman et al., 1978; McKenzie and Rhodes, 1982). By the virtue that the exercise intensity at
which rowing events are performed has been shown to approach 100% of VO2 max, it has been postulated that there may be a strong relationship between peak parameters obtained during an incremental test on a rowing ergometer and rowing performance
(Womack et al., 1996).
48 The purpose of this study, therefore, was to determine the relationship between measures of rowing performance and selected physiological variables.
2. ETHICAL CONSIDERATIONS
All experimental procedures were cleared by the ethical committee of Northwick Park
Hospital. Prior to participation in the study, each subject completed an informed consent form (Appendix B).
3. SUBJECTS
Eighteen members of the Great Britain mens heavyweight rowing squad participated in this experiment. All subjects were instructed to maintain their normal dietary intake and to perform light, steady-state training (< 2 hours per day) in the 48 hours immediately prior to testing.
4. ANTHROPOMETRIC MEASUREMENTS
Complete data for 13 anthropometric parameters were obtained on the 18 elite male heavyweight rowers. These parameters were, body mass, stature (standing and sitting),
4 skinfold thicknesses (bicep, tricep, subscapular and suprailiac), 3 breadths
(biacromial, biiliac, and wrist) and 3 girths (thigh, upper arm and forearm). In addition,
body mass and skinfold measurements were taken on 2 other occasions during the
training cycle. All measurements were taken by the investigator to avoid inter-tester
error.
49 4.1. Body Mass and Stature
Prior to undertaking any physiological tests, body mass (kg) as well as standing and sitting height (cm) were measured using weight and height scales (W.N.T. Avery Ltd,
UK.). For the purpose of these measurements each subject removed their shoes and wore only a pair of shorts.
4.2. Body Composition
Body composition was assessed using skinfold thickness measures. Repeat skinfold measurements were taken at four skinfold sites, biceps, triceps, sub scapular and suprailliac, using a Harpenden skinfold calliper (British Indicators Ltd, St. Albans) to determine the percent change in body fat. The Harpeden skinfold callipers are designed to provide a constant pressure of 10 g'mm^ of the calliper’s jaw surface area on varying skinfold thicknesses, with an accommodation up to a thicknesses of 50 mm.
The width of the skinfold measurement was determined on a dial indicator incorporated into the apparatus with the 1.0 mm increments being interpolated to the nearest 0.5 mm.
The calliper is designed to obtain a skinfold thickness, which includes a double layer of
skin and the underlying adipose tissue, with care being taken to avoid pinching the
muscle. The thumb and index finger of the left hand were used to raise a double fold of
skin about 1 cm proximal from the site of measurement, with the calliper being applied
at right angles to the fold. Once the pressure was released the measurement was
recorded after approximately 4 seconds with the skinfold being held throughout the
measurement.
50 All skinfolds were measured on the right side of the body, following the procedures outlined by Dumin and Rahaman (1967). The sum of the 4 skinfold measurements were used as an overall indicator of body density using the following equation:
Y= 1.1610-0.0632 (X)
Where:
Y= Body density
X= The log of the sum of the 4 skinfold measurements
(source : Dumin and Rahaman, 1967)
Calculations for percent body fat were subsequently determined by the equation:
Fat (%) = [(4.95/body density) - 4.5] x 100
(source : Siri, 1956)
* À
Illustration 1 Body compostion measurement using skinfold callipers
51 4.3. Breadths
4.3.1. Biacromial Breadth
Following the technique utilised by Cameron (1978), biacromial breadth was measured from the rear with the subject standing, arms hanging by the sides and the shoulders relaxed downward and slightly anteriorly to attain a maximal reading. The blades of the anthropometer (British Indicators Ltd, St Albans) were applied firmly to the most lateral border of the acromium. The width was measured to the nearest O.Icm.
4.3.2. Biiliac Breadth
Biiliac breadth was measured following the procedures outlined by Cameron (1978).
The measurement was taken from the rear with the subject standing with the feet about hip width apart for stability. The arms were folded across the chest and the anthropometer blades were brought into contact with the iliac crest so the maximum breadth was recorded. The measurement was recorded to the nearest 0.1 cm.
4.3.3. Wrist breadth
The most medial aspect of the ulnar styloid process and the lateral aspect of the radial
styloid process were located with the thumb and index finger. An adapted engineers
calliper (3M UK Ltd) was used to measure the distance between these bony
landmarks. The use of a flat blade calliper enabled accurate placement and minimised
the risk of movement when necessary pressure was being applied. This breadth was
recorded to the nearest 0.1 cm.
52 4.4. Circumferences
All girth measurements were standardised to the right hand side of the body, with each measurement being repeated three times and the highest score being recorded. All circumferences were recorded to the nearest 0.1 cm.
4.4.1. Thigh Circumference
Midthigh circumference was assessed utilising the procedure outlined by Lohman et al.
(1991). The measurement was taken midway between the midpoint of the inguinal crease and the proximal border of the patella, with the subjects knee extended. The measurement was made using an anthropometric tape (Country Technology Inc, Gays
Mills, USA.) with each subject standing, feet parallel and hip width apart, weight evenly distributed between both feet and legs relaxed.
4.4.2. Upper Arm Circumference
With the subject seated, the midpoint of the upper arm was located by flexing the elbow at an angle of 90 degrees with the palm supinated. The midpoint was determined as being midway between the superior surface of the spinous process of the scapular and the most distal point on the acromial process (Lohman et al., 1991).
With the arm relaxed and resting on the thigh the anthropometric tape was placed around the arm perpendicular to its long axis at the midpoint so that it was touching the skin but not compressing the underlying tissues.
53 4.4.3. Forearm Circumference
The subject was seated with the arm slightly flexed at the elbow and held in moderate abduction, with the palm supine. With the anthropometric tape placed at right angles to the long axis, repeat girth measurements of the forearm were taken to establish the maximum circumference (Lohman et al., 1991).
5. CARDIORESPIRATORY EVALUATION
5.1. Ambient Conditions
Ambient temperature and humidity were measured before each test using a Hygromer
A1 digital handheld temperature and humidity indicator (Rotronic instruments, Horley,
Surrey, England.). The Hygromer A1 contains a Pt 100 sensor for measurement of temperature and a Hygromer® C 80 sensor for measurement of relative humidity. The operating temperature range is -10 to +60°C and 0 to 100% for relative humidity. At
25°C the measurement error is ±0.3°C and ±2% relative humidity. In order to control laboratory conditions temperature was regulated between a range of 18-22 C.
5.2. Submaximal Discontinuous Incremental Test
In order to facilitate the 6 minute performance test undertaken on the same day each
subject performed a submaximal incremental test as opposed to a maximal protocol.
On completion of a standardised warm up, which consisted of 10 minutes rowing at
200 Watts, each subject performed a submaximal discontinuous incremental step test
on a Concept II air braked rowing ergometer (Concept II, Nottingham England). The
test consisted of five 3 minute bouts of work at a fixed exercise intensity followed by a
54 30 second recovery (Table 1). The use of a discontinuous incremental test on the rowing ergometer enabled capillarised earlobe blood samples to be taken at the end of each 3 minute exercise increment to determine the blood lactate concentration The final increment was designed to elicit a blood lactate concentration between 4-6 mmoi r^ which has been found to be above the level tolerable during long-duration steady state rowing (Hartmann, 1990b).
Table 1 Exercise intensities and stroke rates used in the incremental test
Step Watts Stroke Rate
1 256 18-20
2 283 20-22
3 311 22-24
4 338 24-26
5 366 26-28
In order to standardise the test, the gearing for the ergometer was set on the large cog with the fan open. Fixed stroke rates were controlled during the test with each subject being instructed to remain as close to the predetermined rates as possible. Each subject was instructed before and during the test to maintain the required work output as precisely as possible. The increment for each step was 27.5 ± 0.29 W (mean ± S.E.).
Power output was calculated from the acceleration of the flywheel and was displayed on a LCD monitor (Hagerman et al., 1988). The total time for the test, including recovery periods, was 17 minutes.
55 Illustration 2 Blood lactate sampling during the discontinuous incremental test
5.3. Respiratory Analysis
Gas exchange was measured continuously, via an open circuit method, using a Jaeger
EOS Sprint on-line gas analysis system (Jaeger, U.K.) for the determination of minute ventilation ( VE ), oxygen uptake ( VO2 ) and carbon dioxide production ( VCO2 ) which were averaged over 30 second intervals. Subjects inhaled ambient air through a two- way low resistance valve (Hans Rudolph 2700, Hans Rudolph, inc. Kansas City.
U.S.A.). The mixed expired gas samples passed through a pneumotachograph with ventilation {VE) being determined by the pressure change across the pneumotachograph. The mixed expired gas samples then passed through a sampling
56 bag where fractional concentrations of oxygen and carbon dioxide were sampled and measured by a paramagnetic oxygen analyser and infra-red carbon dioxide sensor respectively. The values were corrected to standard temperature, pressure and dry
(STPD) to calculate the VO2 and VCO2 . The analyser was calibrated before each testing session with precision alpha gas mixtures containing 15.0 ±0.01% O 2 and 5.0
±0.01% CO2, while ventilation was calibrated using a 2 litre manual syringe at varying flow rates.
5.4. Maximal Oxygen Uptake (VO2 max)
Expired air was collected throughout the 6 minute performance test (Dist6), by the method previously described, from which each subjects maximal oxygen uptake
(ÛO2 max) was obtained. ÛO 2 max values were expressed relative to body mass
(ml kg min \ in absolute terms (I min ^) as well as independent of body size, which
- 2/3 required the variable to be divided by a reduced proportion of body mass (ml kg min ) as previously proposed by Neville et al. (1992b). Hagerman (1984) and Secher -1 (1982b) have suggested that it may be more meaningful to express VO2 max in 1 min since body mass is supported by the boat.
5.5. Rowing Economy
Following the procedures outlined by Warrington et al. (1992), rowing economy was
determined from the mean VO2 values measured over the last minute of the first and
fourth of the 3 minute exercise bouts. These equated to 256 W and 338 W,
respectively, and represented 50% and 66% of the mean peak power output achieved
in the 6 minute performance test.
57 5.6. Fractional Utilisation
Fractional utilisation was determined from the mean submaximal VOi reading collected during the last minute of the 3 minute exercise bout at 388 W and the FO 2 max obtained during the 6 minute performance test. Percent VO2 max was subsequently derived from the VO2 IVO2 max ratio.
5.7. Heart Rate Measurement
Heart rate was measured continuously by radiotelemetry using a Polar Sports Tester
(Polar, Kempele, Finland). This consists of a chest band transmitter and a wrist watch microcomputer. The heart rate transmitter has an operating temperature range o f -10° to +60®C.
Impulses are picked up from the heart by the chest band sensor and transmitted to the microcomputer via telemetry. Heart rate data were displayed continuously, recorded every five seconds and stored in the microcomputer worn by each subject. The heart rate data were later down-loaded via a Polar computer interface for analysis.
5.8. Blood Lactate Analysis
A capillarised earlobe blood sample was taken at the end of each exercise increment to
determine the blood lactate concentration. The samples were analysed by an Analox
GM7 lactate analyser (Analox Instruments, London). The GM7 is a quantitative
device for the measurement of lactate in whole blood, lysed whole blood and plasma.
Whole blood samples were used in this study and extracellular lactate was measured.
58 An earlobe capillary blood sample was collected into a 100 pi capillary tube,
containing heparin, fluoride and nitrite, (Analox Instruments, London). The earlobe
was thoroughly cleaned before each sample to avoid any sweat contamination. The
blood sample was then mixed with the reagents in the capillary tube for four minutes
using a specially designed tilting device. A 7 pi blood sample was then micro-pipetted
from the capillary tube and injected into the lactate analyser.
The operating principle of the Analox GM7 analyser is to employ substrate-specific enzymes in an open chamber incorporating a membrane covered amperometric oxygen electrode (Clark PO2 electrode). The polypropylene membrane, which is oxygen permeable, protects the electrode head whilst also defining the diffusion path (Figure
1). The electrode consists of a platinum cathode, at a constant potential of -650mv, and a silver chloride anode.
cathode: j*'*-0.65 V platinum wire
glass rod
plastic holster
electrode housing
anode: 0 V (Ag/AgCl)
phosphate buffer
- 0-ring
sample inlet m m m ^ sample outlet
Pt -cathode (exposed end of wire) b 2*permeable membrane (polypropylene) cuvet gloss window
Figure 1 Schematic illustration of a Clark PO2 electrode
59 Oxygen change is measured by the electrode when oxidoreductase enzymes (oxidases) react with their substrate under controlled semi-anaerobic conditions via the the following reaction:
Lactate + O2 Lactate Oxidase (LOP) Pyruvate + H 2O2
Analytical conditions are such that the maximum rate of oxygen consumption, which is electronically detected from the second differential of the oxygen-time relationship -d^
(0 2 )/dt^, relates directly to sample lactate concentration.
The lactate analyser was calibrated at the start of testing, during and directly afterwards with known controls of 3, 5 and Smmolf^ (Analox Instruments, London).
5.9. Determination of Fixed Blood Lactate Concentrations
Power output associated with reference blood lactate concentrations of 2 and 3 mmolf^ were determined from the curvilinear rise in the power-blood lactate relationship, by interpolation, using cubic splines which use a least squares polynomial curve fit written into a computer programme (Simfit, W.G. Bardsley, University of
Manchester).
60 6. ROWING PERFORMANCE TESTS
6.1. 6 Minute "All-Out” Test
The 6 minute "all-out" performance test was completed on the same day as the submaximal ergometer test with at least two hours recovery between the tests. The purpose of this test, which is essentially a time trial, was to simulate competitive rowing over 2000 metres (Hagerman et al., 1983) and establish the VOi max for each individual rower. The test protocol, which required each subject, to exercise maximally over a 6 minute period was familiar to all subjects. Oxygen consumption was measured throughout the test using an on-line gas analysis system (Jaeger, U.K.), as previously described. Post-exercise capillary blood lactate samples were taken at 2 and 5 minutes to establish peak lactate levels. The samples were analysed in an
Analox GM7 lactate analyser (Analox Instruments, London).
Illustration 3 Cardiorespiratory evaluation on the Concept II rowing ergometer
61 In contrast to the incremental maximal-type protocol utilised for laboratory evaluation of aerobic capacity, the pacing strategy in the 6 minute "all-out" test was determined by the subject. During the test, peak power output and total distance covered were recorded from the visual display unit.
Strictly, the VO2 peak values achieved during the 6 minute "all-out" test may not represent true maximal values for oxygen uptake (FOzmax). VOimax is usually reported for a standardised graded test. However, it has been shown that the actual measurement of VO2 max during a progressive incremental exercise test to exhaustion on a variable-resistance rowing ergometer has produced almost identical values to the peak VO2 obtained in the 6 minute "all-out" protocol (Mahler et al, 1984a; Mickleson and Hagerman, 1982). In reality, peak VO2 values during 6 minutes of "all-out" rowing may be more relevant practically as they may provide a greater insight into an individual's physiological limitations to rowing exercise (Hagerman, 1984).
6.2. 2500 metre Test
Following completion of the laboratory tests, 12 of the rowers subsequently completed a 2500 metre time trial on a Concept II rowing ergometer during a squad training camp one month later. Distance covered during each minute of the test was recorded together with the total time to complete the 2500 metres. Heart rate was recorded throughout the test using radiotelemetry by means of a Polar Sports tester (Polar,
Kempele, Finland). A post-exercise capillary blood sample was taken at 5 minutes and was analysed for blood lactate concentration using an Analox PGM7 portable lactate
analyser (Analox Instruments, London).
62 The 2500 metre test is frequently used by the coaches as one of the selection criteria for crews and had been performed by each subject on a number of occasions prior to this study.
7. STATISTICAL ANALYSIS
The data are presented as means ± S.E. The relationship between the distance covered in the 6 minute performance test (DIST6), time taken to perform the 2500m test
(T2500) and the descriptive and laboratory variables were compared using simple linear regression. Being the criterion measurements, DIST6 and T2500 were taken as the dependent variables. The strength of the linear regressions between the dependent and the independent variables was established by the coefficients of determination
(R^). Multiple regression analysis was then performed to determine the most important contributors to the dependent variables. F-tests were employed to determine if any of the dependant variables should be included in the model. T-tests were then used to evaluate whether the corresponding variable should be retained or excluded from the current model. The significance level 0.05 was accepted in all statistical comparisons.
All statistics were performed using commercially available software (Data desk'^. Data
Description, Ithaca. New York).
63 RESULTS
Descriptive statistics for the various physiological and rowing performance variables are summarised in Table 2. Before performing simple regression analysis the relationship between the dependent and independent variables were examined for evidence of non linearity and abnormal distribution.
Table 2 Means and standard errors for variables measured
Variable______Mean------SE Rowing Performance DIST6 (m) (n=17) 1923.5 9.3 T2500 (s) (n=12) 463.4 2.9
Descriptive Variables (n -17) Age (yrs) 24.4 0.9 Mass (kg) 90.5 1.3 Height (cm) 193.8 1.6 Sitting height (cm) 99.3 0.7 Upper arm circumference (cm) 31.0 0.2 Forearm circumference (cm) 29.8 0.2 Thigh circumference (cm) 57.6 0.6 Bicromial breadth (cm) 45.6 0.4 Biiliac breadth (cm) 2R7 0.3 Wrist breadth (cm) 5.81 0.1 0.5 Body Fat (%) 12.7 Sum of Sldnfolds (mm) 30.19 1.1
Laboratorv Variables (n=17) 0.10 VO2 max (1 min ) ^ 5.81 0.96 VO2 max (ml kg min ) ^ 64.3 4.10 VO2 max (ml kg min 28R3 Rowing economy (1-min ^) @ 256 W 3.79 0.05 Rowing economy (1 min ) @ 338 W 4 86 0.06 Fractional utilisation (%) @ 388 W 83 8 1.06 Power output (W) @ 2 mmol l ^ 312.1 5.60 Power output (W) @ 3 mmol l ^ 337.1 4.50 14.9 Peak Power (W) 510.1 Peak Lactate (mmolf^) R39 0.41
64 The first regression considered was the simple linear regression of DIST6 against -1 VQimdx (Imin ) (Figure 2). A scatterplot of studentised residuals against the
predicted values from the regression fit should not display any strange behaviour
(Figure 3). The scattergram revealed one possible outlier (marked x). On closer
examination it was revealed that subject 16 was not in fact selected for the final squad
for the World Championships and thus was classed as sub-elite. It was therefore
decided to remove this observation before pursuing with the data analysis. A
scatterplot of residuals against DIST6 showed no unusual patterns after the removal of
the outlier.
1960 - I 1920 I «
t—(K 1880 Q 1840 -
5.6 6.0 6.4 -1 VOi max (Imin )
Figure 2 Individual values for DIST6 plotted against VOi max (1 min ) including outlier (marked x). .
2 + SR 1 0 -I -2
1900 1925 1950 1975 predicted
Figure 3 Studentised residuals (SR) plotted against predicted values for DIST6.
65 The regression output of DIST6 against absolute VOi max (Imin ) is illustrated in
Table 3. The data plot revealed a strong linear relationship with absolute VOi max explaining 62% (P <0.01) of the total variance in DIST6 (Figure 4a).
Table 3 Output for regression of DIST6 on VOi max (Imin ). Dependent variable is; DIST6 18 total cases of which 1 is missing (no outlier)
R squared = 61.7% R squared (adjusted) = 59.2% s = 24.43 with 17-2=15 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 14455.3 1 14455.3 24.2 Residual 8954.94 15 596.996
Variable Coefficient s.e. of Coeff t-ratio prob Constant 1505.62 85.12 17.7 0.0001 ÛO2 max (Imin ) 71.8969 14.61 4.92 0.0002
A similar finding was observed when T2500 was taken as the dependent variable with absolute VOimax (1 min ^) accounting for 76% (P<0.01) of the variance in rowing performance (Table 4).
-L xauic‘t vyuL^Lii. X V/kJkJAV.» A.*. ------Dependent variable is: T2500 18 total cases of which 6 are missing (no outlier)
R squared = 76.5% R squared (adjusted) = 74.1% s = 5.108 with 12 - 2 - 10 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 847.664 1 847.664 32.5 Residual 260.925 10 26.0925
Variable Coefficient s.e. of Coeff t-ratio prob Constant 574.379 19.53 29.4 0.0001 FDz max (1 min ) -18.8704 3.311 -5.70 0.0002
66 The simple linear regressions of DIST6 and T2500 on VOi max expressed relative to body weight (ml kg min and in dimensionless terms (ml kg min ) were also calculated and are illustrated in Tables 5-8. The plots of residuals against predicted values did not demonstrate any unusual patterns. The scatterplots of the measures of rowing performance against relative VOi (ml kg-min \ which are illustrated in Figures
4b and 5b, showed a weak linear relationship, this is probably accounted for in the low
R^. This was only found to be significant in the case of DIST6 (P<0.05). A much stronger linear relationship was found when FOz max, expressed in dimensionless terms (ml kg'^^ m in '\ was retained as the independent variable, accounting for 49% and 58% (P<0.01) of the variance in DIST6 (Figure 4c) and T2500 (Figure 5c), respectively.
67 1980 -- g' 1950 -- g 1920 - n= 17 00 5 1890 +, r=0.78(P<0.01) o o y=71.89x + 1505.62 1860
5.6 6.0 6.4
VO2 max (I min )
Figure 4a Relationship between DIST6 and VO2 max (I min ).
1980 - 1950 - È2 1920 +0 n=17 5 1890 + r=0.55(P<0.05) y=5.35x + 1579.22 1860 -
60 63 66 69
-1 FO2 max (ml kg min )
Figure 4b Relationship between DIST6 and VO2 max (ml kg min ).
1980 - g- 1950 -T S 1920 + = n=17 5 Q 1890 + r=0.70 (P<0.01) O O y=1.58x + 1467.02 1860 -
270 285 300 315
VO2 max (ml kg ^ min ) -2/3 -1 Figure 4c Relationship between DIST6 and VO2 max (ml kg min ).
68 472.5 n=12 r=-0.87 (P<0.01) T 465.0 y=-18.87x + 574.38 2 457.5 5 0 450.0 0 (s) 5.6 6.0 6.4
-1 VO2 max (I min )
Figure 5a Relationship between T2500 and FO2 max (1 min ).
n=12 o 472.5 - o r=-0.57 (P>0.05) y=-1.47x + 558.93 j 465.0 I 2 457.5 § 450.0 + 0 (s) 62.5 65.0 67.5 70.0
FO2 max (ml kg min )
Figure 5b Relationship between T2500 and FO2 max (ml kg-min ).
n=12 472.5 - r=-0.76 (P<0.01) y=-0.44x + 591.30 T 465.0 - 2 457.5 4 5 0 450.0 - 0 (s) 270 285 300 315
FO2 max (m lkg-m in')
Figure 5c Relationship between T2500 and VO2 max (ml kg -min ).
69 Table 5______Output for regression of DIST6 on VO2 max (ml kg-min ) Dependent variable is: DIST6 18 total cases of which 1 is missing (no outlier)
R squared = 30.6% R squared (adjusted) = 26.0% s= 32.90 with 17-2 = 15 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 7171.61 1 7171.61 6.62 Residual 16238.6 15 1082.57
Variable Coefficient s.e. of Coeff t-ratio prob Constant 1579.23 134.0 11.8 0.0001 VO2 max (ml kg min ) 5.35416 2.080 2.57 0.0212
- 2/3
Dependent variable is: DIST6 18 total cases of which 1 is missing (no outlier)
R squared = 49.0% R squared (adjusted) = 45.6% s = 28.22 with 17 - 2 = 15 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 11460.8 1 11460.8 14.4 Residual 11949.5 15 796.632
Variable Coefficient s.e. of Coeff t-ratio prob Constant 1467.03 120.5 12.2 0.0001 FD2 (ml kg min ) 1.58294 0.4173 3.79 0.0018
70 Table 7 Output for regression of T2500 on VO2 max (ml kg-min ). Dependent variable is: T2500 18 total cases of which 6 are missing (no outlier)
R squared = 32.7% R squared (adjusted) = 25.9% s = 8.640 with 12 - 2 = 10 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 362.089 1 362.089 4.85 Residual 746.500 10 74.6500
Variable Coefficient s.e. of Coeff t-ratio prob Constant 558.934 43.47 12.9 0.0001 FO2 max (ml-kg-min ) -1.46983 0.6674 -2.20 0.0522
- 2/ 3 .
Dependent variable is: T2500 18 total cases of which 6 are missing (no outlier)
R squared = 57.8% R squared (adjusted) = 53.6% s = 6.839 with 12- 2 - 10 degrees of freedom
Source Sum of Squares df Mean Square F-ratio Regression 640.840 1 640.840 13.7 Residual 467.749 10 46.7749
Variable Coefficient s.e. of Coeff t-ratio prob Constant 591.295 34.62 17.1 0.0001 -3.70 0.0041 FD2 (ml-kg min ) -0.438641 0.1185
71 The individual contributions to R made by each independent variable is listed in Table
9. The best single predictor variable for both measures of rowing performance (DIST6 and T2500) was absolute VOi max (1-min \ For the other predictor variables, the highest R^ were found for VOimax (ml kg min \ power output generated at 2 mmoir^ reference blood lactate level (REF2mM), fractional utilisation at 338 W
(FU338) and peak power.
Table 9 Relationship between physiological variables and rowing performance
Variable DIST6 (n=17) T2500(n=12) r ' R^
Rowing Performance DIST6 (m) 0.82** T2500 (s) 0.82**
Descriptive Variables Age 0.06 0.06 Mass 0.16 0.31 Height 0.06 0.26 Sitting height 0.02 0.15 Upper arm circumference 0.07 0.11 Forearm circumference 0.02 0.19 Thigh circumference 0.04 0.06 Bicromial breadth 0.14 0.21 Biliac breadth 0.18 0.45* Wrist breadth 0.15 0.30 0.01 Body fat 0.04 Sum of skinfolds 0.01 0.01
Laboratorv Variables 0.76** FO2 max (I min ) ^ 0.62** 033 VO2 max (ml kg-min ) ^ 0.31* 0.58** VO2 max (ml-kg min 0.49** Rowing economy (1-min^) @ 256 W 0.23 0.37* Rowing economy (1-min ) @ 338 W 0.17 0.27 Fractional utilisation @ 388 W 0.43** 0.57** Power output @ 2 mmol f^ 0.46** 0.67** Power output @ 3 mmol l'^ 0.22 0.29 Peak power (W) 0.39** 0.57** Peak lactate (mmolf^) 0.16 0.12
* P<0.05, **P<0.01.
72 Multiple linear regression was then used to determine the combination of variables that could best predict rowing performance as determined by DIST 6 and T2500. Multiple
-K regression analysis indicated that a combination of VOi max (1-min ) and peak lactate accounted for 77% of the variance in DIST 6 and 83% in T2500. However, in the case of T2500 although the addition of peak lactate to the model did lead to an increase in the (Table 10) this was not found to be significant (P=0.09).
Table 10 Prediction of Rowing Performance
Rowing performance Dependent variable Predictor variable R2 t-ratio P value
DIST6 (m) (n=17) 1 . VOi max (1-min ) 6.05 0 . 0 0 0 1 2. Peak lactate 0.77 3.00 0.0096
1 . VOi max (1-min ) 0 62 5.09 0 . 0 0 0 1 1. REF2mM 6.69 0 . 0 0 0 1 2. Peak lactate 0.80 4.87 0 . 0 0 0 2 1. REF2mM 3.57 0.0028 2. Peak power 0.62 2.37 0.0324
T2500 (s) (n=1 2 ) 1 . FO2 max (1-min ) -6.17 0 . 0 0 0 2 2. Peak lactate 0 83 -1.90 0.0898
1 . FO2 max (1-min ) 0.76 -5.70 0 . 0 0 0 2 1. REF2mM -6 .0 1 0 . 0 0 0 2 2. Peak lactate 033 -239 0.0180 1.FU338 335 0.0062 2. Peak power 0 82 -3.59 0.0059
Further potential explanatory variables, in addition to VOi max, were considered and
included in the model (Table 10). However, the addition of other laboratory and
73 descriptive variables to either model did not significantly increase the predictive power of the multiple R^. Consequently, when the number of independent variables added to 2 the model exceeded two for DIST 6 and one for T2500, the increase in R was negligible.
Other combinations of descriptive variables were evaluated to determine their ability to predict either measure of rowing performance. The combination of REF2mM and peak lactate accounted for 80% and 83% of the variation in DIST 6 and T2500, respectively. This, however, offered no advantages over the selected models.
REF2mM (P<0.01) and peak power (P<0.05) were found to significantly account for the variance in DIST 6 , however, the observed R^ was no greater than when VO2 max
(1 min was exclusively included in the model. In contrast, the amalgamation of
FU338 and peak power explained 82% of the difference in T2500 but no reciprocal relationship was found for DIST 6 .
Analysis of both models revealed that absolute VO2 max was found to be the best single predictor variable. A combination of FD 2 max (I min ) and peak lactate is recommended for the prediction of rowing performance as determined by DIST 6 .
However, when T2500 was adopted as the criterion measure only VO2 max (1-min ) was found necessary to predict rowing performance. In the case of the latter, the best combination of predictor variables offered little advantage in predicting rowing performance than when only absolute VO2 max was retained in the model.
74 Rowing performance, as determined by DIST 6 or T2500, could be predicted (P<0.01) by the following regression equations;
DIST6 (m) = 1435 + 71.36 VO2 max (Imin^) + 8.78 Peak lactate
(R^ = 0.77, S.E. = 19.73)
T2500 (s) = 574.38 - 18.87 VO2 max (I min ^)
(R^ = 0.76, S.E. = 5.11)
Table 11 illustrates each subjects actual and predicted rowing performance data as determined by the above regression equations for DIST 6 and T2500.
Table 11 Actual and predicted rowing performances as computed from the regression equations
DIST6 (m) = 1435 + 71.36 VO2 max (1-min ) + 8.78 Peak lactate
T2500 (s) = 574.38 - 18.87 VO2 max (1-min ^)
DIST6 (m) T2500 (si Difference Subject Actual Predicted Difference Actual Predicted (%) (%) 461.2 + 0 . 6 1 1968 1953.6 - 0.7 458.6 454.6 448.0 - 1.4 2 1965 1982.5 + 0.9 + 0 . 2 3 1962 1931.3 - 1 .6 461.8 462.9 + 1.3 4 1986 1957.5 - 1.4 444.6 450.6 - 0 .1 5 1926 1919 - 0.4 4683 467.8 6 1923 1907.3 - 1 .0 - 1 .1 7 1899 1914.5 + 0 .8 468.6 463.6 473.7 473.2 - 0 .1 8 1881 1878.1 - 0 .1 9 1894 1910.2 + 0.9 475.4 474.4 - 0 . 2 1 0 1860 1870.3 + 0.5 471.0 - 1.4 11 1869 1883.1 + 0.7 477.8 469.3 + 2 . 2 1 2 1935 1934.3 - 0.04 459.3 + 0.04 13 1952 1921.3 - 1 .6 465.3 465.5 14 1911 1928 + 0.9 15 1928 1931.8 + 0 .2 17 1882 1889.4 + 0.4 + 0 . 2 18 1958 1986.1 + 1.4 452.3 453.1
75 DISCUSSION
Success in international rowing has been shown to be not only related to technical skill
(Henry et al, 1995; Smith et al, 1993; Smith and Spinks, 1990; 1995), but also to a high level of physical fitness (Hagerman et al, 1979; Hollings and Robson, 1992;
Mahler et al, 1984b; Secher, 1983; Steinacker, 1993). Due to the methodological problems involved in the physiological assessment of rowers on the water, monitoring has been primarily performed in the laboratory using simulated rowing on an ergometer (Hagerman, 1984; Mahler et al, 1984a; Secher, 1993). The 6 minute performance test (Dist 6 ) on a rowing ergometer has been frequently used to evaluate competitive rowing performance (Faff et al, 1993; Hagerman et al, 1979; Hollings and Robson, 1989; Mickelson and Hagerman, 1982; Williams, 1978) and has been validated as a method of determining VO2 max in rowers (Mahler et al, 1984a). Dist 6 was initially developed to replicate the duration, intensity and pacing strategy of competitive rowing over 2000 metres (Mahler et al, 1984b). From an international perspective, amongst elite rowers, the 2500 metre time trial (T2500) has been adopted as the standard for inter-individual comparison and is used during rowing ergometer competitions (Kramer et al, 1994). Despite the popularity of the two rowing ergometer tests in terms of physiological assessment and performance evaluation, no previous comparision has been made between Dist 6 and T2500 as measures of rowing performance. Furthermore, there is a dearth of information comparing ergometer performance test data to actual rowing performance. Klusiewicz et al. (1991) reported
a strong relationship between Dist 6 and and a 2000 metre race time (r=-0.90). This
finding was supported by Urhausen et al. (1993) and Steinacker et al. (1987), who
both observed a comparable relationship between the blood lactate-heart rate response
for ergometer and on-water rowing.
76 Rowing ergometers have been shown to accurately replicate the rowing task and physiological demands of on-water rowing (Chenier and Leger, 1991; Hagerman,
1984; Hagerman et al., 1979; Henry et al., 1995; Lamb, 1989; McKenzie and Rhodes,
1982; Smith and Spinks, 1995; Steinacker et al., 1987; 1991; Tumilty et al., 1987;
Urhausen et al., 1993). Whilst serving to provide reliable and valid data, the rowing ergometer offers a more easily controlled environment than on-water rowing, which allows a ready comparison of performance between rowers (Hagerman, 1984; Smith and Spinks, 1990). Due to these considerations, rowing ergometer tests are widely used in the assessment of training, performance and as part of the selection criteria of crews for competition (Hollings and Robson, 1992; Lormes et al., 1993, Morton et al.,
1984; Smith and Spinks, 1990).
In the present investigation, the strong relationship observed between DIST 6 and
T2500 (R^ = 0.82, P<0.01) indicated that one measure of rowing performance on an ergometer may be a strong predictor of the other. This is further supported by the similar trend of the regressions between predictor variables and the two measures of rowing performance denoting a strong relationship between DIST 6 and T2500. A comparison of the 1 2 subjects that completed both performance tests indicates that the ranking of rowers based on DIST 6 test is almost identical to the performance times in the T2500 test. Although DIST 6 and T2500 are frequently used to evaluate rowing
performance they are by no means identical, the duration of the latter test typically
taking 7-8 minutes as opposed to a standard 6 minutes for the former. In the present
study the mean duration of the T2500 test was 7 minutes 43 seconds. This would place
a greater emphasis on the aerobic energy pathway (Hagerman, 1975; Hagerman et al.,
1978; 1979) and may explain the stronger linear relationship between T2500 and
VO2 max observed in the current study.
Irrespective of which dependent variable was used as the criterion measurement of
rowing performance, absolute FOimax (1 min ) was found to be the best single
77 predictor variable. Therefore based on these findings, the two null hypotheses for this experiment were rejected (see page 4). Absolute VO2 max values may be more important than relative readings because the rowers weight is supported by the boat
(Hagerman, 1984; Secher et al., 1982b). The relationship between ÛO 2 max (I min ) and rowing performance observed in the present study is comparable to previous findings. Secher et al. (1982b) reported a direct relationship between placing in an international rowing regatta and the average absolute VO2 max for the crew (r=0.87).
In accordance with the current study, Secher et al. (1982b) also observed that when
ÛO2 values were expressed relative to body weight (ml kg min ^) no significant relationship existed (r=0.38). This may reflect the large physical dimensions of the oarsmen and the non weight-bearing nature of rowing. Kinch et al. (1994) and Nevill et al. (1992) independently reported that absolute ÛO 2 max (1 min ^ was the best determinant of rowing performance in varsity level oarsmen (r=0.86). Similarly,
Kramer et al. (1994) observed a strong relationship between absolute VO2 max and rowing ergometer performance in a group of oarswomen (r=0.77). The lower correlation reported by Kramer et al. (1994), may in part be due to the mixed ability and competitive experience of the subjects. The findings of the present study using elite male rowers, and other reported papers, support earlier observations that a high
ÊOz max is fundamental to success in rowing (Clark et al., 1983; Hagerman, 1984;
Hagerman et al., 1978; 1979; 1983; Mahler et al., 1984b; McKenzie and Rhodes,
1982; Secher, 1983; Secher et al., 1982b; Steinacker et al., 1991).
Overall, the relationship between the majority of laboratory variables and rowing
performance were found to be significant. In contrast, those for the descriptive
variables were poor with only biiliac breadth proving to be significantly related to
T2500 (P<0.05). In addition to VO2 max, the other predictor variables that were found
to be significantly related to both measures for rowing performance included FU388,
REF2mM and peak power. Although there is little information relating these variables
to success in rowing, a number of studies in other sports, particularly running, have
78 found a strong relationship amongst these variables and performance. It would appear that the strength of the relationships observed between physiological parameters and performance are strongly dependent on the interrelationships among predictor variables and the size and heterogeneity of the sample group (Sparling, 1984).
Fractional utilisation, or the percentage of peak aerobic power utilised at a given submaximal work intensity, has been highly correlated with running performance
(Conley and Krahenbuhl, 1980; Costill et al., 1973; Unnithan et al., 1995 ). Similarly, the fraction of VOimax, at average race pace, has been found to be significantly related to marathon performance (Maughan and Leiper, 1983; Peronnet et al., 1987).
The significant relationship between fractional utilisation and rowing performance observed in the present study is supported by earlier research (Hagerman et al., 1978;
McKenzie and Rhodes, 1982), which reported extreme values of the fractional utilisation of ÛO2 max (93-98%) during simulated rowing. Hagerman et al. (1978) suggested that this was the most critical factor in maintaining a high mean workload during a 6 minute performance test. Furthermore, the oxidation of lactate during 6 minutes of maximal ergometer rowing was proposed by Hagerman et al. (1978), who observed, after a peak in the second minute of exercise that there was no increase in lactate accumulation until completion of the test.
In accordance with the current findings, several studies have observed that indices of blood lactate response to submaximal exercise, such as lactate threshold and reference
blood lactate concentrations, are highly correlated to endurance performance in
runners (Farrell et al, 1979; Kumagai et al, 1982; Lafontaine et al, 1981; Sjodin and
Jacobs, 1981; Tanaka and Matsuura, 1984; Williams et al, 1983). However, the
amount of data relating blood lactate to rowing performance is limited. In contrast to
the present research, a number of studies (Faff et al, 1993; Klusiewicz, 1993,
Klusiewicz et al, 1991; Steinacker et al, 1991) have reported that power output
attained at the anaerobic threshold (defined as a blood lactate concentration of 4
79 mmoir^) is the best parameter for determining rowing performance. Conversely,
Womack et al. (1992) observed that the rowing velocity at fixed blood lactate concentrations and VO2 max (1 min ^) were equally good predictors of 2000 metre rowing performance.
The strong relationship between peak power output and the two measures of rowing performance observed in the present study, are in agreement with a number of earlier investigations which have indicated the importance of maximal muscle power as a predictor of performance (Hawley and Williams, 1991; Noakes, 1988; Noakes et al.,
1990). Several studies have suggested that the primary variable predicting performance, at least in running (Daniels et al., 1986; Morgan et al., 1986; Morgan et al., 1989; Noakes, 1988; Noakes et al., 1990) and cycling (Hawley and Noakes, 1992) is the maximum velocity or workload that an athlete can achieve during a VO2 max test. Similar findings have been documented in swimming studies, where peak arm power has been used to predict performance in middle distance and sprint swimmers
(Hawley and Williams, 1991; Sharp et al, 1992).
Regression analysis revealed that no significant relationship existed between peak lactate and either of the rowing performance variables. A similar finding was reported by Klusiewicz et al. (1991), who found a weak relationship between post-exercise lactate concentration and time to row 2000 metres (r=0.29). However, in the present
study, when peak lactate was combined with absolute ÊO 2 max (Imin ) in the
predictor model it was found to increase the R^ but this was only significant in the
case of DIST6 (P<0.01). The combination of VO2 max (Imin ) and peak lactate
accounted for 77% of the variance in DIST 6 and 83% of the variance in T2500.
Although there is considerable debate over the merits of using blood lactate
measurements to evaluate the overall anaerobic energy contribution to specific exercise
(Hagerman, 1984), the contribution of anaerobic metabolism during maximal rowing
has been estimated to be between 20 and 30% (Grujic et al, 1987; Hagerman et al.
80 1978; 1979; Steinacker, 1988; Szogy and Cherebetiu, 1974). Hagerman et al. (1978) reported that during 6 minutes of maximal work on a rowing ergometer, the high anaerobic and aerobic capacities of oarsmen allowed them to work at the upper limits of the anaerobic metabolism, normally associated with shorter maximal efforts. In contrast, other studies have reported that a high anaerobic capacity is of limited value and is not among the most essential factors determining rowing work capacity
(Klusiewicz, 1993; Klusiewicz et al., 1991; Lormes et al., 1991; Steinacker et al.,
1991). Klusiewicz et al. (1992) observed a significantly higher peak lactate concentration following a simulated race in senior rowers compared to juniors. This finding was further supported by Secher et al. (1982b), who suggested that blood lactate accumulation was volume dependent and should increase to the third power of a characteristic linear dimension of the subject. Thus, larger rowers should have an advantage over their smaller counterpart due to their higher anaerobic potential.
When T2500 was taken as the dependant variable, the best combination of predictor variables had no great advantage in predicting rowing performance compared to when only absolute VO2 max was retained in the model. The combination of FU388 and peak power was found to account for 83% of the variance in rowing performance compared to 76% for absolute VO2 max. For the purpose of predicting T2500 including more
than one variable in the model does not offer major benefits, but necessitates further
physiological analysis.
A number of the predictor variables, in addition to absolute VO2 max (I min ) and peak
lactate, were found to be significantly associated with performance. Their inclusion in
the model did not lead to any further significant increase in and offered no
advantages over the two variable model. A combination of VO2 max (1-min ), peak
power and REF2mM resulted in a relatively high R^ which accounted for 6 8 % of the
variance in DIST6 . Although the F-ratio was significant, on closer examination the P
values for each of the 3 predictor variables were found to be non-significant. A simple
81 -1 linear regression of VOimax (I min ) on REF2mM revealed a high degree of colinearity between these variables, as they were found to be significantly related (R^ =
0.65). This would indicate that, in some way, this variable interacts with absolute
VO2 max during rowing competition. It has been suggested that a high level of oxygen utilisation may delay the possible deleterious effects of lactate accumulation during high intensity exercise (Âstrand and Rodahl, 1986; Hagerman et al., 1978; Hagerman,
1984). In a review of physiological determinants of distance running performance.
Sparling (1984) suggested that when a strong colinearity exists between such predictor variables, they should not be treated as separate unrelated determinants. Sparling
(1984) went on to suggest that where inter-relationships among predictor variables are unreported, interpretation of data is problematical.
The number of physiological predictor variables included in the present study is by no means exhaustive. Different strength measurements have been used to evaluate rowing performance but the results have been conflicting and, therefore, inconclusive.
Yamakawa and Ishiko (1966) reported a significant correlation between various measures of muscular strength and rowing performance, while Secher (1975) observed that of 8 strength parameters measured, only grip strength significantly correlated with isometric rowing strength. In contrast, a number of other studies have reported a weak relationship between strength and rowing performance (Bloomfield and Roberts, 1972;
Hagerman et al., 1972; Hay, 1968; Kramer et al., 1991; 1994). Furthermore,
Hagerman et al. (1972) proposed that more specific and fimctional measures of rowing strength might be more appropriate. Few studies have investigated the relationship between isokinetic strength and performance in rowers. Pyke et al. (1979) reported a strong positive relationship between specific isokinetic leg torque and rowing ergometer performance. Conversely, Kramer et al. (1991; 1994) found isokinetic leg strength to be poorly related to rowing performance. Additionally, in a study comparing the morphological muscle characteristics of national and international
82 calibre rowers, Larsson and Forsberg (1980), observed that isokinetic strength did not, in general, separate good from less skilled oarsmen in terms of their performance.
SUMMARY. CONCLUSIONS AND RECOMMENDATIONS
In contrast to other more popular endurance activities, analysis of the current literature revealed that there is little information available discerning physiological predictors of rowing performance. The present study is the first to measure such a wide range of physiological and descriptive variables, and relate them to rowing performance.
The findings of the present study revealed that of the 22 descriptive and physiological variables measured, it was found that VO2 max expressed in absolute terms (Imin^) was the single best predictor of rowing performance for both of the rowing performance tests used. Based on these observations, the two null hypotheses were rejected. A number of other physiological variables were found to be significantly related to rowing performance. However, when these variables were included in the predictor model, additional increases in were small.
It was concluded that the combination of absolute VO2 max and peak lactate were recommended for the prediction of rowing performance as determined by DIST 6 .
When T2500 was adopted as the criterion measure, only absolute VO2 max was found necessary to predict rowing performance. Further analysis of the data revealed that other combinations of the physiological variables measured had a strong relationship with rowing performance. However, closer examination using simple linear regression revealed a high degree of colinearity between these predictor variables, indicating that these variables somehow interact with each other during rowing competition.
In light of the findings of this study, further research is required to determine whether a similar relationship exists between the various physiological variables measured and rowing performance in lightweight rowers. Additionally, analysis should be extended to comparison with on-water rowing for single sculls and crew boats during actual
rowing competition to determine the relationship between mean crew VO2 max and
83 performance. Now that it has been established which physiological variables are important to performance in rowing, a natural progression for this study would be to monitor and evaluate changes in these variables in response to training. The next section addresses this question.
84 CHAPTER 4
Experiment 2. An analysis of the variation in selected physiological parameters during a 3 month period of training.
MATERIALS AND METHODS
1. INTRODUCTION
Rowing competitions are traditionally performed over 2000 metres with the race
duration lasting between 6 to 8 minutes, depending on the boat class. The energy
demands of which, have been shown to be derived primarily from aerobic sources
(Hagerman, 1974; Hagerman et al., 1978; Mickelson et al., 1982; Mahler et al., 1985).
Training should, therefore, be focused on improving anaerobic, but more particularly aerobic power and capacity which is the mainstay of success in rowing. During the early phase of the training cycle a high percentage of training is focused on aerobic training with primary emphasis on long slow distance workouts which may formulate over 80% of total Winter training volume (Mader et al., 1986).
Physiological testing has been adopted by various rowing nations, in order to establish physiological profiles and assist the coach in selection of crews (Secher et al., 1982b).
Perhaps the greatest potential of physiological testing, however, is to aid in the planning of training and competition strategy (Hagerman, 1984; Vermulst et al.,
1991). This is particularly relevant to rowing when considering the seasonal variation of most training programmes in terms of intensity and duration. Although several
85 studies have investigated the physiological and training characteristics of rowers and their influence on rowing performance most publications have dealt with male rowers
(Wright et al., 1976; Hagerman et al., 1978; Hagerman and Staron, 1983; Mahler et al., 1984b). As a result there is a lack of information concerning the female rower.
The purpose of this study, therefore, was to evaluate any physiological changes in rowing performance in elite female rowers during the early phase of the training cycle.
2. ETHICAL CONSIDERATIONS
All experimental procedures were cleared by the ethical committee of Northwick Park
Hospital. Prior to participation in the study, each subject completed an informed consent form (Appendix B).
3. SUBJECTS
For the purpose of this study fourteen members of the Great Britain women’s heavyweight rowing squad participated in this experiment. All subjects were instructed to maintain their normal dietary intake and to perform light, steady-state training (< 2 hours per day) in the 48 hours immediately prior to testing.
4. TEST PROCEDURES
Selected physiological variables were measured twice (November and February) during the early phase of the training cycle. All measurements were taken by the investigator to avoid inter-tester error. Many of the test procedures have already been
86 outlined in experiment 1 and, therefore, to avoid repetition, detailed explanation has been restricted to additional test assessments. The test procedures were as follows.
5. ANTHROPOMETRY
5.1. Body Mass and Stature
Prior to undertaking any physiological tests, body mass (kg) as well as standing and sitting height (cm) were measured using weight and height scales (W.N.T. Avery Ltd,
UK.). For the purpose of these measurements each subject removed their shoes and wore only a pair of shorts and singlet.
5.2. Body Composition
Body composition was assessed using skinfold thickness measures. Repeat skinfold measurements were taken at four skinfold sites, biceps, triceps, subscapular and suprailliac, using a Harpenden skinfold calliper (British Indicators Ltd, St. Albans) to determine the percent change in body fat. The Harpeden skinfold callipers are designed to provide a constant pressure of 1 0 gmm'^ of the calliper’s jaw surface area on varying skinfold thicknesses, with an accommodation up to a thicknessess of 50 mm.
The width of the skinfold measurement was determined on a dial indicator incorporated into the apparatus with the 1 .0 mm increments being interpolated to the nearest 0.5 mm. All skinfold measurements were taken on the right side of the body, following the procedures outlined by Durnin and Rahaman (1967).
87 6. CARDIORESPIRATORY EVALUATION
6.1. Ambient Conditions
Ambient temperature and humidity were measured before each test using a Hygromer
A1 digital handheld temperature and humidity indicator (Rotronic instruments, Horley,
Surrey, England.). The Hygromer A1 contains a Ft 100 sensor for measurement of temperature and a Hygromer© C 80 sensor for measurement of relative humidity. The operating temperature range is - 1 0 to +60°C and 0 to 1 0 0 % for relative humidity. At
25°C the measurement error is ±0.3°C and ±2% relative humidity. In order to control laboratory conditions temperature was regulated between a range of 18-22 C.
6.2. Maximal Discontinuous Incremental Test
On completion of a standardised warm up, which consisted of 10 minutes rowing at
120 Watts, each subject performed a maximal discontinuous incremental step test on a
Concept II air braked rowing ergometer (Concept II, Nottingham England). The test consisted of 3 minute bouts of work at a fixed exercise intensity followed by a 30 second recovery.
In order to standardise the test, the gearing for the ergometer was set on the large cog with the fan open. Fixed stroke rates were controlled during the test with each subject being instructed to remain as close to the predetermined rates as possible. Each subject was instructed before and during the test to maintain the required work output as precisely as possible. The increment for each step was 16.7 ± 2.3 W (mean + S.E.).
Power output was calculated from the acceleration of the flywheel and was displayed
88 on a LCD monitor (Hagerman et al., 1988). The test was terminated upon volitional exhaustion or when the subject failed to maintain the appropriate exercise intensity.
In addition to heart rate and blood lactate measurements, oxygen uptake (FO2 ) during both submaximal and maximal exercise was measured by a Jaeger EOS Sprint on-line gas analysis system (Jaeger, U.K.). Heart rate was measured throughout the test by means of radiotelemetry using a Polar Sports Tester (Polar, Kempele, Finland). The use of a discontinuous incremental test on the rowing ergometer enabled capillarised earlobe blood samples to be taken at the end of each 3 minute exercise increment to determine the blood lactate concentration. The blood samples were analysed by an Analox GM7 lactate analyser. (Analox Instruments, London). The lactate analyser was calibrated at the start of testing, during and directly afterwards with know controls.
Power outputs associated with reference blood lactate concentration of 2.5 and 4.0 mmolT^ were determined from the curvilinear rise in the power-blood lactate relationship, by interpolation, using cubic splines which use a least squares polynomial curve fit written into a computer programme (Simfit, W.G. Bardsley, University of
Manchester). The VO2 values at the corresponding power outputs for the reference blood lactate concentrations were also determined to establish any changes in rowing economy over the 3 month training period. Rowing economy, similar to running economy, is considered to be the steady-state oxygen consumption (I min'^) for a standardised submaximal exercise intensity (Farrell et al., 1979; Conley and
Krahenbuhl, 1980).
89 7. TRAINING PROGRAMME
The training programme was designed by the Great Britain Head Women’s Coach and a diary documenting all training undertaken during the study was completed by all the rowers. The training volume was evaluated in terms of monthly trained hours (MTH) and comprised of a combination of rowing training (RT) and land-based training
(LET). The former consisted of on-water and ergometer training and the latter of weight training, circuit training, running and cycling.
Illustration 4 Members of the Great Britain women’s squad during training
90 The results obtained from Novembers test enabled the determination of the individual lactate threshold (ITLac) for each rower, from the curvilinear rise in the power-blood lactate relationship. Based on this data, individual training guidelines were provided using heart rate ranges to gauge exercise intensity during the 3 month training period.
8. STATISTICAL ANALYSIS
The data are presented as means + S.E. For statistical analysis of differences between the first test (November) and second test (February), a two-tailed Student’s t-test for paired observations was used. Significant differences were accepted at the 5% level.
All statistics were performed using commercially available software (Data desk'^. Data
Description, Ithaca. New York).
91 RESULTS
1. Physical Characteristics
The physical characteristics of the subjects are presented in Table 12.
Table 12 Characteristics of study group (n=14)
Age (yrs) Mass (kg) Height (cm) VOi max (Imin"^) Sum of Skinfolds (mm)
25.9 + 0.9 72.9 ±1.5 177.8 + 1.3 3.99 + 0.06 39.0 + 2.6
Means + S.E.
2. Training Data
The estimated training volume, expressed as monthly training hours (MTH), for both rowing training (RT) and land based training (LET), is illustrated in Figure 6 . During the 3 month training period, the total monthly volume of LET remained constant at 19 hours. In contrast the total monthly volume of RT progressively increased from 19 hours in November to 30 hours in January. A detailed breakdown of the 3 month training programme is provided in Appendix C.
92 30 -- □ LBT ERT 5 25
20 --
15 --
10 --
5 --
November December January Month
Figure 6. Total training volume expressed as monthly trained hours (MTH)
3. Anthropometric and Physiological Measures
Table 13. summarises the main results of the anthropometric and physiological variables measured before and after the 3 month training period. Analysis of the mean anthropometric data revealed that there was a slight, but non significant, decrease in the sum of skinfolds for the group. Body mass did not change throughout the course of the study.
Table 13 Changes in selected anthropometric and physiological variables measured pre- and post- the 3 month training period (w=14).
November February
Body mass (kg) 72.9 ± 1.5 72.8 ±1.6
Sum of skinfolds (mm) 39.0 + 2.6 36.7 ±2.3 Power output @2.5 mmol.l'^ (W) 217±5.0 220.5 ±2.6 Power output @ 4.0 mmol.l'^ (W) 243 ± 4.0 247.7 ±1.8*
VO2 (I min ^) @2.5 mmol.l'^ 3.43 ±0.09 3.26 ±0.03**
VO2 (Imin^) @ 4.0 mmol.l'^ 3.75 ±0.07 3.59 ±0.03**
VO2 max (Imin^) 3.99 ±0.06 3.97 + 0.05
Means ± S.E.; *=f<0.05, ** =P<0.01
93 In November the power output at the 2.5 mmoll'^ and 4.0 mmoll’^ blood lactate reference points were 217 ± 5.0 W and 243 ± 4.0 W, respectively. From November to February, there was a significant increase in the exercise intensity attained at 4.0 mmoir^ (4.71 ± 1.79 W, P<0.05), while there was no significant change at the 2.5 mmol 1'^ reference value.
Prior to the 3 month training period, the VO2 at 2.5 mmoll'^ and 4.0 mmolf^ was 3.43
± 0.09 and 3.75 ± 0.07 lm in'\ respectively. FO 2 significantly decreased from November to February at both blood lactate reference points of 2.5 mmol l'^ (0.17 ± 0.03 Imin'\ P<0.01) and 4.0 mmolT^ (0.16 ± 0.03 Imin'\ P<0.01). In contrast to submaximal values, there was no significant change in FO 2 max between November and February.
94 DISCUSSION
The purpose of this study was to evaluate selected physiological changes in rowing performance in elite female rowers during the early phase of the training cycle. The results of the present study indicate that the training programme undertaken during the
3 month conditioning phase was sufficient to elicit an improvement in rowing economy as determined by a decrease in VO2 at the two reference blood lactate concentrations and to also register a significant increase in the exercise intensity attained at a blood lactate reference of 4 mmolT\ This enhanced ability to generate power is considered essential to improving rowing performance (Mahler et al., 1985).
The benefits of using a discontinuous incremental test protocol, as opposed to a conventional continuous test, is that it allows the accurate evaluation of rowing economy, VO2 max and the exercise intensity attained at fixed blood lactate reference points. All the subjects were fully habituated to the test procedures as they had all performed the tests on a number of occasions prior to the study. It is important to examine changes in physiological parameters that result from training in order to evaluate the effectiveness of specific training techniques and programmes.
The issue of what is the optimal exercise intensity for eliciting aerobic training adaptations, which ultimately lead to an improvement in performance, is controversial. Several studies investigating rowing, have claimed that aerobic training is only effective if it is performed at a blood lactate concentration of between 2.5 and 3.5 mmolT^ (Urhausen et al., 1986; Lormes et al., 1988; Steinacker, 1988) or 4 mmol.l'^ (Fritsch, 1981; Hirsch, 1977). Detailed examination of the training programme performed by the rowers, revealed that the majority of the work consisted of aerobic conditioning with a greater emphasis being placed on rowing specific training as the volume progressively increased over the 3 months (Appendix C). In an earlier training study, Mader et al. (1986) reported that between 8 6 % and 94% of total Winter training was performed at a blood lactate level below 2 mmoH'\ As the 3 month training period progressed, in the current study, there was a shift away from long
95 steady state training (blood lactate < 2 mmolT^) and a greater reliance placed on higher intensity exercise around the lactate threshold, which has previously been shown to be between 2 and 4 mmoU'^ in rowers (Hagberg, 1984; Hartmann et al, 1990b). This in part may explain why there was no significant increase in the exercise intensity attained at the 2.5 mmoll’^ reference point. In trained rowers, the power output attained at a blood lactate reference value of 4 mmol 1’^ is reported to be of high predictive value in determining competition performance (Wolf and Roth, 1987).
The significant improvement in rowing economy, as determined by the decrease in
VO2 at both blood lactate reference points, indicates that for a given VO2 , a greater velocity may be attained up to and including VO2 max (Womack et al;, 1996), with a subsequent improvement in performance. The failure of the training programme to elicit any improvement in VO2 max may reflect the training state of the subjects before they commenced the training programme. Similarly, it is likely the high training status of this elite group of female rowers, which included a number of World Championship medalists, precluded them fi-om large physical improvements in response to training. Nevertheless at this elite level, small but non significant differences in training state may impact on performance and could determine the difference between success and failure. Being that there was no change in VO2 max during the course of the study, this would imply that rowing economy is a more sensitive measure of change in aerobic conditioning. The cause of the significant improvement in rowing economy is unclear, although it could be influenced by variations in stroke mechanics (Womack et al., 1996). It has been suggested that rowing economy may be influenced by changes in stoke rate (Di Pramprero, 1986; Di Pramprero et al., 1971). This factor can be excluded, however, as stroke rate was strictly controlled for each rower in the pre- and post- tests. Technical error in measurement of VO2 may also be considered, however procedures for the calibration of the on-line gas analysis system were strictly adhered to both before and after each test.
For international level rowers, peak conditioning is normally targeted for the Summer. In the present study, the Winter phase of the annual training cycling in which the
96 rowers were trained and physiologically assessed, focused primarily on base endurance and strength conditioning and was not designed to achieve peak performance. This may explain why there was an improvement in a number of submaximal variables such
as rowing economy and the velocity attained at a blood lactate reference value of 4
mmolT% while no improvement was observed for VO2 max.
SUMMARY. CONCLUSIONS AND RECOMMENDATIONS
Periodical assessment of work capacity is essential in monitoring the physiological adaptations to training. Over recent years there has been an increase in the availability of information concerning the physiological effects of exercise on trained athletes. Nevertheless, there is a dearth of information evaluating the effects of specific training programmes on elite athletes. Analysis of the limited data available relating to rowing reveals gaps in the knowledge relating to the physiological and metabolic responses to training. This may well reflect the complexity of training, as well as the on-water nature of rowing which makes such analysis difficult. In this context, the present study sought to determine the effects of a specific phase of training on selected physiological variables in a group of elite rowers.
It was concluded that the training programme undertaken during the 3 month conditioning phase was sufficient to elicit an improvement in rowing economy, and also register a significant increase in the exercise intensity attained at a blood lactate level of 4 m m olf\ As a consequence of these findings, the null hypothesis for this experiment was rejected (see page 4). In contrast, no significant change was observed
for the sum of skinfolds or PD2 max in response to training. Previous studies incorporating exercise testing of rowers have shown that a high aerobic capacity is an essential criteria for success in international rowing (Secher et al., 1982b). The present findings suggest that fractional utilisation, enhanced ability to generate power and
rowing economy, in addition to a high VO2 max, may be important to actual rowing performance, in elite rowers. In order to enhance performance, the specific training
97 undertaken by rowers should therefore focus on improving these physiological variables.
Further work is required to identify optimal training intensities and to evaluate the specific effects of training and the subsequent impact on rowing performance. The use for more standardised training programmes by elite rowers training in the national squad should allow a more specific evaluation of the physiological responses to the training undertaken. Additionally, the duration of such longitudinal training studies should be extended to evaluate seasonal variation in training response. This should include analysis of other modes of training commonly used by rowers such as altitude training.
98 CHAPTER 5
Experiment 3. An Analysis of Selected Physiological Adaptations in Response to Altitude Training in Preparation for Competition at Sea Level.
MATERIALS AND METHODS
1. INTRODUCTION
The rationale for training at altitude in order to enhance sea level performance, is based on the adaptive responses of the body to a period of exposure to a reduced oxygen tension. Despite the lack of evidence supporting its efficacy, altitude training is commonly used by National rowing teams to enhance sea level performance (Steinacker, 1993). Grobler (personal communication) reported that about 50% of rowing nations used altitude training in their preparation for the 1993 World Championships. Nevertheless, use of altitude training in terms of improved performance on return to sea level remains questionable. To date there is a lack of research investigating the effect of altitude training on rowing performance. Furthermore, few studies have closely monitored the physiological adaptations that occur at altitude, therefore interpretation of training and performance data in response to altitude training may prove difficult.
The purpose of this study, therefore, was to evaluate the responses and adaptations of selected physiological variables during a period of altitude training and to determine whether any observed changes had an effect on submaximal work capacity on return to sea level.
99 2. ETHICAL CONSIDERATIONS
All experimental procedures were cleared by the ethical committee of Northwick Park
Hospital. Prior to participation in the study, each subject completed an informed
consent form (Appendix B).
3. PHYSIOLOGICAL MONITORING AT ALTITUDE
Physiological monitoring of the Great Britain National Rowing Squad took place during three altitude training camps between 1991 and 1993 as part of their preparation for subsequent World Championships and Olympic Games. The location of the training venue was Silvretta, a lake some 2.5 km long, situated in the Austrian Alps at an altitude of 2030 metres. The duration of each camp was 17-19 days.
Illustration 5 Squad members undergoing training whilst at altitude
100 3.1. Climatic Conditions
Ambient temperature and humidity were measured each day using a Hygromer A1 digital handheld temperature and humidity indicator (Rotronic instruments, Horley, Surrey, England.). The Hygromer A1 contains a Pt 100 sensor for measurement of temperature and a Hygromer® C 80 sensor for measurement of relative humidity. The operating temperature range is - 1 0 to +60®C and 0 to 1 0 0 % for relative humidity. At
25°C the measurement error is ±0.3°C and ± 2 % relative humidity.
4. GENERAL MEASUREMENTS
For the purpose of this phase of the study a number of anthropometric and physiological parameters were measured prior to and daily during 19 days altitude training in 11 subjects (2 female rowers and 9 male rowers).
4.1. Body Mass
Utilising a calibrated electronic weighing scales (Krups U.K. Ltd), daily recordings of weight were taken for each subject on rising in the morning in order to avoid diurnal variation. Measurement was taken with the subject wearing a pair of rowing shorts only.
4.2. Resting Heart Rate
Daily resting heart rate was taken using palpation. The tips of the index and middle fingers were placed either on the carotid artery in the neck just lateral to the larynx or on the radial artery on the anterolateral aspect of the wrist directly in line with the base of the thumb.
101 Upon waking each subject was required to lie motionless for 5 minutes before taking a manual pulse reading for a 30 second period. All subjects were familiar with the above technique of heart rate measurement and many were already undertaking this procedure for recording in their training diary.
5. HAEMATOLOGICAL ANALYSTS
All blood samples were taken from the subjects in a supine position and under fasting conditions at the same time of day (first thing in the morning). This eliminated potential changes caused by circadian rhythms, diet, stress or environmental influences (Hakkmen et al., 1988; Steinacker et al., 1993; Urhausen et al., 1987). Post exercise samples were avoided as it has been previously shown that it is difficult to standardise measurements due to variations in plasma volume (Remes et al., 1979). In order to monitor the duration and process of acclimatisation and subsequent adaptations and responses to altitude training the following haematological measurements were made.
5.1. Blood Gas
A blood sample was collected into a 100 pi capillary tube from an hyperaemic earlobe previously treated with a vaso-dilator cream (Ralgex) to promote peripheral blood flow before sampling. Prior to sampling the cream was thoroughly cleaned-off the earlobe with a medical swab. The puncture was deep enough to ensure that the blood flow was free and rapid. Immediately after collection, the blood samples (> 60 pi) were analysed in a Ciba-Corning 238 pH/blood gas analyser (Ciba-Corning Diagnostics Ltd,
Halstead, England) for determination of PO 2, PCO2, pH and HCO 3' . The measurement technology of the 238 pH/blood gas analyser is based on electrochemistry. Each electrode is designed to selectively measure the activity of a specific substance. The potential generated at each electrode is converted into an electrical signal by a
102 transducer mechanism. The electronic signal is then filtered, smoothed, and converted into a concentration measurement expressed in standard units.
Samples were analysed as soon as possible after collection in order to minimise errors due to metabolic changes. This was particularly important for PO 2 samples, as oxygen is consumed during storage. Results were displayed within 60 seconds of sampling. The blood gas analyser was calibrated at the start of testing and directly afterwards with a known control. The 238 microprocessor continuously monitors system stability and adjusts autocalibration of the analyser accordingly.
Two gas standards were used to calibrate the PO 2 and PCO 2 sensors:
1) Cal Gas Provides the calibration point for 1 and 2 point PO 2 and PCO 2 calibrations. The cal gas contained 12.00 ± 0.05% oxygen and 5.00 ± 0.05% carbon dioxide, balanced with nitrogen.
2 ) Slope Gas Provides the slope point for 2 point PO 2 and PCO 2 calibrations. The cal gas contains 10.00 ± 0.05% carbon dioxide balanced with nitrogen.
5.2. Haemoglobin
The subject was seated comfortably with the middle sampling finger warmed under a hot tap to increase blood perfusion. The puncture site was cleaned with a medical swab and wiped dry. Light pressure was applied to the finger tip until a few blood droplets appeared which were wiped away with a dry absorbent pad. This helped stimulate fiarther blood fiow. The resulting blood drop was collected into a disposable microcuvette (10 pi) containing reagents deposited on its inner walls. This reagent, which consisted of sodium deoxycholate, sodium nitrite and sodium azide, converts the haemoglobin to methaemoglobin azide, without dilution (Vanzetti, 1966). The blood sample was drawn into the cavity of the cuvette by capillary force and spontaneously mixed with the reagents whereby the erythrocyte membranes were disintegrated by
103 sodium deoxycholate, releasing the haemoglobin. Sodium nitrite converts the haemoglobin iron from the ferrous to the ferric state to form methaemoglobin, which then combines with azide to form to methaemoglobin azide (Vanzetti, 1966; von Schenck et al., 1986).
Care was taken to make sure that there were no visible signs of air bubbles within the microcuvette as this has previously been shown, on occasions, to cause a discrepancy in results (Johns and Lewis, 1989). The sample was then placed in a HaemoCue® Photometer (HemoCue®, Leo Diagnostics AB, Angelholm, Sweden) in which haemoglobin concentration was measured photometrically at 565 nm and 880 nm. Combining this two-wavelength determination with the direct sampling method of collecting capillary blood into the 10 pi microcuvette makes the HemoCue equipment even more reliable than the widely used photometric cyanmethemoglobin method due to any potential error caused by dilution of sample is avoided (van Kampen and Assendelft, 1975; von Schenck et al., 1986). The high dilution of the blood (1:251) with the photometric cyanmethemoglobin method confers an intrinsic imprecision in measurement of haemoglobin (van Kampen and Assendelft, 1975). Additionally, turbidity from proteins and lipid particles (Creer and Ladenson, 1983; Sharma et al., 1985) due to high sample dilution may also influence the results from photometric analysis.
The HemoCue® photometer was calibrated before testing and immediately afterwards by means of a control cuvette fitted with a red filter. Three samples were taken with the mean value being recorded. If there was a discrepancy in readings > 0.3 g/dl the procedure was repeated. Results were displayed digitally after approximately 45 seconds.
Evaluation of the HemoCue® against measurements by filter photometer, which is the recommended laboratory reference method of determining haemoglobin (International Committee for Standardisation in Haematology, 1978 [ICSH Standard EP 6/2: 1977]), have demonstrated good comparability (Cohen and Seidl-Friedman, 1988; Von Schenck et al., 1986). Bridges et al. (1987) have shown the HemoCue® system to be
104 precise, accurate and reliable when compared against the Coulter S-880® (Coulter Electronics, Hialeah, USA), using 87 samples with haemoglobin levels between 110 and 170 g/1 (r=0.99). Similarly, comparisons undertaken by Johns and Lewis (1989) in the reference laboratory of the WHO, following guidelines established by the ICSH (International Committee for Standardisation in Haematology, 1984), revealed the HemoCue® to be a reliable instrument for haemoglobinometry with the following results: i) Precision: coefficient of variation, 1.2% ii) Linearity: linear in the range 0-170 g/1 (Fig. 1) iii) Comparability with the ICSH reference method: in range to 200 g/1, r=0.996, in range to 170 g/1, r=0.998. (source: Johns and Lewis, 1989).
5.3. Haematocrit
In order to monitor the relationship between increases in haemoglobin and changes in haemoconcentration resulting from a fall in plasma volume, measurements of haematocrit were made. This also facilitated the monitoring of dehydration, as measured by the fall in plasma volume, and the effectiveness of subsequent rehydration programmes. Changes in plasma volume (PV) were calculated from the Hb and Hct data according to Dill and Costill (1974), as opposed to the computation of changes in plasma volume based solely on changes in Hct (Van Beaumont, 1972). The latter method may be unreliable due to distortions caused by alterations in the volume of the red blood cells (Dill and Costill, 1974). Dill et al. (1969) reported that since only small divergence rates between calculated and observed values for PV were found, it was possible to predict PV changes as frequently as Hb was determined so long as cell volume (CV) remained unchanged.
The sampling procedure adopted was similar to that used for haemoglobin analysis. With the subject sitting, an arterialised capillary blood sample was taken fi-om a
105 warmed finger tip into a pre-heparinised capillary tube. The capillary sample was then spun-down in a centrifuge (Hawksley and Sons Ltd, Lancing, England) for 3 minutes to obtain the packed cell volume. Red blood cell (RBC) count was then measured using a Hawksley micro haematocrit reader (Hawksley and Sons Ltd, Lancing, England).
6. MONITORING OF TRAINING INTENSITY
In order to detect the level of physiological stress placed on each individual rower during daily training at altitude a number of parameters were measured.
6.1. Urea and Creatine Kinase
Total urea and creatine kinase (CK) concentrations were determined from capillary whole blood samples, collected fi*om an earlobe. The samples were analysed by means of a Refiotron® portable dry-chemistry analyser (Boehringer Mannheim, Mannheim, Germany). Using an automated pipette, 30 |il of whole blood were dispensed onto a test strip containing reagent pad (Figure 7), which was then immediately inserted into the analyser.
The separation pad appears to be very effective and results from whole blood samples have been shown to be comparable with that of plasma measurements (Price and Roller, 1988). The glass fibre layers under the protective mesh separate the erythrocytes from whole blood. Due to the special geometric design a plasma reservoir forms below the reagent layers. The test strip contains different reagent layers which are pressed into the plasma reservoir at the start of the reaction. The colour change occurring during the test strip reaction is measured by Ulbricht sphere reflectance photometry using a reference beam for compensation. Analysis time was approximately 3 minutes.
106 Protective mesh .
Magnetic strip
Plasma-separating layer
Reagent layers
Plasma reservoir
Figure 7 Refiotron® test strip
Prior to testing a "Chek" tab (Boehringer Mannheim) was used to assure that the instrument's reflectance photometer was operating within prescribed limits. The Refiotron® was calibrated at the start of testing and directly afterwards with magnetic control strips provided by the manufacturer. The Refiotron® calibration method (Boerma et al., 1988b) and the precision and accuracy of measurement corresponding to laboratory methods have previously been established (Boerma et al., 1988a; Price and Roller, 1988). Additionally, the Refiotron® system using whole blood samples
107 provides results concordant with the results obtained from conventional wet chemistry methods (Price and Roller, 1988).
6.2. Blood Lactate and Heart Rate
In order to detect the individual stress placed on each rower at altitude, daily lactate and heart rate analyses were performed during land-based and on-water training. The restricted size of the lake required training to be performed in a 5 km loop with the rowers coming into a landing stage as they turned at the end of each loop in order that a lactate sample could be obtained. A capillarised earlobe blood sample was taken and analysed in an Analox GM7 lactate analyser (Analox Instruments, Hammersmith). The lactate analyser was calibrated at the start of testing, during and directly afterwards with known controls of 3, 5 and 8 mmoH'^ (Analox Instruments, London).
Illustration 6 Squad members undergoing blood lactate testing and heart rate monitoring during a training session at altitude.
108 Heart rate was monitored throughout training by radiotelemetry using a Polar heart rate monitor (Polar Sports Tester, Finland). Heart rate data were recorded every 5 seconds, stored on the watch and down-loaded onto a computer at the end of each session. From the data collected, it was possible to gain a comprehensive training profile which enabled training intensity to be evaluated, controlled and revised where necessary.
7. EVALUATION OF CHANGES IN AEROBIC CONDITIONING IN RESPONSE TO ALTITUDE TRAINING
For the purpose of this phase of the study nineteen male members of the Great Britain Rowing squad participated in 17 days altitude training (2030 m) in preparation for the Barcelona Olympics (mean ± S.D.: age 25.9 + 0.9 years; height 194.1 ±1.5 cm; body mass 91.0 ± 1.5 kg). Immediately prior to going to altitude and 7 days after returning to sea level each subject performed a 10 min submaximal exercise bout, at a fixed intensity, on a rowing ergometer (Concept II, Nottingham). Heart rate was measured continuously throughout the test (Polar Sportstester, Kempele, Finland). Following a standardised warm up, a capillarised earlobe blood sample was taken at rest, 4 and 10 minutes (Figure 8 ).
4 min rowing 6 min rowing at ITlac at ITlac WARMUP
1 I I — 1 1 1 ...... 1 1 1 1 1 3 4 5 6 10 min. min. A
CAPILLARY BLOOD CAPILLARY BLOOD CAPILLARY BLOOD SAMPLE SAMPLE SAMPLE
Figure 8 Schematic Representation of Experimental Design
109 The samples were assayed using an Analox GM7 analyser (Analox Instruments, Hammersmith) for whole blood lactate concentration. The intensity of the 10 minutes exercise bout was designed to equate to the subjects individual lactate threshold (ITlac). The ITlac was determined from the curvilinear rise in the power-blood lactate relationship in a previously performed discontinuous incremental step test, with work- rates increasing by 38.4 ± 8.4 W every 3 minutes. This has been described in detail by Warrington et al. (1992). Blood bicarbonate (HCOs") and haemoglobin (Hb) concentrations were measured before, during and after the period of altitude training.
8. STATISTICAL ANALYSIS
The data are presented as means (± S.E.) unless otherwise stated. All statistics were performed using commercially available software (Minitab, Minitab Inc). Confidence intervals (± 2 S.E.) were used to determine mean daily changes in the physiological variables measured during the period of altitude training. Repeated-measures analysis of variance was then used to study the significance of day to day changes. Where significant main effects were found, a Tukey post hoc test was used to assess differences between means. Differences in variables pre- and post- altitude training were assessed using dependent t-tests. The relationship between the differences in haemoglobin and haematocrit pre-and post-altitude training and initial haemoblobin and haemotcrit were compared using simple linear regression. The strength of the linear regressions were established by the coefficients of determination (R^). The significance level P<0.05 was accepted in all statistical comparisons.
The statistical procedures used in the study were useful for the identification of changes in the biological parameters associated with the 19 days training in a hypoxic environment. The data for the subjects was initially evaluated using confidence intervals at the 95% level, expressed as mean values ± 2 S.E. Although a close relationship exists between the result of a test of significance and the associated confidence interval, the latter conveys more information because it indicates the lowest
110 and highest true effect likely to be compatible with the sample observations.
Confidence intervals are extremely helpful in the interpretation of data, particularly when there is a small sample size, as they reveal the level of uncertainty related to a result. For example the differences between group means irrespective of whether statistically significance is observed.
A repeated measures design was adopted to allow the study of a phenomenon across time as well as providing the opportunity to control for individual differences among subjects, which is probably the largest source of variation in most training studies.
According to Pedhazur (1982), when the assumption of normal distribution is met the use of ANOVA with repeated measures is more powerful than multivariate tests.
Additionally, if the number of subjects is small, only the ANOVA of repeated measures test can be used.
I ll RESULTS
1. PHYSICAL CHARACTERISTICS
The descriptive characteristics of the subjects are presented in Table 14.
Table 14 Characteristics of study group (n=l 1)
Sex n Age (yrs) Mass (kg) Height (cm) VO2 max (Imin ^) Body Fat (%)
F 2 25.5+2.5 74.5 + 6.0 179.0 ±5.0 4.6+ 0.2 22.0 ± 0.2
M 9 23.8 + 1.4 91.9 + 3.1 191.8 + 1.6 6.2 ±1.2 12.4 ±0.3
Means + S.E.
2. CLIMATIC CONDITIONS
Data for ambient temperature and relative humidity measured daily at midday are presented in Figure 9. During the course of the altitude training camp there was considerable variation in daily temperature (mean 14.8°C, range 9.5-21.5°C) and relative humidity (mean 68.5%, range 40-81%) which highlighted the changeable weather conditions experienced.
112 25 -r 90 - 80 20 -- 70 S -- 60 t E -- 50 3 X -- 40 g ti 10“ -- 30 1 —C — Ambient Temperature -- 20 V —♦ — Relative Humidity -- 10 H 1 h 4 f- H 1 h H H -- 0 CMCO^lOtOh-ODOO Day
Figure 9 Climatic conditions during the altitude training camp
3. TRAINING DATA
Training intensity was graded according to the rowing-specific classification used by
Fischer et al. (1992), based on blood lactate measurements which, in the present study, were taken during each training session. The classification of training for rowing- specific and non-rowing-specific conditioning are presented in Tables 15 and 16.
Table 15 General classification of training intensity [mean (range)].
Training Intensity Lactate (mmolf^) Training Time (min) Training Time (%)
Category I > 8 0 0
Category II 4-8 27.4 (0 - 60) 13.7
Category III 2-4 54.0 (0- 180) 27.1
Category IV < 2 118.3 (0-220) 59.2
113 Table 16 Rowing-specific and non-rowing specific classification of training
intensity
Lactate (mmol.f^) Mean (range)Training Training Time (%)
Time (min)
Rowing-specific:
Category I > 8 0 0
Category II 4-8 16.8 (0-60) 8.4
Category III 2-4 54.0 (0- 180) 27.0
Category IV < 2 69.5 (0-200) 34.8
Non-rowing -specific:
Stretching < 1 7.9 (0-30) 4.0
Walking < 1 22.1 (0-60) 11.1
Running < 1.5 18.9 (0-20) 9.5
Strength 4-8 10.5 (0-50) 5.2
The average daily training time was 200 minutes (range 0-310 minutes), with over
86% of total training being performed at a blood lactate level below 4 mmolf^
(category III and IV). Of the 86% of training performed at categories III and IV, the majority (60%) could be classed as regenerative training (below 2 mmolT^). Over 70% of the total training was on-water rowing-specific with the remainder made up of stretching, walking, running and strength conditioning. The intensity of training was generally lower during the early phase of altitude training and increased in intensity after acclimatisation (Figure 10).
114 Training was performed on a 2.5 day cycle which was followed by a half days rest or active recovery. A detailed breakdown of the altitude training programme is included in Appendix C.
100% o 90% E 80% - O) C c 70% ‘<5 □ Category 4 60% □ CategcryS ■D<0 50% ■ Categcry2 0 40% f □ Category 1 O)(U ts 30% 20% I 1 o. 10%
0% (NcoTfincDNoocnci fMCO-^UO Day Figure 10 Analysis of the training schedule of the elite rowers during the 19 days of altitude training. 4. PHYSIOLOGICAL RESPONSES AND ADAPTATIONS TO THE PERIOD OF ALTITUDE TRAINING Changes in the mean daily values (n=ll) for the physiological variables measured (PaOz, PaC02, HCO3', Hb, Hct, pH, CK, Urea, heart rate and body mass) at rest first thing each morning over the 19 days of the altitude training camp are presented in Figures 10-20. Data are presented as the mean ± 2 S.E.;* = P<0.05, ** = P<0.01, compared with pre-altitude baseline values (day zero). In order to aeeount for possible between-subject variation for the 9 male and 2 female rowers data obtained for body mass, Hb and Het were standardised by subtraeting pre-altitude values from the daily measurement taken during the 19 days at altitude (Figures 18, 20 and 21). 115 4.1. Pa02 and PaCO^ The eflfect of altitude exposure was clearly demonstrated by the changes in PaO] and PaCO]. Within one day of ascent to altitude there was a significant decrease in resting Pa02 and PaCOa, by 34% and 20% respectively, compared to sea level values. PaC02 continued to fall reaching its lowest value of 30.5 mm Hg on day 3. During acute hypoxic phase, there was a marked decrease in both PaO] and PaC 0 2 with a partial restoration towards sea level values with acclimatisation (Figures 11 and 12). The decrease in resting PaC 02 values, which are indicative of respiratory alkalosis, were most pronounced over the first 10 days and then appeared to increase and stabilise during the latter part of the study once acclimatisation had occurred. 4 5 ** ** ** ** ** ** ** ** ** ** I 3 5 d 2 5 0 1 2 3 4 5 6 7 8 910111213141516171819 D ay Figure 11 Changes in PaC02 during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (*=P<0.05;**=P<0.01) The pattern of the Pa02 data was less clear and showed a greater degree of daily fluctuation. This was most evident during the initial period of altitude exposure when acclimatisation was occurring and illustrates the sensitivity of Pa02 measurement. The most significant fall was observed on day 1 at altitude when PaC^ decreased to 72.5 mm Hg. During the following days at altitude Pa02 remained in a reduced state before 116 recovering on day 5 to 99.8 mm Hg, which represented a non-significant decrease of 9.7% compared to pre-altitude values. P49 1—I—I—I—r 1--- 1------1----- 1-----1-----1-----1----- 1----- 1----- 1 I I T 2 3 4 5 6 7 8 910111213141516171819 D ay Figure 12 Changes in Pa02 during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (* <0.05; **=f<0.01) 117 4.2 pH Concomitant with the fall in PaCOz, arterial pH increased and remained above sea level values throughout the period of altitude exposure. Significant increases in pH were observed with acute hypoxia, reaching a peak of 7.45 on day 5, reflecting the expected alkalosis due to the hypoxic ventilatory response. The pattern for pH then gradually decreased towards pre-altitude levels as the acclimatisation process progressed and then stabilised after day 11. Significant increases in pH were again observed towards the end of the study (days 15,17 and 18), possibly reflecting changes in acid base balance as HCOs' was also shown to increase. ** ** ** 7.46 — ** ** 7.45 — S . 7.44 - i 7.43 — 7.42 — 1— I—I—I— 1— I—I—I—I—I—I—I—I—I—I—I—I—I I r 0 1 2 3 4 5 6 7 8 910111213141516171819 D ay Figure 13 Changes in blood pH during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (* =P<0.05; ** =P<0.01) 118 4.3 Blood Bicarbonate (HCOa") The pre-altitude mean resting H C O 3' values fell within the normal range and did not vary significantly at altitude. Resting HCO3’ levels were therefore similar in all conditions both at sea level and at altitude and appear to be independent of altitude exposure or the training regime undertaken. The initial increase of arterial pH was mirrored by a non-significant fall in HCO3* over the same time period, before normalising and remaining relatively stable from day 10 onwards. 27 26 25 I 24 O 23 22 2 1 20 1 9 1 8 0 1 2 3 4 5 6 7 8 9101112131415161718 1 9 D ay Figure 14 Changes in HCO3* during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (*=P<0.05;**=P<0.01) 4.4 Urea and Creatine Kinase In an attempt to monitor the stress of training, serum urea and creatine kinase (CK) levels were measured on a daily basis. Although serum urea levels showed a progressive rise, peaking at 29% (P<0.01) above sea level values, they remained below critical levels (Hubner-Wozniak et al., 1996) throughout the study. Significant increases in serum urea, with the exception of day 5, were observed towards the end of 119 the period of altitude exposure and reached a peak of 7.3 mmoll*^ once acclimatisation had occurred. ** ** ** ** 8 ** ** 7 I 6 5 012345678 9 10 1112 13 14 15 16 17 18 19 Day Figure 15 Changes in serum urea during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (*=P<0.05; **=f<0.01) Similarly there was a significant increase in CK activity reaching a high of 334 U/L, a rise of 217% (P<0.01) above sea level values, peaking after the acclimatisation phase on day 13 before normalising during for the remainder of the altitude study. No significant increase in CK was reported during acute exposure to altitude or during the acclimatisation phase. ** 600 500 400 300 2 00 1 00 0 1 2 3 4 5 6 7 8 910111213141516171819 Day Figure 16 Changes in serum CK during altitude training compared to sea level (day zero) values. Values are means ± 95% confidence intervals (*=P<0.05; **=f<0.01) 120 In order to determine if shifts in PV had any potential effect on the daily variations in urea and CK values, by altering their concentrations, simple linear regression was used to determine if any relationship existed. The data revealed that only a weak relationship existed between changes in PV and the two variables, with PV accounting for only 21% and 28% of the daily variation in urea and CK, respectively. 4.5 Resting Heart Rate Mean resting heart rate increased during acute exposure to altitude and remained above sea level values (48 ± 2 beats min'^) throughout the course of the study with an average daily variation of ± 5 beats min'^ (Figure 17). During the first few days after arrival at altitude there was a progressive increase in the mean resting heart rate. This increase was found to be significantly above sea level values on days 2-6, before beginning to fall and normalise after day 7. The pattern of daily resting heart rate, after the acclimatisation phase was very similar with only a small variation in mean values with the exception of day 12 when again there was a significant increase above pre altitude values (P<0.01). * * * * * I * * e 6 0 I 5 0 4 5 1— I— I— I— I— I— I— I— I— I— I— I— I— I— I— I— I— I— I— r 0 1 2 3 4 5 6 7 8 910111213141516171819 D ay Figure 17 Changes in resting heart rate during altitude training compared to sea level (day zero) values. Values are displayed as means ± 95% confidence intervals (*=f<0.05; **=f<0.01) 121 4.6 Body Mass Despite the implementation of a strict fluid replacement regime during the course of the study, body mass progressively decreased, reaching a minimum at the end of the period of altitude training (Figure 18). Mean body mass loss was 2.7 kg which equated to a mean reduction of 3% (P<0.01) compared to pre-altitude values. The weight loss observed over the duration of the study may be explained by changes in water metabolism which normally occur at altitude. Figure 19 reveals that there was a significant positive relationship between the change in mean daily plasma volume (PV) values and the decrease in body mass (r= 0.64, P=0.003). 0 I ** (/} 1 ** (/} ** (0 ** o 2 m 3 1 2 3 4 5 6 7 8 910111213141516171819 D ay Figure 18 Changes in body mass during altitude training compared to sea level values. Values are displayed as means ± 95% confidence intervals (*=P<0.05; **=f<0.01) 122 0 Y = -1.29588 + 0.198033X r = 0.64 1 E ç 2 ï 1 o 3 1 0 •5 0 Change in P V (% ) Figure 19 Relationship between daily changes in plasma volume (PV) and body mass during the period of altitude training. 4.7 Haemoglobin (Hb) and Haematocrit (Hct) Figures 20 and 21 illustrate the mean standardised pattern of response for Hb and Hct levels for the 11 subjects during the course of the study. Following the 19 days of altitude training there was a significant increase in mean Hb (+6%, P<0.05) while Hct remained nearly constant (+0.4%, ns) when compared to sea level values. * * 00 -i— I—I—I—I—r —T—I— I—I—T" 9 1011 12131415 16171819 D ay Figure 20 Standardised changes in haemoglobin (Hb) during altitude training compared to sea level values. Values are displayed as means + 95% confidence intervals (* =f<0.05; **= f< 0.01) 123 4 3 2 1 X 0 1 2 3 1 2 3 4 5 6 7 8 910111213141516171819 D a y Figure 21 Standardised changes in haematocrit (Hct) during altitude training compared to sea level values. Values are displayed as means ± 95% confidence intervals (* = f <0.05; ** =f<0.01) Further analysis identified that there was a quadratic relationship between pre-altitude Hb values and change in Hb concentration after 19 days altitude training (Figure 22). c 15 0 1 10 I 8 5 X C -726.065 + 104.963X - 3.73224X**2 0 I -0.74 s 13 14 15 16 Initial Hb concentration (g dl'^) Figure 22 Relationship between initial Hb concentration and the change in Hb following altitude training for male and female rowers. When the Hb data for the 2 female subjects was excluded (the two lowest pre-altitude values) simple linear regression revealed that there was a significant negative linear 124 relationship between the magnitude of the increase in Hb and the initial Hb levels (r= - 0.77, P=0.015). This indicated that 59% of the variation in Hb concentrations over the period of altitude training could be accounted for by initial sea level Hb levels (Figure 23). A similar relationship was observed between the increase in Hct after 19 days altitude training and pre-altitude Hct levels (r= -0.66, P=0.05). 20 c 0 1 § 1 0 8 I C i 0 -0.77 ë Ü 13 14 15 16 Initial Hb concentration (g dl‘ ) Figure 23 Relationship between initial Hb concentration and the change in Hb following altitude training for male rowers. 125 6.5 c 0 5.5 ■l 1 B 4.5 O o 3.5 X Y = 1.77754 - 0.471938X 2.5 g Ë o 1 .5 •1 0 ■5 0 Change in P V (% ) Figure 24 Relationship between changes in PV and Hb concentrations during the period of altitude training. Mean pre-altitude PV was taken as a base value of 100, with mean daily values for PV at altitude determined relative to the pre-altitude mean. During the course of the altitude training study, PV fell by 6.2% which almost identically matched the increase in Hb (6%) over the same period. On closer examination simple linear regression revealed a strong relationship between the differences in PV and Hb, with the daily change in PV accounting for 61% of the variation in Hb (Figure 24). 126 5. SUMMARY OF RESULTS Table 17 summarises the average values for the various parameters measured on resting subjects at sea level (pre-training), upon arrival (day 1), midway (day 10) and at the end (day 19) of the altitude training camp. Table 17 Changes in physiological variables pre- and during-altitude training (w=ll) Sea Level Altitude Training Pre-Training Day 1 Day 10 Day 19 Body Mass (kg) 88.7 + 3.38 88.4 ± 3.43 87.1 ± 3.19** 86.1 ± 3.22** Resting Heart Rate 48 + 1.81 52 ± 2.05 52 ± 2.69 52 ± 1.36 (beatmin'^) Haemoglobin 14.7 ± 0.32 15.0 ± 0.32 15.1 ± 0.21 15.6 ± 0.36* (gdf') Haematocrit (%) 44.5 + 0.87 44.7 ± 0.82 44.1 ± 0.50 44.2 ± 0.93 HCOj' (mmolT‘) 24.1 ± 1.36 24.0 ± 1.43 23.4 ± 1.11 23.6 ± 0.86 87.4 ± 7.33 85.3 ± 6.67 PÜ2 (mm Hg) 110.5 ± 6.28 72.5 ± 4.68** 33.4 ± 2.11** 34.2 ± 1.13* PCÜ2 (mm Hg) 43.4 ± 1.31 34.7 ± 2.15** pH 7.42 ± 0.003 7.43 ± 0.006 7.43 ± 0.003 7.43 ± 0.003 Creatine Kinase 105.3 ± 11.9 112.3 ± 10.5 217.6 ± 30.7 224.8 ± 53.3 (pT') Urea (mmol 1'^) 5.69 ± 0.32 5.98 ± 0.32 6.38 ± 0.25 7.02 ± 0.33** Means ± S.E.; * =P<0.05; ** =P<0.01 127 6. CHANGES EV THE SUBMAXIMAL BLOOD LACTATE RESPONSE TO EXERCISE Differences pre- and post- altitude training were assessed using paired Student t-tests, and the data are expressed in Table 18. Table 18 Changes in physiological variables pre-and post- altitude training («=19). Pre- Training Post- Training Lactate (mmolf^) rest 0.86 ±0.27 0.80 ±0.31 Lactate (mmol 1*^) 4 min 2.28 ±0.54 1.90 ±0.52** Lactate (mmolf^) 10 min 2.74 ±0.90 2.61 ±1.0 Heart Rate 4 min (beats'min'^) 158 ±10 161 ±10* Heart rate 10 min (beats min'^) 169 ±10 174 ±10** Hb (g dl'b 15.7 ±1.0 15.3 ±0.9* HCOs- (mmolT') 25.8 ±2.7 25.9 ±2.3 Means ± S.E.; * =P<0.05, ** =P<0.01 There was a significant decrease in blood lactate at 4 min (P<0.01), while no change was observed at rest and 10 min. A significant increase in heart rate at 4 min (P<0.05) and 10 min (P<0.01) was observed pre- and post-altitude training. Following altitude training Hb significantly decreased while no significant change was observed for HCOs'. 128 DISCUSSION Altitude training is frequently used by elite athletes, including rowers, in an attempt to enhance sea level performance. Many endurance athletes now regard altitude training as an integral part of their preparation for major competition. Jurgen Grobler, Director of Coaching for the Great Britain Rowing Team, reported that about 50% of rowing nations used altitude training in their preparation for the 1993 World Championships (personal communication). Despite its popularity among coaches and several attempts to investigate its impact on sea level performance, the effectiveness of altitude training remains unclear. Few studies have used elite athletes and those which have done so generally show no training effect or are inconclusive. Due to logistical reasons, there is a dearth of information relating to elite athletes undertaking prolonged periods of altitude training in preparation for competition. Studies using highly trained athletes are, therefore, not easily controlled. Nevertheless, the nature of rowing (i.e. groups of subjects in one boat) is probably the closest that can be achieved in terms of experimental control in a practical setting. The present study examined the influence of altitude training on a number of physiological parameters in order to evaluate the rate and process of adaptation to a hypoxic environment as well as determining the effect on submaximal exercise performance following chronic altitude exposure. It was hypothesised that there is no significant improvement in aerobic conditioning, as determined by a fall in submaximal blood lactate concentration, as a result of the measured physiological adaptations that occur in response to altitude training. The observed decrease in blood lactate concentration after 4 minutes of submaximal exercise may be explained by lower lactate appearance due to reduced net lactate release by the exercising muscles (Bender et al., 1989; Mac Rae et al., 1992). The possibility of increased metabolic capacity for lactate oxidation may also provide a possible explanation for this reduction seen during acute exercise (Ingjer and Myhre, 1992). However, after 10 minutes of ergometer rowing at a fixed exercise intensity, no 129 significant decrease in blood lactate concentration was observed. The lack of any significant reduction in blood lactate accumulation observed during prolonged submaximal exercise after altitude training compared to sea levels values has been reported previously (Knuttgen and Saltin, 1973; McLellan et al., 1988; Svedenhag et al., 1991; Warrington et al., 1996; Young et al., 1982). Young et al. (1982), reported no difference in the blood lactate response during submaximal cycling exercise following 3 weeks altitude training. Similarly, Svedenhag et al. (1991) found submaximal blood lactate values to be unaltered in a group of elite middle distance runners following 2 weeks training at 2000 metres, which led them to conclude that after re-acclimatisation, altitude training had no effect in these regards. This concurs with a study by Warrington et al. (1996), which found no significant reduction in the blood lactate response during prolonged submaximal exercise, at the individual lactate threshold, following 17 days altitude training at 1850-2000 metres in a group of elite female rowers. The subjects in the present study were highly trained rowers including World and Olympic champions and medalists, who already possessed very high levels of endurance conditioning prior to the period of altitude training. Therefore 17 days of additional training, albeit at altitude, prior to major international competition in world- class athletes would provide only limited potential to elicit further gains in submaximal work capacity. Additionally, altitude training represented approximately 6% of the total annual training programme, in terms of volume, performed by the subjects. Therefore, there may be limited scope for evidence of physiological change as a result. However at this elite level, a small but non-significant improvement in performance may represent the difference between winning and losing in competition. In the final of the men’s heavyweight coxed pairs at the 1992 Olympics, 1.75 seconds spanned the times for the gold, silver and bronze medal winners, a non-significant time differential of 0.4% of the total race duration. Fry et al. (1993) cite a similar example from the 1991 World Canoe Championship where a non-significant performance decrement of less than 2.5% would have excluded the eventual winner of the competition from even qualifying for the final. 130 During the course of the altitude training camp there was considerable variation in daily temperature (mean 14.8“C, range 9.5-21.5°C) and relative humidity (mean 68.5%, range 40-81) which highlighted the changeable weather conditions experienced. Shephard (1991) has previously reported the variations in weather conditions associated with altitude exposure and stated that there is a tendency for ambient temperature to be reduced by approximately 2°C for every 300m ascended. Mean values for haemoglobin (Hb) and haematocrit (Hct) observed in the present study are comparable to those previously reported for elite althletes (Ingjer and Myhre, 1992), with Hb increasing significantly during the course of the study. The magnitude of increase in Hb is similar to previous studies (Balke et al., 1965; Faulkner et al., 1967; Horstman et al., 1980; Ingjer and Myhre, 1992; Reynafarje, 1967), and appears to reflect an increase in haemoconcentration due to a reduction in plasma volume (PV) and to a lesser degree erythropoiesis during the latter part of the study. Terrados et al. (1988) and Weil et al. (1968) have shown that red cell mass does not increase until PaOi falls below 65 mm Hg, which equates to an altitude of 2200-2500 metres. However, this needs to be balanced against a potential detraining effect, because at higher elevations athletes would not be able to train at sufficient intensity to maintain aerobic fitness levels (Jackson and Sharkey, 1988; Levine et al., 1991). Consequently, short-term exposure (2 weeks) to moderate altitudes has not shown an increase in Hct or Hb concentrations (Humpeler et al.,1979; Mairbaurl et al., 1986). Where increases in Hb have been observed, after short-term exposure to altitude, they have been shown to be as a consequence of a reduction in plasma volume as opposed to erythropoiesis (Kaung and Peterson, 1962; Mairbaurl, 1994; Stokke et al., 1986). During more prolonged exposure to hypoxia, it has been speculated that the stimulation of erythropoesis in subjects performing altitude training might be attributed to a repeated loss of red cells due to the increased relative stress of training in hypoxia (Berglund, 1992; Mairbaurl et al., 1983). A more accentuated decrease in plasma volume (PV) in endurance-trained athletes compared to non-endurance trained athletes at altitude has previously been reported (Berglund et al., 1992), which may account for the observed increase in Hb concentration in the present study. Transient changes in Hb and Hct due to changes in PV followed by a parallel but initially slow increase in Hb have 131 previously been reported (Dill et al., 1974; Milledge and Cotes, 1985). This may not only reflect changes in PV and red blood cell (RBC) mass but also a possible synergistic effect between hypoxia and endurance exercise on erythropoiesis (Berglund et al., 1992). In the present study, changes in PV were calculated from the Hb and Hct data according to Dill and Costill (1974) as opposed to the computation of changes in PV based solely on variations in Hct (Van Beaumont, 1972). The latter method may be unreliable due to distortions caused by alterations in the volume of the red blood cells (Dill and Costill, 1974). Dill et al. (1969), reported that since only small divergence rates between calculated and observed values for PV were found, it was possible to predict PV changes as frequently as Hb was determined so long as cell volume (CV) remained unchanged. During the course of the altitude training study, reported here, PV fell by 6.2% which almost identically matched the increase in Hb (6%) over the same period. This would strongly suggest that any increase in RBC volume was a reflection of an increase in haemoconcentration due a shift in plasma volume rather than a true increase in Hb (Dill et al., 1974). It has previously been suggested that the relatively greater increase in Hb compared to haematocrit ratio, as observed in the present study, implies an increase in the mean corpuscular Hb concentration, thereby enhancing the oxygen-carrying capacity without an increase in blood viscosity (Faulkner et al., 1967). Increases in Hb during the period of altitude training demonstrated considerable individual variation and appeared to be dependent on initial Hb levels. When the Hb data for the 2 female subjects was excluded (the two lowest pre-altitude values), simple linear regression revealed that there was a significant negative relationship between the magnitude of the increase in Hb and the initial Hb levels (r= -0.77, P=0.015). This was identical to the relationship observed by Ingjer and Myhre (1992), and indicated that 59% of the variation in Hb concentrations over the period of altitude training could be accounted for by initial sea level Hb values. The findings of both studies indicate that when initial Hb levels were greater than a critical level of 14 g dl'^ then a significant linear relationship exists between initial Hb and the magnitude of increase in Hb concentration following a period of training at moderate altitude. 132 Consequently, those subjects with the lowest pre-altitude Hb experienced the greatest increase in Hb levels and therefore, from a haematological perspective, had the greatest potential to enhance oxygen transport capacity. Immediately upon ascent to altitude, PaOz and PaCOi decreased sharply and then increased gradually during more prolonged exposure. The observed falls in PaOz and PaCOz are comparable to those reported elsewhere for similar altitudes (Levine et al, 1992; Roskamm et al, 1969). The pattern of resting Pa02 exhibited a higher degree of daily fluctuation and highlights the sensitivity of measurement. In the determination of PaOi, measurement errors may result from the use of an ear oximeter or warmed venous blood rather than arterial blood, the calculation of PO 2 from pH and oxygen saturation, and the lack of knowledge of inter-arterial pressure among other factors (Hansen et al, 1967). Since it is not possible to measure intra-cellular oxygen tension, Pa0 2 has become a standard for clinical evaluation of arterial oxygenation status. Although not a measurement of the oxygen content, this provides a measurement tool to evaluate pulmonary gas exchange efficiency from an arterial blood sample. The measurement of PaC02 is essential in determining ventilatory status. Reduced PaC02 values at rest during acute altitude exposure are indicative of respiratory alkalosis (Kayser et al, 1993), and may provide a more reliable marker of the process of acclimatisation to a hypoxic environment (Milledge, personal communication). Exposure to reduced Pa02 results in a Anther increase in pulmonary ventilation at a given exercise intensity. This hypernea will cause a rise in PaÛ 2 and Anther reduce PaC02 in alveolar air. The combined determination of pH and PaC02 provide a more definitive diagnostic tool in assessing respiratory function and can be incorporated into the Henderson-Hasselbach equation to determine HCOs* (Filley, 1971). Since the PaC02 value is proportional to the content of dissolved CO2/ HCO3’, the value for PCO2 can be used with pH not only to calculate H C O 3, but also to aid in the differentiation of acid-base abnormalities (Beetham, 1982). The interplay between the changes in PaC02 and HCOs* during acclimatisation appears to result in a variable degree of correction in arterial blood pH (Gonzalez et al, 1991). Reduced PaC02 and elevated arterial pH during acute altitude exposure, due to respiratory alkalosis, have previously been shown to exert an inhibitory influence on 133 the respiratory system (Âstrand and Rodahl, 1986). In earlier studies, alkalosis caused by hyperventilation has been suggested a factor causing the increase in red cell 2,3- DPG during adaptation to altitude (Lenfant et al., 1968). Although 2,3-DPG was not measured in the present study, significant increases in pH were observed with acute hypoxic exposure, peaking on day 5, reflecting the expected alkalosis due to the hypoxic ventilatory response which has been well documented (Lenfant et al., 1971; Schoene et al., 1984). The acute increase in resting blood pH is similar to that reported in other altitude studies (Kayser et al., 1993; Levine et al., 1992; McLellan et al., 1988). During exposure to altitude, ventilation continues to increase and remains elevated over the first few days, which may extend to weeks of acclimatisation (Levine et al., 1992). The subsequent lowering of pH observed in the present study during more prolonged exposure, is likely to be induced by the decreased blood buffering capacity due to compensatory respiratory alkalosis (Kayser, 1994). The initial increase of arterial pH was mirrored by a non-significant fall in HCO3' over the same time period, before normalising and remaining relatively stable from day 10 onwards. This reflects a gradual renal bicarbonate excretion in response to respiratory alkalosis, caused by the sudden exposure to hypoxia, in an attempt to return pH to equilibrium, which occurs in the acclimatised individual (Boning et al., 1980; Kayser et al., 1993). The resting values for HCO3' fell within the normal range and were in agreement with an earlier study (Roskamm et al., 1969), which reported no significant variation in values recorded during 4 weeks training at 2250 or 3450 metres. Similarly, Warrington et al. (1996), observed no change in HCO3' following 17 days altitude training in a group of elite female rowers. In contrast Lenfant et al. (1971) observed a progressive reduction in HCO3' during 4 days exposure at a higher altitude of 4509 metres. After return to sea level HCO3' reverted to normal. The weight loss observed over the duration of the study may be explained by changes in water metabolism which normally occur at altitude. During acclimatisation a decrease in intra- and extra- cellular water occurs as well reductions in PV. The decreases in PV and in body mass are associated changes often observed at altitude (Dill et al., 1974; Hoyt et al., 1992; Jain et al., 1980; Krzywicki et al., 1971; Wolfel et al., 1991). This was substantiated by the current findings in that there was a strong positive relationship between mean daily variations in PV and body mass (r=0.64. 134 f =0.003). This indicates that 41% of the reduction in body mass could be accounted for by decreases in PV caused by dehydration partly through respiration and/or changes in water metabolism (Boyer et al., 1984; Consolazio et al., 1968; Krzywicki et al., 1971). The 3% reduction in mean body mass observed in the present study is similar to those reported elsewhere for comparable altitudes (Dill et al., 1974; Kayser et al, 1993; Wolfel et al, 1991) and for higher elevations (Guilland and Klepping, 1985; Klausen et al, 1970; Maher et al, 1974). Although reductions in PV and/or alterations in water metabolism may partly explain the decrease in body mass observed during the course of the 19 days of altitude training other mitigating factors may have a role to play. A discrepancy between caloric consumption and expenditure due to a reduction in energy intake in addition to increased basal metabolic rate (BMR) and relative activity levels, particularly in the acclimatisation period, have been reported (Butterfield et al, 1992; Consolazio et al, Kayser et al, 1992). During more prolonged altitude exposure, particularly at higher elevations, a large proportion of weight loss has been associated with a reduction in muscle mass (Green et al, 1989a; Hoppeler et al, 1990; MacDougall et al, 1991; Rose et a l,1988), resulting from an energy deficit which is offset by catabolism of body tissue (Guilland and Klepping, 1985). However, for moderate altitudes up to about 5000 metres losses of fat and muscle appear to be minimised by increasing energy intake (Kayser, 1994). Although a strict fluid replacement regime was implemented over the course of the study, the nutritional and metabolic status of the subjects was not monitored. Food intake has generally been shown to be reduced during the acclimatisation phase of altitude training (Guilland and Klepping, 1985; Hannon, 1981; Kayser, 1992). Therefore, if increases in BMR are not matched by an appropriate rise in energy intake a reduction in body mass will ensue. Strategies which attempt to balance energy intake with increased expenditure at altitude have proved to be successfial in minimising weight loss (Butterfield et al, 1992; Kayser et al, 1993; Wolfel et al, 1991). In addition, it appears that the severity of weight loss is dependent on the duration of sojourn and the height of altitude exposure (Boyer et al, 1984; Butterfield et al, 1992; Guilland and Klepping, 1985; Kayser, 1994). 135 It is well established that during periods of intense training, subjects may experience increases in resting heart rate, serum urea and CK levels (Dressendorfer et al., 1985; Kirwan et al., 1988; Noakes, 1987; Stray-Gundersen et al., 1986; Urhausen and Kinderman, 1992; Verma et al., 1978). Exercise-related increases in urea are associated with enhanced protein catabolism (Haralambie and Berg, 1976; Plante and Houston, 1984) and/or a reduced rate of clearance (Decombaz et al., 1979; Lemon and Mullen, 1980). Variations in serum urea concentrations have been shown to be influenced by nutritional considerations and deficiencies in fluid intake (Haralambie and Berg, 1976; Urhausen and Kindermann, 1992). In order to minimise the effect these factors had on daily serum urea measurements, samples were taken first thing in the morning and under fasting conditions. Additionally, as previously mentioned, a strict fluid replacement regime was implemented over the course of the study. During the study, serum urea levels remained below critical values (Hubner-Wozniak et al., 1996; Urhausen and Kindermann, 1992). The significant rise in serum urea, which peaked and remained in an elevated state towards the end of the study, would indicate that any increases were associated with the progressive increase in training load after the acclimatisation phase rather than the hypoxic stimulus per se. Although training intensity gradually increased as the period of altitude training progressed, the exercise load remained predominantly aerobic in nature with 86% of total training time performed at a blood lactate level below 4 mmol l'\ Additionally, daily training volume remained high throughout the study and averaged 200 minutes per day. Urea concentrations have been reported to increase following prolonged exercise (Decombaz et al., 1979; Haralambie and Berg, 1983; Knuttgen et al., 1971; Rennie et al., 1980). Urhausen and Kindermann (1992) observed that brief periods of high intensity intermittent exercise did not induce any critical changes in blood urea concentration. It appears, therefore, that urea reacts more sensitively to aerobic rather than anaerobic exercise (Urhausen and Kindermann, 1992). Berg (1977), has proposed that where serum urea levels exceed a critical level of 8-10 mmoll'^ for several days, training intensity should be reduced. In support of this contention, Hollman (1994) has 136 suggested that during altitude training there is a decrement in performance when serum urea levels were elevated above 8.5 mmoH'\ In contrast, due to the varying basal urea concentrations observed for different individuals, Lehmann et al. (1985) have suggested that under standardised conditions, a marked increase in blood urea during a particular phase of training might be a more appropriate marker of metabolic strain, resulting in a subsequent reduction in training load. In one training study involving elite female rowers (Kindermann, 1986) elevated urea levels, indicating overstrain, were reduced by immediately undertaking a week of regenerative training at an intensity which elicited blood lactate levels below 2 mmoH'\ Post exercise levels of CK have previously been related to the intensity and type of exercise together with the level of muscular strain (Apple and Rogers, 1986; Clarkson and Tremblay, 1988; Costill et al., 1991; Hortobagyi and Denahan, 1989; Noakes, 1987; Schneider et al., 1995; Urhausen and Kindermann, 1992). The precise mechanisms for CK efflux have not been established, but hypoxia, depletion of energy sources and mechanical disruption at the cellular level have thought to be factors involved in exercise induced CK release from skeletal muscle (Mayer and Clarkson, 1984). In the present study, no significant increase in CK was reported during acute exposure to altitude or during the acclimatisation phase, when the training intensity was generally lower. This would tend to indicate that the significant increases observed on days 12 and 13 were associated with the increased training load during the latter part of the training camp and to a lesser degree the hypoxic environment. However, exposure to altitude has previously been shown to lead to an increase in serum enzyme activity (Highman and Altland, 1960). CK levels measured in the morning primarily representing release during the previous day, are also influenced by the rate of CK clearance and have been shown to display considerable individual variation (Apple and Rogers, 1986; Costill et al., 1991; Hortobagyi and Denahan, 1989; King et al., 1976; Noakes, 1987). Prolonged daily training (> 2 hours) or competition in weight bearing activities has been shown to produce chronically elevated serum CK levels. However, an adaptive response has been suggested, as serum enzyme activities continue to decrease with training (Noakes, 1987). Lower increases in CK activity in non-weight 137 bearing exercise of a predominantly concentric and isometric nature such as cycling (Berg and Haralambie, 1978) and swimming (Costill et al., 1991; Flynn et al., 1994), have been attributed to changes in membrane permeability in fatigued muscle. In contrast, weight-bearing activities where the eccentric component of muscle contraction is accentuated, in particular during running activities, greater increases in enzyme responses have been reported (Fry et al., 1993; Newham et al, 1986; Verde et al, 1992). Several studies have reported an increase in serum CK activity following eccentric exercise, whereas no increase was observed for subjects who exercised concentrically or isometrically (Friden et al, 1989; Schwane et al, 1983). In contrast to other non weight-bearing activities, greater increases in CK levels have been reported after rowing exercise (Altenberg, 1992; Fry et al, 1993). This may reflect the complex nature of the rowing stroke which places a stronger emphasis on isometric, eccentric as well as the concentric component of muscle contraction (Kramer et al, 1991; Mahler et al, 1984b). Although tachycardia during exercise is one of the most commonly observed responses to altitude exposure, few studies have reported data at rest. The increases in resting heart rate observed are in agreement with previous altitude studies and appear to increase in proportion with the severity of acute hypoxia (Dill et al, 1967; Klausen, 1966; Klausen et al, 1970; Lahiri et al, 1967). In contrast to the urea and CK data, mean resting heart rate values seemed to respond independently of training load as they were elevated during acute altitude exposure, when falls in Pa 0 2 were greatest, and normalised as the acclimatisation phase progressed and training intensity increased. Whilst remaining above sea level values, the pattern of mean resting heart rate after an initial significant elevation, normalised and remained very similar, displaying little daily variation, with the exception of day 12. This was supported by an earlier study by Lahiri et al. (1967), which compared the resting heart rates of altitude natives (Sherpas) and sea level residents exercising at altitude. Resting heart rates for the Sherpa subjects were generally lower than the sea level residents for a given altitude. Conversely, the rate of increase in heart rate during cycling exercise at a fixed work rate was greater in the Sherpas at altitude. This would indicate that increases in resting heart rate observed in the lowlanders were associated with the hypoxic stimulus rather than the training undertaken. In contrast to the current finding, a number of sea level 138 based training studies have reported an association between elevated resting heart rates and an increased training load (Dressendorfer et al., 1985; Stray-Gundersen et al., 1986). It has been speculated that such elevations in resting heart rate values are due to increased neuroendocrine influences (Dressendorfer et al., 1985; Kuipers and Keizer, 1988). However, the precise mechanism for elevated basal heart rate remains unclear (Hackney et al., 1990). SUMMARY, CONCLUSIONS AND RECOMMENDATIONS A review of the accumulating body of scientific evidence suggests that altitude training offers little advantage over training at sea level. To date, little research has been published concerning the physiological effects of altitude training in elite athletes. The present study attempted to assess the effectiveness of altitude training in a group of elite rowers by monitoring the physiological responses and adaptations that occur during training in a hypoxic environment and to evaluate the impact of these adaptations on aerobic work capacity on return to sea level. The findings of the present study revealed that there was a significant change in a number of the physiological variables measured during the period of altitude training when compared to sea level values, therefore the null hypothesis (see page 4) was rejected. It appears that those subjects with the lowest initial Hb levels generally experience the greatest increase following altitude training. Any potential increase in Hb in response to a reduction in PaOz appears to reflect an increase in haemoconcentration due to the observed decrease in PV and to a lesser degree erythropoiesis. Although there was a significant increase in mean Hb concentration during the course to the study compared to pre-altitude values, no significant difference was observed for HCO3'. Resting heart rate and blood pH were found to be significantly elevated during altitude acclimatisation before normalising during the latter part of the study. Significant decreases were observed for body mass which continued to fall throughout the period of altitude training and was closely related to changes in PV. CK and urea levels were found to be significantly elevated after the period of acclimatisation, which tended to indicate that any increases were associated 139 with a progressive increase in training load, after this phase, rather than the hypoxic stimulusper se. In a separate part of the study, aerobic work capacity as determined by a reduction in blood lactate concentrations at a fixed exercise intensity was found to be unchanged in response to altitude training. The null hypothesis (see page 4) was therefore accepted. Further research, incorporating matched controls, using highly trained subjects is required. These studies should incorporate submaximal evaluation as well as the use performance tests as a means of determining the effectiveness of altitude training in enhancing the sea level performance of elite athletes. 140 OVERALL SUMMARY In contrast to other traditional endurance activities such as running and cycling, a comprehensive review of the literature revealed there to be a dearth of information relating to rowing. The present study is the first to measure such a wide range of physiological and descriptive variables and relate them to training and performance in a group of elite heavyweight rowers. Over the course of the current study, the three experiments undertaken, have sought address the following issues: 1) To identify what physiological parameters best predict rowing performance 2) To evaluate how these physiological parameters vary with training 3) To monitor the physiological responses and adaptations resulting fi-om a period of altitude training and to identify whether there was any impact on performance on return to sea level. The findings of the first experiment revealed that of the 22 variables measured, VO2 max expressed in absolute terms (Imin^), was the single best predictor of rowing performance for both of the two performance tests used. The addition of further variables to the predictor models added no great advantage but necessitated further physiological analysis. The use of the predictor equations developed to predict rowing performance produced an identical performance ranking order as that achieved in the actual performance test. This underlines the importance of VO2 max to rowing performance. Once it was established which key physiological variables were most closely related to performance, a natural progression was to identify how these parameters varied in response to training. Following the 3 month training period it was revealed that there was no significant change in FD 2 max. In contrast, submaximal variables including 141 .1-1 rowing economy and the exercise intensity attained a blood lactate level of 4 mmol l where found to have significantly improved. This might suggest that such submaximal variables are more sensitive measures of responses to training as they reflect peripheral adaptation. The lack of increase in VO2 max may reflect the phase of training and also training status of the subjects which would preclude them from large physical improvements. The findings of the first two experiments therefore suggest that fractional utlisation, enhanced ability to generate power and rowing economy, in addition to a high VO2 max, may be important to actual rowing performance in elite rowers. The difficulty to elicit further training gains in elite rowers has led many to experiment with alternative training methods. One such method commonly used by endurance athletes is altitude training. The final experiment sought to examine the impact of a period of altitude training on a number of physiological parameters in order to evaluate the process of adaptation to a hypoxic environment as well as determining its effect on submaximal work capacity on return to sea level. The findings of this experiment revealed that there was a significant change in a number of physiological variables measured during the period of altitude training when compared to initial sea level values. This included a marked individual variation in a number of parameters including CK, urea and Hb. In a separate part of the study, no significant improvement was observed in submaximal work capacity on return to sea level. 142 FUTURE RESEARCH DIRECTIONS In light of the current findings future research should focus on the following areas: • Further research is required to determine whether a similar relationship exists between the various physiological variables measured and rowing performance in lightweight rowers. • Specific tests to evaluate the importance of strength and anaerobic capacity in rowing need to be developed in order to determine their contribution in predicting rowing performance. • Laboratory analysis should be extended to on-water rowing to establish whether a similar relationship exists between actual rowing performance and the various physiological parameters measured. • Further work is required to identify optimal training intensities and to evaluate the specific effects of training and the subsequent impact on rowing performance. • The use of more standardised training programmes by elite rowers training in the national squad should allow a more specific evaluation of the physiological responses to the training undertaken. • The duration of longitudinal training studies should be extended to evaluate seasonal variation in training response. » Any observed improvements in physiological parameters in response to training should be further investigated to determine whether they are associated with improvements in performance. 143 Further altitude training studies are required incorporating matched controls, using highly trained subjects. 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The testing will involve some or all of the following 4 main areas of examination; 1) Anthropometric Assessment 2) Maximal Aerobic Power (FO 2 max) Assessment 3) Determination of the individual lactate threshold (ITl a c ) 4) Performance testing The anthropometric profiling will incorporate measurements of height, weight, circumferences, breadths and body composition. Body composition will be determined by skinfold measurements. These measurements will require pinching small folds of skin at 4 different sites. The purpose of the lactate profile and VO2 max test is to measure your endurance capacity, assess the effectiveness of your past training, establish appropriate training intensities and help to identify priorities for fixture training programmes. This is done by measuring the amount of oxygen you inhale/exhale, your heart rates and blood lactate accumulation during a test on a rowing ergometer. The tests will consist of two main sections; (1) to establish a lactate profile (2) to establish maximum aerobic power (ÊO 2 max). Prior to the test: You will be given instructions on and allowed to familiarise yourself with the test procedures/equipment, about rowing on the ergometer and breathing through the collection system and you will be allowed to practice. A belt with built in electrodes will be strapped to your chest for the purposes of recording heart rates. This will be worn throughout the test. To assess blood lactate, blood sampling will be performed by a skilled professional pre, during and post test. For this purpose an ear lobe will be pricked and a small drop of blood will be drawn. There will be little discomfort associated with the procedure, there may, however, be slight bruising at the point of puncture. Test Protocol: Prior to the test there is a standardised warm up. The test will start at a predetermined comfortable pace and stroke rate will be controlled for each increment. To establish a lactate profile you all be asked to perform a number of 3 minute increments on the ergometer. After each 3 minute stage heart rates will be recorded, and a lactate sample will be taken. Following a 30 second recovery the test will re-commence with an increased workload of 27.5 watts. Heart rate and oxygen uptake will be measured throughout the test. The testing session may also include a 6 minute maximal test to determine VO2 max. The VO2 max test protocol will be performed following a minimum 2 hour recovery period. This will involve a 6 minute maximal under competition conditions. Again heart rate and oxygen uptake will be recorded throughout the test. At the end of the 6 minutes the test is terminated and blood samples are taken at 2 and 5 minutes post exercise to determined peak blood lactate concentration. Although you will be undergoing exercise to the point of exhaustion, there is very little risk involved if you are a normal healthy individual. This test will be administered using the same procedures and protocols as the 4 minute maximal test and the same conditions apply. Any questions about the procedures used in the exercise testing is encouraged. If you have any doubts or questions, please ask for a further explanation. Information you possess about your health status or previous experiences of unusual feelings with physical effort may affect the safety and value of the testing. Your prompt reporting of feelings with effort during the testing itself is also of great importance. You are responsible to hilly disclose such information to the testing staff. I have read and understood the explanation of the test purpose and procedures. I consent to participate in the tests. I confirm that I am in a normal healthy state to perform the tests and there is no reason why I should not participate in this testing session. I also understand that I am free to withdraw my consent at any time. Date: Signature of Athlete Signature of Witness APPENDIX C Training Programmes 3 Month Training Programme (November - February) 4 î l 3 > m î m J Ô 1 . lî 9l O' c/) cj or c r c r Ol c r ^ â o- oJ cT o. c r % o O oJ cr - q <2^ H a •f— 0 )^ 0 . ^C.W gS\>-»-fe: K VV€Av’^*^feVSH*ÿ\« <• (Vmw) ofi Civfeft %oJT6^ 3\rtAcw,^j(^ _JZIm_\>6)CjALL6if^S-J2ML_eÆ.Znm--Se&&LÇj:A_J*^U :JIG&sw — L>a,Hr(^ . _ & Ï M i t o 4 > ------ 4> "^uGjN^ im*:][(L4k\<44t4.Qy. . . - AfM v.*^.M t t~~\ A v 'H (-iM ^ I f 4^?" A u - TtH- \A5C- , -7T- :z:__ L f r G ? ...... r%A)CR- PoùU" CtfeAjL T w t o - --_ Vfi_tXX_ 6 yg) ÊXG S . 2 % ^ KG G K G 2 S ^ ^o/^^ C ’ tc ,'9 l é K S # G K S S.s^ G x ^ G k S" Z j a . ^ , <■ k 1 Mju M V ( p o S . MA t// v< ÊKU VO 7 X 4 ^o/o V lA o.< î( ? 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B (2ZA*o _ h I'.wr—'^A^'S.o = A r "THuO. ■?-'^-9 ï_ B _ ^ ( 2 c \C \L ^ = <2.0 T -^ ’3> - 5k«y. j2«^_r% Sc.V V ^ 'o U r % HS.-T. dj&'r\V\.CevST^ t\%C- '^S'CVs^G- y/^ No?_V^/&t^>t 'W 'O ovj^ dcCAfi 1 ^ . 3 ^ '•^ e M (Lvv^ "TANCU % .SLG. ' !» ' 9 1 . "7x w Sl\o^ sc r-'M cttdft.IHES FOR WEEKLY EKDOBAKCE TSAlUim S E S S I ^ PREPARATION COHPETITIOM PEEK® CODE PERIOD Late General S p e c ific Early (UteT SEPTEHBER FEB-Î1AR (2) "(I) OUH - T OUD - T AT OT LT ALT - T TOTAL NO 14 - 8 SESSIONS 12-6 NOTES; 1. Denotes overlap of training effect. 2. Additional Sessions should be OÜÎI or ODD Training 3. This excludes all modes of Strength Training. IS DRAFT: FOR DISCUSSION - AUTUMN 199 (APPEKDIX-IV) . m s FD& KEEXLY STSEPGÎH TEAIMIjIg PREPARATION PERIOD CCmPETITION PERIOD TRANSITION ------— PERIOD 7tPgTL/ M Y—TtmETStOTST ------CSEPTT" 6S - T BS - T m ES - T SE - (2 - 0) mTES: FS - T May be modified towards Strength Retention during the Competition Period. Front Squat/Power Clean/Horizontal Rowing should be done 3 X -per week (to minimise stiffness) with only 2 - 3 sets per session* SE - T Can be continued throughout the Competition Period instead of/as well as OT - T in the boat. 1-1 CO osas «0 o o s i X V) % r* o o o c H u • M M to *o. i M M W» to fa. It* « It* Ü o *> x> o o X3Cw *-» -r* w M o ^ fa. •< o o O) * A m .«-I* -c-* DUO r 4 C M (-« U w => *<____ a CO M M o as o . 40- toM •o : CM CO O r > CM - O CM CM COCO CO CM p.- ■g w v-c f CM o ** t: *» CO o • CM CO to kltc mw o X o ■ CM o o u 4C 0> JQ o OtfM C vM O C H > , v i -rC «M . O =3 Q f-* O Û DRAFT: FOR DISCUSSION - AUTÜWI 1991 (AFFJSKDIX-III) REA - CTASSIFICRTIOH OF STBEKGIg RKD FLEXIBILITY TRAINING - 1990 SE - T GF - T GS-T MS - T FST ES - T Huscle Groig Eophasls 1 Legs 3 2 1 2 3 ---- 2---— -Legfl-6-5stck ------2 ------■ "2•> 0- 1 Back 2 1 1 1 1 Mxiomin&ls 2 1 1 Ana Flexion 2 1 1 1 Ana Extension 1 1 1 1 3 - 5 4 - 6 TOTAL 10 - 12 6 - 8 4 — 6 6 - 7 40-60% % tSaximua Body Wt - 65-75% 60-95% 60-75% Body Wt a ^centriu — 40/50%- - 40- —- 70 Ho. Repetitions 20 30 10 15 3 - 8 -0.-10 10— 20 Ko. Sets/ 2 - 5 Circuits 2 - 4 3 - 4 4 - 6 3 - 5 2 - 4 Explosive Fluent Speed of Fluent Fluent Fluent Fast a 24 - 28 Kovement Fluent a Fluent Reps/Bin CIRCUIT/ KETHOD 1 CIRCUIT CIRCUIT STATION CIRCUIT CIRCUIT STATION INTER HETHOD 2 CONTINUOUS INTER INTER INTER INTER MITTENT MITTENT MITTENT MITTENT MITTENT/ CONTINUOUS 1:1 Recovery/ None 1:2 2:3 1:2 1:2 (1-2 Rest (3-4 (3-5 (2-3 (3-4 rains) mins) Bins) Bins) Bins) 600-1000 TOTAL NO. 500-1500 400-500 220-240 180-210 100-300 REPS notes: These circuits are tabled in the general developmental orderu s e d th rou gh out thilnnual training cycle. The table gives guidelines to the main emphasis and method of execution. Altitude Training Programme (1992) CM CJ a 0» o> 3 CM UÎ X L (£> O _ e I OJ ^ lO to o to <0 o * - CM 04 0 E o O) 01 X 5 _X T- o o L CM a CD a CD 3 OJ c OJ 3 cn Ml Ml E c CM CO E o Ml 1 o> \ CD o CO «3 rt <0 o I e CM 3C 3 : 3c CM <0 ■M >V E •— cO E CO E 3c -M o i-t - 5 X - X CX o o a: o o cx o o Li. OJ OJ X ex CO CM X cr O J OJ o o to CX fO <0 +-> CM *-) 1 CD Q) 1 CD (M a L. 1 C O) 3 £ CM to > to O Ul 1 .X J— E o lO U 1 o o CM 1 o> CM CO 1 <0 CM (d CM CM CM 1 3 : O 3 : i n \ ^ V. 3 1 O)X 00 X 3 3 . 1 Î J *- o 1 tf) X o o cx u i O o 1 o 1 r~ J— CM CM X (X »“ 1 CM X ex to CM o OJ o . CM () \ o> cn 3 OJ 3 to c (£> B P B E O "M CO 03 L O to o O OJ CM OJ ttj o CM m f*0 OJ g OJ I I I o 3 : CM 'ic OJ •M' lO V E - 4 Q ' JiC X CM OJ OJ a X X CM X lU o o LU o o o 3c OJ OJ 07 £E 3C CM CM CM ex T- to CM CX to OJ 3 +-> OJ CM a CO s : If) CD 3 to O) r - CM E X L. 1 o I C7> «r- to E O O o CO <0 CM CM CM CM CM 1 o en CM 1 CO je en 1 1 1 M3 O o I 1 CM X o (U M- o CO O 00 XJ o o m M 1 _ X N 03 E 1 § 0) u j e 1 . 2 CO o 4-> o 00 o ac » «o 1a t/3 o «o > CM X t T- CM <— CM CM cr> en UOO 03 E o 0) O >» tn X CO C3 0) E - o h-4 1 X CO X o o q : «0 «o I (0 O u . CM CM I > »“ CM X CO CM E en O 1 o o 1 lO o e Ift o 1 ü o 03 1 1 en o M? o r> 1 M tn C3 10 X 1 M c o 01 E ob 1 E CO X sz LÜ j e CO CM 1 -X u fd o 1 1 CO OC o o > CM CM cc X o: »- ro ! CM CM a. en en ■M en (O CM X3 r - 03 o e 1 C3 m ro lO 0) je CM CM X CL CO to C3 m t/3 o (U CM f- en E O O i- 1 je X û , ^ CO LU CO (O ce CD I <0 LU o o I O 3c > r - X û ; 00 CM CM CM (O CM en Q) CM (0 en CM N- 03 O lO l . F m a e V (0 X CM >N o CO f > CM <71 iJj h- 1 Ê CM X z> CD cc o - ^ X CO X => »— X ce CO o o ^ 2 H- o CM CM CM a : E in 1 co 1 CM a ! CM CM o en =3 CM en z> O tO 1 tO c - en T- in 1 o J «V V è 2 ? 1 VD ^ C'^ N ^ %\ Ci ^ ^ 8^:% § i ^ vto o », ' cY % I s V > 5 ^ , . ^ ^ ^ VÇ v^ (^ V ' 1 | i # l r . V § I > j Vi (\| CO ) > 1 > 1 Vf L \ 4 1 M :K Oo Vi> 4J V\, <0 . X \ to f\j «3 % (O .■ f j A ■Orv: il i? 4* •H 2ts cv w ''■ i Cm v U4 zs 'CCÎ >1 > 1 flj . . *d •o ^ sê to . - 4 cx> js \ >1 >1 K e