The Effects of Wearing a Wetsuit on the Thermoregulatory And

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1990 The effects of wearing a wetsuit on the thermoregulatory and cardiovascular responses observed during a triathlon in elite male competitors Herbert Groeller University of Wollongong, [email protected]

Recommended Citation Groeller, Herbert, The effects of wearing a wetsuit on the thermoregulatory and cardiovascular responses observed during a triathlon in elite male competitors, Master of Science (Hons.) thesis, Department of Human Movement Science, University of Wollongong, 1990. http://ro.uow.edu.au/theses/2841

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The Effects of Wearing a Westuit on the Thermoregulatory and Cardiovascular Responses Observed During a Triathlon in Elite Male Competitors.

Herbert Groeller

A thesis presented to the Department of Human Movement in partial fulfillment of the requirements of a Masters of Science (hons) at the University of Wollongong August, 1990 i i

Except where specifically stated or acknowledged, this thesis is the original work of the author. No part of this thesis has been submitted previously in any form to this or any other University.

Herbert Groeller i i i

DEDICATION

I would like to dedicate this thesis to my late mother, Cecilia, a caring, selfless person who I'm sure would be very proud of what I have achieved with this piece of work.

In loving memory, Herb. i v

ACKNOWLEDGEMENTS

I would like to give my supervisor Dr Karen Chad a very big thank you for all the encouragement, support, and most importantly her time in bringing this thesis up to standard. I thank Mr Harry Fuller for his shuttle service in the movement of equipment during the study and for his enthusiasm for exercise physiology over the years, which has rubbed off in part on myself.

Obviously with a study of this size I would not have been able to complete it without the help and expertise of the students of the Human Movement Department at the University of Wollongong. A special thanks goes to Nikki Murray who helped me throughout the study. I would also like to thank the other postgraduates who are all now going through the same trials and tribulations. I've enjoyed working with you.

Last, but definitely not least, I would like to thank the subjects from the lllawarra and Cronulla triathlon clubs. Without donating their time effort and good humour, this study would have never gone past the drawing boards. V

ABSTRACT

The effects of wearing a wetsuit, during the swimming leg of a triathlon, on the thermoregulatory and cardiovascular responses, were investigated in 15 trained male triathletes (X ± S.D.) (aged 29.6 ± 3.8yrs). Prior to the simulated triathlons each subject completed a maximum oxygen uptake test (MVO2): (swim = 52.9 ± 5.13 mlkg-1-min-1; bicycle = 67.1 ± 4.79 ml-kg-1- min-1 and run = 68.7 ± 4.08 ml-kg"1-min~1 ) to determine relative workloads for each phase of the triathlon.

Subjects in the triathlon swam tethered in a pool (20.0 ± .68 °C) for 30 minutes followed immediately by a 70 minute ergometer cycle and 40 minutes of treadmill running in a climate chamber with the environmental conditions of 25 °C (dry bulb), 21.5 °C (wet bulb) and 73% relative humidity. Subjects exercised between 65 - 70% of MVO2 for the swimming, bicycle and run stages.

The results showed that in the swimming stage the NW (non wetsuit) treatment had a significantly (p<0.05) lower core and skin temperature but a trend toward higher oxygen consumption and increased heart rates than the W (wetsuit) treatment. The afterdrop in the NW treatment was significantly (p<0.05) greater (0.4-0.5 °C) than the W treatment (0.1 °C) in the first 20 minutes of the bicycle stage. During the cycling phase a significant (p<0.05) increase in core and skin temperature was seen in the W and NW treatment, however, no significant difference was seen vi between the W and NW treatment in heart rate and oxygen consumption. During the run phase, although a significant (p<0.05) increase in core temperature was observed in both treatments, no significant difference was seen between the W and NW treatment in core and skin temperature, heart rate and oxygen consumption.

Results from the study indicate that significantly different thermoregulatory and cardiovascular responses occur when wearing a wetsuit during a triathlon. Furthermore, triathletes appear most vulnerable to hypothermia, and therefore possible injury, in the initial stages of the bicycle phase which may be accelerated when competitors do not wear a wetsuit during the swimming stage. The findings also suggest that in the latter stages of the running phase competitors can suffer from excessive thermoregulatory heat strain due to the continual rise in core temperature. vii

TABLE OF CONTENTS

Acknowledgements i v Abstract v Table of Contents v i i List of Tables ix List of Figures x

CHAPTER I: INTRODUCTION 1

CHAPTER II: REVIEW OF RELATED LITERATURE Temperature regulation 9 Thermoregulatory and cardiovascular responses to immersion in water 1 6 Afterdrop response to swimming in water 30 Wetsuits 36 Precooling 38 Prolonged exercise in heat 4 6 Plasma volume changes due to exercise 57

CHAPTER III: METHODS Definitions 63 Delimitations 65 Limitations 6 6 Testing procedures 67 Statistical Analysis 81

CHAPTER IV: RESULTS 8 2 viii

CHAPTER V: DISCUSSION 11 5

CHAPTER VI: CONCLUSIONS AND RECOMMENDATIONS 1 39

CHAPTER VII: REFERENCES 1 45

APPENDICES A: Informed Voluntary Consent Form 168 B: Medical History Questionaire 170 C: Statement of Human Experimentation 174 D: Food Diary 1 78 E: Training Diary 1 80 F: Raw data 182 ix

LIST OF TABLES

CHAPTER II

TABLE 1 Thermoregulatory responses to changes in core temperature 1 0

CHAPTER IV

TABLE 2 Physical characteristics of subjects in the study (n=15).... 84

TABLE 3 Maximal cardiovascular responses of subjects in the study (n=15) Swimming 85

TABLE 4 Maximal cardiovascular responses of subjects in the study (n=15) Cycling 86

TABLE 5

Running X

LIST OF FIGURES

CHAPTER 1

FIGURE 1 Overall tissue insulation (as percent Imax) plotted as a function of metabolic rate. Modified from "Tissue heat transfer: lessons from korean divers." (Rennie C, 1988) S178 .20

CHAPTER IV

FIGURE 2 Core temperature during 30 minutes of tethered swimming in the wetsuit (n=15) and non wetsuit (n=10)subjects. Rest marked on the X axis indicates resting core temperature prior to immersion in the water. Zero "0" time core temperature indicates core temperature after 5 minutes of immersion in the water 88

FIGURE 3 Core temperature during 70 minutes of bicycle exercise in wetsuit (n=15) and non wetsuit (n=13) subjects. Initial core temperature illustrated is the final core temperature obtained upon the completion of the swimming stage 89

FIGURE 4 Core temperature during 40 minutes of treadmill running in wetsuit (n=13) and non wetsuit (n=9) subjects 9 0 xi

FIGURE 5 Afterdrop upon the completion of the swimming stage in wetsuit (n=15) and non wetsuit (n=10) subjects 94

FIGURE 6 Skin temperature during 30 minutes of tethered swimming in the wetsuit (n=15) and non wetsuit (n=14) subjects 96

FIGURE 7 Skin temperature during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects 97

FIGURE 8 Skin temperature during 40 minutes of treadmill running in wetsuit (n=15) and non wetsuit (n=13) subjects 98

FIGURE 9 Heart rate during 30 minutes of tethered swimming in wetsuit (n=12) and non wetsuit (n=11) subjects 101

FIGURE 10 Heart rate during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects 1 02

FIGURE 11 Heart rate durng 40 minutes of treadmill running in wetsuit (n=15) and non wetsuit (n=13) subjects 1 03 XII

FIGURE 12 Oxygen consumption (VO2) during 30 minutes of tethered swimming in the wetsuit (n=14) and non wetsuit (n=13) subjects 1 05

FIGURE 13 Oxygen consumption (VO2) during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects 106

FIGURE 14 Oxygen consumption (v*02) during 40 minutes of treadmill running in wetsuit (n=15) and non wetsuit (n=13) subjects 1 07

FIGURE 15 Percentage change in plasma volume (%A Plasma Volume) after 30 minutes of tethered swimming and 70 minutes of cycling in wetsuit (n=13) and non wetsuit (n=15) subjects 110

FIGURE 16 Percentage change in plasma volume (%A Plasma Volume) after 30 minutes of tethered swimming, 70 minutes of cycling and 40 minutes of treadmill running in wetsuit (n=13) and non wetsuit (n=13) subjects 111

FIGURE 17 Water intake in 10 minute intervals during 70 minutes of cycling and 40 minutes of running (n=15) 114 1

CHAPTER 1

INTRODUCTION 2

The growth of multievent sports (triathlons) in Australia has been rapid. The first event in Australia was held in 1979 and by 1988 there were well over 100 triathlons staged during the triathlon season (Triathlon, 1988). Triathlons are now a popular recreational activity for a large number of participants as well as a highly professional and competitive sport for the athlete. Although the consistent rise in prize money and increase in status for triathlon events (which has seen triathlons become a Commonwealth Games event in Auckland, 1990) has helped to increase the level of competition, the physical demands placed on athletes in the sport is becoming excessive. The combination of stages and distances involved in the triathlon event can place excessive thermoregulatory and cardiovascular strain on athletes, thus affecting optimal performance. Furthermore, Australia's hot humid coastal climatic conditions may augment the thermal demands placed on triathletes which may pose potential health risks. Thus thermoregulation is of considerable importance in triathlon participation and competition.

A triathlon consists of three events all completed in succession and in the same order: a swim, bike and run. Each leg of a triathlon is separated by a transition period whereby athletes change into the correct attire for the next leg of the race (eg, for the bike leg, cycling shoes and a helmet). Although the order of triathlon legs remain the same in all events, distances for each phase varies with each event. More specifically, triathlon distance and duration may vary from 400 m - 3.8 km (swim), 10 km - 180 km (bike) and a 4 km - 42 km (run) demanding 1-14 hours to complete. The popularity of triathlons may be attributed 3 to the combination of 3 events which has enabled competitors to come from a wide variety of sporting backgrounds and still be successful.

Despite triathlons growing popularity as a sport, the combination of three events in succession has placed high demands on athletes to regulate their body temperature. Significant changes in body temperature may adversely affect exercise performance and thus cause a less than optimal race result (Nadel, 1977, Rowell, 1974). More specifically, variations in core temperature can be seen in the swimming leg of a triathlon. In the swimming leg of a triathlon a triathlete is likely to have a reduction in core temperature which may lead to hypothermia. However, the symptoms of hypothermia for the athlete will be most severe upon the completion of the swim and the commencement of the bicycle leg. At this stage core temperature will be further lowered due to the phenomenon of afterdrop which may leave the athlete susceptible to injury due to the highly co-ordinated task of bicycle riding.

Furthermore, average open water temperatures in Australia are below those suggested for optimal swimming performance. Average water temperatures range in Australia's capital cities during summer from a maximum of 26.3 °C (Brisbane) to 17.5 °C (Hobart) and during winter from a maximum of 20.8 °C (Brisbane) to 11.4 °C in Hobart (Pickard, 1978). It is therefore likely that triathletes will swim in water with temperatures below those required for optimal swimming performance (28 °C - 30 °C) (Nadel et al., 1974a). Lower water temperatures have been shown 4 to decrease swimming performance and increase oxygen consumption (Holmer and Bergh, 1974; Nadel et al., 1974a; McArdle, Katch and Katch, 1986). Triathletes are also more susceptible to hypothermia than other groups of athletes due to their linear physique and low levels of subcutaneous body fat at 7% - 10% (Pugh and Edholm, 1955; O'Toole et al., 1987; Holly et al., 1986). This susceptibility to lowered levels of body temperature was highlighted in the 1985 Great Lakes Triathlon in Australia where 28 competitors were removed from the water (14.5 °C) suffering symptoms of hypothermia (Hazel, 1985). Due to such responses in cold water temperatures, temperature regulation has become an important issue to the triathlete. In order to overcome the detrimental effects of cold water, a majority of triathletes wear wetsuits during the swimming leg.

Although the swimming leg poses immediate difficulties for the bodies thermoregulation system the later stages of a triathlon also place heavy thermoregulatory demands on the body. Apart from the potential difficulties that a triathlete is likely to 5 encounter when swimming in cold water, the athlete must also contend with thermoregulatory problems upon leaving the water.

After completing the swimming leg the athlete will be exposed to ambient temperatures for the commencement of the bike leg. It is during this period of transition between the swim and bike that triathletes after swimming in cold water are likely to experience an afterdrop in core temperature. Afterdrop is the continued lowering of core temperature after immersion in water and is augmented by the subsequent removal and rewarming of the subject (Webb, 1986; Angell, 1982). Thus, afterdrop is most likely to occur to triathletes upon completion of the swim phase and the commencement of the bicycle phase. The magnitude of core temperature change when exposed to rapid cooling and rewarming has been reported to result in a further lowering of core temperature by 1 - 2 °C (Lowdon, 1987, Giesbrecht et al., 1987; Webb, 1986; Savard et al., 1985). The effects of afterdrop were highlighted in the Great Lakes Triathlon (1985) where 4 athletes had to withdraw from the bike leg due to the continued lowering of their core temperature (Hazel, 1985). If the athlete continues the bike stage they are likely to experience lowered core temperatures for a period of 15 - 30 minutes after the completion of the swimming stage (Webb, 1986; Savard et al., 1985; Giesbrecht et al., 1987; Costill et al., 1967). Thus core temperature is likely to be lowered for a significant period of the bike leg and therefore influencing exercise performance for a considerable amount of time in a triathlon. 6

Upon the athlete overcoming the effects of an afterdrop (through the progressive rewarming of the body), the athlete must then contend with the possible effects of hyperthermia in high ambient temperatures during the bike and run stages of a triathlon.

Exercise which is prolonged in the heat has been noted to cause several physiological responses termed collectively as cardiovascular drift (Kreider et al., 1988b; Nadel, 1987; Rowell, 1974; Saltin and Stenberg, 1964). Physiological changes (cardiovascular drift) such as reduced stroke volume, increased heart rate, reduction in blood pressure and pulmonary arterial pressure are a direct consequence of increased blood flow to the skin for the purpose of thermoregulation (Shaffrath and Adams, 1984; MacDougall et al., 1974; Senay, 1987). In addition, the magnitude of cardiovascular drift in prolonged exercise is enhanced by increases in thermal stress. As thermal stress is heightened a deterioration in work capacity occurs, thus directly affecting exercise performance in a triathlon (MacDougall et al., 1974; Saltin and Stenberg, 1964; Kreider et al., 1988a). It is therefore of importance for the triathlete to limit the cardiovascular drift experienced during a triathlon. It has been noted that cardiovascular drift can be eliminated or reduced through lowered skin temperatures, and additionally work capacity may be enhanced by prior cooling (0.5 °Q of the body's core (Hessemer et al., 1984; Olschewski and Bruck, 1988; Rowell, 1969; MacDougall et al., 1974). The triathlete therefore may use the swim leg as a precooling period to reduce the effects of cardiovascular drift during the bike and run stages. 7

When looking overall at the likely thermoregulatory effects of completing a triathlon it would seem that the triathlete is placed in a precarious position in the attempt to maintain core temperature. During the swimming leg the athlete must attempt to maintain or slightly lower core temperature whilst trying to swim as fast as possible. However if core temperature is lowered significantly a decriment in swimming performance may occur (Nadel et al., 1974a). If fluxes in core temperature can be prevented in the swimming leg it will enable the triathlete to enhance performances in the bike and running legs which account for the majority of time in triathlons. However, at present there has been a paucity of data on the phenomenon of afterdrop and its subsequent effect on the performance of triathletes. The limited data on triathlons has resulted in limited guidelines concerning the thermal demands placed on athletes when participating in a triathlon.

Therefore, the purpose of this study is to examine the effect of thermoregulatory and cardiovascular variations during the swimming leg of a triathlon on the performance of a complete triathlon in competitive triathletes (swim, bike and run). The variance in core temperature will be manipulated by the triathletes wearing a wetsuit during the swimming leg of the triathlon. The study will thereby help to gain an understanding of the thermal demands placed on the body during a triathlon which will better prepare athletes and organizers for safer triathlon participation in the future. 8

CHAPTER 2

REVIEW OF RELATED LITERATURE 9

Temperature Regulation

Temperature regulation is of primary importance to the human species as survival is dependent on keeping core temperature at 37 °C. Humans are therefore called a homeotherm due to the ability of the body to regulate internal temperature when there are variations in the external environment. This ability enables humans to be relatively independent of the environment that he interacts in (Brooks and Fahey, 1984). The thermoregulatory system is designed to keep internal body temperatures at a relatively constant level. This has its disadvantages as man can only tolerate a drop in deep body temperature of 10 °C and a rise of 5 °C (Brooks and Fahey, 1984). The small range of internal temperatures that man operates indicates the importance of both dissipating heat produced by the body and retaining heat in a cold environment (McArdle, Katch and Katch, 1986).

The need for temperature regulation can be further illustrated when the body is performing work. Although environmental temperature can affect the ability of the body to regulate core temperature, exercise however also places large demands on the body to dissipate heat and thus to maintain an internal equilibrium. The high thermal demands placed on the body due to exercise occur due to the low efficiency of the body in converting chemical energy to work, resulting in considerable amounts of heat being produced (Jessen, 1987a). Without avenues in which to dissipate heat produced through work the core temperature of the body during exercise would rise by 1 °C every 5 minutes. In a marathon this would mean a core temperature in excess of 70 °C (Mc Ardle, Katch and Katch; Harrision, 1986). It should be noted, however, that marathoners rarely finish with a core temperature above 40 °C which indicates the effectiveness of the thermoregulatory system (Harrision, 1986).

Table 1 Thermoregulatory responses to changes in core temperature

(Modified from Brooks and Fahey (1984). The effects of alterations in core temperature)

Core Physiological responses Temp (°C)

4 4 Upper limit for survival Impaired thermoregulation Heat stroke, brain damage 42

40 Extreme physical exercise 38 Normal range 36 Intense shivering and impaired co-ordination 34 Violent shivering; speech and thought impaired 32 Decreased shivering; erratic movements; incoherent 30 Muscular rigidity; semiconscious 28 Unconscious; cardiac arrythmias 2 6 Thermoregulation absent 11

Table 1 illustrates the detrimental effects that small changes in core temperature (1-3 °C) have on the functioning of the body. Similar fluctuations in core temperature can be encounterd by athletes competing in a triathlon.

The regulation of the internal temperature of the body (core temperature) is under the control of the temperature regulatory center in the hypothalamus. The hypothalamus is situated just above the optic nerve at the base of the brain stem, and attempts to keep core temperature at an equilibrium (Lamb, 1984). The hypothalamus is able to maintain the control of core temperature by serving three roles. Firstly, the hypothalamus acts as a thermal sensor, in which the temperature of the hypothalamus is determined by the arterial blood that is passing through it (Nadel, 1977). The flow of arterial blood through the hypothalamus lets the hypothalamus assume the temperature of the body. Secondly, the hypothalamus acts as an integrator of information from other locations of the body (ie skin), which integrate information from nerve endings or receptors that are located near the skin surface. The nerve endings are temperature sensitive receptors to hot and cold thermal inputs. The hot receptors are situated close to the skin surface, and the cold receptors are situated deeper under the skin surface (McArdle, Katch and Katch, 1986). The receptors act as an early warning system for the hypothalamus which is believed to work on a "set point" principle; as body temperature rises above the set point the anterior hypothalamus is stimulated (Haymes and Wells, 1986; Brooks and Fahey, 1984). The anterior hypothalamus employs mechanisms to increase the loss of heat from the body. When core temperature is below the set point the 12

posterior hypothalamus is stimulated. Once this has occurred the posterior hypothalamus employs mechanisms which reduce the amount of heat loss from the body. Finally the hypothalamus acts as the controller of a number of effector mechanisms (Haymes and Wells, 1986). The effector mechanisms attempt to either increase heat loss (vasodilation and sweating) or reduce the loss of heat from deep body tissues through vasoconstriction and shivering. Thus the effector mechanisms control core temperature through the manipulation of the avenues of heat exchange.

The ability of the body to balance core temperature is through the control of heat production (metabolism) and heat exchange avenues (convection, conduction, radiation and evaporation). Metabolism is the only source of internal heat production and the amount of heat produced is dependent on the work performed by the muscles of the body (Brooks and Fahey, 1984). At rest heat production is low, however, when the body is exposed to cold conditions the metabolic rate can increase 3-5 fold through shivering. Therefore shivering enables the body to maintain internal temperature through increased heat production. Vigorous exercise as seen in triathlons can further increase the total metabolic rate by 20-25 times on resting levels . Therefore, exercise due to the large increases in metabolic rate, is capable of producing a large thermal stress on the body. This thermal stress must be dissipated in order to prevent a rise in internal temperature which may hinder optimal exercise performance (McArdle, Katch and Katch, 1986). Unlike heat production the body has a number of ways to exchange heat with its environment. The 13 first of these avenues is evaporation which helps in the exchange of heat by turning the water that is present on the skin surface (in the form of sweat) into vapor. Through evaporation the body is able to lose 0.58 Kcal of heat for every gram of water that is turned to vapor (Brooks and Fahey, 1984). As ambient temperatures increase the importance of evaporation as a means of heat loss is also increased. At 35 °C evaporation accounts for 90% of the heat loss to the environment (Haymes and Wells, 1986). However in cold conditions heat loss due to evaporation is small and accounts for a minority of the heat lost by the body. In cold conditions there is a large increase in respiratory heat loss which increases with rises in the rate of ventilation. Respiratory losses of heat due to evaporation are increased in cold conditions but are more than counter balanced by the reduced sweating response that occurs in cold environments (Haymes and Wells, 1987).

The second form of heat exchange available to the body is convection. Convection involves the conduction of heat from the skin surface due to the movement of air or water particles. As the air or water particles are heated by the surface of the skin, they move away from the surface of the skin to be replaced by cooler particles, thereby continuing the heat loss from the body. Although convective heat loss in hot environments is small (6%), in cold environments, heat loss due to convection is large and is increased sharply when the body is exposed to wind (Haymes, Dickson, Malville and Ross, 1982). Wind prevents the body from forming a warmer insulative layer of air or water around the periphery surface of the body. The insulative layer reduces the 14 thermal gradient that the periphery is exposed to and thus reduces heat loss due to convection. Wind however prevents the formation of an insulative layer and thus an increase in the thermal gradient occurs resulting in larger heat loss due to convection. Triathletes are therefore susceptible to heat loss due to convection. When the swimming leg is completed and the bike stage commenced, triathletes will be exposed to wind velocities up to 40 kmh (speeds reached whilst cycling). High effective wind speeds, combined with a lack of clothing insulation and wetted skin, will result in large levels of heat loss due to convection (Haymes et al., 1982; Horvath, 1948; Vanggaard, 1975).

The third form of heat exchange is conduction. Conduction can be viewed as the exchange of heat through contact with another object. As the difference between the temperatures of the two objects is increased (ie the thermal gradient is increased) heat exchange due to conduction will also increase. Radiation is the final form of heat exchange available to the body and can be seen as the exchange of heat through electromagnetic or infrared rays that radiate from one object to another. An example of heat loss through radiation is when body temperature is greater than the surrounding environment. Heat in this situation will be radiated out of the body to objects of a lower temperature.

The contribution of each avenue to heat loss or gain in the body is dependent on the ambient temperatures surrounding the body (Nadel et al., 1979). Each avenue of heat loss conforms to the partitional heat exchange equation: 15

0 = M-E±C±K±R±S where M= metabolic heat production; E= Evaporative heat loss; C= Convective heat loss or gain; K= Conductive heat loss or gain; R= Radiative heat loss or gain; and S= Body heat storage or loss (Brooks and Fahey, 1984)

The effective use of the avenues of heat exchange is dependent on the ability of the body to transfer the heat stored in the core of the body to the surface of the skin. This is due to the rate of heat loss from the body which is dependent on the core temperature skin temperature gradient (Nadel et al., 1979; Haymes and Wells, 1986). 16

Thermoregulatory and Cardiovascular responses to Immersion in Water

Water is capable of placing a large thermal load on the bodywhilst exercising due to the high specific heat per unit volume which is approximately 4000 times greater than air (Horvarth, 1981). Even though vigorous swimming can result in an increased heat production of 15 times, this increase may not be enough tostop the efflux of stored heat from the body (Nadel, 1977). The efflux of heat from the body is the result of the lack of an insulative layer surrounding the body at the skin water interfacewhich is due to the high thermal conductivity of water. (Horvath,1981; Nadel, 1977; Brooks and Fahey, 1984; McArdle, Katch and Katch, 1986; Haymes and Wells; 1986). The high thermalconductivity of water is further reflected by the differences in critical temperatures (lowest temperature at which a shivering response is not evoked). The critical temperature for water is 33 °C as opposed to air which has to be 6 - 9 °C lower to evoke the same response (Keatinge, 1969). The lack of insulation offered by water is due to the high convective heat transfer co-efficient (rate of energy exchange per unit of surface area) which removes heat rapidly from the body. Nadel et al., (1974a) calculated that at rest there was a heat transfer coefficient of 230 W.m2.°C which rose to 580 W.m2.°C whilst exercising in water. Such a rise in the heat transfer coefficient indicates that whilst swimming there is likely to be a twofold increase in the heat loss from the body. Nadel et al., (1974a) found that the heat transfer coefficient was not a function of water velocity. He surmised that this value stayed the same due 17 to the high convective currents that result when humans are swimming in water. The rapid removal of heat from the body is especially evident when skin temperature is higher than that of water temperature. When this occurs skin temperature lowers to assume the temperature of the water surrounding the body resulting in an increased heat loss due to conduction (Lowdon 1982; Pendergast 1988). At rest.however, skin temperature does not always simulate water temperature due to the formation of a warmer insulative layer around the body. The insulative layer around the body results in a 1 - 2 °C difference between skin and water temperature (Nadel,1977). However when exercising in water the insulative layer does not exist due to high convective currents around the body and thus explains the increased heat loss found when swimming by Nadel et al. (1974a).

The high heat transfer co-efficient of water and lowering of skin temperature means that water offers little resistance to the efflux of heat. Therefore when immersed in water the body has only two means to influence the rate of efflux of heat from the body: sweating and vasodilation. The magnitude of resistance to heat flow from the body is dependent upon the thickness of the subcutaneous fat layer and the degree of vasoconstriction (Horvath, 1981; Keatinge, 1960; Keatinge, 1969; Nadel et al., 1974; Holmer and Bergh, 1974). Since the body is made up of approximately 40% muscle mass and 15% subcutaneous body fat, it will be primarily these tissues that will have a major influence on the rate of heat loss by the body (Brooks and Fahey, 1984; Pendergast, 1988). This was made evident by Pugh and Edholm (1955), who compared two individuals, one with a high percentage of body fat and the other individual with a low percentage of body fat. Pugh and Edholm found that the subject with a large amount of subcutaneous body fat (average adipose depth of 12.1 mm) was able to swim in water of 16 °C for several hours without any significant change in core temperature. This response was directly compared to the subject with much less subcutaneous body fat (2.9 mm skinfold thickness). The subject with the lower percentage body fat was only able to swim in the 16 °C water for a period of 30 minutes. The same subject had a lowering in core temperature of 3.3 °C. Furthermore the subject upon exiting the water could not stand and was shivering violently. This was opposed to the subject with a greater level of subcutaneous fat who was able to run up the beach after more than 6 hours of swimming in the same water temperature. Pugh and Edholm (1955) noted that the subject with a high percentage of body fat had extremities that were very pale indicating the effectiveness of vasoconstriction to the periphery to reduce heat loss and lowering the heat flow from the skin to the water (Nadel, 1977).

The findings by Pugh and Edholm (1955) were further investigated by Holmer and Bergh (1974) with the aid of swimming flume. Holmer and Bergh (1974) studied 5 subjects exercising at 50% of their maximum oxygen uptake (MVO2) for 20 minutes in water of varying temperature. Holmer and Bergh (1974) found that core temperature measured at the esophagus was inversely proportional to the skinfold thickness (the subject with the lowest percentage body fat had the largest decrease in core temperature of 1.6 °C in18 °C water). No correlation coefficient 19 was given for the relationship between skinfold thickness and core temperature. This change is in agreement with studies by Keatinge (1960), Keatinge, (1969) and Nadel (1974)a who both found similar relationships between core temperature and body fat. Although it appears from research conducted by Nadel (1974a) Holmer and Bergh, (1974), Pugh and Edholm (1955) and Keatinge (1960) indicated that subcutaneous fat plays an important role as an insulator for the body, Pendergast (1988) has questioned whether it is the sole source of insulation available to the body. Pendergast (1988) suggested that body fat will only account for 10% - 30% of the total body insulation at rest. The major insulative tissue of the body at rest is the unperfused skeletal muscle mass that accounts for 70 - 90% of total body insulation (Pendergast, 1988; Veicstenous, 1982, Rennie, 1988). Therefore to maintain total body insulation it is important to reduce blood flow (vasoconstriction) to the skeletal muscles if resistance to efflux of heat is to be preserved (Haymes and Wells, 1986). The reduction in blood flow enables the muscle mass to act as an extension of the insulative effect of the subcutaneous body fat.

The role of vasoconstriction in the body is also supported by Nadel (1977), as a decrease in skin vascular resistance will increase the core to skin gradient resulting in a greater heat loss. Keeping the warm blood of the deep tissues away from the periphery is very important as blood has a high specific heat content and thus can cause substantial losses in heat (Nadel, 1977). Therefore it seems the body is well equipped to resist the flux of heat from the peripheral surfaces through vasoconstriction when at rest. Although the resistance to the efflux of heat is high at rest, during exercise however the resistance to the efflux of heat reduces dramatically. The change in insulation offered by the different body tissues during exercise is illustrated in Figure 1.

% max

METABOLIC RATE (mets)

Figure 1. Overall tissue insulation (as percent Imax) plotted as a function of metabolic rate. Modified from "Tissue heat transfer in water: lessons from l&rean divers." (Rennie C, 1988) S178 21

Figure 1 shows the effect of exercise intensity on insulation offered by muscle mass which becomes perfused with blood. As exercise intensity increases the insulation by the muscle mass is diminished leaving only the superficial shell to resist the efflux of heat from the core of the body to the water. However as exercise intensity is further increased the value of the insulation for the superficial shell is decreased due to increased convective currents associated with greater movement of the extremities. Therefore at rest the muscular tissues of the body offers the majority of insulation in water. However as exercise intensity is increased the muscle mass becomes perfused with blood, which reduces insulation available from the superficial shell of the body. This would explain the finding by Pugh and Edholm in (1955) and support that statement by Nadel et al. (1974a), that subcutaneous body fat is a fixed resistance against the efflux of heat from the body. However it is the attempt of the body to reduce blood to the working muscles that accounts for a significant portion of the cooling.

Research conducted by Toner, Sawka and Pandolf (1984) indicated that the specific muscle mass used in exercise may influence the rate of cooling. Toner et al. (1984) incorporated three forms of exercise (arm only, leg only, arm and leg combined) on a arm leg ergometer in water of varying temperatures (20 °C, 26 °C, 33 °C). Toner et al. (1984) found that of the three exercise activities the arm activity resulted in the greatest lowering of core temperature. Toner et al. (1984) concluded that this was due to: (1) the upper body limbs have a larger surface area to mass ratio resulting in an increased interface between the skin and the water; (2) proportional to muscles mass there was a greater blood flow per unit volume of muscle; and (3) exercise intensity effects the loss of heat from the core of the body. The greater efflux of heat from the body is a result of an increase in the gradients between limb-core and skin temperature. The results imply that swimming may result in larger increases in heat loss (due to the predominant upper body activity) and thus be more susceptible to a lowering core temperature.

The observations of Toner et al. (1984) were suppported by research from Layton, Mints, Annis, Rack and Webb (1983) and Tikuisis (1989). Both studies found that most of the heat loss when swimming water occurred in the limbs due to increased blood flow to the active muscles (Layton et al., 1983; Tikuisis 1989).

Oxygen Consumption when Swimming in Water of Varying Temperatures.

Swimming or exercising in cold water has been shown to increase the metabolic cost of that activity when compared to the same form of exercise is warmer water (McArdle, Magel, Lesmes and Pechar, 1976; Nadel et al. 1974a; Nadel, 1977; Holmer and Bergh,1974). The methods used for testing athletes whilst swimming involves a variety of techniques and equipment. In the literature there are 3 predominant methods of testing physiological parameters of swimming: (tethered, flume and free swimming). When comparing the three methods of evaluating swimming metabolic cost, it was found that there was a high correlation (r = 0.99) between the different testing methods (Bonen, Wilson, Yarkony, and Belcastro; 1980). One of the testing methods (tethered swimming device) was devised by Costill (1966), which allowed the subject to remain stationary whilst physiological measurements were taken. A pulley system with an adjustable weight was used to allow the subject to perform a known value of work. Although there is a high correlation between ail three testing methods the tethered swimming device is highly favorable for use as it requires little expense and is easily erected. However as highlighted by Nadel (1977) work intensity of tethered swimming is varied primarily by manipulating stroke rate. The variation in stroke rate however was not accompanied by an increase in water resistance as expected in free swimming (Nadel, 1977). Bonen et al. (1980) reported that all swimmers tested favored the use of the swimming flume as a means of testing aerobic capacity than tethered swimming.

An improvement on the tethered swimming device was the swimming flume, which permitted water to be recirculated around the subject (similar to the belt on a running treadmill). This allowed both water velocity and temperature to be varied whilst the subject swam unhindered and stationary in the flume (Astrand and Englesson, 1972). One further method of assessing swimming fa>2 is via backward extrapolation (Costill, Kolvaleski, Porter, Kirwan, Fielding, and King, 1985; Lavoie and Montepetit, 1986; Dengel, 1989). Backward extrapolation involves assesing the last breath of the subject upon the completion of 365.8 m of freestyle swimming (Dengel, 1989). This method was shown to be both valid (r=.99) and reliable (r=.97) when compared to tethered swimming. Other methods of measuring oxygen consumption whilst exercising in water have involved the use of arm and leg

ergometers (McArdle et alM 1976; Toner et al., 1984). The use of the arm leg ergometer has enabled physiological measurements to be easily monitored as work is being performed. Although the swimming flume is superior to the tethered swimming device the high costs associated with a swimming flume make it impractical for use and difficult to acquire.

Nadel et al. (1974a) and Holmer and Bergh (1974) conducted studies on swimming performance at varying water temperatures through the use of a swimming flume. Nadel et al. (1974a) and Holmer and Bergh (1974) observed that submaximal exercise in water of 18 °C caused an increase in VO2 as compared to the oxygen consumption when swimming in water of 33 °C and 34 °C respectively. Furthermore, Holmer and Bergh (1974) noted a 500 ml increase in 02 consumption at a temperature of 18 °C which was proportional to a decrease in core temperature measured at the esophagus (below 37 °C ). Nadel et al. (1974a) also found similar results but larger than those recorded by Holmer and Bergh (1974), with a ^02 increase of 400 - 500 ml whilst swimming in 18 °C water as compared to swimming in 26 °C water. However Nadel et al. (1974a) also noted that two lean subjects had an increase in VO2 (200 - 300 ml) when swimming in 26 °C water as opposed 33 °C water. Later studies by McArdle et al. (1984a) and McArdle et al. (1984b) showed similar changes in metabolic rate using an arm-leg ergometer. McArdle et al. (1984a) divided subjects into three groups according to body fat (Low, 12%, Average 15-18% and High 22%). McArdle noted that over all temperature ranges (20 °C , 24 °C and 28 °C ) the Low group showed the largest thermogenic response and lowering of core temperature (rectal). At rest oxygen consumption for the Low body fat group rose from 0.651 I.min-1 after 20 minutes immersion to 1.071.min-1 after 40 minutes. In a similar experiment McArdle et al. (1984b) had the same subjects exercise at 36 W. He noted similar increases in V02 as previous investigators which were accompanied with falls in rectal temperature of 1.7 °C and 0.9 °C in 20 °C and 24 °C respectively. Both the Average body fat and High body fat group showed much smaller changes in metabolic rate and core temperature response. Although Holmer and Bergh (1974) and Nadel et al., (1974a) found significant changes in oxygen consumption when swimming in water of different temperatures, Costill, Cahill and Eddy (1967) and Costill (1966) found no significant difference in oxygen cost when exercising in water of different temperatures.

Costill et al., (1967), had subjects swimming for a period of 20 minutes using a tethered swimming device in 17.4 °C , 26.8 °C and 33.1 °C in three trials. Although no significant changes were noted in VO2 in different water temperatures the results obtained by Costill et al., (1967) agree in part with previous investigations. During the 20 minute exposure to the water, rectal temperature did not lower when compared to resting levels, and in some cases increased during testing. As \f02 seems to be a function of lowered core temperature, it would be expected that no changes in oxygen consumption would be noted (Nadel et al., 1974a; Holmer and Bergh, 1974). The lack of change in core temperature may be associated with the short duration of exposure to the water and also the greater exercise intensity which was used in comparison to McArdle et al. (1984b) and Holmer and Berg (1974). Variations in water temperature not only influence submaximal performance but also reduce maximal swimming capacity. When subjects were required to swim maximally similar changes to submaximal oxygen consumption was noted (McArdle et al., 1984b).

Furthermore when lean subjects swam maximally they could only reach 85% and 92% of their maximum VO2 in 18 °C and 26 °C water respectively (Nadel et al., 1974a). This reduction in MVO2 has been associated with decreased maximal heart rates with no apparent increase in stroke volume (McArdle et al., 1976; Haymes and Wells, 1986). Therefore a reduction in heart rate may result in a reduction in cardiac output and reduce blood flow to the working muscles. The reduction in cardiac output in cold temperatures is also combined with the lowering of the temperature of the blood. The lowered blood temperature results in a reduction in the dissociation of oxygen from the hemoglobin. In turn the reduction in the dissociation of oxygen causes a decrease in oxygen levels present at the site of the working muscles (Haymes and Wells, 1986; McArdle, Katch and Katch, 1986; Pendergast, 1988). The reduction in oxygen to the working muscles is believed to be augmented by a decrease in muscle blood flow. Pendergast (1988) predicted that there is a plateau in the blood flow to the muscle at below 70% of MVO2. The lowered levels of oxygen and blood flow at the site of the muscle possibly accounts for the increased lactic acid present in the muscles after swimming in colder water temperatures (Nadel et al., 1974a, Pendergast, 1988).

The explanation for the increase in VO2 in cold water temperatures is that shivering is employed to increase the level of heat production when core temperature and skin temperature lowers (Holmer and Bergh, 1974; Nadel et al., 1974a). Exercise in cold water, however does not negate the contractions of the muscles associated with shivering. Shivering was found to be superimposed over the contractions necessary for the work performed (Nadel et al., 1974a). This was indicated by the similar rise in metabolic rate with shivering at rest and when exercising in cold water. Furthermore linear increases in metabolic rate were found with decreases core temperature (Nadel, 1977; McArdle et al., 1984a; Pendergast, 1988). Generally a lowering in core temperature by 0.5 - 2.0 °C will result in an increase in VO2 of 10 - 30% (Pendergast, 1988).

Other reasons for an increase in ^02 may be attributed in part to the increased viscosity of the water and an increase in drag caused when shivering is initiated. Therefore shivering results in a reduction in mechanical efficiency and increased oxygen cost (Nadel, 1977, Pendergast, 1988, McArdle et al., 1984a). The reduced performance and increased oxygen cost of swimming in colder water may affect the chemical and physical processes of the body to be inefficient at a cellular level (Holmer and Bergh, 1974). Nadel et al. (1974a) noted that subjects after swimming in 18 °C water complained of tiredness and the inability to contract their muscles effectively, even though the subjects did not complain of cardiorespiratory stress or fatigue. The inability to contract the working muscles may be due to a reduction in nerve conduction and recruitment of muscle fibres that is associated with lower levels of muscle temperature (Haymes and Wells, 1986). Accompanying the reduced contractility of the working muscles, it was noted that a generally higher level of lactic acid accumulation occurred, 1.4 mmol.l"1, 2.3 mmol.l"1 and 3.6 mmol.l"1 in 34 °C , 26 °C and 18 °C water temperature respectively (Nadel et al., 1974a; Holmer and Bergh, 1974). The increased levels of lactic acid accumulation may account for the symptoms (such as muscle soreness) displayed by the subjects when swimming in the colder water.

Costill et al., (1967), Holmer and Bergh (1974), Nadel et al., (1974a), McArdle et al., (1976) observed that lower heart rates were exhibited in exercise and recovery whilst swimming in colder water. The lower heart rates are believed to be caused by peripheral vasoconstriction associated with exposure to cold water. Vasoconstriction of the periphery causes the transfer of blood to the working muscles and the deep tissues of the body (Costill et al., 1967). Costill et al., (1967) found that there was only a slight variation in heart rate during exercise, but lower heart rates were recorded in recovery when subjects swam in the coldest water temperatures. Conversely Costill (1976) found that exercise in the warmest water produced the highest heart rate response during recovery. Holmer and Bergh (1974) noted a 8 beat drop per minute in heart rate when subjects swam in water 26 °C as opposed to 33 °C water. McArdle et al., (1976) found that heart rate was linear to VO2 when exercising in 33 °C water. However when swimming in colder water temperatures (18 °C and 25 °C ) he noted a considerable decrease in heart rate in subjects when compared to ^02- A lower heart rate would be expected to result in a decreased cardiac output. However in cold water there exists an inverse relationship between heart rate and stroke volume which results in the maintenance of cardiac output (McArdle et al., 1976). The vasoconstriction response associated with cold water causes an increase in peripheral resistance resulting in a greater venous return of blood to the heart and thereby an increase in stroke volume results. Increases in stroke volume were only found at submaximal exercise intensities and reduced to values equivalent to warmer water temperatures as intensity increased (McArdle et al., 1976).

The reduction in stroke volume as exercise intensity increases may be a contributing factor to lower M>>02 reported by other investigators. Swimming in cold water therefore posses a problem for athletes that are immersed for an extended period of time. Decreases in water temperature have been identified with similar decreases in performance and body temperature (Nadel et al., 1974a). However swimming in cold water not only possess problems when the athlete is immersed in the water but also upon exiting the water athletes are likely to experience further physiological changes. The Afterdrop Response to Swimming in Water

Afterdrop can be defined as the continued lowering of core temperature after immersion in water and the subsequent removal of the person from the environment that has caused the individual to become hypothermic (Webb, 1986; Angell, 1982).

The phenomenon of afterdrop is well recorded from incidents at sea where men had fallen over board and been exposed to low water temperatures (Lloyd, 1986). In some instances rescued seamen have still perished due to incorrect rewarming techniques carried out to bring core temperature back to normal levels of 37 °C (Angell, 1982; Burton and Edholm, 1955; Lloyd, 1986; Currie, 1798). It was noted that even though the seamen were alive after being rescued from the water they still perished due to the continued lowering of core temperature (Burton and Edholm, 1955). The phenonmen of afterdrop was documented as early as 1798 by Currie, who in an attempted to explain the effects of cold stress on seamen. Currie (1798) conducted a series of experiments in which subjects were exposed to water temperatures of 44 F for up to 45 minutes. Oral temperatures were taken throughout the immersion of the subject in the water. Currie (1798) observed the gradual decline of oral temperatures when the subjects were immersed in the water. However Currie (1798) stated his suprise in the rapid lowering in oral temperature after the subject was removed from the water indicating that an afterdrop had taken place. 31

Although afterdrop was noted to occur to seamen after immersion in water, recent evidence suggests that afterdrop occurs only under certain conditions. Webb (1986) examined three different conditions for body cooling and rewarming: (1) rapid cooling followed by immediate rewarming; (2) rapid cooling followed by a delay in rewarming of 2 hours; and (3) slow cooling over a period of 5 - 6 hours. Webb found that a rapid cooling of the body for a 60 minute duration followed immediately by rewarming resulted in an afterdrop, (lowering of core temperature during rewarming) that lasted for a period of 10 - 30 minutes. This is also supported by other authors (Lowdon, 1987; Costill, 1967; Giesbrecht, 1987) who found a continued lowering of core temperature upon the removal of subjects from cold environments.

The magnitude of afterdrop can be quite large as seen by Lowdon (1987) who recorded a 2 °C drop in core temperature in the first 10 minutes after removal of the a subject from 16 °C water. Similar afterdrops of core temperature in magnitude and duration were recorded by Giesbrecht (1987) who compared three methods of rewarming (shivering, exercise and shivering and a heatpac). Giesbrecht (1987) noted that of the three methods of rewarming the magnitude of the afterdrop was greatest when exercise and shivering was used as the method of rewarming. Exercise and shivering as a form of rewarming is likely to be experienced by athletes when completing the swimming stage of a triathlon. The exercise that was performed in the study by Giesbrecht (1987) involved walking on a treadmill whereas triathletes exercise intensity is much higher. Cycling speeds of up to 45 kph would be expected in a triathlon race resulting in a much larger heat loss due to convective currents. Therefore it could be predicted that the afterdrop experienced by triathletes may be larger due to the greater exercise intensity undertaken. Also due to the nature of the event, afterdrop is most likely to occur upon the completion of the swimming leg and into the first half of the cycling leg.

In the past the phenomenon of afterdrop has been explained by the circulatory theory (Webb, 1986). The circulatory theory for afterdrop uses changes in peripheral blood flow to explain the continuing drop in core temperature. Skin temperature at the time of removal will have assumed the water temperature that the person was immersed in. Exposure to cold water will cause vasoconstriction of the peripheral blood vessels, preventing blood from being cooled by the shell of the body. Thus the vasoconstriction of the peripheral blood vessels effectively increases the insulation of the body (Brooks and Fahey, 1984).The reduction in skin temperature results in a significant gradient between the deep tissues of the body and the skin surface. The gradient between skin and core temperature increases as the temperature of the water lowers resulting in greater potential for heat loss (Costill, 1967).

Burton and Edholm (1955) suggests that upon rewarming skin temperature will rise rapidly to approximate the external environment, resulting in a rapid increase in blood flow to the periphery and muscles. The increase in blood flow causes the warm blood to be cooled by the cooler shell of the body which results in the continued drop in core temperature after rewarming. (Angell, 1982; Giesbrecht, 1987; Cox, 1985; Smith, 1973; Costill, 1967).

The rapid rise in skin temperature associated with the increase in blood flow to the periphery reported by Burton (1955) was not found by Costill (1967). Costill (1967) found that once subjects had been removed from the water skin temperature did not return to normal levels for over 15 minutes indicating perhaps the lack of peripheral blood flow for these subjects. The circulatory theory is therefore dependent on changes in peripheral blood flow to account for the continued lowering of core temperature. The circulatory explanation of afterdrop was discounted by Webb (1986) and Savard (1985) who have offered an alternative explanation to the physiological cause of afterdrop. Webb (1986) and Savard (1985) surmized that afterdrop is caused primarily by the conduction of heat from the body rather than changes in peripheral blood flow as believed in the circulatory theory. Afterdrop due to conduction occurs when a direction of heat loss has been established (such as heat loss from the deep tissues of the body to the skin surface due to the dissipation of heat to cooler tissues of the body). However if there is a reversal in the direction of heat loss through increases in skin temperature, the deeper tissues of the body will not react immediately to increases in skin temperature as the surrounding tissues in the body are cool. Therefore the lowering of core temperature will still occur until the tissues surrounding the deep tissues of the body are of a greater temperature. Thus the core of the body will increase in temperature due to the conduction of heat by the warmer surrounding tissues. Webb (1986) supported this theory by constructing two models that contained no peripheral circulation (a bag of gelatin and a side of beef). Both of the models when cooled exhibited an afterdrop, indicating no circulatory mechanism was responsible for the continued fall in deep tissue temperature despite peripheral rewarming.

To further examine the specific effects of conduction on the two models Webb (1986) extended his model by having temperature probes at different levels in the bag of gelatin and the side of beef. He noted that the deeper probes within the two models were the ones to exhibit a delay in rewarming. The probes that were placed closer to the surface of each model exhibited less afterdrop and responded more quickly to changes in ambient temperatures. This observation further supports the theory of conduction of heat from the body as the primary cause of afterdrop. Conduction as a mechanism of afterdrop is also supported by Savard (1985) who closely monitored blood flow in the calf, foot, hand and forearm. Savard (1985) discovered that vasodilation in the extremities during rewarming did not occur during the afterdrop, as predicted by Burton and Edholm, (1955). However peripheral blood flow did increase once core temperature was on the rise. Reduced blood flow to the periphery gives a possible explanation to the reported "slow rise" in skin temperature after swimming in cold water by Costill et al., (1967). Therefore conduction may be viewed as the primary cause of afterdrop according to Webb (1986), Lloyd (1986) and Savard (1985) due to the occurrence of afterdrop when circulation is not intact.

From the current literature however, it does appear that circulation can contribute to the afterdrop phenonmen (Savard et al., 1985; Hong and Nadel, 1979; Lloyd, 1986, Giesbrecht et al., 1987). The contributory effect of exercise in increasing the magnitude of afterdrop has been termed as secondary afterdrop. (Lloyd, 1986). Webb (1986), however did not account for the effect of exercise on core temperature drop after rewarming. Savard (1985) whilst in agreement with Webb on the mechanism of afterdrop, indicated that increase in muscular blood flow due to movement may have assisted in the drop in core temperature. Movement of the lower body causes a shift of blood to the cold limbs of the body resulting in the lowering of core temperature and adjustments in metabolic rates (Hong and Nadel, 1979; Savard, 1974; Glaser and Holmes-Jones, 1951). Hong and Nadel (1979) found when subjects exercised (bicycle riding) after resting in a cold environment there was an increase in the metabolic rate as a result of the shift of blood to the cooler working muscles from the warmer viscera. Accompanying the increase in metabolic rate there was a decrease in core temperature in all subjects. The drop in core temperature was larger when a greater work load was performed. When subjects cycled after rest at 60 watts there was a corresponding drop in core temperature of 0.6 °C in 3 minutes.

This was compared to a cycling intensity of 30 watts which resulted in a drop in core temperature 0.3 °C in 5 minutes. The variation in afterdrop responses to exercise intensity indicates that triathletes are most likely to augment the continued lowering of core temperature due to higher work rates when in race conditions. Savard (1985) also noted that the change in core temperature upon rewarming may be attributed to the muscular activity of walking between the cold and hot water environments by the subjects. Thus upon the completion of the swimming leg triathletes will be exposed to warm ambient temperatures which will promote the continued lowering of core temperature.

Although the precise mechanisms of afterdrop are unclear both theories support the rapid onset of cooling followed by the immediate rewarming of subjects as the primary cause of afterdrop. (Webb, 1986; Savard, 1985; Burton, 1955 and Hong, 1979). This pattern for the cause of afterdrop would indicate that triathletes would be susceptible to afterdrop due to the cooling effect of the swim leg in open water (lakes, rivers and oceans) and the immediate rewarming effect of ambient air temperatures and bicycle exercise. Furthermore it appears from the current literature that exercise enhances the effect of afterdrop which is related to the intensity and duration of exercise (Lloyd, 1986; Hong and Nadel, 1979). Thus triathletes are likely to experience a secondary afterdrop due to the intensity of exercise during the bicycle stage.

Wetsuits: thermoregulatory and cardiovascular responses

The adverse effects of cold water have been noted by triathletes and as a result these athletes have protected themselves from hypothermia by wearing a wetsuit. Triathletes have been observed as being of predominantly an ectomorphic somatotype and therefore they are susceptible hypothermia when swimming in cold water (Dengel, 1989; OToole, 1987 and Holly, 1986). Due to that susceptibility and possible performance advantages wetsuits have become a necessary piece of equipment for the swimming leg of a triathlon.

Wetsuits are able to provide protection from the effects of cold water by trapping a thin layer of water between the body and the neoprene of the wetsuit (Parson and Day, 1986). The layer of water between the wetsuit and the body quickly heat up, thus reducing the thermal gradient and heat loss between the shell of the body and the surrounding water. Kang, Park, Lee, Yeon, Lee, Hong, Rennie and Hong (1983) showed the positive thermoregulatory effects of wearing a wetsuit in cold water. Kang et al., (1983) showed that Korean women divers in 22.5 °C water were able to work for two hours with a 0.4 °C drop in core temperature. However when the divers were unprotected they were only able to last 60 minutes and were removed from the water when core temperature reached 35 °C . When skin temperatures were examined protected divers (wearing a wetsuit) had skin temperatures that were 7 °C higher than unprotected divers explaining therefore the reduced heat loss found in protected swimmers (Kang et al., 1983).

The wearing of a wetsuit not only reduces the efflux of heat from the body, but also it has been identified to decrease swimming times (Brassil, Axford and Holt 1986; Parsons and Day, 1986; Toussaint, Bruinink, Coster, Looze, Rossem, Veenen and Groot, 1989). The decrease in swimming times (in the order of 7%) has been largely attributed to a reduction in drag due to the increases in buoyancy (Parson and Day, 1986; Toussaint et al., 1989). Furthermore Brassil et al., (1986) studied the effect of wearing a wetsuit on subjects of differing swimming ability. Brassil et al., (1986) found that the greatest performance improvements were linked to those of lower swimming ability. The immediate performance advantages has lead to the common use of wetsuits to improve swimming times. Although there may be several disadvantages of wearing a wetsuit indiscriminately when water temperatures are not cold. Due to the high insulative properties of neoprene, if a wetsuit is worn in warm water it may be possible that swimmers exiting the swimming leg will be hyperthermic. Increases in core temperature whilst swimming is disadvantageous due to increases in cardiovascular drift that will be experienced in the bicycle and running legs. It therefore may be beneficial for athletes to forego the performance advantages of wearing a wetsuit in warm water so that cooler body temperatures will enhance the bike and run phases. There appears to be no current research specifically investigating the effects of wearing a wetsuit in warm water

Thermoregulatory and cardiovascular responses to precooling

Studies that involve cooling of the body in water have shown an increased oxygen cost and decreased mechanical efficiency when exercising or swimming due to the lowering of core and skin temperatures (Nadel et al., 1974a; Holmer and Bergh, 1974; McArdle et al., 1984b). However several other investigators using a cooling procedure (decrease core temperature slightly) prior to exercise have shown results that conflict with exercising in a cold environment (Schmidt and Bruck, 1981; Olschewski and Bruck, 1988; Hessemer, Langusch, Bruck, Bodeker, Breidenbach, 1984; Myler, Hahn and Tumilty,1989, Falls, 1972; Goff, Brubach, Specht and Smith, 1956). Precooling is a procedure where body temperatures are lowered prior to commencement of a physical activity. The subject then commences an exercise activity with lower body temperatures than when no precooling was used. Precooling in part would simulate the effect of the swimming leg in cold water of a triathlon prior to the commencement of the bike and run legs. Thus it may be possible for triathletes to use the swimming phase as a form of precooling for the bike and running phases of a triathlon. Therefore research in the area of precooling is likely to be directly applicable to the performance of competitive triathletes. Studies conducted in precooling generally have shown that slight decreases in core temperature (0.5 - 1.0) result in increased work output, increased work duration and reduced thermoregulatory strain (Schmidt and Bruck, 1981; Olschewski and Bruck, 1988; Hessemer, Langusch, Bruck, Bodeker, Breidenbach, 1984; Myler, Hahn and Tumilty, 1989). This would indicate that triathletes may benefit from a lowered core temperature in the swimming phase when completing the bicycle and running phases.

Prior to discussion of the possible benefits of precooling it is neccessary to examine the cooling procedures and experimental designs in the current literature. The precooling procedure used by Olschewski and Bruck (1988) involved subjects sitting in a thermoneutral environment for a period of 30 minutes (26.2 - 28 °C ). Temperature in the climate chamber was then lowered to 5 - 10 °C for a period of 15 minutes. Ambient temperature was then raised until oxygen uptake values reached resting levels after which temperature of the climate chamber was decreased again to 5- 10 °C for 15 minutes. Temperature was then raised to 18 °C where an exercise protocol was followed. Schmidt and Bruck (1981) and Hessemer et al., (1984) had similar precooling protocols but did not have such rigid control of the lower temperatures as Olschewski and Bruck (1988). To examine the effect of precooling on work capacity Olschewski and Bruck (1988) used an exercise protocol consisting of an incremental increase in work rate which consisted of 80% peak maximum oxygen uptake. The work load was increased from 0.1, 0.25, 0.4, 0.5 and 1.0 of 80% Mv*02- Schmidt and Bruck (1981) and Hessemer et al., (1984) used slightly different exercise protocols. Schmidt and Bruck (1981) used an incremental test load throughout, until exhaustion. Hessemer et al., (1984) used a 60 minute protocol in which subject work rate was manipulated by the subject. Hessemer et al., (1984) had subjects working initially at 50% MVO2 however when pedal rate increased out of the range 60 - 100 r.min-1 workload was adjusted to maintain cadence within this range.

The administration of the precooling maneuver prior to exercise results in several physiological responses to occur. The precooling maneuver resulted in a decline in sweat rate during 41 the prolonged exercise protocol. Decreases in sweat rate of 37% and 20.3% after precooling were noted by Olschewski and Bruck (1988) and Hessemer et al., (1984) respectively. Accompanying the decrease in sweat rate was also a decrease in sweat secretion after precooling which may be a result of lower body temperatures exhibited by subjects throughout the testing protocol. The earlier onset of sweating response allows for the flux in core temperature to be controlled earlier and thus maintenance of lower core temperatures when exercising. Schmidt and Bruck (1981) noted that the sweating response started at a lower body temperature, but was accompanied by a higher work rate. The earlier sweating response after precooling may indicate that thermoregulatory responses occur due to stimuli other than thermal factors (Schmidt and Bruck, 1981). However Schmidt and Bruck (1981) noted that the increased workload due the precooling maneuver may have resulted in high muscle temperatures which in turn may have provided the thermal stimuli to initiate sweating.

A secondary response to precooling found by Hessemer et al., (1984) and Myler et al., (1989) was higher blood lactate concentrations. Hessemer et al., (1984) surmised that increases in blood lactate concentrations after precooling were due to the higher work rate achieved when subjects had been precooled. It is suggested therefore that when comparing work rate with blood lactate concentration, the precooled group may have had lower levels of blood lactate than the control group at any given workload. This conclusion was given support from an earlier study by MacDougall, Reddan, Layton and Dempsey (1974). Lower blood lactate levels were supported by MacDougall et al., (1974) who used three different thermal conditions (hyperthermal, normal and hypothermal) during continued prolonged exercise at 70% Mv"02 MacDougall et al., (1974) found that during hypothermal conditions (18 °C with a water perfused suit) that after 30 minutes of exercise subjects had significantly lower blood lactate levels than when exercising in normal (23 °C) and hyperthermal conditions (mirrored rectal temperature with a water perfused suit). Myler et al., (1989) in a precooling study of elite rowers used a different protocol for both the precooling and the exercise regime. Precooling was carried out by the intermittent application of ice packs to the head, face, neck, arms and thighs for a five minute period. Two six minute work capacity tests were performed involving a precooling procedure prior to a six minute work capacity test. Myler et al., (1989) found that after precooling there were higher blood lactates concentrations present. However the levels of blood lactate present were not significantly different when compared to the control levels where no precooling took place. Hessemer et al., (1984) summized that the lower relative blood lactic acid levels present were due to the increase in central blood volume. An increase in central blood volume would have occurred due to the reduction in peripheral blood flow as a result of decreased skin temperatures (Rowell, 1969). The increased central blood volume enables an increase in blood flow to the working muscle which may aid in the removal of lactic acid from the muscle.

A decrease in lactic acid production at colder temperatures opposed to observations made by Nadel et al., (1974a) and Bergh and Holmer (1974). Nadel et al., (1974a) and Bergh and Holmer (1974) noted increased blood lactate levels when swimming in 18 °C water as compared to colder temperatures. The findings made by Nadel et al., (1974a) and Bergh and Holmer (1974) however did not consider the effect of cold water temperatures on performance once the subject was removed from the water. Thus comparisons between precooling and swimming in subnormal temperatures is limited. However it does raise several questions directly applicable to the performance of athletes in triathlons.

Swimming in cold water is likely to decrease performance during the swimming phase of a triathlon however the lowered core and skin temperatures may enhance exercise performance during the bicycle and running phases. A third effect of precooling is the reported increases in work rate and work capacity when subjects were precooled prior to exercise. Hessemer et al., (1984) found that subjects worked at a significantly higher workload after the precooling phase when exercising as compared to the workloads selected when no precooling took place. Jessen (1987a) believed that higher work rates were attributed to the delaying of the reduction in central blood volume as a result of lower skin and core temperatures.

Schmidt and Bruck (1981) and Olschewski and Bruck (1988) noted increased work times up to exhaustion of 40 sec and 2.3 minutes respectively with precooling,however the increases in work time were not significant (p<0.05). Increased work times up to exhaustion were also found by MacDougall et al., (1974) who noted that there was an increase of 42.50 minutes in work tolerance time when exercising in hypothermal conditions as opposed to the hyperthermal conditions. The increases in work time may be attributed to the increase in central blood flow which was a result of reduced blood flow to the shell of the body. Earlier studies involving the application of cold stress (ice packs, cold showers) during the rest period of intermitent exercise, have observed an increase in work output and duration when compared to no treatment (Goff et al., 1956; Falls, 1972; Roundy and Coomy, 1968; Sills and O'Riley, 1956).

In summary, therefore precooling suggests that triathletes may be at an advantage to have a slight lowering of core temperature (0.5 °C ) upon the completion of the swim leg. This view appears to be supported by Falls (1972) P147 stated "Consequently any cooling modality that reduces mean body temperature sufficiently would be expected to reduce the physiological strain of combined heat-exercise stresses." The lowering of core temperature effectively gives the athlete an extended buffer before thermoregulatory responses are employed (Baum, Bruck and Schwennicke, 1976). The buffer period then allows increasedcentral blood volume to be directed to the working muscles possibly accounting for the improved exercise work capacity (MacDougall et al., 1974).

Precooling is also likely to allow the athlete to maintain lower mean core temperatures throughout the race, thereby reducing the competition between the thermal and metabolic demands of the exercising body (Rowell, 1974; Jessen,1987a). The possible importance of precooling was noted by Baum et al., (1976), who stated " Even slight lowering of resting body temperatures may become significant in the end phases of a run." (Baum et al., 1976 p. 410).

It may be necessary for triathletes to forgo a performance advantage in the swim leg associated with wearing a wetsuit (Lowdon, 1987). By not wearing a wetsuit a slight decrease in core temperature may result, thus enabling the athlete to capitalise on increases in performance during the bike and running legs. Further research is needed to specifically ascertain whether the increased performances that are associated with wearing a wetsuit outweigh the possible advantages of a lower body temperature. Prolonged Exercise in Heat

Exercise in cool conditions can cause a rise in metabolic rate of 20-25 times resulting in a heat production exceeding 1000 watts (Nadel et al., 1987, Gisolfi and Wenger, 1984). Exercise therefore produces a great deal of heat which the body must dissipate in order to maintain effective functioning (Jessen, 1987b). When humans are exposed to moderate to high ambient temperatures and exercising for prolonged periods, thermoregulatory responses, are of critical importance to prevent a change in thermal gradients throughout the body.

The body has two major mechanisms that assist in the regulation of body temperatures in heat: (1) sweating in which heat is lost through evaporation; and (2) vasodilation or the redistribution of blood to the periphery (Brooks and Fahey, 1984; Haymes and Wells, 1986). Both mechanism are of primary importance in the regulation of body temperatures in man as they increase the thermal gradient between the core and the skin, aiding in the dissipation of heat. The following review will deal with sweating and blood responses to exercise in the heat.

Sweating

Sweating is an effective means for the body to dissipate heat, however, for heat to be lost the sweat must first be evaporated. The body is capable of losing 0.58 kcalmin"1 through evaporation and is able to maintain a whole body sweat rate of 20- 25 ml.min-1, although peak values of 66.7 ml.min"1 have been observed (Taylor, 1986; Nadel, 1977). Sweating therefore enables considerable amounts of heat and body fluids to be lost (Haymes and Wells, 1986). The reliance on sweating as the major mechanism of heat loss at high ambient temperatures (greater than skin temperature) occurs due to the body being in predominatly a heat gain situation. Under such conditions heat loss through the others avenues of heat exchange (convection, conduction and radiation) are negligible and may even add to the thermal load placed on the body (Haymes and Wells, 1986).

The sweat that appears on the surface of the skin for evaporative cooling is secreted by two types of sweat glands, apocrine and eccrine sweat glands (Haymes and Wells, 1986; Taylor, 1986; Fortney and Vroman, 1985). Apocrine sweat glands are found primarily in the hands, feet, groin and armpits and are predominantly involved with insensible heat loss (Taylor, 1986; Fortney and Vroman, 1985). Thus apocrine sweat glands do not play an important role in the dissipation of heat from the body during exercise (Haymes and Wells, 1986). Eccrine sweat glands are distributed throughout the body and are mainly involved in the secretion of sweat when stimulated by the anterior hypothalamus. Eccrine sweat glands are regarded therefore as the thermal sweat glands of the body (Haymes and Wells, 1986). Sweat gland activity is primarily a function of body temperature when exercising in hot conditions (Nadel et al., 1980; Fortney and Vroman, 1985).

The sweat rate and evaporative power of the body are affected by several variables that can both increase or decrease the capability of the body to dissipate heat to the environment. These components are physical fitness and the environment.

(1). Physical fitness.

Training results in the initiation of a sweating response at a lower core temperature (Taylor, 1986). The increase in the sensitivity of the sweating mechanism allows for the athlete to control the flux in core temperature earlier and thus avoid subsequent rises in core temperature. Endurance athletes also display a greater sweat output and therefore an increased capacity for heat loss through evaporation (Taylor, 1986). The increase in sweat output due to training has been postulated to be caused by structural changes at the site of the sweat gland. The sweat gland with training becomes larger and thus less prone to blockage when the skin is wetted (Taylor,1986).

(2). The environment.

Environmental temperatures have a direct influence on the heat loss mechanisms of the body. As environmental temperature increases the body is more prone to the storage of heat, thus influencing rectal temperature and the initiation of a sweating response to combat the heat gain by the body. However the effectiveness of the body to dissipate heat through evaporation is influenced by water vapor pressure or humidity in the environment (Brooks and Fahey, 1984; Haymes and Wells, 1986). High levels of humidity (70-80%) are associated with the eastern coastline of Australia (Bureau of Meteorology, 1988) where a predominant number of triathlons are held. Thus not only do athletes have to contend with high ambient temperatures and prolonged metabolic demands, but also reduced thermoregulatory capacity due to elevated humidity levels. High levels of humidity are associated with lower sweat rates and evaporative capacity (Frye and Kamon, 1983; Shvartz and Benor,1972a and 1972b; Fox and Goldsmith, Hampton and Hunt, 1967; Gonzalez, Pandolf and Gagge, 1974).

The lower evaporative power of the environment results in increased skin wettedness which in turn causes the physical suppression of sweat output (hidromeiosis). Hidromeiosis results in the blockage of the sweat glands due to the absorption of water by the stratum corneum (Taylor, 1986; Frye and Kamon, 1983; Fortney and Vroman, 1985). Increased skin wettedness and reduced evaporative power result in elevated skin temperatures. The higher skin temperatures reduce the thermal gradient between the core and the skin thus causing the body to increase blood flow to the periphery to assist in thermoregulation. However vasodilation is contrary to the needs of the exercising organism as it results in a compromise in blood flow to the working muscles (Rowell, 1974).

Blood Flow Redistribution due to Exercise

Vasodilation involves the directing of blood from the core of the body to the peripheral tissues, which influences the core to skin temperature gradient (Nadel et al., 1987). Increasing the skin temperature has two major effects: (1) it will initiate sweating in which heat loss will be promoted via evaporation; and (2) the shifting of blood to the periphery will result in an increase skin temperature. Therefore the gradient between the skin and the environment will be greater and thus increase the amount of heat dissipated from the body via conduction (Nadel et al., 1987). However such changes come at an expense, directing sufficient blood to the skin for thermoregulation at the expense of muscles will result in anerobiosis (Nadel et al., 1980). The body overcomes the effect of anerobiosis through vasoconstriction of non-working areas of the body which results in a reduction in splanchnic adrenal blood flow. Vasoconstriction to the adrenal and splanchnic regions enables an extra 2.2 I.min-1 of blood to be used by the working muscles resulting in an increased central blood volume to be distributed to the working muscles (Rowell, 1974; Fortney and Vroman, 1985). The vasoconstriction of vital organs permits an extra 600 ml.min""' of 02 to be delivered to working muscles. Thus vasoconstriction can accommodate for a significant rise in v"02 without an additional increase in CO2 (Rowell, 1974). Vasodilation is believed to be an active process and not just passive after the vasoconstrictive tone of the body has been reduced (Fortney and Vroman, 1985). Nadel et al. (1979, 1980) noted that cardiac output was 1.3 I.min"1 greater when exercising at 26 °C than at 20 °C. The increase in cardiac output observed by Nadel et al. (1979, 1980) may therefore be due to the need to distribute blood to the skin and the periphery which was not needed in the cooler ambient temperatures. 51

Thermoregulatory and Cardiovascular Responses to Prolonged Exercise

Prolonged exercise places several demands on the cardiorespiratory system. Rowell (1974) observed 4 changes found to prolonged exercise: (1) a continuous rise in heart rate but no change in cardiac output; (2) a continuous fall in stroke volume (Senay 1987; Ekelund, 1967; MacDougall et al. 1974); (3) a progressive reduction in blood pressure, pulmonary arterial pressures, right ventricular and diastolic pressure (Senay 1987; Ekelund, 1967); and (4) a VO2 and a arterio-venous difference rise by 5%, with no significant changes in blood volume. Rowell (1974) therefore concluded that plasma volume changes do not account for this cardiovascular drift. Shaffrath and Adams (1984) noted changes in plasma volume only occurred in the first 12 minutes of exercise. Thus blood volume changes did not initiate cardiovascular drift (Shaffrath and Adams, 1984). The changes noted by Rowell (1974) during prolonged exercise are the physiological changes that occur during cardiovascular drift (Shaffrath and Adams, 1984).

Saltin and Stenberg (1964) noted a decrease in working capacity but no reduction in VO2 after prolonged exercise. Saltin and Stenberg (1964) examined 6 subjects in a prolonged exercise protocol (180 min) that elicited 75% VO2 max at 19 °C. Subjects rested for 90 minutes and then proceeded to work maximally. Saltin and Stenberg (1964) noted that v*02 max was unaffected by prolonged exercise prior to VO2 max test. However there were a number of changes that indicated a drift due to the prolonged exercise. Heart rate was seen to rise on average 23 beats per minute. An increase in cardiac output resulted, although it was not as large as the increase in heart rate. The smaller increase in cardiac output was presumed to be caused by a reduction in stroke volume of 4 - 23 ml. The increase in cardiac output was also mirrored by a 5% increase in in submaximal 02 consumption. Saltin and Stenberg (1964) noted that there was a decrease in arterial pressure indicating that there may have been a decrease in peripheral resistance. The decrease in peripheral resistance was due to vasodilation of the skin in order to balance heat and thermoregulation of core temperature which increased by 0.6 of a degree.

Sawka, Knowlton and Critz (1974) noted similar changes to Saltin and Stenberg (1964); an increase in heart rate, a slight increase in cardiac output and a significant reduction in stroke volume. Such changes have been supported by Sawka et al. (1979) as being caused by competition between the skin and muscle due to the thermoregulatory demands of the body to dissipate heat. Rowell et al. (1969) supports the theory put forward by Saltin and Stenberg (1964). Through direct heating of the skin, Rowell (1969) found that when the skin temperature was increased lower levels of oxygen uptake reduced peripheral venoconstriction that was normally associated with an increase in exercise intensity. The reduction in resistance due to an increase in skin temperature caused a dramatic increase in blood moving to the periphery. The movement of blood to the periphery causes a lag in venous return and results in a reduction in central blood volume (Rowell et al., 1969). Furthermore, MacDougall et al. (1974) found that prolonged exercise caused a reduction in stroke volume but the reduction in stroke volume was augmented by an increase in ambient temperature. The reduction in stroke volume indicates two points: (1) that an increased venous compliance had resulted in a reduction in ventricular filling pressure; and (2) vasoconstriction to non working muscles and the splanchnic region as indicated by Rowell (1974) is not sufficient to prevent a deficit in venous blood flow (MacDougall et al., 1974; Senay, 1987; Shaffrath and Adams, 1984). Increased peripheral venous supply increases the time available for heat exchange with the skin. Increased peripheral blood flow also reduces the exchange of heat to arterial blood being carried to the working muscles (Gisolfi, 1984; Fortney and Vroman, 1985).

Cardiac output is then maintained by increasing heart rate due to the reduction in stroke volume (MacDougall et al., 1974; Senay, 1987). However this is further complicated by the drift that is associated with prolonged exercise (Kreider et al., 1988a; Saltin and Stenberg, 1964). The theory that the cardiovascular drift experienced in prolonged exercise is due to thermoregulation devices is supported by Rowell et al. (1969). Through cooling of the skin he found that cardiovascular drift was eliminated and that this occurred due to the vasoconstriction that resulted when the skin temperature was lowered. The elimination of cardiovascular drift through lower skin temperatures is of direct significance to this study. Athletes who complete the swimming leg of a triathlon without a wetsuit would be likely to have lower skin and body temperatures than those who wore a wetsuit. Thus the lower skin temperatures would reduce the effects of cardiovascular drift during the bicycle and run stages of the triathlon. Through manipulation of airflow on the body and thus lowering of skin temperatures cardiovascular drift was eliminated when exercising for 70 minutes (Shaffrath and Adams, 1984). When the skin was cooled after 70 minutes of exercise (by a fan 4.3 m.s"1) for 5 minutes it was found that a reversal in the cardiovascular drift had occurred resulting in a 10 beat lowering of heart rate. This indicates the positive effects that an increase in central blood volume due to lower skin temperatures has on cardiovascular drift (Roberts and Wenger, 1979).

When exercise intensities were manipulated (43.4% MVO2 and 62.2% MVO2), rather than skin temperature, it was noted that a larger cardiovascular drift occurred when exercise was of a higher intensity. This could be explained due to the higher metabolic thermal load that caused increases in rectal temperature and thus stimulated increased blood flow. When the skin was heated it was noted that vasodilation occurred and cardiac output was affected (MacDougall et al., 1974). The vasodilation resulted in a decrease in stroke volume and aortic pressure. It therefore seems that skin temperature directly influences peripheral blood flow (Rowell et al., 1969; Bergh and Ekblom, 1979). It appears however that at high intensities (68% VO2 max) the level of blood flow was found to be similar and even smaller than lower intensity activities (Rowell et al., 1969). That is, when exercising at high intensities in the heat, blood flow to the periphery does not increase significantly and may even constrict reducing the bodies ability to dissipate heat. The findings of Nadel et al. (1979) support Rowell et al. (1969) that exercise at relatively low intensities (40% of MVO2) resulted in an increase in cardiac output. However under heavy exercise intensities they found no increase in cardiac output. Nadel et al. (1979) summized that the body found it extremely difficult to increase cardiac output to meet the extra demand. Thus when intensities are high, the blood flow to the muscular system influences the blood flow to the periphery for thermoregulation. The reduced ability of the body to dissipate heat at high intensities was noted also by Davies (1979). Davies (1979) found that at high workloads (85% Mv'02) skin temperature did not vary substantially which resulted in a reduction in the sweating capacity of the body. Due to the reduced sweating capacity of the body rectal temperature became much more sensitive to changes in ambient temperature resulting in a reduction in heat dissipation. The reduced ability of the body to dissipate heat at high intensities may indicate that metabolic demands are given a priority over thermoregulation during exercise. Nadel et al. (1980) indicated that heavy exercise in cool conditions results in high heart rates and cardiac output. It is therefore difficult for the body to augment cardiac output in hot environmental temperatures. Thus to maintain cardiac output under high intensities and thermal conditions the body reduces the relative blood flow to the periphery enabling exercise to continue at the cost of increasing core temperature.

Roberts and Wenger (1985) suggested that the reduction in skin blood flow may be initiated by baroreceptors activated due to a lowering in central venous pressure. When the baroreceptors are activated this may override cutaneous vasodilator reflexes resulting in lower skin blood flow (Roberts and Wenger, 1985). The reduction in peripheral blood flow occurs however at the expense of the thermoregulation. Such changes to blood flow are significant to this study as triathletes will be working at exercise intensities similar to Kreider et al. (1988a) and Rowell et al. (1969). Thus according to Rowell et al. (1969) thermoregulation will be secondary to the performance of the exercise activity. Thus large changes in core temperature and cardiovascular drift would be expected when competing in a triathlon. This was supported by Kreider, Boone, Thompson, Burkes and Cortes (1988a) who examined the thermal and cardiovascular responses of completing a triathlon. Kreider et al. (1988b) and Boone and Kreider (1976) noted that cardiovascular drift was associated with the performance of a sprint distance triathlon and biathlon. Furthermore, core temperature rose significantly during the triathlon by 2.7 °C supporting previous research on the effects of prolonged exercise and thermoregulation (Kreider et al., 1988a).

Blood flow during prolonged exercise is of critical importance to exercise performance. Under high thermal demand the body directs a large portion of blood from the muscles to the skin (Rowell,1974; Nadel et al., 1980; Haymes and Wells, 1986). The shift of blood to the shell prevents a large flux in core temperature (Nadel et al., 1979). However to compensate for increased blood flow to the periphery there is a resulting increase in cardiac output which is augmented by higher ambient temperatures (Nadel et al., 1979; Nadel et al., 1980). Prolonged exercise at different ambient temperatures has been shown to influence both endurance time to exhaustion and peak aerobic power (MacDougall et al., 1974; Bergh and Ekblom, 1979; Saltin, Gagge, Bergh and Stolwijk, 1972). If the flux in core temperature is not controlled exercise will have to be discontinued (Nadel et al., 1979). Prolonged exercise in the heat not only causes changes in the distribution blood flow and cardiovascular drift but also affects the distribution and quantity of body fluids present for thermoregulation.

Plasma Volume Changes due to Exercise

The effects of heat and exercise on blood volume are determined mainly by changes in the forces between absorption and filtration acting along the capillary beds (Harrison, 1986). Prolonged exercise in the heat is noted to cause a reduction in blood volume through plasma volume changes as a consequence of fluid shifts in the body (Senay, 1985). Plasma volume changes are affected by 3 factors: exercise intensity, posture and the state of hydration of the body (Senay, 1985).

Research in the area of plasma volume changes in exercise has been noted for the continual disagreement among researchers of the responses that are initiated for different types of exercise under certain conditions. (Wells et al., 1987; Senay, 1985; Harrison, 1985). However such dispute in the findings over plasma volume changes may merely highlight the transient nature of body fluids and the effects of intersubject variability when exercising (Harrison, 1985; Wells et al., 1987). Body fluids make up a major part of total body weight, with average total body water consisting of approximately 40 - 70% of total body weight. Approximately 3 kg of this weight is made up of plasma water, which is in close contact with other compartments of water throughout the body (Senay, 1985). The transient shifts of fluids in and out of the vascular spaces causes hemodilution, the progressive gain of interstitial fluid and hemoconcentration which is the progressive loss of plasma water (Harrision, 1985). The primary cause of changes in plasma volume appears to be due to increased capillary and hydrostatic pressure which occurs when exercise is initiated (Convertino, 1987; Hahn, 1988; Harrison, 1985). Hemoconcentration or hemodilution is predominately affected by the severity of the thermal strain the body is placed under (Harrison, 1985).

Hemoconcentration is believed to result when vasodilation occurs which is stimulated by the rise in core temperature. The rise in core temperature thus increases capillary perfusion and hydrostatic pressure leading to the efflux of plasma water (Harrison, 1985, Senay, 1985). Less severe thermal stress causes venodilation but not vasodilation and as such leads to a drop in hydrostatic pressure and thus hemodilution results (Harrison, 1985). The shift in body fluids is very rapid initially; stabilization of plasma volume is usually achieved after 10 minutes of activity (Convertino, 1987; Harrison, 1985). The continued loss of plasma volume is avoided through several protective mechanisms of the body. Vasoconstriction of inactive tissues as noted by Rowell (1974) reduces capillary hydrostatic pressure and thus potentially increasing the amount of plasma proteins entering the vascular spaces (Harrision, 1985; Harrison, 1986).

As previously found during prolonged exercise in the heat, demands for cardiac output are very high leading to the eventual compromise of thermoregulatory mechanisms in order to meet the increased exercise metabolic demands of the body (Rowell et al., 1969). Thus a reduction in the plasma volume and therefore effectively a reduction in blood volume will result in increased demands being placed on cardiac output (Hahn, 1988). The increased demands for cardiac output will hamper the ability of the body to dissipate heat and delivery sufficient O2 to the working muscles (Harrison, 1985).

As stated previously posture, exercise intensity and hydration will affect plamsa volume changes, thus different exercise activities are likely to cause specific responses to plasma volume. As triathlons are a combination of three activities an examination of each of the activities in relation to plasma volume is warranted. Swimming exercise was found by McMurray (1983) to cause hemoconcentration when compared to a resting semi supine position in water. As the relative body position was the same between the resting and exercise state changes in plasma volume were then due to the activity itself. McMurray (1983) found that the cause of efflux of plasma from the extracellular compartment was due to the higher mean arterial blood pressure which is associated with upper body arm activities (Holmer, 1974; McMurray, 1983). Furthermore, McMurray (1983) noted that plasma volume shifts when swimming were similar in nature to those experienced when performing a cycling activity. Bicycle exercise generally has been shown to decrease plasma volume up to 8 - 15%. Such decreases in plasma volume have been found to be directly proportional to exercise intensity within the range of 40% - 90% of maximum oxygen uptake (Harrison, 1985). Thus triathletes would undergo a substantial decrease in plasma volume during the cycle stage due to the prolonged nature and likely intensity of the leg. Such a reduction in plasma volume would therefore hamper thermoregulation and exercise performance (Wells et al., 1987).

Wells et al. (1987) in a study examining the fluid shifts of triathletes performing successive running and bicycle activities, found significant changes in plasma volume. Wells noted that a 10km run followed by an 40km bike resulted in a greater decrease in plasma volume (9%) than when the legs were reversed (7.75%). The difference in plasma volume losses found by Wells et al. (1987) would likely be due to the ability of the body to maintain plasma volume during running activities (Wells et al., 1987; Senay, 1985; Harrison, 1985).

Two variables which are used to measure plasma volume changes are hematocrit (the percentage of packed red blood cells) and hemoglobin. The use of hematocrit and hemoglobin as means to calculate plasma volume changes is dependent on several factors (Costill and Fink, 1974): (1) that the volume of red corpuscles is constant; (2) the ratio between the red blood cell size is constant; and (3) the ratio of hematocrit and whole body hematocrit remains unchanged (Costill and Fink, 1974; Harrison, 61

1985). These assumptions are believed to be reliable indicators of changes in plasma volume (Harrison, Edwards and Leitch, 1975). However it is believed that if water is lost from the red blood cells due to exercise, that hematocrit measures may in fact underestimate plasma volume changes. Harrison (1985) therefore suggests the use of both hemoglobin and hematocrit to obtain accurate estimations of changes in plasma volume.

Large thermal and cardiovascular demands appear to be placed on athletes when performing a triathlon. Specific investigation into the thermal demands and the possible way athletes may manipulate these demands through the use of wearing a wetsuit therefore is warranted. At present there is a paucity of information on the thermoregulatory effects of afterdrop and precooling on triathlon performance. With this in mind the following research was designed to establish more clearly the thermal and cardiovascular responses when core temperture is manipulated through the application of a wetsuit in the swimming leg. 62

CHAPTER 3

METHODS DEFINITIONS

Afterdrop

Conceptual definition: The continued lowering of core temperature after immersion in water. Operational definition: The continued lowering of rectal temperature after completion of 30 minutes of tethered swimming in 20 °C ±0.68 °C water. The subsequent 2 minute bicycle rectal temperatures are subtracted from the final (30 min) rectal temperature reached in the swimming stage of the triathlon.

Triathlete

Conceptual definition: A person that has competed in an event consisting of swim, bike and run stages. Operational definition: A male athlete that has competed in triathlons over the last two years. The athlete has been training consistently for triathlons and has a MV02 between 60 - 80 ml-kg-1-min_1.

Triathlon

Conceptual definition: A race involving three successive events (swim, bike and run) in the same order without rest. Operational definition: An event in which subjects exercised at 65-70% of M\>02 in the swim, bike and run legs for the following durations respectively (30 minutes, 70 minutes and 40 minutes). Each leg was simulated using the following equipment: A tethered device for the swimming leg, a bicycle ergometer for the bicycle leg and a motor driven treadmill for the running leg.

Core temperature.

Conceptual definition: The temperature of the deep tissues of the body. Operational definition: The temperature of the body 10 cm within the anal sphincter as measured by a Y.S.I 400 series rectal probe and telethermometer.

Skin temperature

Conceptual definition: The mean temperature of the bodies periphery. Operational definition: The mean temperature taken from 4 sites (chest, arm, shin, thigh) of the body using Y.S.I 400 series skin termistor probes and telethermometer. DELIMITATIONS

1. Conclusions drawn from this study were only applicable to the characteristics of the subject population used in this study.

2. Physiological responses measured and monitored were only directly applicable to those environments (25 °C dry bulb and 73% relative humidity) that the athletes were tested in. It should be noted however 25 °C dry bulb and 73% relative humidity are the climatic conditions likely to be experienced at 9.00 am along the Australian Eastern Coast Line.

3. The duration of the testing simulated a triathlon of 1.6 km swim, 40 km bike and a 12 km run. Responses in triathlons of a longer or shorter duration may not reflect the findings found in this study.

4. Windspeed was controlled during the bike and running legs at 7.5 m.s'1 and 4 m.s"1 respectively. Therefore heat loss due to convective currents were specific to wind velocities present in this study.

5. Water temperature was controlled at 20 ±0.68 °C whilst subjects completed a full triathlon. The water temperature was one that triathletes were likely to experience. Physiological responses measured were specific to this water environment. LIMITATIONS

1. Variations in diet and training regimes outside the constraints placed on each athlete may account in part for changes in performance during testing.

2. Fluctuations in temperature of the climate chamber were assumed to be equal for all subjects. Therefore identical thermal stress was assumed to be placed on each subject.

3. The use of ergometers were only a simulation of each stage of a triathlon and therefore conclusions drawn from the study were limited to use of this equipment.

4. Ambient temperature fluctuations may influence the rate of heat loss experienced by each subject whilst swimming. However there exposure was limited due to the constant submersion of the body in the water.

5. Movement of the rectal probe did not allow for all subjects to be included into the statistical analysis, resulting in smaller subject numbers than originally anticipated.

6. Three subjects during the testing protocol had to stop and void their bladder. Subjects completed this during the transition period and the third stopped during the treadmill run between oxygen consumption samples. The volume was measured and recorded to be used in the calculation of weight losses. METHODOLOGY

Subjects

The subjects selected for the study were 15 trained males. Each subject finished in the top 60 places in the major triathlons within N.S.W and Q.L.D. in the 1988-1989 season. Participants in the study were aged between 24 - 35 years with a mean age of 29.6. ±3.8 yrs. The subjects in the study were engaged in physical activity specific to triathlons on a daily basis. Prior to participation, all subjects in the study completed an informed voluntary consent form (Appendix A) and a medical questionnaire (Appendix B). Ethical clearance was obtained from the University of Wollongong Human Experimentation Committee and adhered to the guidelines presented in the Statement on Human Experimentation produced by the National Health and Medical Research Council (Appendix C).

TESTING PROCEDURES

Anthropometric Measurements

Anthropometric measurements were taken of variables which were likely to affect temperature regulation. The height of the subjects was measured on a Holtain stadiometer and recorded to the nearest 0.1cm. The mass of the subject (wearing swimming costumes) was measured on a precision balance scale (AND FW- 105K) and recorded to the nearest ±20 g. Body mass area was calculated according to Dubois method: surface area (m2) = 0.00718 x WtO-425 x Ht°725 (Dubios and Dubois, 1916). Skinfold thickness (triceps, subscapular, suprailiac, umbilical, biceps, thigh, medial calf, axillary) was measured using Harpenden skin calipers with the sum of eight skinfold sites being recorded (Telford et al., 1984) An experienced tester was used to take all skinfold measurements on the all subjects in order to improve reliability . Percentage body fat was also calculated as indicated by Brozek et al. (1963) and Durnin et al. (1984) for comparison to current literature.

Cardiovascular test

Cardiovascular fitness has been related to an individual's thermoregulatory responses and is specific to the type of exercise that is performed (Thoden, 1982; Kohrt, Morgan, Bates and Skinnner, 1987). Therefore, the maximum oxygen uptake (MV02)of every subject was measured for each of the stages of a triathlon: a. Swimming maximum oxygen uptake

A tethered swimming device was used to determine maximum oxygen uptake whilst swimming, (Costill, 1966; Bonen et al., 1980, Borchers and Buckenmyer, 1987). The swimming protocol consisted of a continious incremental exercise test. Swimmers were required to swim with a 2.5 kg load for 3 minutes which acted as a warm up and a familarisation session. The subject was then stopped and any adjustments to the breathing apparatus were made. The test then commenced on a 3 kg workload which was increased by 0.5 kg or 1.0 kg depending on swimming ability, every 2 minutes (Kohrt, Morgan. Bates, and Skinner, 1987). Gas samples were taken for one minute in the final minute of each workload. The test was completed when volitional exhaustion had been reached and or the athlete was unable to maintain a stationary position in the pool. V02 peak was considered to be obtained when: (a) a plateau (less than 100 ml-min-1) or lowering of VO2 ml-kg~1min~1 as workload increased beyond the workload that first resulted in a maximum value, (b) a respiratory ratio greater than 1.00, and (c) a heart rate reaching age predicted maximum (Thoden, 1982). The swimming maximum oxygen uptake test was held in a 25 metre pool heated to 27 °C to assist the subjects in attaining their MVO2 (Holmer and Bergh, 1974; Nadel et al., 1974a). b. Bicycle maximum oxygen uptake

After at least 7 days of rest, following the swimming MVO2 a stepwise incremental maximum oxygen uptake test according to Craig and Walsh (1989) was used to determine cardiovascular fitness on a cycle ergometer. The cycle ergometer used was a modified air brake Repco Cycle Ergometer (Model No HP5209) with the following modifications being made on the bike: (a) a compound gearing system with a single 48 tooth chain ring driving a 14 tooth sprocket; (b) the 14 tooth sprocket inturn drived a 18,19,20,21,24 or 26 tooth cluster on the wheel. The gear ratio was selected by a handle bar control lever connected to a conventional deurailler; (c) on the opposite side of the hub was a magnetic sensor mounted adjacent to a 60 tooth steel sprocket 70 which enabled a Repco Ex50 Exertech Work Monitor Unit to be utilized; (d) the chain wheel had attached 170 mm cranks in which Look (PP66) quick release competitive cycling cleats were connected. The subject then adjusted the bike according to comfort. All measurements (ie. seat height, handle bar length) were recorded to allow for identical bike dimensions throughout the study. The work monitor was calibrated to record work at an atmospheric pressure of 760 mm Hg and an ambient temperature of 22 °C. The formula as stated by Craig and Walsh (1989) was used to calibrate the work monitor unit for differing ambient conditions.

The subject was required to exercise at 125 watts for three minutes. The workload was then increased by 25 watts every minute until volitional exhaustion was reached or the work load could no longer be maintained (subjects were in the final minute required to complete the minute regardless of the work output). Maximum oxygen uptake was reached when subjects met the criteria according to the swimming MV02- c. Running maximum oxygen uptake

After 7 days of rest, following the bicycle Mv*02 subjects performed a maximum oxygen uptake test on a motor driven treadmill to test cardiorespiratory fitness whilst running according to Thoden (1982). The test was preceeded with a 5 min warm up period at a speed that was increased slowly until determined comfortable by the athlete (10.0-14.0 kph). Once a comfortable speed had been established, the test started at 0% grade for 2 minutes followed by a 2% increase in grade every minute until volitional exhaustion was reached. Prior to testing the motor driven treadmill was calibrated for belt speed (10 - 20 kph) at I kph intervals over 25 revolutions with a subject on the treadmill. The treadmill was also calibrated for grade and changes in speed at aforementioned speeds.

All ventilatory measurements recorded during all three M\Jr02 tests were made by standard open circuit spirometry. Subjects wore nose clips and breathed through a Hans Rudolph low resistance, low deadspace valve which was connected to a mixing chamber via light weight tubing. The volume of air was measured by a turbine Ventilation Monitor (Morgan Mark 2) and corrected to Standard Temperature Pressure Dry (STPD) via a computer. The ventilation turbine was calibrated using a 1 litre syringe before and after each test. The ventilometer placement in the swimming V0 2 analysis was via a 0.5 m snorkel arrangement (thus preventing water entering the ventilometer) similar to that used by Holmer (1972). Oxygen (Morgan Mk 701) and carbon dioxide (Morgan) analyzers, calibrated by 3 gravimetrically weighed standard gases (throughout the physiological range) were used to measure the fraction of oxygen and carbon dioxide in a sample of respiratory gases which was taken from a mixing chamber. Expired gas samples were taken every minute and dried prior to analysis. They were then analysed by the gas analysis system indicated above. The fraction of expired oxygen and carbon dioxide and ventilation were manually entered into a computer programme which calculated oxygen consumption for the minute. Heart rate was recorded during the last 10 seconds of every minute with the use of a Sports tester (Model PE3000s). Testers used in the calbration of the equipment were kept the same in order to improve the reliability of the procedures used.

Confirmation of Workload.

Upon the completion of each MVO2 in the swim, bicycle and run, the subject was required to exercise for 10 minutes to confirm the workload that would elicit 70% of MVO2. This was performed approximatly 20 minutes after the MVO2 test. In the bicycle stage the confirmation of workload allowed for the athlete to change gears, cycling at a preffered cadence to simulate more closely race conditions.

RESEARCH PLAN

Upon completion of the MVO2 tests subjects were required to complete two triathlons that were separated by at least 7 days (Wells et al., 1987). At least 7 days after the MVO2 subjects were randomly allocated in the wearing of a wetsuit (Ocean 1 5 mm "Long John" smooth triathlon suit) in the swimming leg of one of the triathlons.

PROCEDURE PRIOR TO TESTING

The subjects were required to monitor their training and diet 14 days prior to the commencement of testing and continued to monitor diet and training throughout the testing period. Subjects filled out a dietary diary prior to testing which required the subject to record all foodstuffs and fluids consumed (Appendix D). Subjects also completed a record of training undertaken 2 weeks prior and during the testing protocol. The record included the total distance trained on each day, heart rates at each training session and type of training used (Appendix E). The subjects were recommended to maintain a similar diet and training regime throughout the entire testing protocol. The diary was a means to assist the subjects in achieving this goal.

TRIATHLON TESTING PROCEDURES

Subjects were required to fast for a 4 hour period prior to testing and not engage in any physical activity on the day of testing (Shaffrath and Adams, 1984). The subjects, upon arrival to the laboratory, voided both the bladder and bowels. The subjects were then given instructions on the correct method of inserting a rectal thermistor. Following the insertion of the rectal thermistor subjects consumed 400 - 500 ml of water which ensured optimal hydration. Subjects were weighed on a precision balance scale to the nearest ±20 g whilst wearing a swimming costume. Following the weighing, subjects were attached with skin thermistors and a heart rate monitor (Pe 3000 with Micro Pellet Electrodes attached) whilst seated. After the completion of the preparation subjects were reweighed. Prior to the commencement of the test protocol subjects had blood samples taken whilst being seated on a chair for at least 20 minutes.

Upon the completion of the preparatory section the subjects were then ready to commence the test protocol which consisted of five phases: a swim; a transition period; a bike; a transition period and a run.

Swim

Prior to the commencement of the swimming leg subjects were fitted with a belt which was placed on the waist and attached to the tethered swimming device. Subjects then entered the water (wearing a "Speedo" single layer rubber cap and goggles) and were standing (at rest) neck deep for a period of 5 minutes. This simulated the wait of an athlete prior to the commencement of a triathlon race. Upon the completion of the 5 minute rest period the subjects commenced the swimming simulation with the use of the tethered swimming device. Subjects were required to exercise at 70% of their MV02 for a period of 30 minutes. The 30 minute period equated to the approximate time period needed to complete 1600 metres whilst free swimming. During the 30 minute period core temperature, skin temperature and heart rate were taken every 5 minutes. Expired gases during the swimming phase were sampled in the 4 - 5 minute, 14-15 minute and the 29 - 30 minute. VO2, HR and al temperatures were taken while the subject was performing the activity.

The pool used in this study was a U.F.i. free standing hydrotherapy pool 6 m x 1.4 m deep. This type of pool was chosen due to its relative portability which allowed it to be situated close to the climate chamber, thus simulating the distance that would be covered in a transition period during a triathlon. The pool was of adequate dimensions to allow for swimming to be unimpended. Temperature of the pool was regulated through the application of a cover to maintain heat when not in use and the application of ice prior to testing when pool temperature was too high. Water temperatures were only taken when the water was well stirred.

Transition swimming stage to bicycle stage

At the end of the swimming period the subjects were assisted by testers to remove the belt and commence the transition phase. Core temperature and skin temperature were monitored every 2 minutes in the first 20 minutes of exercise on the bicycle ergometer. No fluids were allowed to be consumed during the swimming leg or transition period. However, once the subject had commenced the cycle leg water was allowed to be consumed ad libitum. The transition was timed from the moment the swim leg had been completed. The transition required the athlete to place a helmet (Bell V1 Pro) on the head and cycling shoes on the feet. The subject wore no clothing other than the costumes worn in the swimming leg and was not allowed to towel down during the transition period. The subject then proceeded to the bicycle ergometer which was set to the correct dimensions as determined by the subject in the MvX>2 test. The transition period ended when the subject had both feet clipped into the pedals of the bicycle and was looking straight ahead. The subject was then required to wait for a period of 3 minutes (including the transition period) before cycling was commenced. The fixed 3 minute period allowed standardization of the exposure to the environment and rest between each leg of the triathlon. No blood samples were taken from the subjects during the swim-bicycle transition due to the difficulty of obtaining a sample from cooled extremities found during the pilot testing. On the commencement of the bicycle stage, a fan was switched on which caused a wind speed of 7.5 m.s"1. Wind velocity was measured by an Izuzu aneometer (OSK 7116 OGAWA SEIKI) at a distance where the body would be expected to interface with the convective currents of the fan. The wind velocity simulated the convective currents that cyclists are exposed to whilst racing 27 km.h-1 in still air. The wind vanes of the cycle ergometer were not exposed to the convective currents of the fan so that workload would be unaffected (preventing spilling of air over the wind vanes).

Bicycle

After the 3 minute transition period, the cycling stage consisted of 3 minutes cycling at 50% MVO2 followed by 67 minutes at 70% M>)02- The warmup period (50% MVO2) simulated in part the accomodation period that occurs after the swimming leg in a real triathlon event. Skin temperature, core temperature and heart rate were taken every 5 minutes, except the first 20 minutes of the cycle as metioned above. Calibration of the Repco Ex 50 Work Monitor was completed prior to the commencement of each subject test. Subjects were allowed to drink freely during the cycling phase which was administered through water bottles. The water bottles were refilled to a known value and the difference was used to calculate the water consumed during a 10 minute period. In the subsequent triathlon subjects were given the identical amount of water that they consumed in the first triathlon which effectively equated the thermal demands placed on each athlete. Oxygen uptake was measured during the 4-5 minute, 14-15 minute, 29-30 minute, 44-45 minute and the 59 - 60 minute. Every 5 minutes during the cycling stage the subjects were given constant information on the time remaining in the leg. Throughout the cycle phase subjects were required to work on the same cadence and gearing (as selected in the familiarization session).

Transition from the bicycle stage to the run stage

Transition phase was started on the completion of the cycling period and stopped as soon as the subject was standing on the running treadmill. During the transition period subjects changed into running shoes (elasticized laces or velcro attachments). No socks, singlet or shorts were worn during the running phase. Upon the completion of the cycling phase blood samples were obtained, afterwhich subjects commenced their transition phase.

Run

Subjects commenced running at a treadmill speed that ellicited 50% MV02 for 3 minutes. Treadmill speed was then increased to ellicit 70% MVO2 which the subject maintained for 37 minutes. Upon the start of the running phase a fan was switched on at 4 metres per second which simulated convective currents present during running in a race (Adams, Fox, Fry, MacDonald, 1975; Shaffrath and Adams, 1984). Wind velocity was measured at the distance where the body would interface with the convective currents of the fan. The grade of the treadmill was set at 0% throughout the testing period. Treadmill speed and grade were calibrated prior to and during testing (as noted in cardiovascular tests measurements). During the running period of 40 minute duration, rectal temperatures, skin temperatures and heart rate were recorded every 5 minutes. Oxygen uptake was measured during the 4-5 minute, 14-15 minute, 29-30 minute and the 39 - 40 minute. Upon the completion of the running period subjects were required to remain standing whilst blood samples were taken.

THERMOREGULATORY MEASUREMENTS

Total Body Sweat Rate Total body sweat rate was calculated using the difference between weight prior to and after triathlon testing. Subjects were asked to void their bladder and bowels prior to the start of testing. The weight after testing was taken when all thermistors had been removed and the subject had towelled down to remove any sweat on the skin surface. Correction for glycogen lost was not made in total body sweat rate calculations

Temperature Measurements. a) Climatic conditions The water temperature was mainatined at 20 °C ± 0.68 °C for the swimming leg of the triathlon. Ambient temperature, relative humidity and water temperature were measured prior and immediately following the swimming phase of the triathlon. The bike and run phases were held in a computer (Hyundai IBM compatible) driven climate chamber in which temperature and humidity were constantly monitored and controlled. Ambient air temperature was kept at 25 °C dry bulb, 21.5 °C wet bulb, WBGT = 22.5 °C with a relative humidity of 73%. In the bicycle leg wind speed was 7.5 m.s-1 and for the running leg this was reduced to 4 m.s-1. The fans were not started until each leg had commenced.

b) Skin temperature Skin thermistors were placed at 4 sites of the body (upper arm, shin, thigh, chest) according to Olesen (1984). Prior to placement of the skin thermistors subjects had the general area shaved to remove body hair and then wiped with alcohol. The specific point at which the thermistor was attached to the skin was marked by a water soluble marker. Skin thermistors were attached to the skin by a porous tape (Transpore, 3M) which was then anchored to the skin by waterproof tape (B.D.F. Leukoplast) so as not to create a micro climate on the skin surface. The following formula was used to estimate mean skin temperature: Sk = 0.3 x (left Chest + right upper arm) + 0.2 x (right anterior thigh + right shin) (Olesen, 1984). c) Core temperature Core temperature was measured by a Yellow Springs Instrument (Y.S.I) 400 series rectal thermistor inserted beyond the anal sphincter to a depth of 10 cm (Neilson and Neilson, 1962).

All thermistors were calibrated prior to testing each subject. A glass thermometer was placed in a stirred water bath at the following temperatures 10°C, 20°C, 30°C and 35°C. and 41 °C. All thermistors were attached to a precalibrated Y.S.I telethermometer. f) Plasma volume Changes in plasma volume were measured by a finger prick sample using a Ames Autolet lancet. Prior to the sample the finger was wiped with alcohol to clean the site. When the finger was pricked the first portion of blood was wiped from the finger and then a Aris Heparinised Micro Haematocrit Tube was filled. No priming of the finger through pressure was used to obtain a sample. The Micro Haematocrit Tube once filled was plugged at one end and placed in a centrifuge (Clements Australia). The sample was then spun down for a period of 3 minutes. Plasma volume was then estimated according Costill and Dill (1974). Plasma volume was also calculated from hematocrit and hemoglobin values in a formula from Harrison (1985). g) Hemoglobin Hemoglobin was measured by a blood sample from a finger prick as mentioned above. The skin was sterilized at the site and an incision was made using a Ames Autolet lancet. The first drop of blood was wiped away. A sample was taken and filled a Vitrex 20 u,l pipette to the calibration mark (with no air bubbles). The blood was then expelled into a test tube containing 3 mis of diluent. The diluent consisted of 0.8 ml of Ammonia (0.88 S.G. concentration) mixed with 1999.2 ml of distilled water in a two litre volumeteric flask. The solution was then placed in a cuvette and analysed in a Delphi Portable Haemoglobin Meter. The solution 81 was measured until two identical readings were obtained. The hemoglobin meter was calibrated prior to each testing session.

STATISTICAL ANALYSIS

All experimental data from the study was presented as means and standard deviations. An analysis of variance (ANOVA), both factorial and with repeated measures on time was used to examine variations between the wetsuit and the non wetsuit groups. Differences were considered significant at p<0.05. A post hoc Scheffe test was used to identify specific mean differences when a significant F ratio was observed. 82

CHAPTER 4

RESULTS Physical characteristics

The physical and cardiovascular characteristics of the subjects in the study are presented in Tables 2, 3, 4 and 5. The data is presented as means and standard deviations. The subjects (aged 29.6 ±3.8 yrs) had a height of 175.84 ±1.53 cm with a mass of 71.74 ±6.86 kg. The sum of skinfolds for the subjects was 51.00 ±11.59 mm, with a percentage body fat of 11 ±2 %. The mean training distances per week of subjects in the present study were observed to be 7.8 ±2.22 km for the swimming stage, 167.2 ±48.05 km for the bicycle stage and 33.5 ±6.72 km for the running stage.

Core Temperature

Figures 2, 3 and 4 represent the core temperature responses measured during the swimming, bicycle and run phases of the triathlon. When core temperature was measured at rest (resting ambient core temperature), prior to the immersion of the subject in the water, no significant difference was found between the Wetsuit (W) treatment and the Non Wetsuit (NW) treatment. The W treatment and the NW treatment had a resting core temperature of 37.5 ±0.31 °C and 37.6 ±0.25 °C respectively.

Swimming Stage

Following the measurement of resting core temperature in ambient conditions, a second resting core temperature was taken TABLE 2

Physical characteristics of subjects in the ^'HY

Subject Age Height Mass Sum of Body B.S.A Skinfolds Fat

(yrs) (cm) (kg) (mm) (%) (m2 )

1 34 181.9 80.3 41 9.1 2.03 2 25 172.8 60.7 52 11.9 1.72 3 24 185.2 78.2 51 11.6 2.02 4 32 177.3 66.4 41 8.8 1.82 5 33 183.7 77.2 42 9.4 2.00 6 33 180.7 68.4 49 11.4 1.87 7 35 178.7 77.0 35 7.5 1.95 8 31 168.9 67.7 75 13.2 1.77 9 28 168.2 65.7 53 10.6 1.75 10 26 171.8 77.3 64 13.5 1.90 1 1 33 178.9 78.3 53 11.9 1.97 12 32 179.5 81.2 41 9.4 2.00 13 25 171.6 68.0 73 14.9 1.80 14 27 166.8 64.4 48 10.6 1.72 15 26 171.6 65.4 46 10.5 1.77

X 29.6 175.8 71.8 51 11 1.87 S.D. ±3.8 ±5.9 ±6.7 ±11.6 ±2.0 ±.12 85 TABLE 3

Maximal Cardiovascular Responses of Subjects in Study

SWIMMING

1 1 Subject VE V02 VC02 R V02ml.kg- .min- rfl

1 127.6 5.25 4.96 .94 64.1 156 2 102.9 3.58 4.25 1.18 58.2 188 3 155.8 4.10 4.44 1.08 51.4 162 4 101.2 3.38 4.15 1.11 55.8 165 5 122.8 4.77 5.21 1.09 60.8 157 6 92.5 3.40 4.19 1.22 49.3 164 7 83.6 3.49 3.10 .89 45.5 144 8 127.2 3.49 4.09 1.17 50.6 183 9 137.0 3.41 3.75 1.10 51.1 152 10 131.1 3.92 4.46 1.14 51.3 180 11 149.1 4.23 4.92 1.16 54.6 155 12 127.6 3.92 4.37 1.11 47.3 145 13 90.5 3.45 3.77 1.09 53.1 165 14 116.3 3.49 4.03 1.16 53.3 185 15 95.0 3.21 3.21 1.00 47.6 181

X 117.3 3.81 4.19 1.1 52.9 165 S.D. ±22.1 ±.577 ±.59 ±.09 ±5.13 ±14.6 86 TABLE 4

Maximal Cardiovascular Responses of Subjects in Study (,n = 1S)

Bicycle

1 1 Subject VE V02 VC02 R V02mi.k&- min- FR

181.4 5.47 6.73 1.23 67.4 170 140.8 4.07 5.10 1.25 67.2 192 136.1 5.16 7.00 1.24 66.3 184 130.0 5.00 6.12 1.22 75.3 176 166.0 5.30 6.78 1.28 66.2 159 136.8 4.46 5.73 1.29 65.3 174 183.3 5.36 6.52 1.22 69.5 166 150.0 4.25 5.21 1.23 62.5 196 157.5 4.41 5.58 1.27 66.3 186 172.7 5.15 6.45 1.25 66.7 196 167.6 5.30 6.78 1.28 67.4 166 191.7 6.39 7.62 1.19 77.6 175 138.7 4.18 5.14 1.23 62.4 181 156.1 4.42 5.32 1.20 68.4 195 127.8 3.75 4.72 1.26 57.7 201

X 155.8 4.84 6.05 1.24 67.1 181 S.D. ±20.67 ±.70 ±.86 ±.03 ±4.79 ±13.0 87 TABLE 5

Maximal Cardiovascular Responses of Subjects the Study (n = 1$)

Running

Subjects VE V02 VC02 R V^^W" ~S~

155.9 5.30 6.02 1.14 65.6 168 139.2 4.55 5.35 1.18 73.3 198 140.4 5.16 6.14 1.19 66.1 182 126.6 4.70 5.15 1.10 70.7 186 154.0 5.96 7.09 1.19 75.0 168 130.5 4.57 5.48 1.20 65.9 179 160.7 5.64 5.91 1.05 73.1 174 142.6 4.45 5.19 1.17 65.7 198 148.6 5.00 5.68 1.14 75.2 199 173.5 5.41 6.35 1.17 69.7 203 152.8 5.37 6.08 1.13 69.0 167 163.9 5.59 5.97 1.07 69.0 174 129.4 4.31 4.98 1.16 64.6 185 153.9 4.27 4.89 1.15 66.0 203 123.3 4.09 4.73 1.16 61.9 209

X 146.4 4.96 5.67 1.15 68.7 186 S.D. ±14.88 ±.58 ±.64 ±.04 ±4.08 ±14.5 88

JB.O-I ^_^ . uo 38.0-

UJ • DC 37.5- 1- < • DC UJ 37.0- CL • II5I K 36.5- UJ DC WETSUIT o 36.0- NO WETSUIT o >" I rest 10 TIME (min)

Figure 2. Core temperature during 30 minutes of tethered swimming in the wetsuit (n=15) and non wetsuit (n=10) subjects. Rest marked on the X axis indicates resting core temperature prior to immersion in the water. Zero "0" time core temperature indicates core temperature after 5 minutes of immersion in the water. * Significant difference (p<0.05) between wetsuit and non wetsuit subjects. o o UJ DC I- < DC UJ 0- 5 -*• WETSUIT UJ -D- NO WETSUIT l- UJ DC —\—r- -l—'—l— —I—i—l—> O 55 65 U 15 25 35 45 TIME (min)

Figure 3. Core temperature during 70 minutes of bicycle exercise in wetsuit (n=15) and non wetsuit (n=13) subjects. Initial core temperature illustrated is the final core temperature obtained upon the completion of the swimming stage. * Significant difference (p<0.05) between the wetsuit and non wetsuit subjects 90

40.0 -i • WETSUIT 1 • r O -o NO WETSUIT 1 o 39.5- T UJ DC i T 1 i i § 39.0- DC UJ • Q. JL^^^^i I x s 38.5- UJ UJ DC —i • r- O o4 -5 15 25 35 O TIME (min)

Figure 4. Core temperature during 40 minutes of treadmill running in wetsuit (n=13) and non wetsuit (n=9)

subjects. 91 after the subjects were immersed in the water (resting water core temperature) for a five minute period. The five minute period at rest in the water acted to simulate a triathlon race start. The core temperature of the NW treatment (0.2 ±0.19 °C) lowered significantly (p<0.05) after 5 minutes rest in the water when compared to the W treatment which showed a 0.1 ±0.14 °C drop in core temperature. Upon commencement of the swimming phase the NW treatment showed a rapid decline in core temperature which was significant (p<0.05) after 5 minutes of swimming when compared to resting ambient core temperature. Furthermore, the NW treatment showed a significant (p<0.01) 1.0 ±0.6 °C lowering in core temperature throughout the 30 minutes of the swimming phase when compared to resting water core temperature. The W treatment however during the 30 minutes of swimming showed no significant lowering (0.1 ±0.5 °C) in core temperature when compared to the resting water core temperature. When specifically examining the changes in the core temperature between the W and NW treatment it was shown that the NW treatment had a significantly (p<0.05) lower core temperature after 5 minutes of swimming than the W treatment.

Bicycle Stage

The initial core temperature reading illustrated in Figure 3 for the W (37.4 ±0.68 °C) and NW (36.6 ±0.89 °C) treatments is the final swimming core temperature obtained prior to the subject leaving the pool. The final swimming core temperature reading has been included to highlight changes in core temperature throughout the transition period and early stages of the bike which will be discussed in more detail in the "afterdrop" section of the results. During exercise in the bicycle stage the NW treatment had a significantly (p> 0.05) lower core temperature than the W treatment throughout 65 minutes of the bicycle phase. Both the W and the NW treatment under went a significant (p<0.01) increase in core temperature throughout the bicycle phase. However, the NW treatment had a 2.4 ±1.5 °C rise in core temperature during the bicycle phase (from the commencement of the bicycle phase to the completion of the cycle phase) which was significantly (p<0.05) greater than the 1.2 ±1.0 °C rise in core temperature in the W treatment.

Running Stage

Figure 4 shows the core temperature response of the W and the NW treatment during the running stage of the triathlon. Both the NW treatment and the W treatment showed a significant (p<0.01) increase in core temperature from the beginning to the end of the the running phase of the triathlon. Specifically, the W treatment showed an increase of 0.5 ±0.31 °C and the NW treatment showed an increase of 0.7 ±0.27 °C during the 40 minutes of running. Although a significant increase in core temperature was seen in both treatments, no significant difference was noted between the NW treatment and W treatment during the running phase. Afterdrop

Afterdrop, the continued lowering of core temperature after immersion in water, is shown in Figure 5 for the W and NW treatments. It should be noted that the afterdrop is derived from the final swimming core temperature and subsequent subtraction of the bicycle core temperatures. The NW treatment showed a significantly (p<0.05) greater afterdrop than the W treatment in the first 20 minutes (other than the 2 minute period where the afterdrop was at a significance level of p>0.10). The NW treatment showed a significant (p<0.05) afterdrop of approximately 0.4 °C and 0.5 °C during the first 12 minutes of the bicycle stage. After the initial 12 minutes of cycling it then took the NW treatment a further 8 minutes of cycling before core temperature rose above that of the final swimming core temperature. The W treatment showed a similar afterdrop response, however, it was less in magnitude and duration than the NW treatment. The W treatment showed a non significant lowering in core temperature of approximately 0.1 °C in the first six minutes of cycling. After the 6 minute period of cycling the core temperature of the W treatment rose above the final swimming core temperature achieved by the W treatment. 94

0.8-1 ir y • WETSUIT * 0.6- • o H NO WETSUIT * * T 0.4- * • UJ DC 0.2- * * *

< -O.O-i DC UJ -0.2- Q. -0.4- 1 •1 91 I 2 ] UJ -0.6- DUJC l- o -0.8- o -1.0-- 0 2 4 6 8 10 12 14 16 18 20 TIME (min)

Figure 5. Afterdrop upon the completion of the swimming stage in wetsuit (n=15) and non wetsuit (n=10) subjects. * Significant difference (p<0.05) between wetsuit and non wetsuit subjects Mean Skin Temperature

The mean skin temperature responses, were measured during the swimming, bicycle and run phases and are illustrated in Figures 6, 7 and 8.

Swimming Stage

After 5 minutes of rest in the water a significantly (p<0.01) lower skin temperature of 22.1 ±1.1 °C was observed in the NW treatment as compared to the W treatment (27.9 ±1.9 °C). Upon completion of the first five minutes of swimming a significant (p<0.05) lowering in skin temperature from rest was noted in the W (2.5 ±1.5 °C) and NW (1.2 ±1.0 °C) treatments. The W treatment also showed a significantly (p<0.05) greater reduction in skin temperature after 5 minutes of swimming than the NW treatment. In the remaining 25 minutes of swimming the NW treatment showed no significant changes in skin temperature. This was opposed to the W treatment which showed a significant (p<0.05) lowering in skin temperature after 30 minutes of swimming when compared to the 5 minute skin temperature reading. However, despite the lowering of skin temperature after 30 minutes of swimming, the W treatment (24.01 ± 1.04 °C) had a significantly higher (p<0.01) skin temperature than the NW treatment (20.9

±0.74 °C). 30-] WETSUIT NO WETSUIT 29 " 28- 27 -

26 " 25- 24 -j 23 -j

22 ~ 21 - 20- ^ n • 1— 5 15 25 TIME (min)

Figure 6. Skin temperature during 30 minutes of tethered swimming in wetsuit (n=15) and non wetsuit (n=14) subjects. * Significant difference (p<0.05) between wetsuit and non wetsuit subjects i—i—i—i—<—i—i—i—i—i—i—i—'—r 5 15 25 35 45 55 65 TIME (min)

Figure 7. Skin temperature during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects. * Significant difference (p<0.05) between wetsuit and non wetsuit subjects. 98

35-i

O 34- o UJ DC I- 33 - < DC UJ 32- Q. UJ 31 - • WETSUIT CO -D- NO WETSUIT £ -> r , 1— -T" —T" 5 15 25 35 TIME (min)

Figure 8. Skin temperature during 40 minutes of treadmil running in wetsuit (n=15) and non wetsuit (n=13) subjects. Bicycle Stage

Figure 7 indicates the skin temperature responses of the W and NW treatments during the bicycle stage of the triathlon. Significant increases in skin temperature (p<0.01) were seen in both the W and the NW treatments throughout the bicycle stage of the triathlon. The NW treatment, however, underwent a significantly (p<0.01) greater increase in skin temperature (6.4 ±1.2 °C) than the W treatment (4.1 ±1.1 °C). The greater increase in skin temperature in the NW treatment than the W treatment led to a nonsignificant difference between the two treatments in skin temperature after 30 minutes of cycling which was maintained for the remainder of the bicycle stage.

Running Stage

Figure 8 illustrates the mean skin temperature responses between the NW treatment and the W treatment in the running phase. Although there was a trend in both the NW and W treatments for an increase in skin temperature of 0.3 ±0.6 °C and 0.6 ±0.7 °C respectively, no significant difference in increased skin temperature was observed between the two treatments. 1

Heart rates

Heart rate responses during the swimming, bicycle and running stage are represented in Figures 9, 10 and 11.

Swimming Stage

No significant difference in heart rate was seen between the W and NW treatment during the swimming stage. However, the heart rate response during the swimming stage showed a trend to be lower in the W treatment throughout the swimming stage when compared to the NW treatment. More specifically, the W treatment showed a lower heart rate of up to 8 beats per minute throughout the swimming stage than the NW treatment. This may indicate a reduced effort required whilst swimming with a wetsuit as opposed to without a wetsuit.

Bicycle Stage

Heart rate response in the bicycle stage showed that both the W and the NW treatment had a significant (p<0.01) rise in heart rate over the 70 minutes of the bicycle stage. More specifically, an increase in heart rate of 20 ±14 min and 14 ±14 min was found in the NW and W treatment, respectively. No significant difference, however, was found in the rise in heart rate between the NW and W treatment throughout the bicycle stage. 101

150- •*- WETSUIT -a- NO WETSUIT

C* 140- I UJ 130- DC DC < UJ 120 - X * 0^1 U "1r . i • i 0 10 20 30 TIME (min)

Figure 9. Heart rate during 30 minutes of tethered swimming in wetsuit (n=12) and nonwetsuit (n=11) subjects. • 170- " c 160- E w> • UJ 150- < DC • OC 140- < UJ X WETSUIT 130- NO WETSUIT

0^ ~~r~ —r- •>—T" -l ' 1 ' 1 10 20 30 40 50 60 70 TIME (min)

Figure 10. Heart rate during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects. 185- WETSUIT • • 180- NO WETSUIT 175- 170- 165- 160- 155- 150 - ^™ 145 -

n • rj "i i • i i • • CI 10 20 30 40 TIME (min)

Figure 11. Heart rate during 40 minutes of treadmi running in wetsuit (n=15) and non wetsuit (n=13) subjects. 1

Running Stage

A significant (p<0.01) increase in heart rate was seen in both the W and NW treatment during the 40 minutes of the running stage. More specifically, a 12 ±5 min and 11 ±6 min increase in heart rate was found in the W and NW treatment, respectively. No significant difference, however, was found in the rise in heart rate between the W and NW treatment.

Oxygen consumption

Figures 12, 13 and 14 show the metabolic responses of the W and NW treatments during the swimming, bicycle and running stages of the triathlon.

Swimming Stage

The NW treatment showed a significantly (p<0.05) higher oxygen consumption during the swimming stage than the W treatment which suggests that a reduced effort was required to swim when wearing a wetsuit. Both the W and NW treatment showed no significant change in oxygen consumption throughout the swimming stage. More specifically, the W treatment exercised at 62% of M^02 which increased after 30 minutes of swimming to 64% of MVO2. The NW treatment exercised at 72% of MVO2 which was maintained after 30 minutes of swimming. 105

5 15 30 TIME (min)

Figure 12. Oxygen consumption (VO2) during 30 minutes of tethered swimming in the wetsuit (n=14) and non wetsuit (n=13) subjects. 106

WETSUIT NO WETSUIT

15 30 45 TIME (min)

Figure 13. Oxygen consumption (VO2) during 70 minutes of cycling in wetsuit (n=15) and non wetsuit (n=13) subjects. 107

4 n

2- • WETSUIT H| NO WETSUIT

1 -

15 30 40 TIME (min)

Figure 14. Oxygen consumption (VO2) during 40 minutes of treadmill running in wetsuit (n=15) and non wetsuit (n=13) subjects. 1

Bicycle Stage

No significant difference was observed between the W and the NW treatments during the bicycle stage. There was a trend, however, for the NW treatment to have a lower oxygen consumption during the bicycle stage than the W treatment. The W treatment also showed a significant (p<0.01) rise in oxygen consumption between the 8 minute (3.102 ±0.37 l-min"1) and 70 minute (3.39 ±0.42 l-min_1) period. No significant changes in oxygen consumption were seen in the NW treatment during the bicycle stage. More specifically, the oxygen consumption of the W treatment was 64% of MVO2 after 8 minutes of cycling which increased to 69% of MVO2 after 70 minutes of cycling. The NW exercised at 64% of MVO2 after 8 minutes which increased to 67% of M^02 after 70 minutes of cycling.

Running Stage

No significant difference in oxygen consumption was noted between the W and NW treatments during the running stage. However there was a trend toward lower oxygen uptakes in the NW treatment when compared to the W treatment during the running stage. Both the W and NW treatment under went a significant (p<0.05) increase in oxygen consumption during the running phase. The W treatment exercised at 69% of MVO2 at 8 minutes which was maintained after 40 minutes of running. The NW treatment worked at 66% of M>^02 which increased to 69% of M^02 after 40 minutes of running. 1

Plasma Volume Changes

Plasma volume changes were assessed through three blood samples. A finger prick blood sample was taken at rest prior to the triathlon, immediately after the bicycle stage whilst seated on the bicycle and immediately upon completion of the running leg whilst standing on the treadmill. Figures 15 and 16 illustrate the percentage change in plasma volume after the bicycle and running stages. A significant change in plasma volume was seen in the W treatment (-5.8 ±8.8%) when compared to the NW treatment (0.8 ±7.6%) upon the completion of the bicycle phase. No significant difference was seen between the W (4.2 ±9.52%) and NW (4.5 ±9.97) treatment upon completion of the running phase.

Haemoglobin

At rest prior to immersion in the water, no significant difference was seen between the W (15.4 ±1.6 g/l) and NW (15.2 ±1.1 g/l) treatment in hemoglobin concentration. However, after the cycle stage the W (16.3 ±1.6 g/l) treatment showed a significantly (p >0.05) higher concentration of hemoglobin than the NW (15.1 ±0.9 g/l) treatment. At the completion of the triathlon the W (15.4 ±1.1 g/l) treatment had a higher but not significant hemoglobin concentration than the NW (14.9 ±0.6 g/l) treatment. No significant changes in hemoglobin were observed between the rest, cycle and run samples for the W and NW treatment. There was, however, a trend for a concentration in hemoglobin to occur 110

5 o E O 0 > CD E -5 (0 J5 WETSUIT Q. -10 NO WETSUIT <

-15

Figure 15. Percentage change in plasma volume (%A Plasma Volume) after 30 minutes of tethered swimming and 70 minutes of cycling in wetsuit (n=13) and non wetsuit (n=13) subjects. * Significant difference (p<0.05) between wetsuit and non wetsuit subjects 111

15-i

a> E 10- 3 WETSUIT O NO WETSUIT > « E 5- « a. < 0

Figure 16. Percentage change in plasma volume (%A Plasma Volume) after 30 minutes of tethered swimming, 70 minutes of cycling and 40 minutes of treadmill running in wetsuit (n=13) and non wetsuit (n=13) subjects. 1 during the cycle stage when compared to resting levels for the NW treatment.

Haematocrit

At rest prior to immersion in the water, no significant difference was seen between the W treatment (46.8 ±2.2%) and the NW treatment (46.6 ±2.2%). Upon completion of the cycle phase both W and NW treatment showed a concentration in haematocrit of 47.2 ±1.6% and 46.8 ±1.9%, respectively. No significant difference in the concentration of haematocrit was found between the W and NW treatments during the cycle stage. At the completion of the triathlon both the W and NW treatment showed a dilution in haematocrit of 45.1 ±2.1% and 45.5 ±1.9%, respectively. No significant differences in haematocrit concentration was observed between the W and NW treatment upon completion of the triathlon. However, both the W and NW treatment had a significant (p<0.01) lowering in haematocrit during the running stage when compared to the resting and cycling haematocrit levels obtained.

Total body sweat loss and water consumption

Weight loss was calculated as the difference in weight prior to and upon completion of the triathlon. No significant difference was found between the W (1.5 ±0.7 kg) and the NW (1.5 ±0.6 kg) treatments. A negative correlation of 0.66 was found between weight loss and water consumption during the triathlon for both the W and NW treatments. Total body sweat rate was calculated 1 as weight lost during the triathlon in addition to water consumed during the triathlon. No significant difference in total body sweat rate was observed between the W (2.3 ±0.51 I) and the NW treatment (2.3 ±0.46 I). Subjects, upon commencement of the bicycle stage, were allowed to drink freely during exercise. Each subject drank exactly the same amount of water when in the W and NW treatments. When the cumulative total was compared a significantly (p<0.01) greater water consumption during the bicycle stage (703 ±376 ml) than the running stage (150 ±125 ml) were found. Figure 17 illustrates the water intake in 10 minute intervals during the triathlon. Mean water consumption in 10 minute intervals was observed to be 100 ml and 35.5 ml in the bicycle and run stages respectively. 114

300-i

250 -

200 - T

. _ mM T H Water Intake

0 |BS^,B8^,RM,Wiil,IMiM,IMM,l^ 1,1 1,1 10 20 30 40 50 60 70 10 20 30 40 i Bicycle Stage 11 Run Stage i

TIME (min)

Figure 17. Water intake in 10 minute intervals during 70 minutes of cycling and 40 minutes of running (n=15). 115

CHAPTER 5

DISCUSSION 116

The present study has shown that there are several significant thermoregulatory and cardiovascular changes that occur to a competitive athlete when completing a triathlon. The data collected in this study has also highlighted significant changes in the thermoregulatory and cardiovascular responses when subjects wear a wetsuit during the swimming stage of a triathlon.

The age of the athletes used in the present study support earlier research (OToole et al., 1987; Kreider et al., 1988a; Rodgers et al., 1986; Kohrt et al., 1989; Roalstad 1987) which suggest that the triathlete tends to be of an older age treatment than seen in other sports (OToole et al., 1989). Anthropometric and M>^02 data used to calculate relative workloads of each stage of the triathlon was also found to be in agreement with the current research on triathletes (Kreider et al., 1988a; Kohrt et al., 1989). These studies found that mean height and weight of triathletes ranged between 176 - 182cm and 69.4 to 76.6 kg, respectively, with a percentage body fat of 7.1 - 10.5. These values, supporting the similar anthropometric measures found in the present study, indicate that triathletes tend to have a linear physique and carry low levels of body fat (Kreider et al., 1988a; OToole et al., 1987). Such a linear physique with low levels of body fat makes the triathlete suited to exercise in hot conditions. The increased body surface area and higher percentage of lean muscle mass aids in the dissipation of heat from the body during exercise. It should be noted, however, that this linear physique and low level of body fat may also make the triathlete vulnerable to environmental hypothermia, especially when swimming in cold water or when exposed to lowered ambient temperatures. Therefore when 117 exercising in water, the triathlete has very little functional insulation and must rely on the heat produced through metabolism to stabilize core temperature which is difficult to achieve when in cool water (Nadel et al., 1974a; Holmer and Bergh, 1974).

In the current literature, the reported MV02 of triathletes in each of the three stages of a triathlon shows that whilst triathletes have a lower MVO2 than elite single sport athletes, their MVO2 does compare favourably to that of the elite single sport athlete in each stage (OToole et al., 1987; Roalstad,1989). The lower MVO2 values obtained by triathletes compared to single sport athletes may indicate the necessary division of time to train for three events as opposed to one event in specialist athletes. Kreider et al. (1988a), Kohrt et al. (1987) and Dengel et al. (1989) reported a M>^02 of 49 - 56.7 ml-kg-1min-1 for the swim stage; 64 - 66.7 ml-kg-1-min-1 for the bicycle and 65.3 - 68.8 mlkg-1min-1 for the run stage of a triathlon. Although these oxygen uptake findings are similar to the observed M^02 of the present study the swimming VO2 values in this study may be slightly lower than those reported by Kohrt et al. (1987), Dengel et al. (1989) and Kreider et al. (1988a). The slight variation in swimming M^02 values may be attributed to variations in methodology used to measure swimming oxygen uptake as compared to that utilized in the present study. Kohrt et al. (1987) used an arm cranking machine in the M\>02 to simulate swimming and found lower M^02 values. This may be explained by the reduced muscle mass involved in the arm cranking activity as compared to swimming. Although Kreider et al. (1988a) performed a tethered swimming protocol similar to that used in the present study, the swimming 118

MVO2 in a water temperature of 23 °C as opposed to 26.5 ±0.5 °C in the present study. Holmer and Berg, (1974) and Nadel et al. (1974a) found that subjects with low levels of body fat had difficulty achieving their MV02 in the pool at temperatures below 26 °C. Due to the low levels of body fat present in the triathletes used by Kreider et al. (1988a) it is possible that the athletes may not have been able to reach their true M^02 levels. This may highlight some of the problems that triathletes face when exercising in water without sufficient insulation. The higher MVO2 values obtained by Dengel et al. (1989) may have been influenced by the backward extrapolation method used to determine M^02 when swimming.

The mean training distances per week in the present study compare favourably with the current literature. The current literature has observed training distances of 3.2 - 10.5 km swimming, 140 - 304 km cycling and 39.4 - 72.6 km running (Kohrt et al., 1988; Wells et al., 1987; Millard-Stafford, Cureton, Ray, 1988; Kreider et al., 1988a, OToole et al., 1987 and Kreider et al., 1988b) for the swimming. The triathletes in the present study indicated that their total training mileage would increase as the competitive season progressed.

In the present study, results in the swimming stage of the triathlon suggest that swimming without a wetsuit in 20 °C water imposed a large thermal load on the body, due to the inability of the NW treatment to maintain a thermal equilibrium when exercising in water. The thermal load placed on the NW treatment resulted in the lowering of core temperature due to the 119 high thermal conductivity of water as noted by Nadel (1977) and Horvath (1981). Furthermore, the relatively rapid loss of heat from the body can be attributed to heat loss due to conduction (Nadel et al., 1979). This is highlighted in the increased core to skin surface temperature gradient found in the NW treatment compared to the W treatment.

More specifically, the NW treatment had a skin temperature 17.4 °C lower than core temperature which may be due to the skin temperature assuming values close to the water temperature. Thus a large thermal flux is formed when athletes are swimming in cold water without a wetsuit as shown in the NW treatment. The large potential of heat loss in cool water combined with low levels of body fat leaves the athlete with a minimal amount of insulation to prevent the flux of heat from the body. Therefore, the only effective way to increase insulation levels, other than increase body fat, is the wearing of a neoprene wetsuit which will reduce the core to skin gradient.

The insulative role of neoprene was highlighted in this study with higher core temperatures shown in the W treatment during the swimming stage. The ability of the neoprene to trap a layer of water between the skin and the wetsuit enabled higher skin temperatures in the W treatment (up to 5 °C higher than the NW treatment). The increase in skin temperature thus enabled the wetsuit treatment to have a lower core to skin gradient which may have reduced the heat flux from the body. It appears that the 5 mm neoprene wetsuit enabled the W treatment to maintain a 1 thermal equilibrium, due to the relative stability of core temperature in the W treatment during the swimming stage.

The effectiveness of the W treatment to maintain high skin temperatures seems dependent on the ability of the wetsuit to limit the perfusion of cold water to the skin surface of the body. The results (Figure 4) suggest that the perfusion of water may have caused the lowering of skin temperatures at two separate points. At the commencement of swimming skin temperature lowered by over 3.0 °C and then plateaued until the last 10 minutes of tethered swimming when skin temperature lowered by 1.5 °C. The lowering of skin temperature in the final 10 minutes of swimming may indicate leakage of water into the wetsuit which reduced the temperature of the water surrounding the skin.

Rennie (1988) and Viecstenous et al. (1982) observed that as exercise intensity increases, the insulative value of the muscle mass decreases due to the increased perfusion of warm blood to the muscle mass and periphery to cool the body. The increased heart rates and oxygen consumption of the NW treatment during the swimming stage indicate that in the NW treatment insulation would have been lowered even more dramatically due to increased blood flow to the working muscles. Therefore, the NW treatment would have had great difficulty in preventing the lowering of core temperature due to the reduced insulation of perfused muscle mass and low body fat levels.

Wetsuits not only provide a thermoregulatory and insulative advantage but they may also lower the metabolic cost of the 121 activity. Although anecdotal evidence (Brassil et al., 1986; Toussaint et al., 1989; Lowdon, 1987) suggests that wearing a wetsuit provides assistance when swimming to date, however, there has been no scientific research on the effects of wearing a wetsuit on the metabolic cost when swimming on the surface of the water. It should be noted, however, that studies have reported improved swimming times and increased swimming distances when subjects have worn a wetsuit. (Parsons and Day, 1986; Brassil et al., 1986). Due to the improved swimming times and distances, it has been suggested that wetsuits may provide an increased efficiency and/or performance advantage to the athlete. Further work by Toussaint et al. (1989) showed that when 12 subjects wore a wetsuit a 12 - 14% reduction in drag was observed at a swimming speed of 1.5 - 1.2 m.s-1, respectively. Toussaint et al. (1989) suggested that the reduced drag would effectively mean a 5% performance advantage due to the increased flotation as a result of the low specific gravity of neoprene in a wetsuit. The results from the present study support the current literature which suggests that tethered swimming with a wetsuit will result in less of an increase in these parameters the metabolic cost and heart rate to a greater extent than with no wetsuit being worn. Wetsuits appear to be advantageous to swimming performance by reducing metabolic cost through improved stroke dynamics and by reducing the thermal strain on the athlete. It would, therefore, appear that the lowering in metabolic cost can be attributed to the increased flotation which provides improved mechanical efficiency and stroke dynamics. The present study also suggests that the increased metabolic cost of swimming without a wetsuit may be 1 attributed to the lowering of core temperature in the NW treatment as compared to the W treatment. This would be in support of Nadel et al. (1974a) and Holmer and Bergh (1974) who found that there was an inverse relationship between core temperature and oxygen consumption. In the studies of Holmer and Bergh and Nadel et al. (1974a) water temperature was varied to account for changes in oxygen consumption. This may be applied to the use of a wetsuit.

The wetsuit effectively changes the water temperature that the athlete has to swim in due to the warm insulative layer of water that is present around the body of the subject. The increased oxygen cost of the activity is also dependent on the body fat of the individual that was observed by McArdle et al. (1984a) who found that those subjects with the lowest percentage of body fat had the greatest increase in oxygen consumption and lower core temperature when exercising in cool water. Thus the triathletes in the present study which are considered to be of a low body fat and without the wetsuit (NW treatment) protection can expect to suffer decreases in core temperature and increases in the oxygen consumption when swimming. This was evident in the NW treatment. It may be concluded therefore that wearing of a wetsuit may provide two advantages: (1) an improved insulation to prevent heat loss due to conduction; and (2) improved mechanical efficiency due to a reduction in drag and increased flotation.

The results from the present study illustrated that upon the completion of the swimming phase subjects in both the W and NW 1 treatment underwent an afterdrop in core temperature. Furthermore, it was observed that the NW treatment had an afterdrop which was of a larger magnitude and longer duration than the W treatment. At present there is no research specific to the effects of afterdrop experienced in triathlons. However, the current literature does indicate the sequence of events and conditions which may cause afterdrop to be more prevalent. Afterdrop is believed to occur primarily when cooling of the body is rapid and followed by immediate rewarming (Webb, 1986; Giesbrecht et al., 1987). Furthermore, afterdrop has been shown to be enhanced when exercise accompanies the rewarming phase (Giesbrecht et al., 1987, Lloyd, 1986; Layton et al., 1983; Savard et al., 1985). The triathlete is likely to experience these conditions of rapid cooling of the body during the swimming stage of a triathlon in cool conditions due to the low levels of body fat present on the athletes. The rapid and immediate rewarming phase indicated by the current literature is analogous to the athlete being exposed to ambient air upon the completion of the swimming phase. The afterdrop experienced by the athlete is likely to be enhanced due to the high intensity exercise immediately following the swim/bicycle transition. Triathletes, due to the nature of the event, can therefore expect to incur an afterdrop when swimming in cold water. The NW treatment in this study was exposed to such conditions and as a result an afterdrop occured. The mechanism responsible for this afterdrop phenomomen has been highlighted by Webb (1986) who proposed that this lowering in core temperature was due to the continued physical conduction from the body. Although the NW treatment seem to support this hypothesis, it should be noted that the the 1

W treatment also had a lowering in core temperature of 0.1 °C during the first 6 minutes of the bicycle stage. Although the W treatment experienced an afterdrop, they did not have the same cold stress placed on them as the NW treatment. Furthermore, the W treatment appeared to have achieved a thermal equilibrium when exercising in the 20 °C water. Therefore, the afterdrop occurring to the W treatment may indicate that something other than the physical conduction of heat was responsible for the afterdrop. It is possible that the afterdrop experienced by the W treatment was due to the circulation of blood to a cool muscle mass as suggested by Giesbrecht et al. (1987), Hong and Nadel (1979), Glaser and Holmes-Jones (1951) and Savard et al. (1985). Giesbrecht et al. (1987) found that exercise enhanced the afterdrop in subjects when compared to the afterdrop experienced when passive warming and shivering were used as methods of rewarming the body. Whilst Giesbrecht et al. (1987) found that exercise enhanced afterdrop in the subjects, several differences exist between the present study and the study conducted by Giesbrecht et al. (1987). Giesbrecht et al. (1987) had a greater lowering in core temperature of the subjects than was evident in the present study (some of the subjects were brought down to 32.9 °C in core temperature). Also the exercise intensity of the subjects in the study of Giesbrecht et al. (1987) following the cooling period of the body was of a much lower intensity (V02 of1.9 l-min"1) than experienced by the subjects in the present study. However, the study of Giesbrecht et al. (1987) may indicate that triathletes are more susceptible to afterdrop as a result of exercise in the bicycle stage. This susceptibility is due to the effect of exercise on afterdrop, which has been found to 1 exaggerate the effects of afterdrop (Giesbrecht et al., 1987; Lloyd, 1986; Savard et al., 1985). The further lowering in core temperature due to exercise has been termed as "secondary afterdrop" which appears to be caused by the circulatory effects of exercise. The movement of cold blood into the warmer viscera of the body is the primary effect of exercising cooled limbs (Kruk, Pekkarinen, Harri, Manninen, Hanninen, 1990; Hong and Nadel, 1979). Thus this response may explain the occurrence of shivering when only the limbs of the body are cooled (Hong and Nadel, 1979). The effect of cooled limbs and exercise observed in the current literature may explain the slight lowering of core temperature in the W treatment upon the commencement of the bicycle stage. Therefore the higher exercise intensity (relative to Giesbrecht et al., 1987) experienced by subjects in the present study may result in a larger drop in core temperature due to increased blood flow to the working muscles.

The afterdrop experienced by subjects in the present study may be attributed to two mechanisms (circulatory and physical conduction) that explain the sudden lowering in core temperature. Proponents of the traditional circulatory theory of afterdrop suggest that the movement of blood to previously non working cold muscle mass is responsible for the continued lowering of core temperature (Burton and Edholm 1955; Giesbrecht et al., 1987; Savard et al., 1985). Other studies, however, have suggested that afterdrop is due simply to the continued physical conduction of heat from the body as result of the skin to core gradient (Webb, 1986; Saltin, 1968). Although no definite answer can be given as to whether the circulatory or physical conduction 1 mechanism is responsible for afterdrop, it may be possible that both of these mechanisms exist simultaneously.

The current literature suggests that afterdrop does not require a circulatory component, however secondary afterdrop is experienced when exercising due to the circulatory component (Lloyd, 1986). It appears that the intensity of the cooling process influences the magnitude of the afterdrop experienced. Therefore, the NW treatment would be expected to have a greater afterdrop compared to the W treatment due to the greater intensity of cooling during the swimming stage. Thus the physical conduction theory may explain the possible differences between the two treatments due to the wetsuit treatment having a less severe cooling process. This theory, however does not explain adequately the reason for such a rapid drop in core temperature experienced by the NW treatment in less than 3 minutes from exiting the water. Had physical conduction alone been responsible for the afterdrop it would be expected that the rate of heat loss would be similar to when subjects were exercising in the water. Thus afterdrop may be due in part to the immediate circulation of blood to the lower limbs in which muscle temperatures are substantially lower than core temperature (Saltin, 1968). This would result in the immediate lowering of core temperature when combined with the high workloads and convective air currents present when riding a bicycle. Thus from the present study and current literature, it appears that afterdrop is primarly due to the physical conduction of heat from the body, which requires no circulation (Lloyd, 1986). However it appears that a secondary afterdrop occurs due to the shift of cool blood into the warmer 1 visera of the body, which results in an increase in the magnitude of afterdrop (Hong and Nadel et al., 1979; Kruk et al., 1990; Lloyd, 1986)

Whilst the lowered core temperature and afterdrop experienced by the NW treatment may appear to be of a disadvantage for exercise in the bicycle stage, current research suggests that prior cooling of the body may assist endurance performance. Results of the present study indicate that the NW treatment had a greater lowering of core temperature which may have placed the NW treatment at a thermal and cardiovascular advantage over the W treatment. When examining the lowered core temperature of the NW treatment it is possible to regard the swimming stage as a "precooling" for the likely increase in core temperature during the bicycle and running stage. More specifically, the significant lowering of core temperature in the NW treatment may have acted as a precooling for the latter stages of the bicycle and run phase.

Current research has found possible advantages of precooling in exercise performance (Hessemer et al., 1984; Myler et al., 1989; Schmidt and Bruck, 1981; Olschewski and Bruck, 1988). It should be noted, however, several important distinctions exist between the current literature and the present study which should be highlighted. Precooling in the current literature is a separate passive procedure performed on the subject prior to exercise in which the precooling treatment ranges from ice packs placed on the skin surface to exposure to low ambient temperatures (Myler et al., 1988; Olschewski and Bruck, 1988). Precooling using these procedures caused core temperature to be lowered between 0.5 - 1

0.9 °C . In the present study a much larger decrease in core temperature (1.5 °C) was involved in precooling than that seen in the abovementioned literature.

However, apart from the non-passive cooling process, several physiological responses occured in the present study that warrant further discussion with the current literature on precooling. The NW treatment in the initial stages of the bicycle leg showed a trend toward lower heart rates in the first twenty minutes of the stage. This may be a result of the increased central blood volume as indicated by Jessen (1987a) due to the decreased peripheral blood flow which is a direct result of a reduction in skin temperature. Not only did the NW treatment experience a trend toward lower heart rates but also the NW treatment was observed to have a trend toward lower oxygen consumption during the bicycle phase despite the higher oxygen consumption during the swimming phase when compared to the W treatment.

The lower oxygen consumption may be explained by the lower core and skin temperature which occured in the NW treatment when compared to the W treatment. The lower skin temperature of the NW treatment suggests that there would have been less peripheral blood flow as the body would still be in a heat gain situation which is supported in the literature by Jessen (1987a) and Hessemer et al. (1984). The increase in central blood flow thus may allow for effective oxygen delivery to the working muscles (MacDougall et al., 1974; Baum et al., 1976). Baum et al. (1976) suggests that the lowering of core temperature effectively gives the athlete an extended buffer period prior to 1 thermoregulatory responses being employed. The buffer period appears to have occured in the subjects in the present study as the NW treatment showed a slower response to increases in skin temperature than the W treatment but also a consistent extended lowering of core temperature. MacDougall et al. (1974), Saltin et al. (1972) and Schmidt and Buck (1981) have suggested that increased body temperature has a detrimental effect on performance. Thus the lower body temperatures observed in the NW treatment during the bicycle stage may have been advantageous to performance.

It should be noted, however that although the wearing of a wetsuit is advantageous in cool water due to the potential beneficial effects of precooling and thermal stability, the wearing of a wetsuit in warm water may have detrimental effects due to increases in body temperature. At present athletes appear to wear a wetsuit in the swimming stage regardless of water temperature due to the perceived performance advantage of a wetsuit as indicated earlier by Brassil et al. (1986) and Toussaint et al. (1989). Thus triathletes will wear wetsuits even in the high water temperatures that are present in the North Eastern Coastline of Australia during the triathlon season. Given the relative thermal equilibrium of subjects when swimming in 20 °C water with a wetsuit in this study, it is possible that swimming in warmer temperatures will result in a net gain in body temperature. The athlete may, therefore, suffer a decriment in performance due to the rise in core temperature. This is supported by the findings of Kreider et al. (1988a) who found that subjects had a significantly raised core temperature after 1 swimming 800m in 23 °C without a wetsuit compared to the control treatment who completed no swimming stage. Given that the subjects wore no wetsuit in the study by Kreider et al. (1988a) may mean that larger increases in core temperature can be expected when swimming in a wetsuit in warm water. Thus a significant level of heat strain may be placed on the athlete prior to the commencement of the bicycle stage.

The thermoregulatory buffer (as discussed earlier) appears not to be prolonged in nature. It was observed that the NW treatment in the present study reduces the buffer or "catches up" to the W treatment in core temperature, skin temperature, heart rate and oxygen consumption. The reduction of the buffer between the W and NW treatment may possibly be explained by the thermoregulatory mechanisms that are employed when exercising in cold ambient temperatures. Nadel et al. (1987) suggested that there are two basic phenomenon that occur to man when attempting to limit the loss of heat from the core of the body: (1) increased metabolic rate through shivering; and (2) vasoconstriction. An increase in metabolic rate manifests itself in the form of pilomotor activity and shivering (Horvath, 1981). An increased metabolic rate was observed in the present study by the NW treatment in the first 8 minutes of the bicycle stage. The increased metabolic rate may, therefore, be attributed to the contraction of nonworking muscles in order to increase the rate of heat production. An extended period of shivering would, therefore, be expected in the NW treatment due to the lower core and skin temperatures observed when compared to the W treatment during the bicycle period (Hong and Nadel, 1979; 131

Nielson, 1976; Haymes and Wells, 1986). The NW treatment would thus be expected to be shivering for longer period of time. The results of the present study in this area concurs with the observations of Schmidt and Bruck (1981), and Kruk et al. (1990). Schimdt and Bruck (1981) and Kruk et al. (1990) noted that there was a lack of sweating and vasodilatory responses in the cooled treatment, which may indicate that there was not a significant thermoregulatory drive to permit heat loss activation. This may account in part for the NW treatment showing a greater rise in core temperature and skin temperature during the bicycle stage than the W treatment.

A secondary mechanism which may explain the reduction of the buffer between the NW and W treatment in core temperature is vasoconstriction of the peripheral blood vessels (Nadel et al., 1987). Vasoconstriction of the periphery would result in a slower heating of the skin surface which was exhibited by the lower skin temperatures observed in the NW treatment. This suggests that the reduced blood flow to the periphery maybe an effective way of increasing tissue insulation, thus helping the body to maintain a heat gain situation and prevent heat loss through increasing the insulation of the body. It could be suggested that the increased skin and core temperatures of the W treatment caused the shift in blood to the periphery to assist in cooling of the body. The increased duration of shivering and vasoconstriction may have caused the NW treatment to show larger increases in core temperature for the bicycle stage than the W treatment. 1

The bicycle stage in the present study acted primarily as a rewarming phase due to the moderate temperature (25 °C and 73% relative humidity) that subjects were exposed to. However if the triathletes were exposed to cooler ambient temperatures, the initial stages of the bicycle phase may have imposed a more severe cooling stress on the body. It is therefore, neccessary to discuss the possible repercussions of cooler ambient temperatures on the triathlete. The triathlete is vulnerable to severe cooling at the start of the bicycle phase for several reasons. Firstly, since triathletes start the bicycle stage with wetted skin, their skin temperatures are lowered due to the evaporation of water from the skin surface. Secondly, triathletes wear a minimal amount of clothing during the bicycle stage (usually only a helmet and cycle pants), which provides a minimal amount of insulation available to athlete when exercising on the bicycle. Thirdly, the wind speeds of up to 45 krr1 reached during the bicycle stage may place the triathlete in a position of high wind velocity with very little thermal insulation being afforded. The chances of injury are, therefore, great due to the high speeds that are involved and the level of co-ordination required for the activity. It has been noted in several studies that cold wet conditions with wind can impose severe thermal strain on the body (lampietro et al., 1958; Haymes et al., 1982; Vangaard, 1975). Even though the climatic conditions observed in the present study were not extreme (25 °C 73%RH), the effect of wet, cold conditions combined with relatively high wind velocities can be seen in the wetsuit treatment whose skin temperature showed a consistent lowering over the 6 minutes of the bicycle stage. The lowered skin temperature may be the 1 effect of evaporation of water from the skin surface, resulting in the partial vasoconstriction of the surface blood vessels. No such lowering in skin temperature was seen in the NW treatment which may be due to the already lowered skin temperature of the body as a result of the cooling of the skin in the water. Wind reduces the total insulation of the body by reducing air insulation and thus increasing heat through convection (Haymes et al., 1982). Haymes et al. (1982) observed that in subzero temperatures clothing which was suitable to maintain a thermal equilibrium was not suitable at the same temperature in the presence of a wind. Furthermore, Haymes et al. (1982) observed that core temperature can be reduced during the downhill portion of cross country skiing due to the high wind velocities and little muscular activity. The lowering in core temperature in this situation may be applied directly to the triathlete and result in a further lowering of core temperature and skin temperature if a downhill section is near the swim-bicycle transition area and little muscular activity is involved.

The initial stages of the bicycle leg may present many problems to the athlete such as afterdrop, cold stress, injury potential and increased core temperature. However the latter stages of the bicycle leg and running phase can impose high levels of heat strain on the body as found in the present study and in the work of Kreider et al. (1988a). Earlier results from the present study suggest that the prolonged nature of the triathlon caused several significant thermoregulatory changes to occur during the bicycle and running stages. Apart from these responses there are also cardiovascular parameters may have to be considered. More 1 specifically, the changes manifest themselves as cardiovascular drift may have to be addressed. Cardiovascular drift is characterized by a continuous rise in heart rate and core temperature, fall in stroke volume and progressive reduction in blood pressure with an increase in oxygen consumption for the activity (Senay, 1985; Harrison, 1985; Sawka et al., 1974; Saltin and Stenberg, 1964). Kreider et al. (1988a) who used a similar protocol to the present study found that the triathlon treatment (which performed the individual stages of the control treatment together as a triathlon) had a significantly higher core temperature and a 13 beat rise in heart rate in the running leg when compared to the control treatment (which performed the bicycle and run stages on different days). Kreider et al. (1988a) also found that, concurrent with the rise in heart rate during the running stage, was a significant reduction in stroke volume when compared to control treatment values.

A similar reduction in stroke volume was found in other studies in which exercise was prolonged (Sawka et al., 1974; Saltin and Stenberg,1964; MacDougall et al., 1974; Rowell et al., 1969). Saltin and Stenberg (1964) and Sawka et al. (1974) found that heart rates increased greater than cardiac output during exercise and concluded that this discrepancy in the relative increases in heart rate and cardiac output was due to a lowering in stroke volume. Therefore, it would appear that rises in heart rate during the bicycle and run phases in the present study may be attributed to a lowering in stroke volume. The reduction in stroke volume has been linked to increases in body temperature which generates 1 competition between the skin and working muscles for the finite blood volume available (Rowell, 1974).

Competition between the skin and working muscles causes a reduction in central blood volume due to increased peripheral circulation, which in turn reduces ventricle filling and thus stroke volume (Rowell, 1974; Sawka et al., 1979). Therefore, a lowering of skin temperature may decrease peripheral blood flow and reduce competition between the skin and the working muscles. A maintenance in stroke volume and reduction in cardiovascular drift can, therefore, be achieved through lower skin temperatures as observed by Rowell et al. (1969) and Shaffrath and Adams (1984). The lower body temperatures observed in the NW treatment throughout the bicycle stage in the present study may have helped to maintain stroke volume and thus reduce the effects of cardiovascular drift. A reduction in cardiovascular drift may have been observed in the NW treatment who displayed a consistently lower oxygen consumption after the first 8 minutes of the bicycle stage than the W treatment. However, both the W and NW treatment showed a 5% and 3% increase, respectively, in oxygen consumption by the completion of the bicycle phase. The magnitude of increase in oxygen consumption observed in the present study during extended exercise is in accordance with other current literature on prolonged exercise (Saltin and Stenberg, 1964; MacDougall et al., 1974).

The similar cardiovascular drift in the W and NW treatments in the latter stages of the bike and the run phase may indicate that 1 skin temperature has a large influence on cardiovascular drift. The skin temperatures in the study after 25 minutes of cycling showed no significant difference between the W and NW treatments. The similarity in skin temperature was also found in the heart rate response during the triathlon indicating that blood flow to the periphery would also be simlar between the groups. The results of this study support investigations by Rowell et al. 1969 and Shaffrath and Adams 1984. The investigators found that skin temperature affects peripheral blood flow acutely and changes in skin temperaure have a large effect on cardiovascular drift.

Kreider et al. (1988a), however, found that subjects had no increase in oxygen consumption during the bicycle stage which was due to the inability of the subjects to keep up to the required workload. This resulted in the subjects exercising at a much reduced intensity in comparison to the present study during the bicycle phase. Which thereby causing a reduction in oxygen consumption values resulting in smaller observed increases in core temperature than was found in the present study. However in the running stage of the Kreider et al. (1988a) study, the subjects worked at a substantially higher percentage of M^02 (78%) than in the present study. During the running stage Kreider et al. (1988a) observed the greatest increases in the cardiovascular and thermoregulatory parameters which may have been due to the much higher exercise intensity used be Kreider et al. (1988) than in the present study. Kreider et al. (1988a) observed a 1.4 °C rise in core temperature during the running stage as opposed to the 0.5 °C and 0.7 °C rise in core temperature in the W and NW 1 treatments, respectively. Another possible reason for the larger overall increase in core temperature of Kreider et al. (1988a) compared to the present study is the higher ambient temperature (29 °C ) that was used during the triathlon by Kreider et al. (1988a). However Kreider et al. (1988a) made no mention of the relative humidity during the triathlons, and therefore it may be questioned whether humidity was controlled for during the study. This may have allowed for variations in thermal stress on each subject which would explain or account for the variations between the two studies. Therefore the different thermal responses reported by Kreider et al. (1988a) and the present study may be attributed to the different relative intensities and variations in ambient temperatures that subjects were exposed to.

The cardiovascular drift which appears to have occured in the present study due to rises in core temperature and oxygen consumption may be accelerated when subjects are dehydrated and thus have a reduction in plasma volume (Kreider et al., 1988). Kreider et al. (1988a) observed a 3% loss in body weight which is similar to the 2% loss in body weight found in the present study. The 2% weight loss may indicate that the subjects in the present study were sufficiently dehydrated to impair performance by compromising circulatory and thermoregulatory function according to Adolph (1947); Haymes and Wells (1986). Kreider et al. (1988a) also observed that subjects averaged 117 ml and 108 ml of water every 10 minutes in the cycle and run stages, respectively. In the present study subjects averaged 100ml and 37.5 ml of water every 10 minutes in the cycle and run stages, 1 respectively. Both studies indicate that the amount of water consumed voluntarily by subjects during the simulated triathlons may not have been sufficient to prevent dehydration during the triathlon. Thus it would be suggested that more water be consumed during the run and bicycle stages to reduce the detrimental effects of dehydration.

Results from the present study indicate that a significant contraction in plasma volume occured in the W treatment when compared to the slight expansion of plasma volume in the NW treatment. The contraction of plasma volume observed in the W treatment is an expected response to cycling exercise (Taylor, 1986). The significant difference in plasma volume observed between the W and the NW treatments may indicate a lower level of heat strain experienced by the NW treatment when compared to the W treatment. This appeared to be the case in the present study as the NW treatment was observed to have lower body temperatures throughout the cycle stage in comparison the W treatment. Upon the completion of the running stage both the W and NW treatment were observed to have an expansion of plasma volume which is in support of the findings by MacDougall et al. (1974), Senay et al. (1980) and Edwards and Harrison (1984). No significant difference in plasma volume change was seen between the W and NW treatment which may be expected due to the similar body temperatures in both the W and NW treatment upon completion of the triathlon. 139

CHAPTER 6

CONCLUSIONS AND RECOMMENDATIONS 1

CONCLUSIONS

On the basis of the results of this investigation, the following conclusions may be drawn:

1. Swimming without a wetsuit in 20 °C water involves a significant reduction in core temperature.

2. Swimming with a 5mm wetsuit in 20 °C water enabled athletes to maintain thermal equilibrium.

3. A reduction in heart rate and metabolic cost is attained when a wetsuit is worn during tethered swimming.

4. Triathletes are likely to experience an afterdrop when swimming in cold water during the early stages of the bicycle phase. However the triathlete is likely to have a greater afterdrop when no wetsuit is worn during the swimming stage as to when a wetsuit is worn.

5. Triathletes undergo significant rises in core temperature during the bicycle and running phases. The increase in thermal strain during this period may become excessive particularly in warmer ambient temperatures. 1

6. The wearing of a wetsuit during the swimming phase significantly effects the thermoregulatory and cardiovascular responses of the bicycle and running phases as compared to no wetsuit being worn.

7. The prolonged nature of exercise in a triathlon results in a weight loss of 2-3% even with voluntary hydration. This may indicate that triathletes may not have an optimal level of water intake. However this does not take into account loss of mass through glycogen depletion which may influence the predicted optimal level of water intake required by an athlete.

8. It is still unclear as to the performance advantage obtained when wearing a wetsuit. from the results of the study there is a trend which indicate a reduced energy cost of swimming with a wetsuit. However the study did not resolve whether there was any effect on performance after the completion of the swimming stage. This section of the study appears to warrant further investigation.

It appears from the study that triathletes are most vulnerable to hypothermia upon the commencement of the bicycle stage. This is due to afterdrop and the increased potential of cooling as a result of heat loss from convection and evaporation. However overall the bicycle phase appears to be a rewarming stage where large increases in body temperatures occur. The running stage appears to cause further increases in body temperature which may result in excessive heat stress being placed on the triathlete. The present study has highlighted the possible advantages of cooler 142 body temperatures during the bicycle and running phases. It appears from the present study that triathletes have to withstand both a loss and gain in body temperature to complete a triathlon. The severity of the heat gain and heat loss appears to be dependent on exercise intensity and relative environmental temperature of the water and ambient air. RECOMMENDATIONS

The results from the present study have highlighted several areas from which practical modifications may be derived and serve as guidelines that which race administrators should consider, when organizing a triathlon event. This study also highlights further avenues of research to be investigated:

1. Due to the thermal vulnerability of triathletes when exercising in water it is suggested that triathletes be required to wear a wetsuit when swimming in water below 20 °C.

2. Due to the effects of afterdrop and possible chances of injury, it is suggested that any athlete suffering symptoms of hypothermia be withdrawn immediately from the event prior to the commencement of the bicycle stage.

3. Race organizers when designing a triathlon course should avoid long downhill sections in close proximity to the swimming/bike transition area. This would help to avoid excessive cold stress on the athlete prior to warming-up after the swimming stage. Due to the large potential for heat loss in the early stages of the bicycle leg it is suggested (particularly in cool ambient conditions) that athletes be encouraged to wear protective clothing (dry sports clothing) to reduce heat loss through convection and exaggerate the possible afterdrop response. 4. Triathletes should be encouraged to monitor their fluid intake during the run leg, as the study has found that large reductions in water intake are seen when running as compared to when cycling. Increased water intake may be encouraged through the provision of water bidions during the running leg as opposed to cups which a very difficult to drink out of when in motion. Likewise athletes should be careful to avoid excessive intake of fluids

5. Due to the beneficial effects of wetsuits in reducing heat loss in water, it would be interesting to establish if a wetsuit has a benefical or detrimental effect on thermoregulatory and cardiovascular responses when used in warm water.

6. The possible beneficial effects of precooling require that more research be completed specific to triathlons as opposed to a passive cooling process prior to exercise. This may be achieved through the direct manipulation of water temperature as opposed to the wearing of a wetsuit.

7. Further research that manipulates temperatures in the bicycle stage (particularly cold temperatures) may reveal more fully the effect of ambient air temperature on afterdrop and also the severity of cooling that triathletes may experience in the initial stages of the bicycle phase in different air temperatures.

8. Further research utilizing a swimming flume would assist in a more motion specific analysis of the effects of swimming with a wetsuit. 145

CHAPTER 7

REFERENCES Adams, W.C.; Fox, R.H.; Fry, A.J.; and MacDonald, I.C. (1975). Thermoregulation during marathon running in cool, moderate and hot environments. Journal of Applied Physiology 38(6): 1030 - 1037

Adolf D.F. (1947). Physiology of man in the desert New York: Interscience

Adolf, E.F. and Molnar, G.W. (1946) Exchanges of heat tolerances to cold in men exposed to outdoor weather. American Journal of Physiology 146: 507 - 537

Angell, J. (1982) Hypothermia : just another word for wet and tired.... except that it can kill you. Yacht Racing and Cruising April

Astrand, P.O. and Englesson S.A. (1972). A swimming flume. Journal of Applied Physiology 33: 514 Baum, E.; Bruck, K. and Schwennicke, H.P. (1976). Adaptive modifications in the thermoregulatory system of long distance runners. Journal of Applied Physiology 40(3): 404 - 410

Behnke, A.R. and Yaglou, C.P.C. (1951) Physiological responses of men chilling in ice water and to slow and fast rewarming. Journal of Applied Physiology 3: 591 - 602 Bergh, U and Ekblom, B. (1979). Physical performance and peak aerobic power at different body temperatures. Journal of Applied Physiology : Respiration. Environmental.Exercise and Physiology 46(5): 885 - 889.

Bonen, A., Wilson, B.A., Yarkony, M. and Belcastro, A.N. (1980). Maximal oxygen uptake during free, tethered and flume swimming Journal of Applied Physiology : Respiration- Environmental. Exercise and Physiology. 48 (2): 232 - 235

Boone, T. and Kreider, R.B. (1976). Bicycle exercise before running: effect on performance. Annals of Sports Medicine 3(1): 25 - 29

Borchers, G.E. and Buckenmeyer, P.J. (1987) Triathlon: the swim to bicycle transition. Abstract. Medicine. Science. Sports and Exercise, (supplement) S49

Brassil, J.; Axford, L. and Holt, J. (1986). The effect of a wetsuit on swim performance. Triathlon Sports 13-15

Brengelmann, G.L.; Johnson, J.M., Hermansen, L. and Rowell, L.B. (1977). Altered control of skin blood flow during exercise at high internal temperatures. Journal of Applied Physiology Respiration. Environmental. Exercise and Physiology. 43(5): 790 - 794 Bristow, G.K., Giesbrecht, G.G. (1988). Contribution of exercise and shivering to recovery from induced hypothermia (31.2°C) in one subject. Aviation. Space and Environmental Medicine 59: 549 - 552

Brooks, G.A.; Fahey, T.D. (1984). Exercise Physiology : Human Bioenergetics and it's Applications Brisbane : John Wiley and Sons

Brozek, J.; Grande, F.; Anderson, J. and Keys, A. (1963). Densitometric analysis of body composition : revision of some quantitative assumptions. Annals of the New York Academy of Sciences. 110: 113 - 14

Bureau of Meteorology. (1988). Climate Averages of Australia. Department of Administrative Services. Meteorological Summary.Australia : Australian Government Publishing Services.

Burton, A.C.; Edholm, O.G.; (1955) Man in a Cold Environment. Physiological and Pathological Effects of Exposure to Low Temperatures. London : Edward Arnold (Publishers) LTD.

Cannon, P and Keatinge, W.R. (1960) The metabolic rate and heat loss of fat and thin men in heat balance in cold and warm water Journal of Physiology (London) 154: 329 - 344 Convertino, V.A. (1987). Fluid and hydration state: Effects of long-term exercise. Canadian Journal of Sports Science 12(supp.1) 136s - 139s

Costill, D.L. (1966). Use of a swimming ergometer for physiological research. Research Quarterly 37: 564 - 567

Costill, D.L; Cahill, P.J. and Eddy, D. (1967). Metabolic responses to submaximal exercise in three water temperatures. Journal of Applied Physiology 22: 628 - 632.

Costill, D.L, and Fink, W.J. (1974). Plasma volume changes following exercise and thermal dehydration. Journal of Applied Physiology 37(4): 521 - 525

Cox, L. (1985). Cold water Caution. Triathlon July PP 14-69

Craig, N. and Walsh, C. (1989) Cycling. In Draper, J. and Telford, R. Sport Specific Guidelines for the Physiological Assessment of the Elite Athlete (pp 21-51). Canberra : National Sports Research Program Australian Coaching Council.

Currie, J. (1798) Medical Reports on the Effects of Water, Cold and Warm, as a Remedy in Fever and Other Diseases Whether Applied to the Surface of the Body or Internally. Caddell and Davies : London App2 pp20 - 25 Davies, C.T.M. (1979). Influence of skin temperature on sweating and aerobic performance during severe work. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology. 47(4): 770 - 777

Dengel, D.R.; Flynn, M.G.; Costill, D.L. and Kirwan, J.P. (1989) Determinants of Success during triathlon competition. Research Quarterly For Exercise and Sport 60(3): 234 - 238

Dill, D.B. and Costill, D.L. (1974). Calculation of percentage changes in volume of blood plamsa, and red cells in dehydration. Journal of Applied Physiology 37(2): 247 - 248

Dixon, R.W.; Faulkner, A.J. (1971). Cardiac Outputs during maximum effort running and swimming. Journal of Applied Physiology 30(5): 653 - 656

Dubois, D. and Dubois, E.F. (1916). Clinical calorimetry. formula to estimate the appropriate surface area if height and weight be known. Archives. International Medicine 17: 863 - 871

Durin, J.V.G.A. and Wormersley, J. (1984). Body fat assessed from the total body density and it's estimation from skinfold thickness : measurements on 481 men, women aged from 16 Edwards, R.J. (1979). Tasman and coral sea ten year mean temperature and salinity fields. CSIRO Division of Fisheries and Oceanography Report No 88.

Edwards, R.J.; Harrison, M.H.; Cochrane, L.A. and Mills, F.J. (1983). Blood volume and protein responses to skin cooling and warming during cycling exercise. European Journal of Applied Physiology 50: 195 - 206

Edwards R.J. (1984). Intravascular volume and protein responses to running exercise. Medicine Science in Sports and Exercise 16(3): 247 - 255

Ekelund, L.G. (1966) Circulatory and respiratory adaptation during prolonged exercise in supine position. Acta Phvsiologica Scandanavica 68: 382 - 396

Ekelund, L.G. (1967) Circulatory and respiratory adaptation during prolonged exercise of moderate intensity in the sitting postion. Acta Phvsiologica Scandanavica 69: 327 - 340

Falls, H.B. (1972). Heat and Cold Applications, (ed) Morgan, W.P. Ergogenic Aids and Muscular Performance New York : Academic Press Fortney, S.M. and Vroman, N.B. (1985). Exercise, performance and temperature control: Temperature regulation during exercise and implication for sports performance and training. Sports Medicine 2: 8 - 20

Fortney, S.M.; Nadel, E.R.; Wenger, C.B.; and Bove, J.R. (1981). Effect of acute alterations of blood volume on circulatory performance in humans. Journal of Applied Physiology: Respiration. Environment. Exercise and Physiology 50(2): 292 - 298

Fox, R.H.; Goldsmith, R.; Hampton, I.F.G. and Hunt, T.J. (1967). Heat acclimation by controlled hyperthermia in hot dry and hot wet climates. Journal of Applied Physiology 22(1): 39 - 46

Frye, A.J. and Kamon, E. (1983). Sweating efficiency in acclimated men and women exercising in humid and dry heat. Journal of Applied Physiology : Respiration. Environment. Exercise and Respiration 54(4): 972 - 977

Giesbrecht, G.G.; Bristow, G.K.; Uin, A.; Ready, E.A. and Jones, iiAu R.A. (1987). Effectiveness of three field treatments for induced mild (33.0 C) hypothermia. Journal of Applied Physiology 63(6): 2375 - 2379

Gisolfi, C.V. and Weger.C.B. (1984). Temperature regulation during exercise: Old concepts, new ideas. Exercise and Sport Science Reviews 339 - 372 153

Glaser, E.M. and Holmes-Jones, J. (1951) The initiation of shivering by cooled blood returing from the lower limbs. Journal of Physiology (London) 114: 277 - 282

Goffs, L.G., Brubach, H.F., Spehct, T., Smith, N. (1956). Effect of total immersion at various temperatures on oxygen uptake at rest and during exercise. Journal Applied Physiology 9: 59 - 61

Gonzalez, R.R.; Pandolf, K.B. and Gagge, A.P. (1974). Heat acclimation and decline in sweating during humidity transients. Journal of Applied Physiology 36(4): 41 - 425

Graham, T.E. (1988). Thermal, meatbolic, and cardiovascular changes in men and women during cold stress. Medicine and Science in Sports and Exercise 20(5): sup S185 - S19

Hahn, A.G. (1988). Avoiding the dangers of exercise in the heat Excel 5(2): 3 - 6 Harrison, M.H. (1986) Heat and Exercise : Effects on blood volume. Sports Medicine 3: 214 - 223

Happ, W.P., Turtle, W.W., Wilson, M, (1949) The physiologic effects of abdominal cold packs. Research Quarterly 20: 153 - 169

Harrison, M.H. (1986) Heat and exercise, effects on blood volume. Sports Medicine 3: 214 - 223 Harrison, M.H. (1985) Effects of thermal stress and exercise on blood volume in humans. Physiological Review 6:149 - 209

Harrison, M.H.; Edwards, R.J. and Leitch (1975). Effect of exercise and thermal stress on plasma volume. Journal of Applied Physiology 39(6): 925 - 931

Haymes, E.M. and Wells, C.L. (1986). Environment and Human Performance Champaign : Human Kinetics Publishers, Inc.

Haymes, E.M; Dickson, A.L; Malville, N. and Ross, R.W. (1982). Effects of wind on the thermal and metabolic responses to exercise in the cold. Medicine. Science. Sports and Exercise. 14(1): 41 - 45

Hazel, J. (1985). How to survive in cold water. Australian Triathlon Sport August/September

Hessemer, V.; Langusch, D.; Bruck, K.; Bodeker, R.H.; and Breidenbach, T. (1984). Effect of slightly lowered body temperatures on endurance performance in humans. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology. 57(6): 1731 - 1737.

Holmer, I (1972) Oxygen uptake during swimming in man. Journal of Applied Physiology 33(4): 502 - 509 Holmer, I. and Bergh, U. (1974). Metabolic and thermal responses to swimming in water at varying temperatures. Journal of Applied Physiology. 37(5): 702 - 705

Holly, R.G.; Barnard, R.J.; Rosenthal, M.; Applegate, E. and Pritikin, N. (1986). Triathlete characterization an response to prolonged strenous competition. Medicine and Science in Sports and Exercise. 18(1): 123 - 125

Hong, S. and Nadel, E.R. (1979). Thermogenic control during exercise in a cold environment. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology.47(5): 1084 - 1089

Horvath, S.M. (1948). Reactions of men exposed to cold and wind. American Journal of Physiology 152: 242 - 249

Horvath, S. (1981). Exercise in a cold environment. Exercise and Sport Science Reviews 221 - 263 lampietro, P.F.; Bass, D.E. and Buskirk, E.R. (1958). Heat exchanges of nude men in the cold: effect of humidity, temperature and windspeed. Journal of Applied Physiology 12: 351 - 356

Jessen, C. (1987a). Thermoregulatory mechanism in severe heat stress and exercise. Hales, J.R.S. and Richards, D.A.B. (eds) Transactions of the Menzies Foundation 14: 7-15 Jessen, C. (1987b). Hyperthermia and it's effect on exercise performance. Hales, J.R.S. and Richards, D.A.B. (eds) Transactions of the Menzies Foundation Hales, J.R.S. and Richards, D.A.B. (eds) Transactions of the Menzies Foundation 14: 103 - 107

Johnson, J.m.; Rowell, L.B.; Brengelmann, G.L. (1974). Modification of the skin blood flow-body temperature relationship by upright exercise. Journal of Applied Physiology 37(6): 880 - 886

Jose, A.D.; Stitt, F.; Collison, D. (1970). The effects of exercise and changes in body temperature on the intrinsic heart rate in man. American Heart Journal 79(4): 488 - 49

Kang, D.H.; Park, Y.S.; Park, Y.D.; Lee, I.S.; Yeon, D.S.; Lee, S.H.; Hong, S.Y.; Rennie, D.W. and Hong, S.K. (1983). Energetics of wetsuit diving in Korean women breath-hold divers. Journal of Applied Physiology: Respiration- Environment. Exercise and Physiology. 54(6): 1702 - 1707

Keatinge, W.R. (1960) The effects of subcutaneous fat and of previous exposure to cold on the body temperature, pheripheral blood flow and metabolic rate of men in cold water. Journal of Physiology (London) 153: pp166 - 178

Keatinge, W.R. (1969). Survival in Cold Water Oxford : Blackwell Scientific Publications Kohrt, W.M.; Morgan,D.W.; Bates, B. and Skinner, J.S. (1987). Physiological response of triathletes to maximal swimming, cycling, and running. Medicine and Science in Sports and Exercise 19(1): 51 - 55

Kreider, R.B.; Boone, T; Thompson, W.R.; Burkes, S. and Cortes, C.S. (1988a). Cardiovascular and thermal responses of triathlon performance. Medicine and Science in Sport and Exercise 20(4): 385 - 390

Kreider R.B.; Cundiff, D.E.; Hammett, J.B.; Cortes, C.W.; Williams, K.W.; (1988b). Effects of cycling on running performance in triathletes Annals of Sports Medicine 3(4): 220 - 225

Kruk, B., Pekkarinen, H., Harri, M., Manninen, K., Hanninen, O. (1990) Thermoregulatory responses to exercise at low ambient temperature performed after precooling or preheating procedures* European Journal of Applied Physiology 59: 416 - 420

Lamb, D.R. (1984). Physiology of exercise New York: Macmillan Publishing Comapny

Lavoie, J.M. and Montpetit, R.R. (1986). Applied physiology of swimming. Sports Medicine 3: 165 - 189 Layton, R.P.; Mints, W.H.; Annis, J.F.; Rack, M.J.; Webb, P. (1983) Calorimetry with heat flux transducers: comparision with a suit calorimeter. Journal of Applied Physiology- Respiration Environmental. Exercise and Physiology 54: 1361 - 1367

Lowdon, B. (1985). Hazards of cold water swims in triathlon events. Sports Health 2(2): 17-19

Lowdon, B. (1987). The speed suit : discovering the wetsuit's advantage. Triathlete June: pp 22 - 24

Lloyd, E.L. (1986) Hypothermia and Cold Stress Sydney : Croom Helm Ltd

McArdle, W.D.; Katch, F.I. and Katch, V.L. (1986). Exercise Physiology: Energy. Nutrition, and Human Performance. Philadelphia: Lea and Febiger

McArdle, W.D.; Magel, J.R.; Lesmes, G.R. and Pechar. (1976). Metabolic and cardiovascular adjustment to work in air and water at 18, 25, and 33 °C. Journal of Applied Physiology 40(1): 85 - 90

McArdle, W.D.; Magel, J.R; Gergley, T.J.; Spina R.J. and Toner.M.M. (1984a). Thermal adjustment to cold-water exposure in resting men and women. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology 56(6): 1565 - 1571 McArdle, W.D.; Magel, J.R.; Spina, R.J.; Gergley, T.J. and Toner.M.M. (1984b). Thermal adjustments to cold-water exposure in exercising men and women. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology. 56(6): 1572 - 1577

McArdle, W.D.; Glaser, R.M. and Magel, J.R. (1971). Metabolic and cardiorespiratory response during free swimming and treadmill walking. Journal of Applied Physiology 30(5): 733 - 738

MacDougall, J.D.; Reddan, W.G., Layton, C.R. and Dempsey, J.A. (1974). Effects of metabolic hyperthermia on performance during heavy prolonged exercise. Journal of Applied Physiology 36(5): 538 - 544

McMurray, R.G. (1983) Plamsa volume changes during submaximal swimming. European Journal of Applied Physiology 51: 347 -356

McMurray, R.G.and Horvath, S.M. (1979). Thermoregulation in swimmers and runners. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology 46(6):1086 - 1092 Mayers, M.A.; Holland, G.J.; Rich, G.Q.; Vincent, W.J.; Heng, M. (1986). Effects of prolonged intense cycle ergometry upon immediately subsequent maximal treadmill running in trained triathletes. Medicine and Science in Sports and Exercise. 18: S86

Millard-Stafford, M.L.; Cureton, K.J. and Ray, C.A. (1988) Effect of glucose polmer diet supplement on responses to prolonged successive swimming, cycling and running. European Journal of Applied Physiology 58: 327 - 333

Myler, G.R.; Hahn, A.G. and Tumilty. D. McA. (1989) The Effect of Preliminary Skin Cooling on Performance of Rowers in Hot Conditions-Unpublished manuscript, Canberrra College for Advanced Education, Centre for Sports Studies, Canberra.

Nadel, E.R. (1987) Prolonged exercise at high and low ambient temperatures. Canadian Journal of Sport Science 12(Suppl.1): 140s - 145

Nadel, E.R.; Holmer, I; Bergh, U.; Astrand, P.-O. and Stolwijk, A.J. (1974a). Energy exchanges of swimming man. Journal of Applied Physiology. 36(4): 465 - 471

Nadel, E.R.; Pandolf, K.B.; Roberts, M.F. and Stolwijk, J.A. (1974b). Mechanisms of thermal acclimation to exercise and heat. Journal of Applied Physiology 37(4): 515 - 520 Nadel, E.R (1977). Thermal and energetic exchanges during swimming. Problems with Temperature Regulation during Exercise. Nadel, E.R. ed New York : Academic Press Inc

Nadel, E.R; Cafarelli, E.; Roberts, M.F and Wenger, B. (1979) Circulatory regulation during exercise in different ambient temperatures. Journal of Applied Physiology 46(3): 430 - 437

Nadel, E.R.; Fortney, S.M. and Wenger, C.B. (1980) Effect of hydration state on circulatory and thermal regulations.. Journal of Applied Physiology 49(4): 715 - 721

Nadel, E.R.; Mack, G.W.; Nose, H. and Tripathi, A. (1987). Tolerance to severe heat and exercise: Peripheral vascular responses to body fluid changes.Hales, J.R.S. and Richards, D.A.B. (eds) Transactions of the Menzies Foundation 14: 69 - 76

Neilson, B. and Neilson, M (1962). Body temperature during work at different environmental temperature. Acta Physiologic Scandinavica 56 : 120 - 129

Olschewski, H. and Bruck, K. (1988). Thermoregulatory, cardiovascular, and muscular factors related to exercise after precooling. Journal of Applied Physiology. 64(2): 803 - 811 Olesen, B. (1984). How many sites are necessary to estimate a mean skin temperature Hales, J.R.S. Thermal Physiology New York : Raven Press.

OToole, M.L; Douglas, P.S. and Hiller D.B. (1989). Applied physiology of a triathlon Sports Medicine 8(4): 201 - 225

OToole, M.L.; Hiller, W.D.B.; Crosby, LO. and Douglas,P.S. (1987). The ultraendurance triathlete : a physiological profile. Medicine and Science in Sports and Exercise19(1) : 45 - 50

OToole, M.L; Hiller, W.D.B.; Roalstad, M.S. and Douglas, P.S. (1988). Hemolysis during triathlon races: its relation to race distance. Medicine and Science in Sports and Exercise 20(3): 272 - 275

Parsons, L. and Day, S.J. (1986). Do wetsuits affect swimmming speed? British Journal of Sports Medicine 20(3): 129 - 131

Pendergast, D.R. (1988). The effect of body cooling on transport during exercise. Medicine and Science in Sports and Exercise 20( sup S171 - S176)

Pickard, R. (1978). Cold water survival. Sports Coach 2(1): 8-10

Piwonka, R.W. and Robinson, S. (1967). Acclimatization of highly trained men to work in severe heat. Journal of Applied Physiology 22(1): 9 - 12 Pugh, L.G.C. and Edholm, O.G. (1955). The physiology of channel swimmers Lancet 2: 761 - 768

Pugh, L.G.C.E. (1967). Cold stress and muscular exercise, with special reference to accidental hypothermia. British Medical Journal 2: 333 - 337

Rennie, D.W. (1988). Tissue heat transfer in water: lessons from the Korean divers. Medicine and Science in Sports and Exercise 20(5): sup S177 - S184

Roberts, M.F. and Wenger, C.B. (1979). Control of skin circulation during exercise and heat stress. Medicine and Science in Sports and Exercise. 11(1): 36 -41

Rodgers, G.; Goodman, C; Mitchell, D. and Hattingh, J. (1986) The responses of runners to ardous triathlon competition. European Journal of Applied Physiology 55: 405 - 409

Roundy, E.S., Coomy, L.D. (1968) Effectiveness of rest, abdominal cold packs, and cold showers in relieving fatigue Research Quarterly 39: 690 - 695

Rowell, L.B.; Murray, J.A.; Brengelmann, G.L. and Kraning, K.K. (1969) Human cardiovascular adjustments to rapid changes in skin temperature during exercise. Circulation Research 24: 711 - 724 Rowell, L.B. (1974) Human cardiovascular adjustments to exercise and thermal stress. Physiological Reviews 54(1): 74 - 159

Saltin, B.; Gagge, A.P.; Bergh, U.and Stolwijk, J.A.J. (1972). Body temperatures and sweating during exhaustive exercise. Journal of Applied Physielpgy 32(5): 635 - 643

Saltin, B.; Stenberg, J. (1964). Circulatory response to prolonged severe exercise. Journal of Applied Physiology 19(5): 833-838.

Savard, G.K.; Cooper, K.E.; Veale, W.L and Malkinson, T.J. (1985). Peripheral blood flow during rewarming from mild hypothermia in humans. Journal of Applied Physiology 58(1): 4 - 13

Sawka, M.N.; Knowlton, R.G. and Critz, J.B. (1979). Thermal and circulatory responses to repeated bouts of prolonged running. Medicine and Science in Sports11(2): 177 - 180

Schmidt, V. and Bruck, K. (1981). Effect of a precooling maneuver on body temperature and exercise performance. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology. 50(4): 772 - 778

Senay, L.C. (1987). Exercise in a hostile world. Canadian Journal of Sports Science 12(supp 1): 127S - 135S Senay, L.C; Rogers, J.R.G.; and Jooste, P. (1980). Changes in blood plasma during progressive treadmill and cycle exercise. Journal of Applied Physiology : Respiration. Environment- Exercise and Physiology 49(1): 59 - 65

Senay, L.C. and Pivarnik, J.M. (1985). Fluid shifts during exercise Exercise and Sport Science Reviews13: 335 - 387

Shaffrath, J.D. and Adams, W.C. (1984). Effects of airflow and workload on cardiovascular drift and skin blood flow. Journal of Applied Physiology : Respiration. Environment. Exercise and Physiology. 56(5): 1411 - 1417

Shvartz, E. and Benor, D. (1972). Heat strain in hot and humid environments. Aerospace Medicine 43(8): 852 - 855

Shvartz, E. and Benor, D. and Saar, E. (1972). Acclimatization to severe dry heat by brief exposures to humid heat. Ergonomics 15(5): 563 - 571

Sills, F. D. and O'Riley, V.E. (1956). Comparitive effects of rest, exercise, and cold spray upon performance in spot-running Research Quarterly 27: 217 - 219

Smith, H.E. and Trowbridge, R. (1973). Survival in the Cold National Fitness Council Victoria Taylor, A.S.N. (1986). Eccrine sweat glands adaptations to physical training and heat acclimation. Sports Medicine 3: 387 - 397

Telford, R.; Tumulty, D. and Damm, D. (1984). Skinfold measurements in well performed Australian athletes. Medicine in Scientific Sports Exercise 14: 471 - 476

Thoden, J.S.; Wilson, B.A.and MacDougall, J.D. (1982). Testing aerobic power. In MacDougall, J.D; Wenger, H.A.and Green,H.J. (eds) Physiology testing of the elite athlete (pp 39-60). New York : Mouvement Publications, Inc.

Tikuisis, P. (1989) Prediction of the thermoregulatory response for clothed immersion in cold water. European Journal of Applied Physiology 59: 334 - 341

Toner, M.M.; Sawaka, M.N. and Pandolf, K.B. (1984). Thermal responses during arm and leg and combined arm-leg exercise in water. Journal of Applied Physiology : Respiration- Environment. Exercise and Physiology 56(5): 1355 - 136

Toner, M.M.; Sawka, M.N.; Foley, M.E.; and Pandolf, K.B. (1986). Effects of body mass and morpholgy on thermal responses in water.Journal of Applied Physiology 60(2): 521 - 525 167

Toussaint,, H.M.; Bruinink, L; Coster, R; De Looze, M.; Rossem, V.; Veenen, R. and Groot, G. (1989). Effect of a triathlon wet suit on drag during swimming. Medicine and Science in Sports and Exercise. 21(3): 325 - 328

Triathlon Magazine (1988) Triathlon fixtures March

Vanggard, L. (1975). Physiological reactions to wet-cold Aviation. Space. Environment and Medicine 46(1): 33 - 36

Viecsteinas, A; Ferretti, G and Rennie, D. (1982). Superficial shell insulation in resting and exercising men in cold water. Journal of Applied Physiology : Respiration. Environment- Exercise and Physiology. 52(6): 1557 - 1564

Webb, P. (1986). Afterdrop of body temperature during rewarming : an alternative explanation. Journal of Appplied Physiology 60: 385 - 390.

Wells, C.L; Stern, J.R.; Kohrt, W.M. and Campbell, K.D. (1987). Fluid shifts with successive running and bicycling performance. Medicine Science in Sports and Exercise 19(2): 137 - 142 168

APPENDIX A 1

INFORMED VOLUNTARY CONSENT FOR TRIATHLON STUDY

The University of Wollongong's Human Movement Department in conjunction with the N.S.W Triathlon Federation is investigating the relationship between changes in core temperature and triathlon performance. The study will involve several parts. The first stage will involve 3 maximum oxygen uptake tests that will be used to determine the fitness level of each subject in each event. The second phase will be the gathering of anthropometric measurements, they being height, weight and percentage body fat. The final phase will involve two testing sessions in which each subject will be required to complete a triathlon at race pace each session. The swim will be iin a pool 6 metres x 1.2 metres in which subjects will be stationary whilst swimming due to a tethered swimming device. Water temperature will be 18 °C in both triathlons, however in the second triathlon subjects will be required to wear a wetsuit for the swimming stage. The bike and run legs will be completed in the University of Wollongong Climate Chamber so that a sprint distance triathlon (1.6km, 40km and 12 km) has been simulated. During this time several physical responses will be measured: body temperature (rectal probe) skin temperature (skin thermistors) heart rate (sports tester) blood volume (finger prick blood sample) fitness (oxygen analysis equipment)

Absolute confidentiality of individual results will be maintained and will only be presented as group or mean characteristics. As a volunteer for this study I understand that I have the freedom to discontinue participation from the study at any stage without penalty.

I have read and understood the above, including the references to instruments used to measure the physical responses and agree to participate in this research project. I regularly take part in strenous physical activity at least as intense as these tests. Any questions that I have concerning the procedures or project in general have been answered to my satisfaction.

Name

Signature Date / /89 170

APPENDIX B MEDICAL HISTORY QUESTIONNAIRE

SURNAME GIVEN NAMES _ DATE OF BIRTH_ SEX M/F

ADDRESS CONTACT PH NO

HEIGHT WEIGHT

1. When was the last time you had a physical examination ?

2.If you are allergic to any medication, food or other substances, please name them.

3. If you have been told that you have any chronic or serious illness, please name them.

4. Have you been hospitalized in the last three years? Please give details

5. During the last twelve months:

a) Has a physician prescribed any form of medication for you? Y/N b) Has your weight fluctuated more than a few kilos? Y/N c) Did you attempt to bring about this weight change through diet and or exercise? Y/N d) Have you experienced any faintness, lightheadedness, blackouts? Y/N e) Have you occasionally had trouble sleeping ? Y/N f) have you had any severve headaches? Y/N g) have you experienced unusual heartbeats such as skipped beats of palpitations ? Y/N h) have you experienced periods in which your heart felt as though it were racing for no apparent reason ? Y/N

6. At present: a) do you experience shortness of breath or loss of breath while walking ? Y/N b) Do you experience sudden tingling numbness, or loss of feeling in your arms, hands, feet or face? Y/N c) Do you experience swelling of your feet and ankles? Y/N d) Do you get pains or cramps in your legs? Y/N e) Do you experience any pain or discomformt in your chest? Y/N f) Do you experience any pressure of heaviness in your chest? Y/N

7. Have you ever been told that your blood pressure was adnormal? Y/N

8. Have you ever been told that your serum cholestrol of triglyceride level was high? Y/N

9. Do you have diabetes? Y/N If yes, how is it controlled dietary means oral medication insulin injection uncontrolled 173

10. How often would you characterize your stress level as being high? occasionally frequently co n stantly

11. have you ever been told that you have any form of the following illnesses: heart disease heart attack aneurysm rheumatic heart heart murmur a n g i n a

12. Has any member of your immediate family been treated ar suspected to have had any of the following conditions ? Please identify their relationship to you (father, mother, etc) diabetes heart disease stroke high blood pressure

S i g n a t u re Date / /89 174

APPENDIX C 1

NATIONAL HEALTH AND MEDICAL RESEARCH COUNCIL STATEMENT ON HUMAN EXPERIMENTATION

The collection of data from planned experiementation on human beings is necessary for the improvement of human health. experiments range form those undertaken as a part of patient care to those undertaken either on patients or on healthy subjects for the purpose of contributing to knowledge, and include investigations on human behaviour. Investigators have ethical and legal responsibilities toward their subjects and should therefore observe the following principles:

(1) The research must conform to generally accepted moral and scientific principles. To this end institutions in which human experimentation is undertaken should have committee a concerned with the ethical aspects and all projects involving human experimentation should be submitted for approval by suvch a committee.

(2) Protocols of proposed projects should contain a statement by the investigator of ethical considerations involved.

(3) The investigator after careful consideration and appropriate consultation must bve satisfied that the possible advantage to be gained from the work justifies any discomfort or risks involved. (4) The research protocol should demonstrate knowledge of the relevant literature and wherever possible be based on prior laboratory and animal experiements.

(5) In the conduct of research, the investigator musta at all times respect the rights, wishes, beliefs, consent and freedom of the individual subject.

(6) Research should be conducted only by suitably qualfied persons with appropiate competence, having facilities for proper conduct of the work; clinical research requires not only clinical competence but also the facilities for dealing with any contigencies that may arise.

(7) New therapeutic or experimental procedures which are at the stage of early evaluation and which may have long-term effects should not be undertaken unless appropriate provision has been made for long-term care, observation and maintenance of records.

(8) Before research is undertaken the free consent of the subject should be obtained. To this end the investigator is responsible for providing the subject at his or her level of comprehension with sufficient information about the purpose, methods, demands, risks, inconvenience and discomforts of the study. Consent should be obtained in writing unless there are good reasons to the contrary. If consent is not obtained in writing the circumustances under which it is obtained should be recorded. 1

(9) The subject must be free at any time to withdraw consent to further participate.

(10) Special care must be taken in relation to consent and to safeguarding individual rights and welfare where the research involves children, the mentally ill and those in dependent relationships or comparable situations.

(11) The investigator must stop or modify the research programme or experiment if it becomes apparent during the course of it that continuation may be harmful.

(12) Subject to maintenance of confidentiality in respect of individual patients, all members of research groups should be fully informed about projects on which they are working.

(13) Volunteers may be paid for inconvenience and time spent, but such payment should not be so large as to be an inducement to participate. 178

APPENDIX D 179

DATE DM TIME ROOD QUANTITY (APPROX)

DATE DAI TIME POOD QUANTITY (APPROX)

DATE QAY TIME ROOD QUANTITY (APPROX) 180

APPENDIX E 181

DATE DAY EVENT TIME TFMP TYPE OF TRAINING LONG SLOW I HIGH TEMPO / INTERVAL / SPRINT DISTANCE REPS TIMEO REP) TIME HEART RATE

DATE DM EVENT TIME TEMP TYPE OF TRAINING LONG SLOW / HIGH TEMPO / INTERVAL / SPRINT DISTANCE REPS TIMEO REP) TIME HEART RATE

DATE DAY EVENT TIME TEMP TYPE OF TRAINING LONG SLOW / HIGH TEMPO / INTERVAL / SPRINT DISTANCE REPS TIMEO REP) TIME HEART RATE

DATE DAY EVENT HMf IEME TYPE OF TRAINING LONG SLOW / HIGH TEMPO / INTERVAL / SPRINT DISTANCE REPS TIMEO REP) TIME HEART RATE

DATE DAY EVENT HME IEME TYPE OF TRAINING LONG SLOW / HIGH TEMPO / INTERVAL / SPRINT DISTANCE REPS TIMEO REP) TIME HEART RATE 182

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Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 7.646 7.646 4.019 .0569 subjects w. groups 23 43.759 1.903 Repeated Measure (B) 6 2.67 .445 8.598 .0001 AB 6 2.79 .465 8.983 .0001 B x subjects w. groups 138 7.143 .052

There were no missing cells found. 4 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... R R5 R 10 R 15 R 20 R 25 1 5 1 5 1 5 1 5 1 5 1 5 Y © 37.467 37.4 37.367 37.353 37.373 37.393 h- 1 0 10 1 0 1 0 1 0 1 0 UJ N 37.36 37.26 37.11 36.96 36.81 36.68 25 25 25 25 25 25 Totals: 37.424 37.344 37.264 37.196 37.148 37.108

Page 2 of the AB Incidence table

Repeated Mea... R 30 Totals: i— 1 5 1 05 Y X 37.373 37.39 © UJ 1 0 70 N 5 36.56 36.963 25 175 Totals: 37.048 37.219 Repeated Measures Swim Skin Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: -> value: WETSUIT (A) 1 932.945 932.945 107.914 .0001 subjects w. groups 26 224.778 8.645 Repeated Measure (B) 6 115.518 19.253 50.858 .0001 AB 6 26.232 4.372 11.549 .0001 B x subjects w. groups 156 59.056 .379

There were no missing cells found. 1 case deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... SK0 SK5 SK10 SK15 SK20 SK25 i— 1 5 15 1 5 1 5 1 5 1 5 Y cn 27.899 25.421 25.183 25.125 25.297 25.05 \- 13 13 1 3 1 3 1 3 1 3 UJ N 5 22.052 20.945 20.883 20.923 20.843 20.848 28 28 28 28 28 28 Totals: 25.185 23.343 23.186 23.174 23.229 23.099

Page 2 of the AB Incidence table

Repeated Mea... SK30 Totals: t— 1 5 105 Y "D 24.01 25.426 LU 1 3 91 N 5 20.867 21 .052 28 1 96 Totals: 22.551 23.395 Repeated Measures Bike Core Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 61.723 61.723 9.318 .0076 subjects w. groups 16 105.983 6.624 Repeated Measure (B) 20 162.931 8.147 163.359 .0001 AB 20 1 1.049 .552 11.078 .0001 B x subjects w. groups 320 15.958 .05

There were no missing cells found. 11 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... R0 R2 R4 R6 R8 R10 1 0 1 0 1 0 1 0 1 0 1 0 Z> Y 00 37.49 37.44 37.45 37.47 37.56 37.6 i— 8 8 8 8 8 8 UJ N 5 36.375 36.4 36.388 36.375 36.375 36.437 18 18 1 8 1 8 1 8 1 8 Totals: 36.994 36.978 36.978 36.983 37.033 37.083

Page 2 of the AB Incidence table

Repeated Mea... R12 R14 R16 R18 R20 R25 1 0 1 0 1 0 1 0 1 0 1 0 Y 3 37.69 37,78 37.87 37.94 38.01 38.2 y— 8 8 8 8 8 8 5 N 36.513 36.612 36.737 36.888 37 37.325 1 8 1 8 1 8 1 8 1 8 1 8 Totals: 37,167 37,261 37.367 37.472 37.561 37.811 Repeated Measures Bike Core Temperature

Page 3 of the AB Incidence table

Repeated Mea... R30 R35 R40 R45 R50 R55 1 0 1 0 1 0 1 0 1 0 1 0 r> Y CO 38.36 38.49 38.59 38.67 38.71 38.75 i— 8 8 8 8 8 8 LU N 5 37.6 37.888 38.025 38.15 38.275 38.413 18 18 1 8 1 8 18 1 8 Totals: 38.022 38.222 38.339 38.439 38.517 38.6

Page 4 of the AB Incidence table

Repeated Mea... R60 R65 R70 Totals: t- 10 1 0 1 0 210 Y =5 38.77 38.77 38.78 38.1 14 cn 8 8 8 1 68 t— N UJ 38.475 38.513 38.55 37.301 18 1 8 1 8 378 Totals: 38.639 38.656 38.678 37.752 Repeated Measures Bike Skin Temperature

Page 3 of the AB Incidence table

Repeated Mea... SK30 SK35 SK40 SK45 SK50 SK55 t- 10 10 1 0 1 0 1 0 1 0 Y GO 31.985 31.92 32.018 32.046 31.879 31.826 h- 7 7 7 7 7 7 UJ N 31.641 32.083 32.149 32.281 32.29 32.216 1 7 17 1 7 1 7 1 7 1 7 Totals: 31 .844 31.987 32.072 32.143 32.048 31.986

Page 4 of the AB Incidence table

Repeated Mea... SK60 SK65 SK70 Totals: t— 1 0 1 0 1 0 210 Y 00 31.693 31.685 31.732 30.405 i— 7 7 7 147 LU N 32.127 31.799 31.914 29.488 1 7 1 7 1 7 357 Totals: 31.872 31.732 31.807 30.027 Repeated Measures Bike Skin Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 72.647 72.647 4.996 .041 subjects w. groups 15 218.119 14.541 Repeated Measure (B) 20 1523.205 76.16 180.497 .0001 AB 20 93.708 4.685 11.104 .0001 B x subjects w. groups 300 126.584 .422

There were no missing cells found. 12 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... SK0 SK2 SK4 SK6 SK8 SK10 i— 1 0 1 0 1 0 1 0 1 0 1 0 X Y 00 27.776 27.547 27.363 27.739 27.976 28.624 i— 7 7 7 7 7 7 LU N 5 25.039 25.593 25.996 26.523 26.809 27.134 1 7 1 7 1 7 1 7 1 7 1 7 Totals: 26.649 26.742 26.8 27.238 27.495 28.011

Page 2 of the AB Incidence table

Repeated Mea... SK12 SK14 SK16 SK18 SK20 SK25 i— 1 0 1 0 1 0 1 0 1 0 1 0 X> Y OO 29.362 30.075 30.712 31 .044 31.627 31.874 (— 7 7 7 7 7 7 UJ N 5 27.624 27.794 28.584 29.051 29.69 30.917 1 7 1 7 1 7 1 7 1 7 1 7 Totals: 28.646 29.136 29.836 30.224 30.83 31 ,48 Repeated Measures Afterdrop Core Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: vlean Square: F-test: P value: WETSUIT (A) 1 6.741 6.741 3.047 .1028 subjects w. groups 14 30.97 2.212 Repeated Measure (B) 13 33.995 2.615 110.722 .0001 AB 13 1.53 .1 18 4.983 .0001 B x subjects w. groups 182 4.298 .024

There were no missing cells found. 13 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... R000 R200 R004 R600 R800 R1000 i— 10 10 1 0 10 1 0 1 0 Y cn -.06 -.1 1 -.1 -.08 .01 .05 t— 6 6 6 6 6 6 LU N -.483 -.467 -.483 -.5 -.5 -.433 1 6 16 1 6 1 6 1 6 1 6 Totals: -.219 -.244 -.244 -.238 -.181 -.131

Page 2 of the AB Incidence table

Repeated Mea... R1200 R1400 R1600 R1800 R2000 R2500 1 0 1 0 1 0 1 0 1 0 1 0 Y In .14 .23 .32 .39 .46 .65 LU 6 6 6 6 6 6 N 5 -.383 -.283 -.15 -.01 7 ,133 .45 1 6 1 6 1 6 1 6 1 6 1 6 Totals: -.056 .038 .144 .238 .338 .575 Repeated Measures Afterdrop Core Temperature Page 3 of the AB Incidence table

Repeated Mea... R3000 R3500 Totals: 1- 1 0 1 0 140 CD Y cn .81 .94 .261 i— 6 6 84 LU N .733 1.017 -.098 1 6 1 6 224 Totals: .781 .969 .126 Repeated Measures Run Core Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: vlean Square: F-test: 3 value: WETSUIT (A) 1 .131 .131 .075 .7879 subjects w. groups 14 24.364 1.74 Repeated Measure (B) 8 5.645 .706 45.659 .0001 AB 8 .135 .017 1.092 .3738 B x subjects w. groups 112 1.731 .015

There were no missing cells found. 12 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... R0 R5 R10 R15 R20 R25 i— 1 1 1 1 1 1 1 1 1 1 1 1 Z) Y 38.718 38.736 38.791 38.882 38.982 39.027 cn h- 5 5 5 5 5 5 l±J N 38.56 38.62 38.68 38.76 38.92 38.98 1 6 1 6 1 6 1 6 1 6 1 6 Totals: 38.669 38.7 38.756 38.844 38.962 39.013

Page 2 of the AB Incidence table

Repealed Mea... R30 R35 R40 Totals: i— 1 1 1 1 1 1 99 Y zo 39.109 39,182 39.218 38.961 cn 5 5 5 45 i— N LU 39.06 39.22 39.26 38.896 5 1 6 1 6 1 6 1 44 Totals: 39,094 39,194 39.231 38.94 Repeated Measures Run Skin Temperature

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 10.723 10.723 1.336 .2621 subjects w. groups 19 152.546 8.029 Repeated Measure (B) 8 13.412 1.677 9.825 .0001 AB 8 1.031 .129 .755 .6428 B x subjects w. groups 152 25.937 .171

There were no missing cells found. 7 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... SK0 SK5 SK10 SK15 SK20 SK25 1 1 1 1 1 1 1 1 1 1 1 1 r> Y GO 32.419 31.929 32.578 32.685 32.4 32.419 I— 1 0 1 0 1 0 1 0 1 0 1 0 LU N 32.6 32.232 33.002 33.188 33.086 32.988 21 21 21 21 21 21 Totals: 32.505 32.073 32.78 32.924 32.727 32.69

Page 2 of the AB Incidence table

Repeated Mea... SK30 SK35 SK40 Totals: i— 1 1 1 1 1 1 99 Y r> 32.574 32.685 32.734 32.491 00 f- 1 0 1 0 1 0 90 LU N 5 33.199 33.182 33,238 32.968 21 21 21 189 Totals: 32.871 32.922 32.974 32.719 Repeated Measures Swim V02

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: vlean Square: F-test: P value: WETSUIT (A) 1 1.03 1.03 2.206 .151 subjects w. groups 23 10.735 .467 Repeated Measure (B) 2 .128 .064 2.584 .0864 AB 2 .006 .003 .118 .8889 B x subjects w. groups 46 1.135 .025

There were no missing cells found. 4 cases deleted with missing values.

The AB Incidence table

Repeated Mea... S 4-5 V02 S 14-15 ... S 29-30 ... Totals: i— 13 13 1 3 39 X Y 00 2.368 2.469 2.45 2.429 1— 12 12 12 36 LU N 2.616 2.715 2.66 2.664 5 25 25 25 75 Totals: 2.487 2.587 2.551 2.542 Repeated Measures Run Heart Rate

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 1289.752 1289.752 1.068 .3127 subjects w. groups 22 26573.914 1207.905 Repeated Measure (B) 7 2437.333 348.19 46.979 .0001 AB 7 17.267 2.467 .333 ,938 B x subjects w. groups 154 1141.4 7.412

There were no missing cells found. 4 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... R5 R10 R15 R20 R25 R30 14 14 1 4 1 4 1 4 1 4 5 Y 156.143 159.571 1 61 162.714 164.429 165.357 oo 1 0 1 0 1 0 1 0 1 0 1 0 t— N LU 150.8 154.8 156.5 158.1 158.7 159.5 24 24 24 24 24 24 Totals: 153.917 157.583 159.125 160.792 162.042 162.917

Page 2 of the AB Incidence table

Repeated Mea... R35 R40 Totals: 1 4 1 4 1 12 X Y 00 166.857 167.786 162.982 t— 1 0 1 0 80 LU N 5 161 .9 161 .5 157,725 24 24 1 92 Totals: 164.792 165.167 160.792 Repeated Measures Bike Heart Rate Page 3 of the AB Incidence table

Repeated Mea... B65 B70 Totals: i— 1 3 1 3 182 3 Y CO 153.615 155.462 153.659 1— 12 1 2 168 LU N 5 157.833 157.583 154.125 25 25 350 Totals: 155.64 156.48 153.883 Repeated Measures Bike Heart Rate

Anova table for a 2-factor repeated measures Anova.

Source: df. Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 18.943 18.943 .009 .9255 subjects w. groups 23 48743.326 2119.275 Repeated Measure (B) 13 6722.997 517.154 14.519 .0001 AB 13 698.686 53.745 1.509 .1128 B x subjects w. groups 299 10650.245 35.62

There were no missing cells found. 3 cases deleted with missing values.

Page 1 of the AB Incidence table

Repealed Mea... B5 B10 B15 B20 B25 B30 i— 13 13 1 3 1 3 13 1 3 Y => 141.769 151.538 153.385 154.923 155.231 156.077 00 \— 12 12 1 2 1 2 1 2 1 2 LU N 5 138.083 146.25 149.75 154.083 155.167 155.917 25 25 25 25 25 25 Totals: 140 149 151.64 154.52 155.2 156

Page 2 of the AB Incidence table

Repeated Mea... B35 B40 B45 B50 B55 B60 i— 1 3 13 1 3 1 3 1 3 1 3 Y 5 155,077 155.692 155.538 155.769 154.077 00 153.07" LL1 1 2 12 1 2 1 2 1 2 1 2 N 5 156.25 158.667 157.417 157.917 155.75 157.083 25 25 25 25 25 25 Totals: 155.64 157,12 156.44 156.8 154,88 1 55 Repeated Measures Swim Heart Rate

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 1680.909 1680.909 2.06 .1667 subjects w. groups 20 16321.333 816.067 Repeated Measure (B) 5 43.273 8.655 .424 .8308 AB 5 149.461 29.892 1,465 .2079 B x subjects w. groups 100 2039.933 20.399

There were no missing cells found. 6 cases deleted with missing values.

Page 1 of the AB Incidence table

Repeated Mea... S5 S10 S15 S20 S25

•— 12 1 2 1 2 1 2 1 2 X Y 00 122.833 124.5 124.417 124.583 126.417 i— 1 0 1 0 1 0 1 0 1 0 LU N 132.7 134.3 131.5 131.6 131.3 22 22 22 22 22 Totals: 127.318 128.955 127.636 127.773 128.636

Page 2 of the AB Incidence table

Repeated Mea... S30 Totals: i— 1 2 72 X Y 00 126.25 124.833 h- 1 0 60 LU N 5 130.6 132 22 132 Totals: 128.227 128.091 Repeated Measures Bike V02

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: P value: WETSUIT (A) 1 .027 .027 .033 .8585 subjects w. groups 23 19.155 .833 Repeated Measure (B) 4 .639 .16 4.624 .0019 AB 4 .053 .013 .381 .8217 B x subjects w. groups 92 3.178 .035

There were no missing cells found. 4 cases deleted with missing values.

The AB Incidence table

Repeated Mea... B 7-8 V02 B 14-15 ... B 29-30 ... B 44-45 ... B 69-70 ... Totals: i— 13 13 13 1 3 1 3 65 X Y 3.064 3.18 3.271 3.244 3.318 3.215 oo t— 12 12 1 2 1 2 1 2 60 N LU 3.115 3.13 3.24 3.191 3.255 3.186 25 25 25 25 25 125 Totals: 3.089 3.156 3.256 3.218 3.288 3.201 Repeated Measures Run V02

Anova table for a 2-factor repeated measures Anova.

Source: df: Sum of Squares: Mean Square: F-test: D value: WETSUIT (A) 1 .357 .357 .758 .3927 subjects w. groups 24 11.311 .471 Repeated Measure (B) 3 .177 .059 4.657 .005 AB 3 .1 .033 2.626 .0569 B x subjects w. groups 72 .913 .013

There were no missing cells found. 3 cases deleted with missing values.

The AB Incidence table

Repeated Mea... R 7-8 VQ2 R 14-15 ... R 29-30 ... R 39-40 ... Totals: t— 1 4 1 4 1 4 1 4 56 Y 00 3.363 3.366 3.433 3.391 3.388 I— LU 12 1 2 1 2 1 2 48 N 5 3.199 3.223 3.279 3.38 3.271 26 26 26 26 1 04 Totals: 3.287 3.3 3.362 3.386 3.334 Factorial Analysis Bike Plasma Volume Change

One Factor ANOVA Xi: WETSUIT Y-j: PLAMS CHANGE PERECENT BIKE

Analysis of Variance Table Source: 3F: Sum Squares: Mean Square: F-test: Between qroups 1 285.786 285.786 4.255 Within qroups 24 1611.924 67.164 p = .0501 Total 25 1897.711

Model II estimate of between component variance = 218.623

One Factor ANOVA Xi: WETSUIT Yi: PLAMS CHANGE PERECENT BIKE

GrouD: Count: Mean: Std. Dev.: Std. Error: Y 13 -5.798 8.757 2.429

N 13 .832 7.592 2.106

One Factor ANOVA XT : WETSUIT Y-): PLAMS CHANGE PERECENT BIKE

Cc^Danson: Mean Diff.: Fisher PLSD: Scheffe F-test: Dunnett t: Y vs. N -6.631 6,635 4,255* 2.063

' Sranificant at 95% Factorial Analysis Run Plasma Volume Change

One Factor ANOVA X-|: WETSUIT Y-): PLASMA CHANGE PERCENT RUN

Analysis of Variance Table Source: DF: Sum Squares: Mean Square: F-test: Between qroups 1 .448 .448 .005 Within qroups 23 2190.085 95.221 p = .9459 Total 24 2190.534

Model II estimate of between component variance = -94.773

One Factor ANOVA X-|: WETSUIT Y-): PLASMA CHANGE PERCENT RUN

Group: Count: Mean: Std. Dev.: Std. Error: Y 12 4.209 9.517 2.747

N 13 4.477 9.974 2.766

One Factor ANOVA X-|: WETSUIT Y-i: PLASMA CHANGE PERCENT RUN

Comparison: Mean Diff.: Fisher PLSD: Scheffe F-test: Dunnett t: Y vs. N -.268 j 8.082 .005 .069