Oxygen Uptake and VO2 Consumption When Training

Introduction

Oxygen uptake kinetics is the rate oxygen uptake responds at the onset exercise and reflects the adjustment of both systemic oxygen transport and muscle metabolism (Xu and Rhodes, 1999). There are three phases of exercise VO2 kinetics that can be identified in the moderate exercise domain (Whipp and Ward, 1990 cited in Xu and Rhodes, 1999). Phase 1 represents the early fast increase in VO2, which usually is usually completed within the first 15 – 25 seconds of exercise (Xu and Rhodes, 1999). It suggests that in phase 1 the increase in VO2 is mainly attributed to the increase in cardiac output (Q) and thus pulmonary flow (Whipp, 1987). Therefore, because phase 1 is mainly a consequence of increased venous return it is often called cardiodynamic phase (Hughson et al, 2000). Phase 2 is the primary phase of the adaptive process, it reflects the change in muscle oxidative metabolism as venous return continues to increase and more O2 is extracted with exercise (Hughson et al, 2000). Following a short delay of phase 1, VO2 increases exponentially towards a steady state level, research has suggested that there is a linear dynamic relationship between VO2 and the work rate (Barstow et al, 1993; Gerbino et al, 1996). Limitations of oxygen transport either or activation of metabolic processes that govern muscle oxygen utilisation may explain phase 2 (Hughson 1990). Phase 3 has been described as an additional phase in which the VO2 adds on top of the metabolic requirements of that work rate (Paterson and Whipp, 1991). Phase 3 is steady state VO2 levels, which are reached after approximately 3 minutes (Whipp, 1987).

For constant-load exercise below lactate threshold, oxygen uptake rapidly increases with exercise onset obtaining a steady state within about 3 minutes. However, during constant-load exercise above the lactate threshold an additional ‘slow component’ VO2 response is present (Gaesser and Poole, 1996). The VO2 slow component represents additional oxygen cost that is superimposed on the rapid phase of oxygen uptake kinetics observed during exercise onset (Gaesser and Poole, 1996). The slow component has been defined as the difference between VO2 measured at 3 minutes of constant-load exercise and end-exercise (Gaesser and Poole 1996; Womack et al, 1995). The magnitude of the VO2 slow component is elevated with increased intensities of exercise above the lactate threshold. Elevated body or muscle temperature has been proposed to contribute to the VO2 slow component; however, these observations are based on the temperatures rise during the constant-load exercise (Poole et al, 1988 cited in Saunders et al, 2000; Poole et al, 1990 cited in Saunders et al, 2000). The duration of exercise have been found to determine the magnitude of the slow component and the cause of the slow component is the increase in blood lactate levels, increases in plasma epinephrine levels, increased ventilatory work (minute ventilation VE), elevation of body temperature and recruitment of type IIb fibres (Xu and Rhodes, 1999). The recruitment of type II muscle fibres during exercise has been found to be an explanation for the slow component phenomenon (Barstow et al, 1996; Whipp 1994). Barstow et al, (1996) demonstrated that the contribution made by the slow component to the total VO2 response to 8 minutes of heavy, constant load cycling was greater in subjects with a high proportion of type II fibres.

Exercise itself results in relative hyperthermia (Febbraio et al, 1996), heat production during exercise is 15-20 times greater than at rest and is sufficient to raise Tc 1°C every 5 minutes if there are no thermoregulatory adjustments (Nadel et al, 1977 cited in Coris et al, 2004). Gonzalez (1988) cited in Cheung et al, (2000) found a hot and/or dry humid environment imposes a major stress on the human body’s ability to maintain physiological stability during exercise, due to decreases in the thermal and water vapour pressure gradients between the body and the environment, therefore impairing heat exchange. Lindinger, (1999) more recently supported this and concluded exercise in the heat imposes additional challenge to maintaining high levels of physical and mental function due to demands placed on mechanisms to regulate thermal and fluid balance. The combination of exercise and heat stress has been found to increase the cardiovascular and thermoregulatory strain on the body because of the requirement to send blood to the skin in these conditions (Sawka and Coyle, 1999). Endurance performance during prolonged, submaximal exercise has been found to be reduced in a hot environment (MacDougall et al, 1974; Adams et al, 1975; Suzuki, 1980 cited in Morris et al, 1998). Morris et al, (1998) more recently supported this, they found that performance during a prolonged, intermittent, high-intensity running test to exhaustion was less in a hot environment (30°C, ∼66%) than a moderately hot (21°C, ∼71%) environment.

When the air is hot, the thermal gradient for heat loss is reduced so that the rate of heat accumulation by the body is increased and fatigue, or an inability to exercise voluntary, occurs sooner than when exercising in cool conditions (Werner, 1993). Rowell (1974) cited in Febbraio (2001) found a reduction in O2, substrate delivery and utilisation because of reduced muscle blood flow during exercise in the heat.

Morris et al, (1998) supported these findings suggesting decline in exercise performance in heat may be due to its impact on Q and mean arterial blood pressure. Sawka and Coyle, (1999) more recently stated cardiovascular and thermoregulatory systems are thought to be primarily responsible for the decrease in exercise performance in a hot environment. A high level of aerobic fitness has been associated with an improved exercise-heat tolerance (Cheung et al, 2000).

Aims:

The aim of this study is to establish if VO2 kinetics and the slow component are when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 1: Participants VO2 will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 2: Participants VE will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 3: Participants HR will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 4: Participants RPE will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Method

Participants

In the investigation conducted 2 healthy participants both aged 21 and of similar fitness levels volunteered to take part. Both participants had their height and weight taken prior to completing the investigation. Participant 1’s height was 158cms and weighted ...

This is a preview of the whole essay

Hypothesis 2: Participants VE will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 3: Participants HR will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Hypothesis 4: Participants RPE will increase when exercising in a heated environment compared to that of a thermoneutral environment.

Method

Participants

Measurements

Participants’ height and weight measurements were recorded prior to starting each experiment. In order to maintain and control the heated environment, of which the participants were to undertake the experiment, a heat tent was used. Tc of the participants was obtained using tympanic probes, which were inserted into each participant’s ear. The participants wore the tympanic probes for the duration of each experiment. In order to obtain the skin temperatures of the participants, skin thermisters were attached at each participant’s thigh, chest, biceps and forehead. Expired air for measuring VE, VO2, VCO2 and RER from each participant was obtained throughout the experiment using a metabolic cart. The participants’ heart rate (HR) throughout the experiment was obtained using a polar HR monitor and RPE values of the participant were obtained via asking the participants to look at a borg scale placed in front of them, and indicating which score was most appropriate to how they were feeling.

Procedure

Prior to starting each experiment, environmental data was taken, these were a room temperature of (23°C) and humidity of (52%) in the experiment 1 (thermoneutral environment) and a room temperature of (35-37°C) and a humidity of (27-30%) in the experiment 2 (heated environment). Resting measurements of the participants were also recorded, these were; height, weight, resting heart rate, expired air for VE, VO2, VCO2 and RER, Tc and Tskin. In the first experiment participants remained at rest in a thermoneutral exercise environment (23°C) for at least 30 minutes prior to commencing exercise, during this period participants were constantly monitored. Participants were then asked to undertake 10 minutes of moderate/heavy exercise using a cycle-ergometer in the thermoneutral environment. This was obtained by using Karvonen’s formula using 70% VO2 max exercise intensity. Tc/ Tskin, HR and RPE were recorded every minute for the duration of the experiment. The participants were allowed fluid on request pre, during and post exercise, which was recorded. In the second experiment participants remained at rest in a heated exercise environment (35-37°C) for at least 30 minutes prior to commencing exercise, during this period participants were constantly monitored. Participants were then asked to undertake 10 minutes of moderate/heavy exercise using a cycle-ergometer in the heated environment. Tc/ Tskin, HR and RPE, again, were recorded every minute for the duration of the experiment. The participants again, were allowed fluid on request pre, during and post exercise, which was recorded. The participants were asked to wear the same clothing as worn in the first experiment (UCW polo shirts and shorts).

Ethical considerations

Each participant was given a pre-test questionnaire and an informed consent form, ensuring their readiness for physical activity, and ensuring there were no other limiting factors to the participants knowledge preventing them from completing the experiment (see appendix I). Stop test indicators were HR >190bpm, a RPE of >17 and a Tc of >39°C.

Data and Statistical Analysis

The data was gathered and put into graphs and tables using Microsoft excel. The data presented for VO2, VE, HR and RPE were presented individually for each participant. Tskin, Tc, and Tbody were calculated using the following equations:

Tskin = (0.1 x Ta) + (0.6 x Tt) + (0.2 x TI) + (0.1 x Th)

Tc = (0.6 x Tr)

Tbody = (0.4 x Tskin) + (0.6 x Tc)

Results

Figure 1. Participant 1’s V02 values in a thermoneutral and heated environment.

Figure 1 shows that participant 1 had a steady state VO2 of 1549ml/min in the thermoneutral environment and a steady state VO2 of 1734ml/min in the heated environment. This showed an increase in VO2 of 185ml/min when exercising in the heated environment compared to that of a thermoneutral environment. Time to steady state in the thermoneutral environment was reached at approximately 3 minutes with a slow component of ΔVO2 150ml/min (10-3). Time to steady state in the heated environment was reached at approximately 4 minutes with a slow component of ΔVO2 205ml/min (10-3).

Figure 2. Participant 2’s V02 values in a thermoneutral and heated environment.

Figure 2 shows that participant 2 had a steady state VO2 of 1492ml/min in the thermoneutral environment and a steady state VO2 of 1643ml/min in the heated environment. This showed an increase in VO2 of 151ml/min when exercising in the heated environment compared to that of a thermoneutral environment. Time to steady state in the thermoneutral environment was reached at approximately 3 minutes with a slow component of ΔVO2 147ml/min (10-3). Time to steady state in the heated environment was reached at approximately 4 minutes with a slow component of ΔVO2 192ml/min (10-3).

Figure 3. Participant 1’s VE values in a thermoneutral and heated environment.

Figure 3 shows that participant 1’s VE increased when exercising in the heated environment compared to that of a thermoneutral environment. The VE increase occurred quicker and maintained a more dramatic increase throughout the experiment in the heated environment compared to that of the thermoneutral environment.

Figure 4. Participant 2’s VE values in a thermoneutral and heated environment.

Figure 4 shows that participant 2’s VE increased when exercising in the heated environment compared to that of a thermoneutral environment. The VE increase occurred quicker and maintained a more dramatic increase throughout the experiment in the heated environment compared to that of the thermoneutral environment.

Figure 5. Participant 1’s Heart Rate in a thermoneutral and heated environment.

Figure 5 shows that participant 1’s HR increased more dramatically in the first couple of minutes of exercise and maintained higher values when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 6. Participant 2’s Heart Rate in a thermoneutral and heated environment.

Figure 6 shows that participant 2’s HR increased and maintained higher values when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 7. Participant 1’s rate of perceived exertion (RPE) using Borg scale ratings in a thermoneutral and heated environment.

Figure 7 shows that participant 1’s RPE increased more rapidly in the heated environment, however, once reaching a plateau, values where the same when exercising in the heat and a thermoneutral environment.

Figure 8. Participant 2’s rate of perceived exertion (RPE) using Borg scale ratings in a thermoneutral and heated environment.

Figure 8 shows that participant 2’s RPE increased more rapidly and maintained higher values when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 9. Bar chart showing the Tskin of Participant 1 obtained using tympanic probes placed on the body.

Figure 9 shows that participant 1’s Tskin increased when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 10. Bar chart showing the Tskin of Participant 2 obtained using tympanic probes placed on the body.

Figure 10 shows that participant 2’s Tskin increased when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 11. Bar chart showing the Tc of Participant 1 obtained using tympanic probes placed on the body.

Figure 11 shows that participant 1’s Tc increased when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 12. Bar chart showing the Tc of Participant 2 obtained using tympanic probes placed on the body.

Figure 12 shows that participant 2’s Tc increased when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 13. Bar chart showing the Tbody of Participant 1 obtained using tympanic probes placed on the body.

Figure 13 shows that participant 1’s Tbody increased when exercising in the heated environment compared to that of a thermoneutral environment.

Figure 14. Bar chart showing the Tbody of Participant 2 obtained using tympanic probes placed on the body.

Figure 14 shows that participant 2’s Tbody increased when exercising in the heated environment compared to that of a thermoneutral environment.

Discussion

In the present study participants steady state VO2 were found to increase in the heated environment (1734ml/min and 1643ml/min) compared to that of the thermoneutral environment (1549ml/min and 1492ml/min), which supported hypothesis 1 (see figures 1 and 2). VO2 increased due to increased demands placed upon the body in the heat. Researchers have stated that increased metabolism by the heart and the skin (MacDougall et al, 1974) could account for increased VO2 reported during exercise in hot conditions (Gisolfi and Copping, 1974; Galloway and Maughan, 1997). There are, however, a number of factors that would have contributed to the increased VO2 in the heated environment compared to that of the thermoneutral environment. Participants VE were found to increase in the heat compared to that of the thermoneutral environment (see figures 3 and 4), which supported hypothesis 2. This is further supported by the increase in duration of the slow component in the heated environment compared to that of the thermoneutral environment, Xu and Rhodes, (1999) stated the slow component is longer with increased VE. In the present study steady state was reached at approximately 3 minutes after starting exercise, however steady state was reached at approximately 4-5 minutes of exercise. Increased VE occurred due to increased demands placed upon the body, requiring more O2 to be transported through the blood (McArdle Katch and Katch 2001; Powers and Howley 2001). Furthermore, VE increased when exercising in heat is due to increased blood temperature, which has been found to directly affect the respiratory control centre (Powers et al, 1982).

Muscles require O2 in order to function, due to increased demands placed upon the muscles, increased ventilation is necessary to transport the oxygen to the muscles in order to ‘fuel’ them and prevent lactate build up (McArdle Katch and Katch 2001; Powers and Howley 2001). In the present study the slow component increased in the heat (P1 = ΔVO2 205ml/min and P2 = ΔVO2192ml/min) compared to that of the thermoneutral environment (P1 = ΔVO2 150ml/min and P2 =ΔVO2147ml/min). This provides evidence that lactate build up was greater in the heated environment. Gaesser and Poole, (1996) stated the slow component is a result of work done above the lactate threshold. This could explain the increase in participants RPE when exercising in the heat compared to that of the thermoneutral environment. Febbraio et al, (2001) suggested that exercise in the heat increased muscle lactate production. With increased muscle lactate production as a result of increased temperature placed upon the participants, their rate of perceived exertion would have increased due to fatigue. Participants RPE was found to increase more dramatically and maintain higher values in the heat compared to that of the thermoneutral environment (see figures 7 and 8), which supported hypothesis 4. Pandolf et al, (1972) cited in Pandolf (2001) found RPE did not differ significantly after 30 minutes of exercise in comfortable (24°C) compared to hot (44-54°C) environments. However, contradictory to this, Galloway and Maughn, (1997) more recently supported the findings of the present study. They found RPE appears to be higher in the heat than in the cold at the same relative intensity, and there is an increased exercise time to fatigue when individuals exercised in cool conditions compared to heated conditions. Research states that voluntary fatigue occurs at a Tc of approximately 40°C (Gisolfi and Copping, 1974; MacDougall et al, 1974; Nielsen et al, 1997). It should be noted however, that these values were obtained using trained athletes, the participants used in the present study were of a general physical fitness, so fatigue among the participants may occur at lower temperature. Improved exercise-heat tolerance has been associated with higher levels of cardiorespiratory fitness (Cheung et al, 2000). Nybo and Nielson (2001) found that RPE increases parallel with rising Tc and HR, which is consistent with the findings in the present study.

Participants HR were found to increase when exercising in the heat compared to that of the thermoneutral environment (see figures 5 and 6), which supported hypothesis 3. Increases in Q occur rapidly during the transition from rest to steady-rate exercise due to increased demands for blood to be transported around the body (McArdle, Katch and Katch, 2001). When exercising in the heat demands are increased further (Cheung et al, 2000), therefore further increasing Q. Q has is increased in an attempt to pump blood around the body quicker. One of primary mechanisms for heat loss during exercise is increased skin blood flow (Watt et al, 2000), the blood is circulated closer to the skin in an attempt to cool down. Research has found that Q and blood flow to the contracting muscles and skin are maintained by decreases in stroke volume (Werner, 1993) and increases in HR (Geor et al, 1995 cited in Lindinger, 1999; Nielson et al, 1997; Savard et al, 1988: Werner, 1993). This supports the findings of the present study, due to the increased demands placed upon the participants body in the heated environment, the Q and blood flow to the contracting muscles was maintained via increases in the participants HR.

In the present study the Tskin and Tc of the participants were greater in the heated environment compared to that of the thermoneutral environment (figures 9 to 12). Nadel et al, (1977) cited in Coris et al, (2004) found that Tskin and Tc rise with exercise. Obviously the heated environment would play a major role in the temperatures recorded for the participants, however, other factors should be considered. The onset of muscular contraction is accompanied by a rapid increase in muscle temperature due to the inefficiency of metabolic energy conversions (Brinnel et al, 1987) causing an increase in body temperature, in order to counteract this the body needs to lose heat. One of primary mechanisms for heat loss during exercise is increased skin blood flow (Watt et al, 2000), the blood is circulated closer to the skin in an attempt to cool down. This will therefore make the skin temperature rise, this can be seen visually, with the face, arms and legs turning red due to the blood being closer to the skin. Werner, (1993) found that when exercising at a ambient temperature of 30°C, approximately 70%-80% of the heat loss occurs by evaporative cooling and approximately 20% is lost through convection and conduction. This again would result in a raised Tskin due to the body trying to maintain a cool temperature.

To conclude, from the data obtained in the present study and the literature research O2 uptake, VE, HR and RPE increase in a heated environment, due to the extra demands placed upon the body. If the study was to be conducted again, a wider range of participants should be used which would ensure more accurate results.

References:

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

Barstow, T.J., Casaburi, R., and Wasserman, K. (1993). O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate. Journal of Applied Physiology, 75, 755-762.

Barstow, T.J., Jones, A.M., Nguyen, P., Casaburi, R. (1996). Influence of muscle fibre type and pedal frequency on oxygen uptake kinetics of heavy exercise. Journal of Applied Physiology, 81, 1642-1650.

Brinnel, H., Cabanac, M., and Hales, J.R.S. critical upper levels of body temperature, tissue, thermosensitivity and selective brain cooling in hyperthermia. Cited in Nielson, B., and Nybo, L. (2003). Cerebral changes during exercise in the heat. Sports Medicine, 33, 1-11.

Cheung, S.S., McLellan, T.M., and Tenaglia, S. (2000). The thermophysiology of uncompensable heat stress. Sports Medicine, 29, 329-359.

Coris, E.E., Ramirez, A.M., and Van Durme, D.J. (2004). Heat illness in athletes: the dangerous combination of heat, humidity and exercise. Sports Medicine, 34, 9-16.

Febbraio, M.A., Snow, R.J, and Stathis, C.G. (1996). Blunting the rise in body temperature reduces muscle gylcogenolysis during exercise in humans. Cited in Febbraio, M.A. (2001). Alterations in energy metabolism during exercise and heat stress. Sports Medicine, 31, 47-59.

Febbraio, M.A. (2001). Alterations in energy metabolism during exercise and heat stress. Sports Medicine, 31, 47-59.

Gaesser , G.A., and Poole, D.C. (1996). The slow component of oxygen uptake kinetics in humans. Ex. Sports Sci. Rev, 24, 35-70.

Galloway, S.D.R., and Maughn, R.J. (1997). Effect of ambient temperature on the capacity to perform prolonged cycle exercise in man. Medicine and Science in Sports and Exercise, 29, 1240-1249.

Geor, R.J., McCutcheon, L.J., Ecker, G.L., and Lindinger, M.I. (1995). Thermal and cardiorespiratory responses of horses to submaximal exercise under hot and humid conditions. Cited in Lindinger, M.I. (1999). Exercise in the heat: thermoregulatory limitations to performance in humans and horses. Canadian Journal of Applied Physiology, 24, 152,163.

Gerbino, A., Ward, S.A., and Whipp, B.J. (1996). Effects of previous exercise on pulmonary gas-exchange kinetics during high-intensity exercise in human. Journal of Applied Physiology, 80, 99-107.

Gilsofi, C.V., and Copping, J.R. (1974). Thermal effects of prolonged treadmill exercise in the heat. Medicine and Science in Sports and Exercise, 6, 108-113.

Gonzalez, R.R. (1988). Biophysics of heat transfer and clothing considerations. Cited in Cheung, S.S., McLellan, T.M., and Tenaglia, S. (2000). The thermophysiology of uncompensable heat stress. Sports Medicine, 29, 329-359.

Hughson, R.L. (1990). Exploring cardiorespiratory control mechanisms through gas exchange dynamics. Medicine of Science in Sports and Exercise, 22, 72-79.

Hughson, R.L., and Morrissey, M. (1982). Delayed kinetics of respiratory gas exchange in the transition from previous exercise. Journal of Applied Physiology, 52, 921-929.

Hughson, R.L., O’Leary, D., Betik, A.C., and Hebestreit, H. (2000). Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake. Journal of Applied Physiology, 88, 1812-1819.

Katch, F.I., Katch, V.L. and McArdle, W.D. (2001). Exercise Physiology: fifth edition. Lippencott Williams & Wilkins, USA.

Lindinger, M.I. (1999). Exercise in the heat: thermoregulatory limitations to performance in humans and horses. Canadian Journal of Applied Physiology, 24, 152,163.

Martin, T.P. (1974). Oxygen Deficit, oxygen debt relationship at submaximal exercise. Journal of Sports Medicine, 14, 252 - 253.

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

Morris, I.G., Nevill, M.E., Lakomy, H.K.A., Nicholas, C., and Williams, C. (1998). Effect of a hot environment on performance of prolonged, intermittent, high-intensity shuttle running. Journal of Sports Sciences, 16, 677-686.

Nadel, E.R., Wenger, C.B., and Roberts, M.F. (1977). Physiological defenses against hyperthermia of exercise. Cited in Coris, E.E., Ramirez, A.M., and Van Durme, D.J. (2004). Heat illness in athletes: the dangerous combination of heat, humidity and exercise. Sports Medicine, 34, 9-16.

Nielson, B., and Nybo, L. (2003). Cerebral changes during exercise in the heat. Sports Medicine, 33, 1-11.

Nielson, B., Strange, S., Christensen, N.J., Warberg, J., and Saltin, B. (1997). Acute and adaptive responses in humans to exercise in a warm, humid environment. European Journal of Applied Physiology, 434, 49-56.

Pandolf, K.B., Cafarelli., Noble, and Metz (1972). Cited in Pandolf, K.B. (2001). Rated perceived exertion during exercise in the heat, cold or altitude. International Journal of Sports Psychology, 32, 162-176.

Paterson, D.H., Whipp, B.J. (1991). Asymmetries of oxygen uptake transients at the on- and offset of heavy exercise in humans. Journal of Physiology, 443, 575-586.

Poole, D.C., Ward. S.A., and Gardener, G.W., and Whipp, B.J. (1988). Metabolic and respiratory profile of the upper limit for prolonged exercise in man. Cited in Saunders, M.J., Evans, E.M., Arngrimsson, S.A., Allison, J.D., Warren, G.L., and Cureton, K.J. (2000). Muscle activation and the slow component rise in oxygen uptake during cycling. Medicine and Science in Sports and Exercise, 32, 2040-2045.

Poole, D.C., Ward. S.A., and Whipp, B.J. (1990). The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise. Cited in Saunders, M.J., Evans, E.M., Arngrimsson, S.A., Allison, J.D., Warren, G.L., and Cureton, K.J. (2000). Muscle activation and the slow component rise in oxygen uptake during cycling. Medicine and Science in Sports and Exercise, 32, 2040-2045.

Powers, S.K. and Howley, E.T. (1994). Exercise Physiology (2nd edition). Boston, Massachusetts: WCB McGraw-Hill.

Powers, S.K. and Howley, E.T. (2001). Exercise Physiology (4th edition). Boston, Massachusetts: WCB McGraw-Hill.

Powers, S., Howley, E., and Cox, R. (1982). Ventilatory and metabolic reactions to heat stress during prolonged exercise. Journal of Sports Medicine and Physical Fitness, 22, 32-36.

Rowell, L.B. (1974). Human cardiovascular adjustments to exercise and thermal stress. Cited in Febbraio, M.A. (2001). Alterations in energy metabolism during exercise and heat stress. Sports Medicine, 31, 47-59.

Savard, G.K., Nielson, B., Laszczynska, J., Larsen, B.E., and Saltin, B. (1988). Muscle blood flow is not reduced in humans during moderate exercise and heat stress. Journal of Applied Physiology, 64, 649-657.

Sawka, M.N, and Coyle, E.F. (1999). Influence of body water and blood volume on thermoregulation and exercise performance in the heat. Medicine and Science in Sports and Exercise, 27, 167-218.

Suzuki, Y. (1980). Human physical performance and cardiocirculatory responses to hot environments during submaximal upright cycling. Cited in Morris, I.G., Nevill, M.E., Lakomy, H.K.A., Nicholas, C., and Williams, C. (1998). Effect of a hot environment on performance of prolonged, intermittent, high-intensity shuttle running. Journal of Sports Sciences, 16, 677-686.

Watt, M.J., Garnham, A.P., Febbraio, M.A., and Hargreaves, M. (2000). Effect of acute plasma volume expansion on thermoregulation and exercise performance in the heat. Medicine and Science in Sports and Exercise, 32, 958-962.

Werner, J. (1993). Temperature regulation during exercise: An overview. Cited in Morris, I.G., Nevill, M.E., Lakomy, H.K.A., Nicholas, C., and Williams, C. (1998). Effect of a hot environment on performance of prolonged, intermittent, high-intensity shuttle running. Journal of Sports Sciences, 16, 677-686.

Whipp, B.J. (1987). Dynamics of pulmonary gas exchange. Cited in Xu, F., and Rhodes, E.C. (1999). Oxygen uptake kinetics during exercise. Sports Medicine, 27, 313-327.

Whipp, B.J. (1994). The slow component of O2 uptake kinetics during heavy exercise. Medicine and Science in Sports and Exercise, 26, 1319-1326.

Whipp, B.J., and Mahler, P.B. (1980). Dynamics of pulmonary gas exchange during exercise. Cited in Xu, F., and Rhodes, E.C. (1999). Oxygen uptake kinetics during exercise. Sports Medicine, 27, 313-327.

Whipp, B.J., and Ward, S.A. (1990). Physiological determinants of pulmonary gas exchange kinetics during exercise. Medicine and Science in Sports and Exercise, 22, 62-71.

Xu, F., and Rhodes, E.C. (1999). Oxygen uptake kinetics during exercise. Sports Medicine, 27, 313-327.

Womack, C.J., Davis, S.E., Blumer, J.L., Barrett, E., Weltman, A.L., and Gaesser, G.A. (1995). Slow component of O2 uptake during heavy exercise: adaptation to endurance training. Journal of Applied Physiology, 79, 838-845.

02003954