/I
/o* I g
RELATIONSHIP BETWEEN VENTILATION AND OXYGEN UPTAKE
AT 40% AND 85% OF PEAK OXYGEN UPTAKE
IN 18-35-YEAR-OLD WOMEN USING
THE ARM CRANK ERGOMETER
THESIS
Presented to the Graduate Council of the
North Texas State University in Partial
Fulfillment of the Requirements
For the Degree of
MASTER OF SCIENCE
By
Peter C. Zervopoulos, B.S.
Denton, Texas
May, 1988 Zervopoulos, Peter, Relationship Between Ventilation and Oxygen Uptake at 40% and 85% of Peak Oxygen Uptake in
18-35-Year-Old Women Using the Arm Crank Ergometer. Master of Science (Physical Education), May, 1988, 135 pp., 8 tables, bibliography, 138 titles.
This study investigated whether or not a relationship exists between ventilation and oxygen uptake at 40% and 85% of V0 2 peak intensity in 30 upper body fit and 30 unfit 18-
35-year-old women. The correlations between ventilation and oxygen uptake at 40% of peak intensity for the fit group (r
= -.51) and the unfit group (r = -.48) were modestly negative. At 85% intensity the relationship between ventilation and oxygen uptake in the two groups was -.44 and
-.66, respectively. The lower correlations between ventilation and oxygen uptake observed at the 85% level of peak intensity among the unfit group could be due to a lower ventilatory threshold (66% = fit; 49% = unfit), lesser local muscle changes, along with reduced lactate and C02 management; all of which would be improved with training. Copyright by
Peter C. Zervopoulos
1987
iii TABLE OF CONTENTS
Page
LIST OF TABLES ...... vi
LIST OF ILLUSTRATIONS ...... vii
Chapter
I. INTRODUCTION AND PURPOSE OF STUDY ......
Statement of the Problem Purpose of Study Limitations and Delimitations
CHAPTER BIBLIOGRAPHY ...... 4
II. LITERATURE REVIEW ...... 5
Arm Ergometry in Exercise and Attaining Peak Oxygen Uptake ...... 5
Optimum Protocol Body Positions in Arm Crank Exercise Arm Crank Exercise Versus Leg Exercises
Ventilation in Exercise ...... 14
Ventilatory Control Hypoxic and Hypercapnic Responses Genetic Versus Trained Responses Exercise Breathing Patterns Ventilation and Oxygen Uptake Comparisons in Exercise
CHAPTER BIBLIOGRAPHY ...... 37
III. PROCEDURES ...... 51
Subjects Testing Instruments Test Administration Determination of Dependent Variables Research Design and Statistical Tests
IV. RESULTS ...... 58
iv V. DISCUSSION AND CONCLUSIONS . ..e 65
Minute Ventilation and Oxygen Uptake Relationship Test, Re-test Reliability Ventilatory Threshold Predicting Peak Oxygen Uptake from Maximum Test Time Conclus ions
CHAPTER BIBLIOGRAPHY...... 0 .0 .0 .0 .0 .0 .0 90
APPENDIX A ...... 0. 0.. . . 103
APPENDIX B 107 . . 0. 0. 0. . . . APPENDIX 109
REFERENCES ...... 114
V LIST OF TABLES
Tables Page
1. Descriptive Statistics for the Fit Group . . 59 2. Descriptive Statistics for the Unfit Group . 60 3. Descriptive Statistics for the Combined Groups 61 4. Pearson Correlation Coefficients for the Test, Re-test Reliability with V0 2 Peak and Ve Peak ...... 62 5. Pearson Correlation Coefficients for Combined Samples for V0 2 Peak, Ve Peak, Maximum Test Time, and Ventilatory Threshold . .0.0 62 6. Pearson Correlation Coefficients for the Fit Sample for V0 2 Peak, Maximum Test Time, and Ventilatory Threshold ...... 63 7. Pearson Correlation Coefficients for the Unfit Sample for V0 2 Peak, Ve Peak, Maximum Test Time, and Ventilatory Threshold . .a.0 63 8. Studies Investigating the Percentage of V02 at Which Ventilatory Threshold Occurs . .I.* 80
vi LIST OF ILLUSTRATIONS
Illustrations Page
Al. Ve/V02 Plots for the Combined Fit and Unfit Samples at 40% VO2 Peak ...... 104 A2. Ve/VO2 at 85% V0 2 Peak for the Fit Sample . . . 105 A3. VO2 Peak vs. Maximum Test Time Plots for Combined Fit and Unfit Groups ...... 106
vii CHAPTER I
INTRODUCT ION AND PURPOSE OF STUDY
With the rise in awareness of paraplegic
athletes -- as seen in the Los Angeles Olympics --along
with the sustaining popularity of sports that involve
the upper body such as swirrmning, cross-country skiing,
and rowing, for example, has come the need to examine
if certain physiological phenomena which occur in lower
body exercise also hold true in upper body exercise.
For instance, it has been known that endurance
athletes, because of a reduced lactate production
through training, breathe less than non-athletes at
equal, heavy, absolute workloads. This has been shown
to be the case among upper body trained athletes also.
More specifically, based on a study utilizing a bicycle
ergometer, researchers suggest a possible inverse
relationship between the ventilatory response to
exercise and the maximum whole body oxygen consumption
value. To perform this experiment in an upper body mode, one would extract the maximum oxygen uptake measure using the arms, or, the V02 peak. This term is
used since VO2 max can not usually be obtained with a
small muscle group. Studies done in this area using
the upper body and involving women are scarce. The
I 2
reason for testing these athletes in an upper body mode
is the impracticality of testing swimmers, cross-
country skiers, and rowers, for example, with a tread- mill or bicycle ergometer -- which can hardly give
objective information concerning the athletes' specific
working capacity (Deboer, Kallal, and Lango, 1982).
The role that low exercise ventilation may play in
endurance performance is unknown. One possible
advantage might be through an influence on the per-
ceived effort of exercise where a close correlation of
ventilation and perceived exertion has been shown
(Pandolf, Billings, Drolet, Pimental, and Sawka, 1984).
If a role were to be found in the ventilation versus
oxygen uptake relationship using other modes and
populations, it is believed that this fact should first
be established, that is, whether or not an inverse
relationship at different V02 intensities holds true
for 18 - 35-year-old athletic and non-athletic women.
Statement of the Problem
The problem under study is whether or not a
relationship exists between ventilation and oxygen
uptake at 40% and 85% of V02 peak intensity in upper
body fit and unfit 18 - 35-year-old women. 3
Purpose of Study
The purpose of the study is to determine the relationship between ventilation and oxygen uptake at 40% and 85% of peak oxygen uptake among 18-35-year-old women using the arm crank ergometer.
Limitations and Delimitations
A limitation of the study is that the upper body trained women are not all trained in the same activity. All are upper body athletes but use their upper body musculature to different extents and in different ways as their sports or activities warrant. Thus the generalizability of the results is affected since all the athletes will be tested in one mode. The subjects are all volunteers. Another possible drawback is that the athletes may not be truthful on their distances swum per week or may not be in competition form which would throw off the athletic data.
Delimitations include the choice of a specific population, namely, 18-35-year-old women. Also each of the subjects used the same calibrated metabolic cart and arm crank ergometer throughout the experiment. CHAPTER B IBLI OGRAPHY
DeBoer, L. B., Kallal, 3. E., & Lango, M. R.
(1982). Upper extremity prone position exercise as
aerobic capacity indicator. Archives of Physical
and Medical Rehabilitation, 63, 467-471.
Pandolf, K. B., Billings, D. S., Drolet, L. L.,
Pimental, N. A., & Sawka, M. N. (1984). Differen-
tiated ratings of perceived exertion and
various physiological responses during prolonged
upper and lower body exercise. European Journal of
Applied Physiology, 53, 5-11.
4 CHAPTER II
LITERATURE REVIEW
Arm Egometry in Exercise and
Attaining Peak Oxygen Uptake
Optimum protocol Choosing the correct protocol is of obvious importance for peak oxygen uptake (V02 peak) determination in a maximum arm crank test. Comparing continuous protocols in 13 untrained males at various cadences, Sawka, Foley, Pimental,
Toner, and Pandolf (1983) found that a 70 rpm cadence elicited significantly higher maximum oxygen consumption
(VO2 max) and maximum ventilation (Ve max) responses than either 50 or 30 rpm. This progressive intensity protocol design started each subject at a power output of 75 W and was increased by 25 W every three minutes. During the continuous 70 rpm protocol, the subject's Ve max, maximum heart rate (HR max), and maximum lactate production (LA max) compared favorably with the highest values previously reported for arm crank exercise (Martin & Stager, 1981;
Sawka, Miles, Petrofsky, Wilde, and Glaser, 1982; Vrijens,
Hoekstra, Bouchaert, and Van Uytranck, 1975). Using 30 untrained males, Davis, et al. (1976) employed a continuous protocol at a cadence of 50 rpm, with a
5 6 zero load the first four minutes of the work bout followed by a .25 kpm increase each minute thereafter. The researchers reported arm crank VO2 values that were 64% of the subjects' cycle ergometer VO2 max value and 59% of the subjects' treadmill V0 2 max values. Pimental, Sawka,
Billings, and Trad (1984) studied nine untrained males also utilizing a continuous protocol but with a cadence of 70 rpm. Their design included an incremental increase of 17 W every three minutes until exhaustion and found on the average that arm crank exercise VO2 values were 72% of the subjects' cycle ergometer VO 2 max values. Vrijens, et al.
(1975) compared five elite kayakers from the Belgian
National Team with nine lower body trained students using the arm crank ergometer. A continuous-progressive protocol at a cadence of 60 cycles/min. was engaged. The load was increased by 40 W every three minutes until exhaustion. The peak VO2 values for the kayakers and students on the arm crank ergometer was 88% and 81% of the subjects' values attained from bike ergometer VO2 max values, respectively. In a discontinous design, Seals and Mullin (1982) studied 12 untrained males at a cadence of 60 cycles/min.
They found arm crank V02 peak values fell between 60-70% of the subjects' VO2 max values attained through cycle ergometry. McConnell, Swelt, Jersaty, Missri, and Al-Hani
(1984) examined 20 untrained subjects (10 male and 10 female) also using a discontinuous protocol. The males 7 began their testing at a load of 300 kpm/min. and the females at 150 kpm/min. Two minutes of each exercise bout was followed by one minute of rest. Different loading schemes were used to keep the test times between 6-12 minutes. The researchers reported the subjects' average arm crank VO2 peak value to be 71% of their VO2 max value attained on a treadmill. In another segment of the Seals and
Mullin study (1982), the researchers observed 43 well trained upper body males using the same discontinuous, 60 cycle/min design. The results showed that the arm crank VO2 peak values for these athletes fell between 80-95% of their
VO2 max values attained on a bicycle ergometer.
Looking at many of these studies, a lack of standardization exists among the protocols which makes it difficult to compare upper body peak VO2 values. Generally, it seems throughout these arm crank ergometry studies that the highest Peak VO2 values elicited are those designs which have a high cadence ( 60 rpm). A possible reason for this is demonstrated in a study by Powers, Beadle, and Magnum.
(1984). By examining the effects of speed and work rate on exercise efficiency during arm ergometry in males, decreases in gross and work efficiency with increasing speed of movement were demonstrated. In comparing continuous 50 rpm,
70 rpm, and 90 rpm cadences, Powers (1984) found the 90 rpm continuous protocol to be the most exercise inefficient.
They also contrasted the continuous 50 rpm and 70 rpm 8 cadences and found the 70 rpm more exercise inefficient.
Thus, the resulting gross and work ineffiency which accompany greater speed of movement on the arm crank ergometer contribute significantly in attaining peak VO2 values in this mode.
Sawka, et al. (1983) explored possible differences between a continuous and an intermittent design in 13 untrained males. Both protocols were carried out at a cadence of 50 rpm. For the intermittent protocol, the initial power output level corresponded (via extrapolation) to 70% of the subjects' predicted maximal heart rate. Each three minute power output level was increased by 25 W.
These work bouts were interspersed with 15 minute rest periods. The continuous protocol started each subject at
75W and increased 25W at each three minute interval. Sawka
(1983) reported that the intermittent design - which he stated could theoretically minimize the effects of accumulated muscular fatigue - has no advantage for maximal effort arm crank testing in that no significant difference was found in the two designs. The continuous and intermittent protocols were not, however, compared at 70 rpm. One might reason that no difference in the protocols exists at the higher (70 rpm) cadence. Washburn and Seals
(1983) compared a continuous, 60 rpm protocol with a discontinuous protocol of the same cadence using 20 conditioned but not upper body trained males. The 9
discontinuous protocol consisted of two minute work bouts
separated by one minute rest intervals. The load was
adjusted based on the assumption that arm crank peak V0 2 was 60% of the subjects' VO2 max on the treadmill. They found
no significant difference between the two protocols. The
only advantage stated would be in total test time
administration which favored the continuous (five to seven minutes) over the discontinuous (14-19 min.) protocol.
Body Positions in Arm Crank Exercise
Along with selecting an optimum protocol, choosing the most advantageous body position in relation to the arm crank
ergometer is important in determining VO2 peak. Cerretelli,
Shindell, d. Prampero, and Rennie (1977) compared supine and
erect body positions in four moderately active subjects
ranging from 29-51-years-old. The subjects' hips and
shoulders were strapped during testing for added
stabilization, and the center of the arm crank ergometer
shaft was positioned at the level of the subjects'
shoulders. The work loads were randomized. A higher V02 peak in the sitting (4.15 L/min.) than in the supine posit-ion (3.58 1/min.) was reported for the four subjects.
In another study, Stenberg and Astrand, et al. (1967) tested
the supine and erect body positions with six male and four
female subjects described as healthy and endurance trained.
They found that in the supine position, the oxygen uptake was generally lower on the heavier but still submaximal 10 workloads than in the sitting position. The researchers also reported higher values for ventilation were generally reached in the sitting position. DeBoer, et al. (1982) studied the feasibility of using a prone position arm crank test to predict the upright cycling V02 max. They used 21 healthy, asymptomatic, adult male volunteers -- each of whom performed an upright cycling and a prone position arm crank test. Using a protocol of a 25 W increase every two minutes, they reported that a VO2 peak measure from prone position arm cranking is a weak predictor of upright bicycling VO2 max.
Another consideration in the endeavor to elicit peak
VO2 measures in arm cranking is that of the height of the arm ergometer relative to the upper body. Cunmins and
Gladden (1983) studied physiological responses to submaximal and maximal arm cycling above, at, and below heart level with five volunteers. The three different levels at which the center of the cycle crankshaft was positioned relative to the xiphisternal joint. Heart level was defined as +5 to
+9 cm, below heart level was -27 to (-35) cm., above heart level fell between +47 and +62 cm. Three of the experi- mental sessions consisted of four, 10 minute periods of arm exercise at one of the three arm positions (above, at, or below heart level). Each bout was interspersed with a 10 minute rest period. The protocol started at 0OW, progressed to 29.6 W, 59.0 W and ended at 88.0W. The second set of 11 three experiments was designed to extract peak V0 2 with maximal arm exercise at each position. The subjects started out at a high wattage and worked in bouts of three minutes
followed by 10 minute rest intervals. Resistance increased with each subsequent work period. DeBoer, et al. (1982)
reported found no significant differences in the responses
(V02 peak included) to either submaximal or maximal arm cycling with the arms positioned above, at, or below heart
level. The authors suggest that arm position during upright
arm exercise is not nearly as important a consideration as
is the amount of isometric or static contraction involved in
the exercise.
Arm Crank Exercise Versus Leg Exercises
Comparing arm crank exercise and leg exercise
performance parameters and physiological measures shows markedly different responses in submaximal vs. maximal
exercise designs.
Examining submaximal VO2 response, Stenberg, Astrand,
Ekblom, Royce, and Saltin (1967) and Vokac, Bell, Bautz,
Holter, and Rodahl (1975) reported a greater V02 response at
a given submaximal power output during arm crank ergometry
compared to leg cycling. Toner, Sawka, Levine, and Pandolf
(1983) stated that a possible explanation for these
differences is that arm crank ergometry requires greater
body stabilization than does leg cycling. This point is
seen in a maximum arm crank whose subjects' torsos were 12 strapped so that only the muscles involved in the actual cranking were measured (Cun-rnins & Gladden, 1983). Using a discontinuous protocol, the subjects' arm crank peak V02 averaged 57%, significantly lower than other studies whose subjects' torsos were not strapped. Therefore, higher V02 responses at a submaximal level of arm crank exercise over
leg cycling are due to a greater exercise component.
During maximal effort, however, arm cranking VO2 was
lower and ranged from 60% to 73% of leg cycling among non-
trained individuals (Astrand & Rodahl, 1977; Davis, Vodak,
Wilmore, Vodak, and Kurtz, 1977; McConnell, 1984; Pimental,
1984; Seals, 1982; Secher, Larsen, Brinkhorst,
Petersen,1974; Vokac, 1975). For well upper body trained athletes, a study of 43 males (Sawka, 1982) showed the athletes attaining between 80-95% of leg cycling V02 max
through arm training. Another study (Scoggin, Dockel,
Kryger, Zwillich, and Weil, 1978) showed an average of between 80-85% of leg cycling among athletes with one
swimmer eclipsing 119% of leg cycling V02 max using the arm crank ergometer. It has been suggested that V02 peak values
in arm crank ergometry are limited more by peripheral
factors than central circulatory factors (Glaser, Swak,
Brune, and Wilde, 1980; Kay, Peterson, and Christensen,
1975; Martin, 1981). These limiting peripheral factors
include a relatively small skeletal muscle mass, possible
restrictions to muscle perfusion, and high levels of local 13
fatigue. Sawka, Glaser, Wilde, and von Luhrte ( 1980) explained that during exercise a smaller skeletal muscle mass would need to develop a greater percentage of its maximal tension to complete a given power output level. He continued to explain that this could result in intramuscular
tensions that could exceed perfusion pressure and thereby
impede 02 delivery, and, as a result of blood flow occlusion, would cause a shift from aerobic to anaerobic metabolism in order to enable muscular contraction to continue (Sawka, 1983). This anaerobic supplementation would be short term, and soon local fatigue would set in and
exercise would terminate.
The anaerobic supplementation was noted in other
studies which reported that arm crank exercise elicits
higher plasma lactate (LA) concentrations than cycle
exercise at a given submaximal V02 level (Astrand, Guharay,
and Wahren, 1968; Sawka, 1982). Sawka et al. (1980)
reasoned that since arm crank exercise elicits a lower peak
V02 , the anaerobic threshold should occur at a lower
absolute V02 level resulting in the elevated LA
concentration at a given submaximal power output level.
After maximal effort, however, blood lactate concentrations were lower in arm cranking than in cycle exercise (Sawka,
1980). Sawka (1980), explained that this difference is due
to the size of the muscle mass involved during the two modes of exercise. Although maximal LA production per unit of 14 muscle mass may be equivalent, total lactic acid production will be greater during cycle than arm crank exercise.
Toner, et al. (1983) found for a given submaximal 02 uptake, arm crank elicited a higher heart rate. They
continued to explain that this elevated response is one
variable that indicates that arm cranking imposes a greater
load on the circulatory system. The elevated heart rate may
result from an increased V02 level, a greater static
exercise component, as well as an increased sympathetic
output. Maximum heart rate values, however, were lower for
arm crank ergometry than cycle exercise (Astrand, Ekblom,
Messin, Saltin, and Stenberg, 1965; Bergh, Kanstrup, and
Ekblom, 1976; Sawka, 1982; Stenberg, 1967).
Ventilation in Exercise
Of clear significance in the study of the relationship
between peak oxygen uptake and ventilation is the
understanding of ventilation during exercise; the factors in
its control, responses to hypoxia and hypercapnia, and
breathing patterns in the different phases of exercise.
This section consists of three parts. The first considers
factors in the control of ventilation along with hypoxic and
hypercapnic responses. The second portion examines
breathing patterns and characteristics at different phases
of maximal and submaximal exercise. The third and final
part recounts the relationships seen between oxygen uptake
and ventilation. 15
Ventilatory Control
West (1985, p. 115) delineates the three basic elements of the respiratory control system. The sensors (first basic element) collect information and pass it to the central controller (second basic element), located in the brain.
The central controllers coordinate the information and send the impulses to the effectors (third basic element), or respiratory muscles, which force inspiration and at times, expiration.
Three main centers of neurons make up the central controller. The medullary respiratory center is located in the reticular medulla and consists of an inspiratory area responsible for inspiration and, an expiratory area, dormant during regular expiration because of its passive nature, but active during exercise (West, 1985, p. 115). Little is known about the apneustic center, located in the lower pons.
The pneumotaxic center, located in the upper pons, is said to regulate inspiratory volume through inhibition and, secondarily, respiratory rate (West, 1985, p. 118). The effectors, or the muscles of respiration include the diaphragm, intercostals, abdominals, and accessory muscles.
Of the numerous sensors in the respiratory control system, the peripheral and central chemoreceptors are most pertinent to this study and will be examined further. Whipp and Wasserman (1980) show the importance of the carotid bodies (peripheral chemoreceptors) in humans in controlling 16 ventilation during muscular exercise. Carotid bodies are
inhibitory interneurons located at the carotid bifurcation
and respond to decreases in pH and P02 (West, 1985, p.
113). Gabel and Weiskopf (1975), studying five normal young men at sea level and simulated altitude, confirm this. They measured ventilatory responses to acute hypoxia after
systematically altering the H+ and PC0 2 at the peripheral
and central chemoreceptors. The authors found the H+ ion to
be the primary agent which interacts during hypoxia at the
chemoreceptors in man. Gabel and Weiskopf (1975) also
demonstrated that the PaCO2 (arterial carbon dioxide
pressure), which under all conditions is normally kept
within a close range (West, 1985, p. 117), has little
influence on the observed sensitivity of the peripheral
chemoreceptors to acute hypoxia. Sorensen and Severinghaus
(1968) studying nine subjects, however, reported that the
peripheral chemoreceptors are also stimulated by hypercapnia
and can account for 20-55% of the ventilatory response. On
a related note, Gray (1971), Hornbein and Roos (1963)
examined ventilatory response time in cats in acidosis and
alkalosis. They demonstrated that metabolic acidosis, which
is known to stimulate the carotid bodies, accelerated the
ventilatory response to exercise - while metabolic alkalosis
appeared to slow the ventilatory response. Wasserman, et
al. (1975) demonstrated the effects carotid bodies had on
the kinetics of the ventilatory response to exercise. He 17 examined six male subjects with resected carotid bodies and
11 others acted as controls. Wasserman, Whipp, Koyal, and
Cleary (1975) found the ventilatory response to exercise faster in normal subjects than in subjects whose carotid bodies had been resected. Griffiths, Henson, Huntsman,
Wasserman, and Whipp (1980) also demonstrated the role of carotid bodies with six male subjects using a bicycle ergometer. They proved that the exercise ventilatory dynamics during normal conditions were appreciably faster during hyperoxic conditions but slower during hypoxia.
Oren, Whipp, and Wasserman (1982) suggest that the carotid bodies exert their influence during the non-steady
state phase of moderate exercise. "The peripheral chemoreceptors subserve an important component of the non-
steady state hyperpnoea of dynamic exercise," Griffiths, et
al. (1980) concluded. Oren, et al. (1982) and Wasserman
(1975) show that the carotid bodies are responsible for the compensatory hyperventilation associated with the metabolic
acidosis at high work intensity. Wasserman (1975) also
concludes that the carotid bodies are partly responsible for
the rate of increase in Ve to steady state.
The central chemoreceptors, located on the ventral
surface of the medulla, also play an important role in the
control of ventilation during exercise. They are the most
important receptors in the minute-by-minute control of
ventilation (Wasserman, Whipp, and Astagna, 1974). Astrand 18
(1977) states that these central receptors are also essential for rhythmic ventilation. These receptors respond to changes in the hydrogen ion concentration of its surrounding extra-cellular fluid (West, 1985, p. 117). In a study cited previously, Gabel and Weiskopf (1975) identified the H+ ion as the primary interacting agent at the central and peripheral chemoreceptors during hypoxia. Byrne-Quinn,
Weil, Sodal, Filley, and Grover (1971) measured 13 athletic and 10 non-athletic subjects and concluded that the medullary (central) chemoreceptors also mediate the ventilatory response to increased C026 The sensitivity of these chemoreceptors is demonstrated by the fact that the composition of the extra-cellular fluid surrounding the receptors is governed primarily by the cerebral spinal fluid
(CSF), which because of its lower protein content has less buffering capacity, and thus is more sensitive than blood to pH change or the presence/absence of H+ (West, 1985, p.
117). Oren, et al. (1982) studying five healthy males as previously mentioned, postulates that the control of ventilation during the steady state condition is possibly the domain of the central chemoreceptors.
Hypoxic and Hypercapnic Response
The study of the control of ventilation in exercise also includes the ventilatory responses to two of the resulting physiological environments that exercise brings: hypoxia and hypercapnia. In comparing ventilatory responses 19 in athletes vs. non-athletes, Martin, Sparks, McCullough, and Grover (1979) studied 23 subjects consisting of eight endurance, eight non-endurance athletes, and seven non- athletes on a modified Balke treadmill test. He found that the endurance athletes have lower ventilatory chemoresponses and lower exercise Ve than non-athletes. Martin, et al.
(1979) adds that the Ve of endurance athletes responds less to hypercapnia and hypoxia than that of non-athletes.
Byrne-Quinn, et al. (1971) compared 13 college varsity male track, swi-ming, and skiing athletes with 10 non-athletes and reported significantly lower Ve responses to hypoxia and hypercapnia in the athletes. Lally, Zechman, and Tracy
(1974) reported similar findings at different exercise intensities in eight divers, 11 non-diving athletes, and nine sedentary non-divers. Martin, et al. (1979) standardized the workloads in the athletic and non-athletic subjects for fitness differences and still found that the endurance athletes breathed significantly less than non- athletes at either exercise intensity. Contrasting responses in different types of athletes, Martin, Weil,
Sparks, McCullough, and Groves (1978) tested eight elite endurance and eight non-endurance athletes using a Balke treadmill test. They reported a failure to find significantly different Ve responses between the two groups.
Looking at the relationship between hypercapnic and hyperoxic response, two previously noted studies, Byrne- 20
Quinn, et al. (1971) and Martin, et al. (1979) showed that low responsiveness to hypoxia was associated with low responsiveness to hypercapnia in endurance athletes. On a related note, Martin, et al. (1978) and Martin, et al.
(1979) in aforementioned studies report that both ventilatory responses (hypoxic and hypercapnic) correlated positively with ventilation during light, heavy, or maximal exercise. Martin, et al. (1978) Wasserman, et al. (1975), and Lally (1974) demonstrated no propensity for low ventilatory responders to progressively underbreathe and thus retain C02 as exercise intensity increased. Rather,
Martin, et al. (1978) explain that lower responders maintained lower relative Ve and a higher arterial PC02 "setpoint" than high responders at any level of exercise.
Genetic Versus Trained Responses
Reflecting on the literature reviewed in the previous section showing attenuated hypoxic and hypercapnic ventilatory responses in endurance athletes, the question arises as to whether these responses are genetic in origin or acquired as a result of training. Saunders, Leeder, and
Rebuck (1976) studying 21 families consisting of 23 swirrmers, 41 parents, and 19 siblings, showed that swirrrning training has little effect on an athlete's ventilatory responsiveness. Saunders, et al. (1976) found no significant difference in ventilatory responsiveness between swirrmers and their non-swirrnming siblings and did not 21 demonstrate a significant relationship between the swirmners'
Ve/PC0 2 (a ventilatory response measure) and duration of
training. The researchers found a strong relationship between Ve/PCO 2 in siblings of the same family, which was
apparently independent of age, sex, and swiirning training.
"Although this may reflect common environmental influences,
the association of Ve/ PCO 2 of children with that of their mothers but not with that of their fathers suggests that
genetic factors are important," the authors explained
(Saunders, 1976). They acknowledged that the design of
their study does not allow clear separation of genetic from
non-genetic familial factors, however, the authors support
the view that genetic factors are major determinants of the
ventilatory response to CO 2 . Scoggin, et al. (1978) also
studied ventilatory responses using five outstanding male
long distance runners ( 2mi), 16 non-athletic parents and
siblings, and 34 non-athletic subjects acting as controls.
They concluded that familial influences make a major
contribution to the decreased hypoxic ventilatory response
seen in long distance runners. The hypercapnic responses were not significantly decreased in runners and their
families. Martin, et al. (1979) suggests that the
athletes' lower Ve/VC 2 as compared with non-athletes is
probably independent of training and may demonstrate
inherently lower ventilatory responses. Studying patients
having low hypoxic responses with accompanying unexplained 22 respiratory failure, Hudgel, & Weil (1974), and Moore,
Zwillich, Battaglia, Cotton, and Weil (1976) found that the responses were also decreased in the patients' healthy family members.
In the studies above, a familial effect is shown in the ventilatory responses. It is not evident, however, whether these attenuated responses are a result of factors within the environment or are under hereditary influence.
Experiments on monozygous (Identical -- same environment, same genes) and dizygous (Fraternal -- same environment, different genes) twins help investigate the importance of heredity in the ventilatory responsiveness to hypoxia and hypercapnia. Collins, Scoggin, Zwillich, and Weil (1978) measured the ventilatory response to isocapnic hypoxia and hyperoxic hypercapnia in twelve pair of identical and twelve pairs of non-identical healthy twins. They found similar ventilatory responses to hypoxia in the identical and dissimilar responses in the non-identical twin pairs, though both groups shared a common environment. This outcome indicates that hereditary factors greatly influence the hypoxic ventilatory response. The authors found no hereditary influence on the hypercapnic ventilatory response. Arkinstall, Nirmer, and Klissouras (1974) studying twelve sets of monozygous and 13 sets of dizygous twins found no significant difference in the ventilatory response to inhaled CO2 between the two groups. Leitch, 23
Clancy, and Flenley (1975) investigated a pair of female monozygotic twin athletes. These two track athletes were tested on an intermittent, short duration treadmill protocol. The authors suggested that genetic roles are minor in determining the carbon dioxide and hypoxic ventilatory response. They cited the difficulty in drawing
firm conclusions studying just one identical twin pair; but
that their experiment on the highly trained twins shows that genetic factors predominate in determining the ventilatory
response to CO2 and hypoxia when physical activity, a major environmental factor, is removed. Thus it may be concluded
that the current literature shows a familial effect on the
ventilatory responses, and that this effect may be more attributed to hereditary than environmental factors.
Exercise Breathing Patterns
In order to examine the relationship between oxygen
uptake and ventilation, observing the breathing patterns at
various times and intensities during exercise is useful.
Since ventilatory response during exercise changes over time
and/or intensity, it is prudent to divide exercise into
three time-related phases: Phase 1, 2, 3 (West, 1982) and
two intensity stages: sub-, supra-anaerobic threshold.
Phase I is described as the time period from the
beginning of work to that point in which the gas tensions in mixed venous blood entering the pulmonary capillaries start
to change (Whipp, amd Ward, 1982; Whipp, 1984). Whipp, 24
Ward, Lamana, Davis, and Wasserman (1982b) explains that the increased rates of pulmonary gas exchange in Phase I therefore reflect alterations of pulmonary blood flow and its distribution, without altered mixed venous composition.
The ventilatory response begins in virtual synchrony and sometimes before the start of work (DeJours, 1964, p. 634).
Different ventilatory responses are shown, however, if exercise begins from a control state of rest or from previous loadless or mild exercise. Broman and Wigertz
(1971) studied six well trained endurance athletes on a cycle ergometer in the supine position and reported abrupt initial ventilatory response increases in exercise starting from rest. Considerably slower breathing responses were seen with the subjects working from previous mild exercise.
Linnarsson (1974), studying eight healthy males on a bicycle ergometer intermittent protocol, confirmed this. He observed a rapid, initial ventilatory response on transition from rest to loadless pedalling and a less abrupt response from loadless pedalling to work. Casaburi, Whipp,
Wasserman, and Stremel (1978) testing ten subjects on a bicycle ergometer described work starting from a background of mild exercise leads to a more gradual rise in breathing during Phase I. Whereas Jensen, Lygger, and Pedersen
(1980), studying five healthy males (one of which was a competitive cyclist) showed that work starting from rest brings on a step-like increase in ventilation on the first 25 breath, which is held relatively constant throughout the remainder of Phase I. The speed of the initial ventilatory response brings into question its origin. DeJours (1974) postulates that because the initial ventilatory response had occurred before a metabolite from the exercising limbs could reach a chemoreceptor site, the response must be neurogenic
in nature, from the limbs and/or the cerebral cortex.
Wasserman, Whipp, and Castagna (1974) experimenting with dogs, however, noticed that when pulmonary blood flow (Q)
rose, so did Ve with no change in alveolar or end-tidal carbon dioxide partial pressures. They hypothesized that any such increase in Ve that was not matched by any suitable
increase in alveolar ventilation would result in a
downstream "error signal" in pH, PC02 , and P02 , thus rapidly
sensed by a chemoreceptor, providing a humoral stimulus to
early exercise hyperpnea. Whipp, Ward, and Wasserman (1984)
partially confirmed this by noting that in Phase 1, changes
in Ve are closely related to the change in pulmonary blood
flow. They add that the magnitude of the pulmonary blood
flow increase appears to significantly influence the magnitude of Ve response. However, Wasserman et al. (1975)
studied six male subjects whose carotid bodies had been
resected and indicated that the magnitude of the ventilatory
response was not affected. Whipp, et al. (1982b) testing
six healthy subjects (five male, one female) on a bicycle
ergometer reports a positive association between the size of 26 the heart rate response in Phase 1 and the corresponding Ve response. The particular heart rate response was accompanied by larger Ve responses when work was initiated from rest.
Phase 2 is described as "the Dynamic Phase following
Phase 1, in which a new steady state is approached, associated with changing mixed venous blood composition"
(Whipp, 1982a). Casaburi,.et al. (1978) studying five subjects cycling for 30 minutes reported that in this phase
Ve, VCQ2 and V02 change as a simple mono-exponential
function. The relative Phase 2 time constant (changes over
time) is different for each function: 35-40 S for V02 , 50-
60 sec. for VC0 2 and Ve (Whipp, 1982a). Whipp (1982a) explains that the time constant for VCO2 , being longer than
that for V02 , reflects the transient storage of C0 2 in the
body stores. The slow time constant for ventilation presumably reflects the influence of this storage, since it
is with VCO2 that Ve is most closely related during this
non-steady state phase (Casaburi, Whipp, Wasserman, Beaver,
and Koyal, 1977; Cassaburi, 1978).
Lind (1984) experimented on 19 male subjects using an
incremental load protocol on a bike ergometer. He reported
that the increase in tidal volume at low work intensities
can be ascribed to enhanced expiratory activity of the
intercostal muscles and/or to raised abdominal pressure
brought on by contraction or increased tone of the abdominal 27 muscles. It has been shown that the carotid bodies play an
important role in the control of Phase 2 ventilation in man.
Studying subjects whose carotid bodies had been resected,
Wasserman, et al. (1975) showed that Phase 2 ventilatory
kinetics are appreciably slower than normal. Griffiths, et
al. (1980) examined six male subjects performing constant
load work on a bicycle ergometer and showed faster
ventilatory kinetics by increasing the gain of the carotid
chemoreflex brought on by hypoxia.
The Phase 3 condition is ventilatory steady state. A
close correlation exists between ventilation and CO2 output
in this phase. Whipp, et. al. (1982a) state that the
arterial isocapnia of the exercise hyperpnea reflects
crucial control in Phase 3. They state that the
proportional contribution of the carotid bodies to
ventilation appears to be somewhat greater than at rest:
15% in moderate exercise, 10% at rest (Whipp, 1982a).
In exercise above the anaerobic threshold, the
ventilatory response is by and large nonlinear. Wasserman,
Van Kessel, and Burton (1967) testing 10 healthy males on a
cycle ergometer also indicate that this non-linearity stems
from the lactic acid build-up that results from these work
rates. No respiratory compensation exists for this
resulting metabolic acidosis. They report that Ve increases at a faster rate relative to work rate than for work below
the anaerobic threshold, especially in work rate increments 28 of four minutes or more. Ve also increases out of proportion to VCQ2 in these work rate increments. Yet for
select exercise work rates of 1 minute or less, Ve increases
in the same proportion as VCO 2 , as seen in work below the anaerobic threshold. Comparing seven elite endurance athletes and 12 non-athletes, Folinsbee, Wallace, Bedi, and
Horvath (1983) found that the elite subjects achieved substantially greater maximum ventilation and CO 2 production.
Other ventilatory measures and responses should also be emphasized when considering breathing patterns in exercise ventilation. Hey, Lloyd, Cunningham, Jukes, and Bolton
(1966) report that when ventilation is increased by stimuli such as C02 inhalation or muscular activity, tidal volume
(VT) is often found to increase with Ve up to a value equal to about half the vital capacity (VC). It then levels off with an increase in frequency becoming more important as the factor responsible for the further increase in Ve. Kay, et. al. (1975) studying five healthy subjects on a bicycle ergometer observed that an increase in respiratory frequency occurs initially with a gradual phasing out of the expiratory pause. Askanazi, Emili, Broeli, Hyman, and
Kinney (1979) studying 30 supine subjects and Jensen,
Christensen, Petersen (1972) studying five male subjects demonstrated that this shortening of the expiratory pause is followed by a shortening in the inspiratory phase. 29
Folinsbee, et al. (1983) in their study investigating seven
elite cyclists and 10 sedentary males report that tidal
volume at maximum exercise was not significantly larger in
athletes vs. non-athletes. They note that the trained
subjects reached higher ventilation volumes through a
significantly higher respiratory frequency. Martin and
Stager (1981) using sustained voluntary hypernea, report
female swimmers and runners exhibiting greater ventilatory
endurance than non-athletes. Jensen, et al. (1972) however, demonstrated that voluntary hyperpnea is controlled
differently than the exercise pattern. Bechbache, Chew,
Duffin, and Orsini (1979) reported the possibility that entrainment of breathing frequency by work rhythm may occur
in treadmill and cycle exercise. Kay, et al. (1975) found no such entrainment studying five healthy males during steady state cycle ergometry.
Ventilation and Oxygen Uptake Comparisons in Exercise
Noting the attenuated hypoxic and hypercapnic ventilatory responses generally seen in the previous section, the focus now turns to the relationship between ventilation and oxygen uptake. Due to an endurance athlete's high VS2 max value, one possibility is that their reduced ventilatory response is in some way related to their higher VS2 max. Morrison,
Van Malsen, and Noakes (1983) studied 587 males and 308 females -- both active and sedentary - in a submaximal bicycle ergometer test. The protocol consisted of 3-5 30 progressively increasing workloads at a rate of 50 rpm. The aim of the study was to determine a possible relationship between the ventilatory response to exercise and the predicted whole body maximum oxygen consumption. The V0 2 max values were predicted from a plot of 02 consumption rates at three or more workloads, against heart rates. The authors conclude that V0 2 max, which is primarily genetically determined, is inversely related to exercise ventilation. They add that at 40% V0 2 max, the ventilatory response to exercise is identical in the trained and sedentary individuals in each V02 max group. At the higher workloads (50-60% and 85% Va2 max), however, the trained subjects demonstrated lower ventilatory responses. The authors reason that this is due to a higher ventilatory turnpoint in the trained athletes, or, increased ventilation due to anaerobic metabolism occurring at a higher work rate.
The suggested reason for others not finding this relationship could be due to the great variability in responses as well as the relatively small populations and limited range in V02 max of these populations. They explain for example, that the lower correlation of the female population studied agrees with the above interpretation because of the small range or V0 2 max values even though a large sample was used. Byrne-Quinn, et al. (1971) examined
13 male athletes from college varsity or national track, swimming, or cross-country skiing and 10 sedentary subjects. 31
All were native to a low altitude. A modified Balke
Treadmill Test was used so that the subjects reached exhaustion at between six and eight minutes from the start of exercise. A significant negative correlation was
reported with both hypoxic and hypercapnic ventilatory
responses vs. V02 at rest. But during exercise, the
increase in ventilation in response to hypoxia was similar
to that seen in the non-athletes. Some of the V0 2 max values of the sedentary sample overlapped those of the athletic population so that these two groups, it was stated, present a continuous spectrum of physical fitness.
Therefore, the investigators combined the two groups and
discovered the relationships seen above. They added that athletes probably have to be born with a natural endowment of high V02 max. Whether their decreased ventilation is
linked to this or is acquired through prolonged training was
not resolved by this study. Martin, et al. (1979) using a modified Balke protocol looked at ventilation in eight endurance athletes, eight non-endurance athletes and seven
non-athletes. They found that endurance athletes breathed
significantly less at either exercise intensity (33% V0 2 max, 66% V02 max) by employing a method that combines three
indices of exercise ventilation: Ve/VCO2 , PAO2 , and PACO2 . Non-endurance athletes have exercise Ve that was between
that of endurance athletes and non-athletes., Hagan, et al.
(1984) looked at 45 male subjects performing a progressive 32
treadmill test at a speed of 90 m/min. The grade increased
from 0 to 2% for the first minute, and 1% each minute
thereafter. Their results show that the greater the maximal
aerobic power, the farther the rightward shift of the Ve/V02
exponential relationships. They added that the results
suggest that individuals with large maximal aerobic power
have a lower minute ventilation for any given V02 level.
Numerous studies have reported minute ventilation
increases in proportion with V02 until heavy work
intensities are reached. Wasserman, et al. (1967) examined
10 healthy males using incremental bicycle ergometer work
and recorded these findings. He reports, however, that Ve
is more linear to VC0 2 than V02 . Koyal, Whipp, Huntsman,
Bray, and Wasserman (1976) compared ventilatory responses on
a treadmill vs. cycle erogometry using 20 normal male
subjects. The protocol designs were of both constant speed
(rpm, m/min) and increasing load (50W, 100W, 150W for cycle;
increase grade for TM). Though minute ventilation is
greater during cycle ergometry than during treadmill work at
comparable levels of 02 uptake the Ve/V02 relationship is
linear at work rates below the onset of metabolic acidosis.
In other studies involving bicycle exercise, when energetics
are predominately aerobic, Ve is linear with V0 2 . Wasserman, Whipp, Koyal, and Bearer (1973) found a similar
relationship studying anaerobic threshold and respiratory
gas exchange in 85 normal men during exercise. Similar 33 findings are also reported by Weltman, and Katch (1979) and
Kay, et al. (1975).
Looking at Ve and VO2 in a temporal sense, Whipp, et al. (1984) explain that in Phase I (from rest to onset of mixed venous gas tensions), Ve does not change as a function of V02 but rather of VCO2 . The increase is more abrupt if work is intitiated from rest. In a different study (Whipp,
1983) they add that V0 2 and VC0 2 change in concert with Ve.
Skinner, et al. (1980) write of a linear increase in oxygen uptake and ventilation in this phase.
In Phase 2 (from mixed venous gas tensions to steady state), Whipp, et al. (1982a) report that Ve and V02 change as a mono-expontential function with a 35-40 S time constant for VO2 , and a 50-60 S time constant for Ve. Whipp (1983) states that the behavior in V0 2 is linear while the behavior
in Ve is non-linear during this phase.
In Phase 3 (steady state), V0 2 continues a near linear
rise until near maximal work loads at which time it begins
to plateau. Also Ve continues to increase until its
"breakaway" (Skinner & McLellan, 1980).
During heavy and severe exercise, ventilation increases out of proportion to V0 2 . This increase in Ve is correlated with the onset of metabolic acidosis (Wasserman, 1967;
Whipp, 1984). Others also report on the non-linearity of
the Ve response in metabolic acidosis (Lally, 1974; Whipp,
1983). 34
The effects of endurance training on the Ve/VO2 relationship was studied by Gaesser, Poole, and Gardner
(1984). They examined six men before and after three weeks
of training. During those three weeks, the subjects cycled
six times per week for 30 minutes each session at 70% VO2 max. The authors report no increase in the ventilatory
threshold but a significant increase in VO 2 max. Other
studies have disclosed increases in ventilatory threshold after exercise (Denis, Fouquet, Poty, Geyssant, Lacour,
1982; McLellan & Skinner 1981; Ready & Quinney 1982). Thus
the effects of training on the ventilatory threshold and on the Ve/VO2 relationship appear uncertain at this point.
Comparing Ve and VO2 in different modes of ergometry reveal different results depending on the exercise intensity employed.
Rasmussen, Klausen, Clausen, and Jensen (1975) examined
10 healthy young males. Five trained with their arm muscles and five trained with their leg muscles for five weeks.
Both before and after training the Ve/VO2 (a ventilation measure) was always greater during arm exercise than during leg exercise at submaximal loads. Sawka, et al. (1982) compared submaximal arm crank and cycling tests using nine healthy males. Progressive intensity, discontinuous tests were used for both modes. The authors report that arm crank exercise elicted higher Ve/VO2 values than cycle exercise at a given power output. Pimental, et al. (1984) while 35 examining responses to prolonged upper body exercise in nine males, compared progressive intensity cycle and arm crank ergometer submaximal protocols. They report that at all
time periods, arm crank exercise elicted significantly higher ventilatory equivalents (Ve /VO 2) of oxygen than cycle exercise. Similar results were reported by Bevegard,
Freyschuss, and Strandell (1966). They examined six healthy males using submaximal graded leg and arm exercise tests.
The authors report that during arm exercise, total ventilation was significantly higher for a given oxygen uptake. Davies and Sargent (1974) also report higher ventilation in arm work as opposed to leg work for a given oxygen uptake in eight male subjects. These results did not hold true for maximal loads, however. Sawka. et al. (1982) state that in maximal tests the Ve and VO 2 responses were significantly lower in arm crank vs. leg cycling for the nine subjects. Bergh, et al. (1976) tested 10 recently trained males in a series of five minute long maximal exercise tests on the bicycle ergometer, treadmill, and with combined arm and leg work. They found pulmonary ventilation during maximal exercise to be the highest in bike ergometry and lowest in arm work. The authors add that the relationship of Ve to VO2 was the same in arm work, bicycling, and arm and leg work but that Ve/VO2 was lower in running. 36
Contrasting two distinct modes of arm ergometry,
Glaser, et al. (1980) examined six wheelchair dependent and
10 able-bodied volunteers on both the wheelchair and arm crank ergometers. Steps were taken to standardize the two modes with respect to energy output. Both modes employed a
progressive intensity, discontinuous test with exercise
bouts of four minutes interspersed with seven minute rest
periods. The authors disclosed similar V0 2 peak and Ve max measures for both modes of ergometry. Sawka, et al. (1980)
also studied seven wheelchair dependent and 10 subjects
exercising on the arm crank ergometer using a discontinuous,
progressive intensity work protocol. They reported that
when Ve was expressed per unit of VO2 at each power output
level, no differences were found among the two activities.
Based on this literature review it can be concluded
that an abundance of literature exists concerning
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Interaction of physiological mechanisms during exercise.
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Wasserman, K., Whipp, B. J., & Castagna, J. (1974).
Cardiodynamic hypernea; hypernea secondary to cardiac
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457-464. 49
Weltman, A., & Katch, V. L. (1979). Relationship between
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Whipp, B. J., & Wasserman, K. (1980). Carotid bodies and ventilatory control dynamics in man. Federation Procedings, 39, 2668-2673. CHAPTER III
PROCEDURES
Subjects
The subjects consisted of 60 female volunteers; 30 fit subjects who were swimmers or other upper body trained athletes and 30 classified as unfit. The participants were
18-35-years-old.
The 30 fit subjects consisted mainly of members of the
Lone Stair Masters Swim Club, Southern Methodist University
Swim Team, and the Texas Christian University Swim Team along with a few unattached swimmers and triathletes. The criterion for being a fit group member was swimming at least
8,000 yards per week, having built up to that distance slowly and having swum 8,000 yards per week for at least three weeks. Two of the fit group had just reached the
8,000 yards per week plateau or were about to. The extra weight training and aerobics they had engaged in along with swimming qualified them in the author's eyes.
The unfit group was extracted from the North Texas
State University population and the Denton, Texas area. The criterion for the unfit sample was a history of minimal or no upper body type rhythmic exercise. Most subjects were sedentary but a few jogged fairly regularly.
51 52
The subjects were asked to refrain from intense upper body exercise for one day, and other heavy exercise, meals, smoking, and ingestion of stimulants for two hours prior to testing. A questionnaire, to be filled out by the subjects, consisted of inquiries into any past cardio-pulmonary difficulties. The participants were acquainted with the risks, test procedures, the extent of their involvement, and signed an "informed consent" statement prior to testing.
Testing Instruments
A Beckman Metabolic Measurement Cart was used to measure the two main variables, Ve peak and V0 2 peak. The
Beckman cart was calibrated prior to each test. A Monark
881 portable arm crank ergometer was used to exercise the upper body. The subjects' heart rate and EKG were continuously monitored via Quinton Instruments. Blood pressure measures were taken before and after each test.
Test Administration
The test was administered by the author in the North
Texas State University Exercise Physiology Laboratory from mid-February through July, 1987. The temperatures in the air conditioned laboratory ranged from 68 degrees to 73 degrees Fahrenheit with the relative humidity of 55 + 5%.
The peak testing times were planned to occur in late morning and mid-afternoon so regular meal times would not be altered -- allowing subjects to more easily comply with the rules prohibiting eating and/or smoking for the two hours 53 preceding the test. Because of work or scheduling conflicts, however, approximately 25% of the tests were not conducted in this time period. Ten subjects from each sample were re-tested for test reliability.
The author arrived at the lab a few minutes before the subjects to prepare for testing. This included replenishing
EKG pads, alcohol, conducting gel, and at times replacing
EKG paper and Beckman Metabolic Measurement Cart (BMMC) tape rolls. The BMMC was calibrated before each test with known gas quantities from a tank. The laboratory, air conditioned in part for the computerized electronic equipment, made for an optimal environment for exercise.
The subjects were asked to report to the laboratory wearing a loose exercise top and comfortable trousers or shorts. Upon arrival, the participant(s) filled out personal health history and informed consent forms. After taking their resting blood pressure, the author then weighed the subjects on an Acme chair scale. In an adjacent room, the author then applied a standard five lead EKG (RA, RL,
LA, LL V5) using Quinton disposable pads and conducting gel.
This time was used for answering questions and trying to ease any anxiety the author sensed in the participant. On three occasions, a group of three or more subjects arrived together. When this happened, the author enlisted the help of an assistant to prepare the others while one of the volunteers was being tested, so as to save time. On only a 54 few occasions, however, was there not a second CPR trained person present (in addition to the author).
The subject was subsequently taken to the testing area of the lab (see diagram) where the author specifically explained the test protocol. The EKG leads were connected to the pads and the breathing mask from the BMC was fitted snugly on the subject's nose and mouth to ensure that her exhaled air was not leaking to the outside. Following a recorded resting EKG, the participant practiced loadless pedalling on the arm crank ergometer for three minutes at a cadence of 60/min. set by an electronic metronome. During this time the author entered the subject's weight (to estimate her resting V02 maximum value) along with some appl icable prograrrming corrmands into the BMMC.
The participants were then instructed to begin this continuous (i.e. no rest intervals) test at OW setting with a cadence of 60/min for the first two minutes. The protocol then called for a lOW load increase every two minutes thereafter until the subject fell more than five rpm's below the 60/min cadence for longer than ten seconds. V0 2 peak,
Ve peak, and heart rate values were recorded at one minute intervals.
The author found it fairly easy to safely conduct the test without assistance. The BMMC automatically printed out
V02 peak and other gas related measures such as RQ, VCO2 , and METS, etc. at every minute. The Quinton EKG machine 55 required one only to activate a switch every minute to obtain a printed EKG readout. Through pilot studies, the author learned that the portable Monark arm crank ergometer used was easily moved during the harder pushing and pulling that occurs while cranking at heavier loads. To correct this, the ergometer was set on an acrylic board to reduce slipping and was anchored to the heavy athletic training table using rope. Thus, turning the knob on the arm crank ergometer every two minutes to increase the load was the only manual task that was needed to be done during the test.
This left plenty of time to watch and encourage the subject and study the EKG screen for the possibility of any abnormalities.
After reaching fatigue, the subject was instructed to cool down with loadless pedalling for three minutes. At one minute the mask was removed and following the third minute of loadless pedalling the participant waited for her heart rate to fall under 100 beats/min. in addition to a blood pressure reading that was near resting before the EKG leads and pads were removed.
The entrance to exit laboratory time for each subject was approximately one hour.
Determination of Dependent Variables
The Ventilatory Threshold was defined as the V02 at which the first non-linear increase in ventilatory occurred and was determined by sight. The V0 2 measures taken from 56
BMMC test readings were plotted on graph paper (20 squares/inch) at one minute intervals, and were connected by line segments. The Ve minute-by-minute measures were also taken from the BMMC test readings and plotted on the same graph. Each one-half inch of the x-axis represented one minute while every one-half inch on the y-axis denoted a unit of ten, either in liters per minute for the peak ventilation plots, or in millilters per kilogram per minute for the peak oxygen uptake plots. The two variables were then compared by sight and the one minute V0 2 interval at which a non-linear increase in Ve began was termed the ventilatory threshold. This V0 2 measure was divided into the V02 peak accrued to determine the percentage of V0 2 at which ventilatory threshold occurred.
Research Design and Statistical Tests
The remainder of the statisical procedures were calculated on the NTSU computer system to analyze the
results. Each of the statistics were calculated for the combined groups and for the separate fitness samples. Means and standard deviations were calculated for age, weight, V0 2 peak, Ve peak, maximum test time, maximum heart rate, and
resting heart rate.
Using upper body exercise, the test was designed to determine the relationship between ventilation and oxygen uptake at 40% and 85% of V0 2 peak intensity in upper body
trained, 18-35 year old fit and unfit women. Independent t- 57 tests were performed to assess differences between fit and unfit performances. Pearson Product Moment correlation procedures were used to determine the relationship between
Ve and V02 at 40% and 85% Va2 peak intensity in the fit and unfit samples.
To assess the reliability of arm crank ergometer, 10 subjects from each group performed a second arm crank ergometer test from two to six days following the initial test. A Pearson Product Moment correlation procedure was employed to assess the reliability of the test results using an arm crank ergometer in female subjects. Paired t-tests were performed to assess the pre-, post-test differences for
V02 and Ve peak. The ventilatory threshold measure defined as the first non-linear increase in Ve from V0 2 peak using this protocol, a Pearson Product Moment correlation was employed between these two variables. CHAPTER IV
RESULTS
The descriptive statistics for the fit, unfit, and combined groups for this study are evidenced in Table I.
Figure 1, Appendix 1, displays the Ve/V02 to V0 2 relationship for the combined fit and unfit samples at 40%
of -.51734 V02 peak intensity. A Pearson correlation (p=0.00171) and -.47930 (p=0.00368) was accrued for the separate fit and unfit samples, respectively. The 85%
A. Ve/V02 to V02 relationship is seen in Figure 2, Appendix
For the unfit group at 85% V02 peak intensity, this relationship was insignificant. Looking at the combined samples at this intensity a relationship of -.16786
(p=.09992) was extracted.
Pearson correlation coefficients for the test, re-test reproducibility with V02 peak and Ve peak are seen in Table
4. Pooled t-values seen in Appendix B, Table 1 indicate a significant difference in means of the fit and unfit samples for V02 peak and Ve peak. The Appendix B, Table 2 t-test indicates similar pre-, posttest means for both V0 2 peak and
Ve peak for the combined fit and unfit groups.
58 59
Table 1
Descriptive Statistics for the Fit Group.a
SED SDc Range Age 25.9 1.0 5.7 18-35
Weight (]Kg) 59.7 1.2 6.6 46-73
VO Peak 31.6 0.8 4.4 24-44 (mi/kg/min)
Ve Peak 66.2 2.2 12.2 48-91 (L/min)
Ventilatory Threshold 20.8 0.8 4.6 14-34 (ml /kg/mn)
Ventilatory Threshold 66.2 1.3 7.1 57-85 (% VO 2 Peak)
Maximum Test Time 15.3 0.4 2.3 11.21
Maximum Heart Rate 175.1
Resting Heart Rate 63.2 1.8 10.0 41-79
n = 30. b SE = standard error. c SD = standard deviation. 60
Table 2
Descriptive Statistics for the Unfit Group.a
SEb SDc Range Age 23.7 0.9 4.8 18-35
Weight (Kg) 58.7 1.4 7.9 46-78
VO Peak 20.2 0.7 3.9 14-29 (mI/kg/min)
Ve Peak 40.1 1.8 9.7 48-91 (L/min)
Ventilatory Threshold 10.1 0.5 2.8 5-16 (ml/kg/min)
Ventilatory Threshold 49.9 1.6 8.9 31-68 (% Vo2 Peak)
Maximum Test Time 9.2 0.2 1.4 6-12
Maximum Heart Rate 164.4
Resting Heart Rate 77.5 1.8 9.7 55-98
n = 30. b SE = s tandar d er r or. c SD = s tandar d deviat ion. 61
Table 3
Descriptive Statistics for the Combined Group.a
SEb SDc Range 0-01 Age 24.9 0.7 5.4 18-35
Weight (Kg) 59.2 0.9 7.3 46-78
VO Peak 25.7 0.9 6.9 14-44 (mi/kg/min)
Ve Peak 53.1 2.2 17.1 26-91 (L/min)
Ventilatory Threshold 15.4 0.9 6.6 5-34 (ml/kg/min)
Ventilatory Threshold 58.0 1.5 11.5 31-85 (% VO2 Peak)
Maximum Test Time 12.3 0.5 3.6 6-12
Maximum Heart Rate 169.8
Resting Heart Rate 70.4 1.6 12.2 41-98 an = 30. bSE = stand ard erro r. cSD = standard deviation. 62
Table 4
Pearson Correlation Coefficients for Test, Re-test Reliability With V02 peak, Ve peak.
VE peak V02 peak Ve peak V02 peak Re-test Re-test
b .7473 a VO2peak .8072 P-=.0000 2=-000 p=. 000
Ve peak .8072 .7616 .9190 2=.0000 R-=.000 P-=.o000
V0 peak, .8932 .7616 .8219 2 0 0 0 Re-test P=-000 P-=.o000 P=.
Ve peak, .7473 .9190 .8219 0 0 Re-test R=. 0 P=.000 P=.000
bn an = 20. - 60.
Table 5
Pearson Correlation Coefficients for Combined Fit and Unfit Samples for V02 peak, Ve peak, Test Timemax, and Ventilatory Threshold. ~
Max Ventilatory Test Threshold Time (ml/kg/min) V02 peak Ve peak
VO2peak .8072 .8035 .9404
Ve peak .8072 .8398 .7696
Max. Test .8035 .8398 .8047 Time Vent i latory . 9404 .7696 .8047 Threshold (ml /kg /min)
n = 60. bp =.000 63 Table 6
Pearson Correlation Coefficients for the Fit Sample V02 peak, YV peak, Test Timemax, Ventilatory Threshold.a -
Max Ventilatory Test Threshold V0 2 peak Ve peak Time (ml/kg/min)
V02 peak .4302 .3485 .8747 .009 P=.030 P=. 000
Ve peak .4302 .4649 .4806 P=. 009 P=. 005 P=.004
Max. Te s t . 3485 .4649 .4425 T ime P=. 030 P=.005 P=.007
Vent i latory .8747 .4806 .4425 Threshold P=.000 P=. 004 P=.007 (ml /kg/min) an = 30.
Table 7
Pearson Correlation Coefficients for the Unfit Sample for V02 peak, Vepeak, Test Timemax, and Ventilatory Threshold.a
Max Ventilatory Test Threshold V02 peak Ve peak T ime (ml/kg/mn)
V02 peak .5965 .4730 .7746 P=.000 P=. 004 P=. 000
Ve peak *5965 .7503 .1859 P=. 000 P=.000 P=. 163
Max. Test .4730 .7504 .1298 Time P= 004 P=.000 P=.247
Vent i latory .7746 .1859 .1298 Threshold P= 000 P=. 163 P=. 247 (ml /kg/min) n = 30. 64
Figure 3, Appendix 1, shows the statistics and plotted points for the V02 peak vs. maximum test time relationship for the combined fit and unfit samples. A fairly accurate prediction of V02 peak using the time to fatigue can be accrued with this test protocol by plugging in the intercept and slope measures seen in Figure 3, Appendix 1. The V02 peak vs. maximum test time relationship along with the ventilatory threshold relationship for the combined, fit, and unfit samples is evidenced in Tables 3, 4, and 5.
The percentage of V02 peak at which ventilatory threshold occurs is 49.711 t 1.620% for the unfit sample, and 66.247 t 1.290% for the fit group. CHAPTER V
DISCUSSION AND CONCLUS IONS
Minute Ventilation and Oxygen Uptake Relationship
The Ve/VO2 to V0 2 comparisons at 40% intensity yielded a slightly stronger inverse relationship in the fit, unfit, and combined groups than did a similar study using bicycle ergometry conducted by Morrison, et al. (1983). Their
results studying 308 females show the Ve/VO2 vs. V02 relationship to be r=-0.26 (p 0.001). Morrison, et al.
(1983) also showed equal ventilatory responses between the
trained and sedentary group at 40% V02 max, noting that both
groups were below their ventilatory turnpoint (threshold) at
this intensity. Since Scoggin (1978) indicated that the
respiratory response below the ventilatory threshold is
independent of training, and, Koyal (1976) demonstrated that
the Ve to VO2 relationship is linear at work rates below the
onset of metabolic acidosis, the slight disparity in this
study seen in the Ve/V02 to V02 relationship between the fit
and unfit groups at 40% (r=-0.52, p=0.0017, r=-0.48,
p=0.0037, respectively) could indicate that the ventilatory
threshold of a few members of the unfit group is below 40%.
65 66
This is so even though the unfit group mean ventilatory threshold measure was 49.711% + 1.620 (SE), well above the
40% intensity.
The Ve/V02 to V02 relationships in this study at 85% intensity show a large disparity between the fit and unfit populations (r=-.443, p=0.00710, r=-.14700, respectively) which indicates a reduced ventilatory response to exercise and a modest inverse relationship between the two variables in the fit population. The reduced ventilatory response seen in relation to V02 agrees with Morrison, et al. (1983),
Hagan and Smith (1984), Martin, et al. (1978) at 2/3 V0 2 max, Ekblom, Astrand, Saltin, Stenberg, and Wallstram (1968) at 75% V02 max, and Rasmussen, et al. (1975). Morrison, et al. (1983) explains that the reason for this Ve reduction would be based on the fact that a higher ventilatory turnpoint is seen in trained athletes. Furthermore,
Rasmussen, et al. (1975) states, "The finding that the decrease in Ve/VO2 was confined to exercise with trained muscles can therefore be taken to indicate that the reduction of Ve/V02 was related to local changes in these muscles. Thus it seems justified to conclude that training causes adaptations in muscle tissue, which during exercise at a given V02 , reduces the increase - in excess of resting value - of Ve." 67
In reviewing the Respiratory Exchange Ratio (R)- the C0 2 produced when the exchange of oxygen and carbon dioxide 02 consumed at the lungs no longer reflects the oxidation of specific foods in the cells - and its higher values at heavier exercise loads, Wasserman (1973) explains that the first consequence of inadequate 02 supply is the formation of lactic acid. This excess lactic acid will be more than 99% dissociated and buffered predominately by the bicarbonate system (Wasserman, 1967) through this set of reactions:
Lactic acid + NaHCO3 - Na lactate + H2 CO3
H 2 0 + CO2
The carbon dioxide released in this buffering reaction is exhaled as the venous blood enters the lungs - thereby preventing accumulation in the body tissues. This
"buffering of lactic acid" process adds extra CO2 to the top of the R equation in addition to that quantity normally released during energy metabolism, and the R moves toward and above 1.00. Skinner and McLellan (1968) mentions that these augmented levels of lactic acid and CO2 stimulate the respiratory center to increase Ve. R should again become equal to the metabolic RQ when CO2 stores reach a steady state (Davis, 1976).
The R values seen at 40% V02 peak (.78 unfit, .84 fit) show a small difference between the fit and unfit samples. 68
Considering the larger early release of lactate seen in arm crank exercise compared to lower body exercise (Cerretelli,
1977), these results would seem to be indicative of arm crank exercise below the ventilatory threshold. The larger early release of lactate could also be attributed to test anxiety (Davis, 1976) and/or the mechanical inefficiency of arm cranking (Davis, 1976). The 85% Va2 peak R value (.91 unfit, 1.02 fit) clearly indicate evidence of hyperventilation and exhaling of additional C02 by the process of lactate buffering. The mechanical inefficiency of arm crank exercise may have more of an effect on high R values at heavier loads (Davis, 1976).
Relating to C02 levels, one reason why aerobically trained athletes breathe less, could be their low responses to hypercapnia and hypoxia (Martin, 1978; Martin, 1979) shown in light, heavy, and maximum exercise. Stegmann and
Kinderman (1982) also reported that endurance athletes generally have a lower ventilatory response to similar levels of alveolar C02 pressure. The lower responses to hypoxia and hypercapnia occurred despite a 3 torr higher average end-tidal PC0 2 in the endurance athletes (Martin,
1979). Martin (1979), whose study was performed at a relative V02 max which would tend to equalize the lactic acid stimulus to Ve for fitness differences, stated that 69 these low ventilatory responses may be inherent. Previous studies have demonstrated no propensity for low ventilatory responses to progressively underbreathe and thus retain C02 as exercise intensity increased (Lally, 1974; Martin 1978;
Wasserman, 1976). Rather, Martin, et al. (1978), explains that lower reponses maintained lower relative Ve and a higher arterial PC0 2 setpoint than high responders at any level of exercise. Heigenhauser, Sulton, and Jones (1983) studying trained and recreational swimmers stated, however, that since the ventilatory responsiveness to C02 was not related to Ve/V02 during either arm or leg exercise, it appears that in addition to the chemosensitivity to C02, other factors play a part in the control of ventilation.
It has been shown that proportional decreases in arterial lactate are accompanied by a decrease in Ve/V02 during exercise of trained muscle (Rasmussen, 1975).
Reduced concentrations of lactate in skeletal muscle and blood are seen in the trained vs. the untrained state during any point in submaximal exercise (Hermansen, Hultman, and
Saltin, 1967; Ekblom, 1968; Henriksson, 1977; Ivy, Withers,
Van Handel, Elger, and Costill, 1980; Pendergast, 1979).
This is true at both absolute and relative intensity
(Hermansen, 1967). Saltin and Karlson (1967) explain, however, that lower lactate values seen after training are 70 not due to a lower lactate production by glycolysis, but some of the formed lactate may be utilized immediately in other parts of the muscles. There exist characteristics of trained muscle that cause the reduction of lactate output and thus, may in part be related to the reduction in ventilation seen in trained individuals.
One of the reasons why muscles of endurance athletes display a reduction of lactate output, even at comparable rates of glycolysis may be the removal of pyruvate through
its conversion to alanine via the reaction catalyzed by alanine transaminase (Holloszy, 1975). The training induced
increases of alanine transaminase may enhance its capacity to compete with lactate dehydrogenase for pyruvate (Mole,
1971). Mole, et al. (1971) showed approximately an 80% and
50% increase (per gram of muscle) in the mitochondrial and cytoplasmic forms of alanine transaminase, respectively, in gastrocnemius muscles of rats tested in a running program.
Felig and Wahren (1971, 1971a) exhibit the quantitative importance of the pyruvate to alanine pathway. While testing men exercising on a bicycle ergometer, they found that alanine release from the legs increased roughly 500% during strenuous exercise (1971). They also estimated that conversion of pyruvate to alanine in muscle occurs at 35-60% of the rate at which lactate is formed during vigorous, submaximal exercise. Looking at an alternative pathway in 71 the removal of pyruvate, via ox-idation, Hermanssen, et al.
(1967) stated that at the same relative work level, the rate of pyruvate oxidation is similar in the trained and untrained states, despite the fact that the trained individual is doing more work and using more oxygen.
Another characteristic of trained muscle that may result from the management of lactate output and reduced ventilation is the increased mitochondrial enzyme activity.
Rises in this activity may be due to an increase in enzymatic protein, seen in the doubling of cytochome c levels (Holloszy, 1967; Holloszy, 1975). Endurance trained muscle has been reported to also have twice as many mitochondrial christae per gram than untrained muscle
(Kiessling, Pichl, and Lundquist, 1971; Morgan, Cobb, Short,
Ross, and Gunn, 1971), which may be responsible for the increase in total mitochondrial protein (Kiessling, 1971;
Morgan 1971). Henriksson and Reitman (1979) demonstrated a gradual augmentation and significant difference in vastus lateralis oxidative enzyme activities (34.7%, p 0.005, total increase) after 3, 5, and 8 weeks of bicycle ergometry training. They concluded that exercise acts as a stimulus for both factors underlying an increased V0 2 max, as well as for oxidative enzyme synthesis in skeletal muscle. Holloszy
(1975) explains that since oxygen uptake is the same in the trained and untrained states during submaximal work at a 72 given intensity, and, as seen above, the size and number of mitochondria per gram of muscle increases with endurance
training, the rate of electron transport and 02 consumption per mitochondrion respiratory assembly needed to balance a given rate of ATP hydrolysis by the myofibrils (muscle cells) must be lower in the trained group. Holloszy (1975)
states:
The greater number of mitochondria per gram of muscle, the lower must be the 02 uptake per mitochondr ion required to maintain a given submaximal level of 02 uptake per gram of muscle. In this context, it seems reasonable that in the process of attaining a given steady state level of 02 consumption, creatine phosphate and ATP concentrations must decrease less, and ADP, Pi, creatine and, perhaps, AMP and anonia levels, must increase to a lesser extent in muscles of trained as compared to untrained individuals (p. 161).
The substances that promote lactate formation, it would appear, are spread more thinly due to an increased mitochondrial activity ensuring less of a "load" for each mitochondrion. It seems that, in the sense of mitochondrial content and lactate management, endurance trained skeletal muscle becomes more like the aerobic model, cardiac muscle.
Another way in which endurance trained skeletal muscle, with its lactate output control, becomes more like heart muscle is the increased percentage of energy derived from
fatty acid oxidation. Mole, et al. (1971) indicated that physically trained individuals derive a much greater percentage of their energy from fatty acid oxidation than do untrained individuals during exercise of the same intensity. 73
In male rat studies, Mole, et al. (1971) found the capacity to oxidize fatty acid (FA) in the gastrocnemius and quadriceps muscle double in response to training. Paul,
Issekutz and Miller (1966) mentioned an inhibitory effect of fatty acid oxidation on glucose metabolism in muscle and vice versa. "The high free fatty acid concentration decreased insulin sensitivity which would in turn impair glucose utilization since it is with insulin that glucose enters the muscle cell," Paul, et al. (1966) stated in their dog leg muscle study. This decrease in glucose metabolism has been associated with the slower rates of muscle lactate formation (1971). Saltin and Karlsson
(1971a), studying 15 subjects in a prescribed running program found that, at the same submaximal work level and 02 consumption, the rise in quadriceps muscle lactate was less after the 12 week running program. The authors stated that the slightly larger breakdown of muscle glycogen at the beginning of the exercise in the untrained subjects could explain the higher blood lactate concentrations as compared with findings in the trained subjects. In a longitudinal study, a significantly lower rate of glycogen depletion was seen and was partly due to lower lactate production.
Applying this to arm work, an even larger disparity in lactate output can be seen between the trained and untrained populations. Cerretelli, et al. (1977) observed, "Arm crank 74 ergometry in untrained subjects resulted in a considerably larger release of early lactate and 02 deficit than did the same absolute or relative leg work, suggesting that the oxidative metabolism of the untrained arms responded particularly slowly during the early minutes of work."
Pendergast, et al. (1979) indicated that the early lactate threshold seems to be an unusually sensitive index of the degree of arm training, which agrees with the results of this study, showing a relationship of r=.94 (p .00000) between ventilatory threshold and V0 2 peak. This is also seen by the fact that, at 40% Va2 peak, some members of the unfit group in the study exceeded their ventilatory threshold. In a similar study using cycle ergometry at 40%
V0 2 max, however, none of the subjects exceeded their ventilatory turnpoints. One reason for this larger lactate difference in arm vs. leg exercise studies may be that untrained arms are used less, generally, than untrained legs. For example, a subject assigned to an untrained group in a leg exercise study still uses his/her legs to walk or climb stairs during the course of a normal day. Whereas, that same untrained subject would probably not engage in any rhythmic arm exercise during a standard day. Therefore, one receives a sense of a study being "all or nothing" when using the arms. Furthermore, since arm exercise involves using a smaller skeletal muscle mass, a greater percentage 75 of its maximal tension (compared to legs) would be needed to complete a given power output (Sawka, 1980). This would probably result in inter-muscular tensions that could exceed perfusion pressure and thereby impede oxygen delivery which would lead to anaerobic metabolism and lactate production
(Sawka, 1980). Since an arm trained subject would generally, have greater strength than a similar untrained
subject (Clausen, Klausen, and Rasmussen, 1973), a less percentage of the trained muscles' maximal tension would be needed to complete a given power output. Coupled with this
is the fact that trained muscle extracts more oxygen than untrained muscle, as seen by an increased arterial-venous oxygen (a-v 02) difference (Saltin, Blomquist, Mitchell,
Johnson, Wildenthal, and Chapman, 1968; Ekblom, 1968;
Ekblom, 1969). Astrand, et al. (1967) shows the importance of this measure by stating that above 70% of maximal oxygen uptake, increased a-v 02 difference contributes relatively more and increased cardiac output relatively less to further
increases in oxygen uptake. Also, since muscle blood flow studies have shown identical (Grimby, Haggendal, and Saltin,
1967) and lower (Varnavskas, Bjornstrop, Fahlen, Prerovsky, and Stenberg, 1970) muscle blood flow in trained vs. untrained subjects using 133Xe clearance methods, it is most probable that increased oxygen extraction and more adequate distribution of capillary blood flow are both responsible 76 for post-training hemodynamic adjustments (Varnavskas,
1970). Ekblom (1969), studying 2 men on treadmill and cycle ergometry, adds that the reduced blood lactate at a given submaximal load may be taken as a criterion as a more effective regulation of the muscle blood flow. Thus it seems that the increased oxygen extraction and the retardation of intramuscular tensions exceeding perfusion pressure, along with a more adequate distribution of capillary blood flow seen in the trained versus the untrained, would in part delay lactic acid build-up in arm exercise.
An additional way to explain the management of muscle lactate concentration brought about by training is that at the same absolute work load, this reduction is due largely to the activation of relatively more red fibers. Animal
(Barnard, Edgerton, and Peter, 1970), morphological
(Kiessling, 1971), and human skeletal muscle enzyme (Bhan &
Scheuer 1972) studies all point to an increase in the number of red fibers. Relatively more of these fibers are activated in trained muscle, while exercising at the same absolute and relative work load (Saltin & Karlsson 1971). 77
Holloszy (1975) explains:
Fast twitch red skeletal muscle, which has a high capacity for glycolsis and glycogenolysis also has a high respiratory capacity. As a result of the adaptive increases in hexokinase activity and respiratory capacity and the decrease in glycogenolytic capacity induced by endurance exercise, fast twitch red skeletal muscle becomes more like the heart in its enzyme patterns. The capacities of slow twitch red muscle for both glycolysis and respiration are lower than those of heart muscle. Slow-twitch red muscle also becomes more like cardiac muscle when it adapts to exercise as a result of increases in both its glycolytic and respiratory capacities ( p. 160).
Test, Re-test Reliability
The test, re-test reliability of the combined group for
V02 peak (r=.893) and Ve peak (r=.919) were slightly lower than the results from Bar-Or and Zwiren (1975) (r=.94, r=.98, respectively). Paired t-tests indicated a probable difference of fit and unfit means for VO2 peak and Ve peak, and also similar means for the combined groups test vs. re- test for both V02 peak and Ve peak.
The non-significant correlation seen in the fit group
VO2 peak (r=.331, p=0.175) in the test vs. re-test is puzzling. Sawka, et al. (1983) using a continuous 50 rpm protocol with seven subjects had a reliability of r=.63 with a p 0.05 level of significance. Bar-Or and Zwiren (1975) studying 59 men, extracted a test, re-test reliability of r=.94 for V02 and r=.98 for Ve. They stated that the high reliability of their all out arm test suggests that a given individual uses the same muscle group in repeated exertions. 78
Perhaps the inconsistent results in the fit group reliability might be related to muscle group adjustments made by the subjects in this re-test. The author noticed in a few of the re-test subjects more trunk twisting movements during the heavy exertion stages, taking some of the load from the arm and shoulder muscles. This adjustment would come with experience on the arm crank ergometer, along with using the chair-back for leverage by forcefully pressing one's backside against it while cranking. Perhaps a breastplate support to help standardize arm position
(Franklin, Vandor, Wrisley, and Rubenfire, 1983) should have been employed. It would seem to follow, however, that these adjustments would lead to higher V0 2 peak values in the re- test. This was not the case, however, in the fit group
(31.26 ml/kg/min t .810 test, 29.67 ml/kg/mi-n t 1.32 retest).
The question arises as to whether the low reproducibility seen in the fit group could be due to the subjects' not reaching their highest V0 2 peak with this protocol. The data on maximum heart rate in this study (175 bpm-fit, 164 bpm-unfit) compares favorably with Vander,
Franklin, Wrisley, and Rubenfire (1984), who extracted a maximum heart rate of 169 bpm in their study of 10 healthy women exercising on the arm crank ergometer. Seals and
Mullin (1982) studying 11 male swirrmers and 12 untrained, 79 acquired a maximum heart rate of 169 bpm and 178 bpm, respectively, in an arm crank study. The respiratory quotient (R.Q.) at exhaustion in this study (1.09-fit, .93- unfit) also compared favorably to other studies - 1.11
(Vander, 1984), 1.06 (Franklin, 1983) - although the R.Q. for the unfit population was somewhat below 1.00.
Another possible explanation for the observed test, re- test differences might be the relaxed adherance to the rules of participation in the study. Approximately six of the fit group re-tests were engaged in triathlon training, coupled with their full-time employment, obviously necessitated the need for efficient use of time to accomodate all aspects of triathlon training. It is possible that the subjects could not comply with the conditions of the study - retesting one day prior to testing. The significant reliability correlation seen in the unfit group (r=.87, p=0.001) could lend credence to this argument since this group, of course, does not train.
Assuming that the test results were obeyed, the most logical reason for the differences seen in the test, re-test reliability of the fit group may be the total length of the test. Buchfurer, et al. (1983) stated that in testing cardiopulmonary function with incremental exercise, a protocol should be selected to bring the subject to the limit of his tolerance in 10 + 2 minutes. Possible factors 80 for declining VO2 max values seen in prolonged tests
include: higher body temperature, greater dehydration, different substrate utilization and subject discomfort
(Buchfurer, 1983).
Ventilatory Threshold
The results of other studies investigating the
percentage of VO2 max where ventilatory threshold occurs are
seen in Table 6. The ventilatory threshold in this
experiment was defined as the first non-linear increase in
Ve from VO2 and was calculated by sight from plotted points
taken from one minute intervals. Davis, et al. (1976)
mentioned limitations using time-based plots in predicting
non-linear Ve increases by noting the low test-retest
reproducibility accrued.
Table 8 Investigating the Percentage of VO Where Ventilatory Threshold Occurs. 2
STUDY SUBJECTS MODE VENTILATORY THRESHOLD (% Vo2 Peak
Present 30 untrained females ACa 49.7+1.6 Study 30 upper body trained females 66.21.3
Paterson and 19 active AC 40.0+0.93 (p .001) Morton (1986) male volunteers CYb incremental 52.01.16 (p .001)
Reybrouck, et al. 3 healthy males AC 65.0 (1975)
Davis, et al. 30 college AC incremental 46.5+8.9 (1976) males CYdncremental 63.879.0 TM incremental 58.65.8
Simon, et al. 6 trained CY incremental 65.8 (1986) 6 sedentary men 51.4 (p .05)
Reybrouck, et al. 8 h ealthy males CY incremental 56.2+9.3 (1983)
Ivy, et al. (1980) 13 males (23.8+5 yrs.) CY incremental 54.28.3
Weltman and 31 relatively high CY incremental 59.5+7.7 Katch (1979) fit males
McClellan and 16 males CY 30 w incremental High VO 2 Group - 53.4% Skinner (1985) (23.8+4.1 yrs.) (56-61 mIs/kg/min) Med VO 2 Group - 52.3% (48-52 mls/kg/min)
Low VO 2 Group - 48.9% (47-51 mIs/kg/min)
Thorland, et al. 10 x-country TM incremental 45.0 (1980) female competitors
Reybrouck, et al. 1 healthy males TM modified Barke 60.4+15.5 (1986)
aAC - Arm Crank, bCY - Cycle Ergometer, CTM - Treadmill 81
The obvious advantage in having a higher ventilatory threshold is, of course, the ability to perform aerobically at a higher percentage of V02 peak. Added to the fact that trained athletes possess a higher V0 2 max than non-trained people, trained athletes also have a higher ventilatory threshold expressed as percentage of V0 2 max than non- athletes (Rusko, 1980; Reybrouck, 1975).
An application of the ventilation threshold seems to be that it is a good predictor of anaerobic threshold under certain conditions. Wasserman, et al. (1973) examining 85 normal subjects, states that Ve is an excellent determinant for the detection of the anaerobic threshold (AT) during an
incremental exercise test. Davis, et al. (1976), in a study involving 39 males using the arm crank, bicycle, and treadmill ergometers, presented similar findings. They mentioned limitations of the prediction being its subjective determination from the time-based plots and the relatively low test, re-test reproducibility of the gas exchange (r=.74 in arm crank) AT measurement. Yoshida, Muro, Takevchi and
Suda along with (1981, 1982), studying 10 and 13 college age males, performing incremental load work, reports a correlation of r=.866 (p 0.01) for the non-invasively determined gas exchange AT versus the invasive lactate AT.
Caizzo, et al. (1982) using 16 subjects on a high cadence, incremental test protocol shows that the Ve/V02 (r=.93, p
0.001) and Ve (r=.88, p 0.001) provide the most accurate 82 and reliable detection of anaerobic threshold of the commonly used ventilatory or gas exchange indices.
Despite the high correlations seen above between the lactate and ventilatory thresholds (VT), a number of studies show an uncoupling of the two parameters, indicating different underlying regulatory mechanism. Gaesser and
Poole (1986) tested six subjects (4 males) "to observe the possibility that the lactate threshold could be increased significantly during the first three weeks of training without any concomitant change in the ventilatory threshold." The investigators report a significant training induced dissociation between the lactate and ventilatory thresholds. The ventilatory threshold, defined as the V0 2 at which the ventilatory equivalent for oxygen (Ve/V02) increased without a simultaneous increase in the ventilatory equivalent for carbon dioxide (Ve/VC02), did not change while the lactate threshold rose significantly. The authors report a high correlation between lactate (Tlac) and ventilatory thresholds (r=.86) post-training though they state the results indicate a coincidental rather than a causal relationship. Looking at this relationship with five subjects in a glycogen depleted state, Heigenhauser, et al.
(1983) found that the ventilation threshold occurred at a lower work rate than the lactate threshold. Hughes, Turner, and Brooks (1982) also compared VT and Tlac in normal and glycogen depleted conditions. The nine male subjects, given 83 a 50 rpm and 90 rpm incremental bike protocol in the normal state and a 50 rpm incremental protocol in the glycogen depleted state, showed a significant uncoupling of the two thresholds (VT and Tlac) in the glycogen depleted state - shifting the VT to a lesser and the Tlac to a greater work rate relative to the normal glycogen state. Hagberg, et al.
(1982) also cast doubt on the causal relationship between the two parameters by examining responses of two males and two females with McArdle's disease. Those with McArdle's disease lack muscle phosphorylase, making them incapable of increasing blood lactate or H+ . Hagberg, et al. (1982) state that hyperventilation occurs during intense exercise, even when there is no increase in plasma H+ . They suggest the possibility that non-humoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise. The authors conclude that the hyperventilation accompanying heavy exercise does not appear to be solely mediated by pH. Simon, et al. (1986) also studied ventilatory threshold, defined as the greatest work rate before the non-linear increase in Ve occurs, and plasma lactate threshold (PLT) comparisons in six trained cyclists and six untrained sedentary men employing a continuous, incremental, 60 rpm bike protocol. The authors found that PLT and VT occurred together for the trained group but that VT occurred at a lesser work rate than the
PLT for the sedentary group. 84
Jones and Ehrsam (1982) sum up this issue:
The relationship between changes in ventilation and changes in plasma lactate concentration is usually close enough to allow the lactate threshold to be estimated from ventilation measurements, as long as care is taken to avoid the possible effects of diet, previous heavy exercise, and acid-base abnormalities. In addition to comparisons between the two entities, are studies that have found high correlation coefficients for regression equations relating plasma lactate concentration to ventilatory in a number of physiological situations, such as exercise in hypoxia. However, despite these close correlations, a number of perturbations have been shown to interfere with the close linkage between ventilation and lactate, leading critics to suggest that the two are not coincidently linked (p. 75). Increasing evidence also indicates that ventilation threshold could play a part in an athelete's training regimen. It has been shown that individuals with similar
V02 max values often perform differently in an endurance event (Costill, Thomason, and Roberts, 1973; Daniels, 1974) and improvement in endurance performance among athletes is evidenced although their V0 2 max has reached a plateau
(Astrand, 1967; Wilmore, 1977). "The athlete is able to improve his performance even after he reaches an upper limit or ceiling for his V0 2 max, by developing the ability to work at a higher percentage of his capacity for prolonged periods of time," Wilmore (1977) explains. Furthermore, ventilation thresholds may occur at a different percentage of V02 max for those with similar V02 max measures (Davis,
Frank, Whipp, and Wasserman, 1979; McLellan and Skinner,
1975). Given the close relationship evidenced above between ventilatory threshold and anaerobic threshold, one might say 85 that exercise at a given percentage of V0 2 max may represent varying degrees of metabolic acidosis for one person compared to another. This, in turn, may lead to a source of unexplained variance for endurance times among individuals
(McLlellan, 1985). McLellan and Skinner (1985) reported a
30% reduction in the standard error of estimation in time to fatigue when intensity was expressed relative to ventilation threshold than relative to V0 2 max. Thus, training a person relative to his/her ventilation threshold could prove useful
in enhancing and predicting performance.
A significantly higher relationship was accrued in this study (r=.94, p=.00000) for ventilatory threshold vs. V0 2 peak for the combined fit and unfit groups as compared to previous studies (Reybrouck, Ghesquierre, Cattaert, Fagard, and Amery, 1983; Davis, 1979; Thorland, Sady, and Refselli,
1980; Ivy, 1980). Ivy, et al. (1980) extracted a relationship of (r=.91) studying 13 healthy males on a cycle erogmeter. Relationships of r=.75 (Davis, 1979) and r=.81
(Thorland, 1980) were observed examining nine middle-aged men and ten females (18-28 yrs.), respectively. Reybrouck
(1983) attributed his higher correlation results (r=.87) to using a rather heterogenous group of subjects with a diversity of V0 2 max determination.
The relationship drawn for ventilatory threshold vs.
V02 peak for the fit population was also significantly higher (r=.87, p=.0000) than other studies observed, r=.85 86
(Weltman, 1979), r=.81 (Thorland, 1980), r=.72 (Davis,
1979).
The fact that lower correlation coefficients were obtained in the studies above using exclusively cycling or
running modalities, could be due to lesser V0 2 peak diversity as compared to arm crank exercise used in this
study. The subjects in this study, as mentioned previously,
represented a full spectrum of upper body fitness from
subjects with no history of rhythmic arm exercise to major
university swim team members.
A large training disparity also existed within the fit
group with members swirrming from 8,000-50,000 yds. per week with a V0 2 peak range of 23.9-43.7 ml/kg/min. This may
account for the higher relationship seen among the members
of the fit group in this study, as compared to others.
Predicting Peak Oxygen Uptake From Maximum Test Time
The relationship accrued in this study for the combined
groups between V0 2 peak and maximum test time (r=.80355,
p=.00000) was slightly lower than McLellan and Skinner
(1985) r=.85, and Vander, et al. (1984) r=.86, who
correlated arm V02 and work load.
The differences evidenced in the relationship between
V02 peak and maximum test time in the fit (r=.35, p=.02956)
and unfit (r=.473, p=.00415) groups could be due to the load
increments which would naturally shorten the test time.
Since the mean fit test ran 15.4 minutes and the average 87 unfit test ran 9.2 minutes, this would agree with Buchfurer, et al. (1983) suggesting selection of a work rate increment to bring the subject to the limit of his tolerance in about
10 1 2 minutes for optimal V0 2 max. Other arm crank studies using male subjects (DeBoer, 1982; Washburn, 1983; Fardy and
Hellerstein, 1978; Bar-Or, 1975; Magel, 1978) employed work increments anywhere from 17W to 40W. The author reasoned that since this study used female subjects, which were shown to have lower arm V0 2 peak than men (Vander, 1984), a lower work increment should be employed. It is possible, then, that the less taxing lOw increments have caused the lower relationship seen in the fit sample.
Some of the subjects' efforts to attain V0 2 peak may have been impeded by complaints of hand and forearm fatigue
in the middle and late stages of their tests. This may have skewed the V02 peak vs. maximum test time relationship.
Though this problem appeared in both samples, it may have more of an effect on the fit sample. Many of these complaints came from those who were exclusively swimmers,
such as the university team participants. They explained
that forearm muscles are not taxed to a great degree while
swimming the different strokes, and thus, would fatigue more
easily considering the static component (of the hands and
forearms) during arm crank exercise. Conversely, six members of the fit population were also regular tennis and
softball players in addition to swimming. These subjects 88 experienced no hand and forearm muscle fatigue until near the conclusion of the test. This may suggest that with any hand and forearm muscle training, those subjects who were exclusively swimmers may have improved their V0 2 peak values. Davis, et al. (1979) also encountered this problem in the early stages of their tests:
During the early stages of the arm crank test the subjects uniformly complained of pain in their forearms with the pain persisting until the cessation of exercise. It seems possible that the forearm muscles, which represents a relatively small amount of the total musculature ultimately involved in the arm crank V0 2 max effort, supported the arm work almost exclusively in the early stages of the test. At some point in time, these muscles are taxed beyond their capability to supply energy entirely aerobically, and thus, lactate is produced. As the work rate is further increased, additional musculature of the shoulder girdle and trunk is recruited until V02 max is finally reached (p. 1044).
Though this does not generally agree with this author's observations in the sense that forearm fatigue occurred later in this study, a "lack of uniform recruitment patterns" (Davis, 1976) in arm work could be a partial reason why some of the subjects' V0 2 peak might not have been reached, which in turn would have skewed the VO2 peak vs. maximum test time relationship.
Conclusions
1. At 40% V0 2 peak, a modest negative, significant correlation exists in the upper body fit, unfit, and combined groups between V0 2 and Ve/V02 for women.
Therefore, at intensities below the ventilatory threshold,
it is reasonable to conclude that V02 is inversely related 89
and to Ve/V02 in arm crank exercise using upper body trained untrained, 18-35-year-old females.
Exercising at 85% V0 2 peak, a non-significant relationship exists between Ve/V02 and V0 2 peak in the unfit and combined groups; but a modest, significant negative correlation is seen in the fit sample. This is due to a higher ventilatory threshold in the fit population, lower ventilatory responses seen in trained populations attributed to training adaptations in exercising muscle and more efficient lactate management.
2. It is reasonable to conclude that this arm crank test protocol showed a significant, moderate to high reproducibility in the combined group. The non-significant reproducibility seen in the fit group could be due to non- adherence to test rules, muscle group adjustments in the re- test, or excessive length of test time, although the RQ and maximum heart rate compared favorably with other arm crank studies involving both men and women.
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Applied Physiology, 49, 223-230. APPENDIX A
103 [104 t0 0
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107 0 0 a 0 <<0 s "-0 0 : 0 1 0 0 1C. o i a Int LU 0D I C) . 0 e C) I C) Li. 00 LU O 0 0 1 ) 0 qz') t1 C14 0 3 In L -4 oco < Lww LU L -) -4 1 - I I A4 it a 0 0 ML >Lw 0 1 c z> w LUJ c.. I -4 14444 N 1 -- .j < -U t r)- CL < 1 . LU Z In > 1 ' 4 t )-4W LL 0 V; 444 * I 1 0 1 0 C) E J-4 0 < 0 I 0 0. uJ 0 0 10 I 0 InCL 0 C Co 0z 1I 0 C o i o 0 1 0 I Co o 0 U 0 o0 0 Ln r- 0 (nOa 1444 Co I Co 4)C * I 4.CL < Lww 'V 5-4 Ci: r0
0 1 a <0 10to W 44 Im 44 N Poo 0 Zce CJ 11- 00 0 1 0 Il I' 0 -4 v C' () 1I mo 1 -4v <0 N 0 1 0. 0) ' 1 o N .1 0. o -4 Inz * - I - C' '1 I -0) N I N
109 Table C-1
Raw Data for the Unfit Sample
Max Max VO2 v Subject Weight Test Heart Peak Peak Ventilatory Threshold ID Age (kg) Time Rate (ml/kg/min) (1/min) (%VO9Peak) (ml/kg/min)
1 27 51.2 8.0 176 15.9 29.6 IR 27 51.6 7.0 155 14.5 27.6 51.72 7.5 2 35 74.0 11.0 165 17.9 41.8 40.78 7.3 2R 35 75.0 11.0 151 16.7 37.9 3 24 51.2 8.0 164 20.6 30.8 60.68 12.5 4 35 50.0 6.0 105 15.8 26.2 44.30 7.0 4R 35 49.5 6.5 111 14.4 26.1 5 26 46.0 8.0 158 22.0 30.9 57.73 12.7 6 20 63.0 9.0 142 18.1 37.1 45.30 8.2 7 21 53.1 8.2 162 20.1 42.6 53.23 10.7 8 22 60.0 11.5 185 25.9 64.2 8R 22 61.0 11.5 182 24.1 58.8 40.06 9.8 9 21 57.5 11.2 149 28.9 49.8 53.98 15.6 10 20 72.0 10.5 188 21.4 56.0 32.24 6.9 1CR 20 72.0 10.5 178 20.5 58.9 11 24 53.0 9.0 176 24.9 41.4 64.32 15.5 12 30 58.8 10.0 160 23.2 39.1 55.60 12.9 13 27 66.5 9.2 155 16.1 45.6 51.55 8.3 14 23 64.5 8.0 160 16.8 28.8 54.17 9.1 15 33 78.0 10.5 163 19.6 51.9 15R 33 78.5 11.0 165 21.2 55.3 47.17 10.1 16 22 61.0 11.0 175 19.9 50.0 47.74 9.5 17 24 53.5 7.5 170 23.2 42.4 52.59 12.2 17R 24 55.0 8.0 153 18.8 36.7 18 21 59.5 10.0 178 18.9 44.6 47.09 8.9 18R 21 60.0 9.0 172 16.5 42.1 19 19 -55.0 9.0 171 19.7 36.9 61.93 12.2 18R 21 60.0 9.0 172 16.5 42.1 19 19 55.0 9.0 171 19.7 36.9 61.93 12.2 20 21 51.0 9.0 165 17.9 32.0 67.60 12.1 21 22 67.0 10.0 165 14.8 40.1 21R 22 67.5 10.0 183 17.1 42.2 30.99 5.3 22 20 62.5 10.0 150 18.7 32.1 50.27 9.4 23 20 52.5 8.0 162 18.2 27.9 42.31 7.7 24 20 64.0 11.0 171 29.3 50.9 56.31 16.5 25 18 60.0 11.5 162 24.1 48.7 34.44 8.3 26 22 52.5 7.5 146 20.6 34.7 54.85 11.3 27 31 66.0 8.0 165 17.8 44.9 48.31 8.6 28 18 52.0 9.0 183 24.6 46.0 47.56 11.7 29 26 53.0 8.0 163 17.2 27.6 42.44 7.3 30 22 52.5 8.5 157 14.1 27.6 30R 22 52.5 8.5 154 14.4 29.0 53.47 7.7 Table C-2
Respiratory Exchange Ratio for the Unfit Group at 40%, 85%, and Peak Oxygen Uptake
Subject ID 40% 85% Peak 1 .95 1.10 1.28 2 .81 1.01 1.03 3 .78 .89 .95 4 .78 .92 .93 5 .63 .78 .82 6 .74 1.02 1.06 7 .77 .93 .95 8 .93 1.14 1.23 9 .63 .86 .90 10 .77 1.04 1.10 11 .62 .76 .80 12 .60 .80 .85 13 .87 1.00 1.04 14 .71 .79 .85 15 .78 .88 .90 16 .72 .92 .95 17 .88 1.06 1.18 18 .90 1.16 1.25 19 .80 .97 1.01 20 .78 .92 1.01 21 .82 1.10 1.10 22 .85 1.05 1.10 23 .81 .91 .95 24 .79 .80 .90 25 .87 .95 .95 26 .69 .84 .90 27 .72 .93 .96 28 .65 .83 .85 29 .69 .87 .90 30 .99 1.15 1.23
.78 7 = .91 x = .93 Fl 2
Table C-3
Raw Data for the Fit Sample
Max Max Vo Ve Subject 2 Weight Test Heart Peak Peak Ventilatory Threshold ID Age (kg) Time Rate (ml/kg/min) (1/min) (%VOPeak) (mi/kg/min) 1 19 63.0 17.0 173 23.3 54.7 69.53 16.2 2 19 53.0 15.5 175 39.6 53.0 57.83 3 22.6 19 63.0 15.0 174 29.4 54.6 70.07 20.6 4 19 61.0 15.7 180 29.7 83.4 57.91 5 17.2 21 59.5 17.4 186 43.7 87.7 78.11 33.9 6 18 72.3 21.0 191 34.6 92.0 76.59 7 26.5 20 69.3 21.0 170 29.2 62.5 68.49 20.0 8 19 60.7 19.0 197 37.1 90.6 84.64 9 31.4 18 64.7 16.0 176 39.5 76.4 76.20 30.1 10 18 63.5 14.0 180 28.7 48.1 74.22 11 21.3 27 63.0 13.0 165 26.2 85.2 61.83 16.2 IIR 27 63.0 16.0 163 22.7 86.5 12 33 57.0 14.0 160 30.5 59.5 13 69.18 21.1 23 60.0 16.0 185 30.2 66.7 66.23 20.0 13R 23 59.5 16.0 175 25.8 66.7 14 26 58.5 12.0 184 27.8 56.7 61.51 17.1 15 33 69.0 17.0 168 26.3 58.1 58.02 15.2 15R 33 68.0 17.0 166 31.6 73.3 16 34 53.0 13.0 171 31.5 62.2 72.38 22.8 16R 34 53.0 15.0 180 33.6 80.3 17 30 54.5 12.5 154 27.7 60.5 67.87 18 18.8 35 58.0 15.0 176 34.4 69.3 61.92 21.3 18R 35 58.0 16.0 172 32.2 75.7 19 33 53.0 12.5 160 28.6 51.7 65.03 18.6 19R 33 53.0 12.0 150 26.4 44.0 20 29 58.0 14.0 175 28.6 56.6 63.64 18.2 20R 29 58.0 14.0 176 29.9 50.4 21 29 49.0 14.5 197 32.5 65.7 66.15 21.5 21 R 29 49.0 14.0 186 26.0 51.7 22 29 57.5 15.0 178 33.4 75.3 61.08 20.4 22R 29 57.5 16.5 170 34.4 82.7 23 33 51.0 11.0 160 23.9 49.0 56.90 13.6 24 29 55.5 16.0 162 32.0 61.4 60.94 19.5 25 32 68.0 16.0 190 29.4 84.0 26 62.93 18.5 28 73.0 16.5 170 30.2 76.2 57.95 27 24 61.0 17.5 16.0 188 3.5 74.2 59.10 19.8 27R 24 61.5 15.0 179 28.5 63.7 28 26 46.0 16.0 162 33.4 60.3 67.37 22.5 29 29 62.5 15.5 163 29.7 64.3 63.64 18.9 30 26 54.0 14.0 183 35.6 64.7 69.00 24.6 13
Table C-4
Respiratory Exchange Ratio for the Unfit Group at 40%, 85%, and Peak Oxygen Uptake
Subject ID 40% 85% Peak 1 .82 .97 1.05 2 .70 .86 .95 3 .79 1.00 1.00 4 .82 .96 1.05 5 .75 .89 .90 6 .86 1.03 1.13 7 .90 1.01 1.04 8 .89 1.00 1.16 9 .71 .81 .90 10 .69 .78 .85 11 .75 1.05 1.08 12 .92 1.06 1.11 13 .92 1.11 1.21 14 .83 .95 .99 15 .84 1.02 1.11 16 .90 1.22 1.23 17 .85 .99 1.03 18 .97 1.18 1.33 19 .76 .94 1.05 20 .84 .93 .95 21 .82 1.09 1.20 22 .96 1.02 1.05 23 .92 1.04 1.04 24 .85 1.02 1.10 25 .95 1.12 1.20 26 .73 1.02 1.16 27 .91 1.11 1.14 28 .90 1.08 1.22 29 .89 1.13 1.14 30 .81 1.11 1.32
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