The capacity of an individual to perform prolonged exercise is influenced by a number of factors, one of which is ambient temperature. A low ambient temperature (approximately 0°C) was first reported to impair endurance performance over 50 years ago (1). Since this early report, a number of authors have examined the metabolic and physiological responses to cold exposure at rest and during exercise at different intensities. Cold exposure of normothermic men at rest has been found to increase mean arterial pressure and cardiac output(32) and to result in a large increase of carbohydrate utilization with moderate increases in lipid oxidation(19,36). During low intensity exercise in the cold, heart rate is lower and oxygen consumption is higher than in a warmer environment (17) with a preferential utilization of lipid when both skin and rectal temperatures have been lowered(17). In the absence of a severe thermoregulatory stress, an increase in carbohydrate oxidation, or possibly a reduction in lipid oxidation, has been reported when comparing a neutral (21°C) environment with a cool (9°C) environment (19). Moderate intensity exercise in the cold (9°C) has been observed to result in a lower utilization of muscle glycogen when compared with that in a hot trial (41°C), with no difference in oxygen consumption between environmental conditions (13). Maximum oxygen uptake(˙VO2max) has been reported to be reduced (4) or unaffected (27) during cold exposure, and performance of high intensity exercise is reduced at lower muscle temperatures(5).
A detrimental effect of heat exposure on performance of prolonged exercise is also well recognized. Brown et al. (8) observed a reduction in exercise capacity at 80% of ˙VO2max when ambient temperature was increased from 20 to 35°C and attributed this reduction to an increased anaerobic contribution to energy production. Heat exposure combined with exercise results in hypo-hydration owing to high sweating rates, but changes in metabolic rate, cardiovascular function, and thermoregulatory failure may also affect exercise capacity in a hot environment(24,31). Nielsen et al.(26) observed that exhaustion from exercise at 60% of˙VO2max at either 20 or 40°C occurred when core temperature reached 39.7°C regardless of acclimation state. These authors suggested that core temperature rather than circulatory failure is the critical factor limiting exercise capacity in the heat. Hypohydration induced before exercise has reduced isometric muscular endurance (35), anaerobic exercise performance, ˙VO2max (9), and endurance exercise performance (2). Other studies have, however, found no change in isometric muscular endurance(33), no change in anaerobic exercise performance(18), and no reduction in ˙VO2max(2).
It is clear from this brief summary that the literature describing the effects of heat and cold exposure on performance and physiological responses to exercise is at best inconclusive. Comparisons between studies are difficult because of methodological differences such as variations in exposure temperature and humidity, clothing worn during exposure, exposure time, fitness levels and acclimation state of subjects, and exercise intensity, all of which will affect the outcome of such studies. It is also clear that there has been little systematic evaluation of the effects of ambient temperature on exercise capacity and on thermoregulatory, cardiorespiratory, and metabolic responses to prolonged exercise. One recent study by Febbraio et al.(12) has addressed this area. The purposes of this study were, therefore, to examine systematically the effects of temperature on exercise capacity and to evaluate the effects of temperature on physiological responses to prolonged moderate intensity exercise.
MATERIALS AND METHODS
Eight healthy male volunteers were studied. The mean (SEM) physical characteristics of the subjects were: 25 ± 2 yr of age, 72.1 ± 3.5 kg body mass, 176 ± 3 cm height, 1.88 ± 0.06 m2 body surface area and 4.01 ± 0.17 L·min-1 maximum oxygen consumption (˙VO2max). The subjects' ˙VO2max was recorded during an initial discontinuous incremental test on an electrically braked cycle ergometer (Gould Corival 300, Sensormedics, Rugby, Warwickshire, UK) and a second test was performed a few days later to verify that a maximum value had been achieved. Expired gas was collected in Douglas bags during the last 1-2 min of each increment. The bags were immediately analyzed by drawing a sample of air through an infrared CO2 analyzer (P.K. Morgan Ltd, Rainham, Kent, UK) and a paramagnetic O2 analyzer (Servomex, Taylor Instruments Ltd, Crowborough, Sussex, UK). The expired volume was drawn through a dry gas meter (Harvard, Edenbridge, Kent, UK) and expired gas temperature was recorded at the dry gas meter inlet. All gas volumes were corrected to STPD.
All subjects were moderately active, but none was heat acclimatized or specifically trained. All subjects were given written information concerning the nature and purpose of the study and gave their written informed consent. This study was approved by the Joint Ethical Committee of Aberdeen University and Grampian Health Board and conformed with the ACSM policy statement regarding the use of human subjects.
Experimental protocol. Each subject completed six rides to exhaustion on an electrically braked cycle ergometer at approximately 70% of˙VO2max. The first two of these tests were conducted at 20.9(± 0.3)°C dry bulb temperature and 49 ± 1% relative humidity(RH) and served to familiarize the subjects with the experimental protocol and with the sensation of exercising to exhaustion. These preliminary trials also allowed evaluation of the power output to ensure that an intensity corresponding to approximately 70% of ˙VO2max was attained and that the subjects were able to exercise for a duration of more than 1 h. The final four rides were the experimental trials and were performed 1 or 2 wk apart and at the same time of day. The ambient dry bulb temperature (Ta) was manipulated for these trials using a climatic chamber and the subjects cycled at 3.6 ± 0.3°C, 10.5 ± 0.5°C, 20.6 ± 0.2°C, and 30.5 ± 0.2°C with a RH of 70 ± 2% and an air velocity of approximately 0.7 m·s-1 on all trials. Air velocity was determined from the cooling power of the environment which was calculated using a katathermometer. The temperature conditions were administered using a Latin square cross-over randomization design. Subjects were instructed to record their dietary intake and physical activity for 2 d before the first experimental trial; their dietary intake and physical activity were then replicated before each of the other three experimental trials.
During the experimental period the subjects attended the laboratory in the morning after an overnight fast, were weighed, inserted a rectal thermistor 10 cm beyond the anal sphincter and then rested in a sitting position for approximately 30 min in a comfortable environment (24.7 (± 0.2)°C). For the last 10 min of this time the subject's hand was immersed in hot(42°C) water to allow arterialized-venous samples to be drawn. A venous cannula was then inserted into a lower forearm vein and two resting blood samples (6.5 mL) were obtained 5 min apart. Thermistors (Comark, Rustington, W. Sussex, UK) for the measurement of skin temperature were attached to the chest, upper arm, thigh, and calf for calculation of weighted mean skin temperature according to the method of Ramanathan (29), and a heart rate monitor (Polar Sport Tester PE3000, Bodycare LTD., Kenilworth, Warwickshire, UK) positioned. Baseline recordings of rectal(Tre) and skin (Tsk) temperatures and resting heart rate (HR) were made at the same times as blood was drawn. Subjects were dressed in only shorts, socks, and shoes on all trials. During the two coldest trials subjects wore a glove on the hand from which blood was being sampled in an attempt to maintain arterialization of the venous blood samples.
All blood samples were collected using a dry syringe: 2.5 mL of blood were immediately dispensed into a tube containing K3-EDTA (1.5 mg·mL-1) and the remaining 4 mL into a plain serum tube. Duplicate aliquots (100 μL) were removed immediately from the EDTA tube and were deproteinized in 1 mL of ice cold 0.3N perchloric acid (PCA) which was then centrifuged and the supernatant used for measurement of blood glucose(glucose oxidase method, Boehringer Mannheim Biochemica, London, UK Cat # 124 036), blood lactate (method of Maughan (21)), and blood glycerol (method of Boobis and Maughan (6). The remaining blood in the EDTA tube was used for determination of hemoglobin(cyanmethemoglobin method) and microhematocrit for calculation of percent changes in plasma volume relative to the second resting sample(11). The serum obtained was divided into two aliquots. One aliquot was immediately stored at -20°C for subsequent determination of serum free fatty acids (FFA, enzymatic colorimetric method, Boehringer Mannheim Biochemica, Cat # 1 383 175). The second aliquot was refrigerated and used for determination of serum electrolytes: sodium (Na+) and potassium (K+) were determined by flame photometry (Corning clinical flame photometer 410C, Essex, UK); chloride (Cl-) by potentiometric titration (Jenway chloride meter, Essex, UK), and serum osmolality by freezing point depression (Gonotec osmomat 030, YSI Ltd, Farnborough, UK). Blood glucose, hemoglobin, and microhematocrit were all determined within 5 h of sampling, and serum osmolality, Na+, K+ and Cl- within 2 d. Remaining samples of plasma, serum, and PCA supernatant were frozen and stored at -20°C until analyzed. All analyses were performed in duplicate except for hematocrit which was performed in triplicate.
Immediately following collection of the second resting sample the subjects transferred to the climatic chamber where they began exercising as soon as possible (within 30 s of entering the chamber). The subjects were asked to maintain a cadence of 60-70 rpm throughout the test and exhaustion was defined as the point at which the subjects could no longer continue or could no longer maintain a cadence above 60 rpm. No preset criteria for termination of exercise based on Tre or HR were required by the local ethics committee and no test was terminated before exhaustion. Subjects were not allowed to consume any fluid from two hours before or during exercise.
Blood samples (6.5 mL) were drawn during exercise at 15-min intervals and at exhaustion. The cannula was kept patent by a slow (approximately 0.5 mL·min-1) saline drip. Expired gas was collected into Douglas bags over a 2-min period every 15 min in the chamber and the bag immediately removed from the chamber and analyzed to determine oxygen consumption(˙VO2) and respiratory exchange ratio (R): these data were used to estimate rates of fuel oxidation. Ratings of perceived exertion (RPE) for both overall perception of exertion and for perceived exertion of the legs were obtained every 10 min throughout the test using the Borg category scale(7). Skin temperature, Tre, Ta, HR, and RH were recorded every 5 min throughout exercise and at exhaustion. Time to exhaustion was noted in all trials, and subjects were not informed either of elapsed time at any stage during each exercise trial or of the total exercise time at the end of the trial. Following exercise, subjects were weighed and weight loss, corrected for respiratory water loss and loss resulting from CO2-O2 exchange (22), was taken as representing sweat loss.
Data analysis. All data are presented as mean (SEM) or median(range) as appropriate following a Shapiro-Wilks test for normality of distribution. A two-way two-factor ANOVA for repeated measures was applied to determine any treatment differences during the exercise protocol. Following observation of a main effect, one way ANOVA or Kruskal-Wallis tests were performed to determine at which time points an effect was observed.Post-hoc analysis by paired t-tests or Wilcoxon tests was performed to determine which trials were significantly different. ANOVA or Kruskal-Wallis tests were applied as appropriate to determine any initial baseline differences in all variables. For examination of changes in serum electrolyte concentration, blood metabolite concentration and changes in plasma volume with time the second resting sample was used as the baseline. In all cases significance was taken at P < 0.05.
The ambient temperature was stable during all trials except for the coldest trial where a rise in temperature of approximately 2°C, from 2.4 ± 0.5°C at the beginning of the trial to 4.7 ± 0.8°C at the end, was recorded. The experimental trials are referred to as 4°C, 11°C, 21°C, and 31°C for clarity of presentation.
Time to exhaustion was significantly influenced by Ta (P = 0.001, Fig. 1) with exercise duration shortest at 31°C (51.6 ± 3.7 min) and longest at 11°C (93.5 ± 6.2 min). Time to exhaustion was similar (P = 0.98) on the trials at 4°C (81.4 ± 9.6 min) and 21°C (81.2 ± 5.7 min) but was significantly different between all other trials (P < 0.05). The range of times to exhaustion in the four experimental trials were 47.8-136.1 min at 4°C, 70.7-121.2 min at 11°C, 49.6-96.0 min at 21°C, and 39.2-65.0 min at 31°C. Significant affects of Ta were also observed on ˙VO2, ˙VE, R, estimated rates of fat and carbohydrate(CHO) oxidation, total CHO and fat oxidation, HR, Tre, [horizontal bar over]Tsk, sweat rate, and overall RPE.
Cardiorespiratory and fuel oxidation responses. There was a significant (P < 0.01) inverse relationship between oxygen consumption and Ta (Fig. 2). The largest mean difference in ˙VO2 between trials (0.80 L·min-1) was observed at the 75-min sample time between the 4°C and 21°C trials. Minute ventilation volume (˙VE, Table 1) was highest during the trial at 4°C and lowest during the trial at 21°C. The other two trials had similar ˙VE responses. Minute ventilation volume increased significantly over the exercise duration in the 4°C trial only.
Respiratory exchange ratio values (Table 1) fell significantly over the duration of exercise in all trials. R values were significantly higher during the trial at 4°C compared with the 11°C trial. Additionally, R values on the 11°C trial were significantly lower(P < 0.05) than those on the 21°C trial. Estimated rates of fat oxidation (Table 1) increased significantly over the duration of exercise in all trials. Fat oxidation rates were higher(P < 0.05) during the 11°C trial compared with those in the 4°C trial at the 30-min sample time. Additionally, at the 45-min sample during exercise at 31°C and at the 60-min sample during exercise at 21°C, the estimated fat oxidation rate was significantly lower than that at 11°C. Estimated rates of CHO oxidation (Table 1) fell over the duration of the test in all trials except for the 4°C trial where no change in the rate of CHO oxidation was observed. The CHO oxidation rate was higher (P < 0.05) during the 4°C trial compared with that of the 11, 21, and 31°C trials at the 30-min sample time and compared with the 11°C and 21°C trials at the 60- and 75-min sample times. No differences were observed in CHO oxidation rates at any other time between any of the other trials.
Total CHO oxidation was significantly (P < 0.01) lower in the 31°C trial (90 ± 6 g) compared with that in the 21°C (149± 11 g), 11°C (166 ± 19 g), and 4°C (168 ± 20 g) trials. A significant difference (P < 0.05) in total CHO oxidation was also observed between the 11°C and 21°C trials. Total fat oxidation in the trial at 11°C (66 ± 9 g) was significantly greater (P < 0.01) than that in the 21°C (43 ± 5 g) and 31°C (22 ± 4 g) trials. No difference in total fat oxidation was observed between the 4°C (51 ± 17 g) trial and any other trial. Total fat oxidation in the 21°C trial was significantly higher(P < 0.01) than that in the 31°C trial.
Heart rate was not different at rest between trials but was significantly higher (P < 0.05) during exercise at 31°C than during the other three trials (Fig. 3) with the differences being observed from the 35-min timepoint onwards and at exhaustion. No differences were observed in HR at any time between the 4, 11, and 21°C trials.
Thermoregulatory responses. No difference was observed in resting Tre before the trials. Rectal temperature was significantly(P < 0.01) influenced by Ta during exercise and values were highest in the 31°C trial and lowest in the 4°C trial(Fig. 4). Weighted mean skin temperature was also not different at rest between trials but was significantly (P < 0.01) influenced by Ta (Fig. 4) during exercise. Weighted mean skin temperature was significantly different (P < 0.01) between all trials at the first data collection point after entering the climatic chamber and remained different between trials at all subsequent sample points until exhaustion.
Mean sweat rate (Fig. 5) calculated on the assumption that it was linear throughout the test was significantly (P < 0.01) affected by the ambient temperature as expected. Sweat rate in the 31°C trial was more than double that observed at 4°C. All trials were significantly different from each other.
Serum electrolyte responses. There were no differences between the different Ta conditions in any of the measured serum electrolyte concentrations or in serum osmolality (Table 2) at rest or during exercise, and no differences were observed between the two resting samples in any of the conditions. Serum osmolality and serum K+ concentration changed significantly over time with values increasing above resting values (Rest2) at all sample times during exercise and at exhaustion in all trials. Serum Na+ concentration during exercise was not consistently increased above the resting value but was significantly higher at exhaustion than at rest in the 11, 21, and 31°C trials. Likewise, serum Cl- concentration was not consistently increased above the resting value during exercise, but was significantly higher at exhaustion than at rest in the 11 and 31°C trials.
Metabolic responses. The blood glucose concentration(Table 3) was not different between the two resting samples or between conditions at rest. Compared with the resting value (Rest2) the blood glucose concentration dropped significantly (P < 0.05) at the 15-min sample time in all trials. In the 4° trial, the blood glucose concentration remained below resting values throughout exercise and was still below resting concentrations at exhaustion. The blood lactate concentration (Table 3) was not different between resting samples and was not different between conditions at rest or during exercise but increased (P < 0.05) from rest at the 15-min sample time in all trials.
The serum FFA concentration (Fig. 6) was not significantly different between conditions at rest or between the two resting samples. After the onset of exercise the serum FFA concentration dropped significantly (P < 0.05) from the resting value over the first 15 min in all trials before increasing again. Blood glycerol concentration(Fig. 6) was also not different between trials at rest or between the two resting samples but the concentration increased after the onset of exercise and was significantly higher (P < 0.05) than the resting value by the 15-min sample time in all trials.
Plasma volume responses. The estimated change in plasma volume(Table 3) was not significantly different between trials at any time. A significant drop in plasma volume was observed in all trials between rest and the 15-min sample time. Plasma volume then remained constant following this initial drop, in the 11, 21, and 31°C trials, but in the 4°C trial there was a small temporary restoration in plasma volume at the 30- and 45-min sample times.
Subjective responses. Overall RPE (Fig. 7) increased with time in all trials and was significantly higher (P< 0.05) during the 31°C trial compared with all other trials at the 20-, 30-, and 40-min time points. A similar effect of temperature was not observed in the rating of exertion localized to the legs, and there were no differences between trials at any time. In the 31°C trial no differences were observed between local and overall perception of effort. However, in the 4° and 21°C trials the perception of local effort was significantly higher than the overall RPE at the 40- and 50-min time points.
The main observation to arise from the present study is the marked effect of ambient temperature on exercise capacity. The results indicate that the optimal temperature for prolonged cycle exercise at moderate intensity is around 11°C under the humidity and air velocity conditions of this study. Although the finding of reduced exercise capacity in the heat and in the cold is not a new concept, this study is one of the first to systematically investigate the effects of Ta on endurance capacity in the laboratory and to quantify the effects of different Ta conditions on exercise capacity at a constant power output in the same subject group.
Physiological responses to exercise in the heat. Exercise capacity was markedly reduced in the heat (31°C): during this trial˙VO2 was lower than that at 4°C and 11°C, and HR was higher compared with that in the other three trials. Increases in HR are invariably observed during exercise in the heat and are most likely a result of increases in skin blood flow and redistribution of central blood volume toward the periphery resulting in a reduction of stroke volume(30). The HR rises in an attempt to maintain cardiac output, but this will eventually decline if exercise persists(16,23) and will lead to circulatory collapse. During exercise at 31°C, Tre and [horizontal bar over]Tsk were significantly elevated relative to the other trials, indicating a larger stress on thermoregulation. Rectal temperature at exhaustion was 40.1(± 0.2)°C in the 31°C trial and, if Nielsen et al.(26) are correct in their suggestion that exercise in the heat is terminated when a critical core temperature is reached, exercise capacity in this trial may have been limited by hyperthermia. Weighted mean skin temperature was much closer to Tre during the trial at 31°C, reducing the temperature gradient between the core and the environment. The higher [horizontal bar over]Tsk in the heat would also reduce the temperature gradient between the skin and ambient air, thus decreasing nonevaporative heat loss. As a result we would expect a large increase in skin blood flow and a high rate of sweat production to promote evaporative heat loss. This was evident in the present study from the much larger calculated sweat rates during the 31°C trial. Despite the higher sweat rates in the heat in the present study, no differences were observed in serum osmolality, serum electrolyte concentrations, or changes in plasma volume between the different temperature conditions, suggesting that there was a similar loss of fluid from the vascular compartments in all trials.
Fortney et al. (14) suggested that peripheral pooling of blood was more important than a decrease in plasma volume in reducing central venous pressure. Therefore, at 31°C in the present study a reduced central venous pressure, secondary to a large peripheral pooling of blood combined with the large evaporative fluid loss, is likely to be the most important factor in limiting exercise capacity (32). It could also be argued that in the trial at 21°C smaller scale effects of a similar nature contributed to the reduction in exercise capacity relative to that at 11°C. In the 21°C trial, Tre, ˙Tsk, and sweat rate were all higher than in the two colder trials indicating a greater thermal stress, yet this stress was not large enough to result in any differences in HR between the 21°C trial and the two colder trials. In addition, the lower total CHO oxidation during the 21°C trial suggests that there may be a significant amount of glycogen still available to the working muscles at exhaustion relative to the trials at 4°C and 11°C.
Rowell et al. (30) observed that at the point of exhaustion during moderate intensity exercise in the heat there was an hepatic outpouring of glucose and a fall in hepatic venous O2 content together with hepatic lactate production, or at least a fall in hepatic lactate removal, suggesting the approach of hepatic ischemia. These observations demonstrated that the thermoregulatory system was stressed between the combined demands for skin blood flow, for the maintenance of cardiac output, and for working muscle blood supply. In the present study blood glucose and blood lactate concentrations appeared to be higher at exhaustion in the 31°C trial than in the other trials, but this may simply reflect the shorter exercise duration in the heat rather than hepatic or muscle ischemia. Although there is no direct evidence of a compromised blood flow to the working muscle mass in the present study, the pattern of change in serum FFA and blood glycerol, which indicates a marked blunting of lipolysis at or near exhaustion at 31°C, suggests a greater reliance on anaerobic energy production near the end of the 31°C trial and/or may reflect a reduced perfusion of adipose tissue near the end of the trial. These changes in metabolism may have contributed to the overall effect of heat on exercise capacity but are clearly secondary to the effects on thermoregulation and cardiovascular function.
Physiological responses to exercise in the cold. The higher˙VO2 observed at 4°C and 11°C above that observed in the trials at 21°C and 31°C is interesting because exercise capacity was similar at 4°C and 21°C, yet oxygen consumption was very different. This difference in oxygen consumption was not likely to be owing to temperature effects on the cycle ergometer as it was an electromagnetically braked bicycle and the physics of the braking system are not affected by temperature changes. The actual resistance was not measured in the present study, but the instrument has been warranted functional by the manufacturer within this temperature range. In addition, a study by Claremont et al.(10) previously observed a higher ˙VO2 response to exercise in the cold (0°C) compared with hot (35°C) conditions, in the absence of a fall in Tre, and this response did not result from an effect of temperature on the cycle ergometer resistance.
The effect of ambient temperature on the oxygen cost of exercise is variable and is influenced by many factors. Fink et al.(13) observed that ˙VO2 was higher when exercising in the heat (41°C) compared to a cold (9°C) environment, yet Beelen and Sargeant (3) observed that if muscle temperature was lowered, ˙VO2 was higher during high intensity exercise indicating a reduced mechanical efficiency. The reason for these different effects of temperature on the oxygen cost of exercise between studies is not clear but may be related to differences in the precise exposure temperature, exercise protocol, or exercise intensity. The effects of cold exposure on the respiratory system may help explain the inconsistent effects of cold exposure reported in the literature, as different ventilatory responses result from airway cooling, core cooling, and peripheral (skin) cooling when these occur alone or in combination (15). If core cooling occurs, ˙VE and ˙VO2 decrease until shivering thermogenesis occurs at which time increases in metabolism,˙VO2 and ˙VE will result in an attempt to maintain core temperature. When the exercise intensity is high enough to maintain core temperature, but skin cooling is still present, there are increases in˙VE and ˙VO2 which are thought to be a result primarily of stimulation of thermal receptors in the skin or increases in muscle tension and/or muscle metabolism (15). Sjödin et al.(34) using a water perfused suit, observed a 4% increase in energy expenditure during exercise at 42% of ˙VO2max when water temperature was lowered from 15 to 10°C. The maximum difference in Tsk between trials was 2.6°C and core temperature was elevated equally in both conditions. In the present study the difference in [horizontal bar over]Tsk was much greater (approximately 12°C) between the 4°C and 31°C trials. The difference in ˙Tsk between the 4°C and 11°C trials was even approximately 3°C. With the much larger difference in [horizontal bar over]Tsk, we might expect a greater effect on energy expenditure than that observed by Sjödin et al.(34).
The observation of significantly higher R, ˙VO2, ˙VE, and CHO oxidation during exercise at 4°C compared with that in the other trials appears to mimic the effects of core cooling and shivering thermogenesis, but this is unlikely to be the case as Tre was above 38.5°C in this trial and metabolic rate was high enough (around 60-75% of˙VO2max) to have prevented a shivering response. The effect on˙VO2 and ˙VE may be the result of the large reduction in skin temperature (12°C) and probably also an alteration in muscle temperature which may reduce mechanical efficiency and thus increase the total energy cost (3,15,28). These alterations would lead to an earlier onset of fatigue. Although muscle temperature was not recorded in this study, the changes in CHO oxidation are consistent with an alteration in either metabolism or mechanical efficiency.
No consistent effect of Ta on the estimated rate of fat oxidation was observed in the present study, but the oxidation rate was typically higher during the trial at 11°C than on any of the other trials. Total fat oxidation was also significantly greater in the 11°C trial than in the 21° and 31°C trials, which may provide an explanation for the increased oxygen cost of exercise at 11°C. Whether this increased utilization of fat resulted in a sparing of muscle glycogen at 11°C is not known. Despite the absence of any observable reduction in the estimated rate of CHO oxidation at 11°C, a sparing of muscle glycogen could explain the prolonged exercise capacity in the 11°C trial over the 4° and 21°C trials.
Many studies have shown decrements in performance during exercise in the heat at temperatures around 30-35°C dry bulb compared with a cooler(20-25°C) environment (8,20,25). The effects of a low ambient temperature on exercise capacity have been less well studied, and no studies have systematically evaluated the effects of ambient temperature on exercise capacity. In the present study exercise duration was longest at 11°C: below this temperature (at 4°C) and above this temperature (at 21° and 31°C), a reduction in exercise capacity was observed. The present results clearly indicate that when the ambient temperature is high (31°C), fatigue during exercise at this intensity is unlikely to be a result of a depletion of endogenous CHO stores. At 4°C, alterations in CHO oxidation and oxygen consumption indicate that mechanical efficiency may have been altered. The reason for a higher oxygen cost of exercise in this trial cannot be elucidated from the present results and requires further investigation. At 21°C there is a reduction in exercise capacity relative to the 11°C trial, and even in this neutral environment(21°C) there are detrimental effects on Tre and sweat rate consistent with a thermoregulatory stress. Further work needs to be performed to determine the mechanisms responsible for the differences in exercise capacity in this range of ambient temperatures.
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SUBSTRATE OXIDATION; THERMOREGULATION; HEAT STRESS; COLD STRESS
©1997The American College of Sports Medicine
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