Neurohumoral responses during prolonged exercise in humans.

This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous glucose difference plus one-half lactate), the cerebral balances of dopamine, and the metabolic precursor of serotonin, tryptophan, were evaluated in eight endurance-trained subjects during exercise randomized to be with or without hyperthermia. The core temperature stabilized at 37.9 +/- 0.1 degrees C (mean +/- SE) in the control trial, whereas it increased to 39.7 +/- 0.2 degrees C in the hyperthermic trial, with a concomitant increase in perceived exertion (P < 0.05). At rest, the brain had a small release of tryptophan (arteriovenous difference of -1.2 +/- 0.3 micromol/l), whereas a net balance was obtained during the two exercise trials. Both the arterial and jugular venous dopamine levels became elevated during the hyperthermic trial, but the net release from the brain was unchanged. During exercise, the O2/CHO was similar across trials, but, during recovery from the hyperthermic trial, the ratio decreased to 3.8 +/- 0.3 (P < 0.05), whereas it returned to the baseline level of approximately 6 within 5 min after the control trial. The lowering of O2/CHO was established by an increased arteriovenous glucose difference (1.1 +/- 0.1 mmol/l during recovery from hyperthermia vs. 0.7 +/- 0.1 mmol/l in control; P < 0.05). The present findings indicate that the brain has an increased need for carbohydrates during recovery from strenuous exercise, whereas enhanced perception of effort as observed during exercise with hyperthermia was not related to alterations in the cerebral balances of dopamine or tryptophan.     

Perceived exertion is associated with an altered brain activity during exercise with progressive hyperthermia.

The present study tested the hypothesis that perceived exertion during prolonged exercise in hot environments is associated with changes in cerebral electrical activity rather than changes in the electromyogram (EMG) of the exercising muscles. Therefore, electroencephalogram (EEG) in three positions (frontal, central, and occipital cortex), EMG, rating of perceived exertion (RPE), and core temperature were measured in 14 subjects during submaximal exercise in normal (18 degrees C, control) and hot (40 degrees C, hyperthermia) environments. RPE increased from 11 +/- 1 units at 5 min to 20 +/- 0 units at exhaustion (50 +/- 3 min) in the trial with progressive hyperthermia, whereas exercise in the control trial was maintained with a stable core temperature for 1 h without exhausting the subjects. Altered EEG activity was observed in all electrode positions, and stepwise forward-regression analysis identified core temperature and a frequency index of the EEG over the frontal cortex as the best predictors of RPE. In contrast, there were no significant correlations between RPE and any of the measured EMG parameters (median spectral frequency, root mean square, or amplitude), and the EMG parameters were not different in hyperthermia compared with control. Thus hyperthermia does not seem to affect the activation pattern of the muscles. Rather, the linear correlation among core temperature, EEG frequency index, and RPE indicates that alterations in cerebral activity may be associated with the hyperthermia-induced development of fatigue during prolonged exercise in hot environments.     

Hyperthermia and central fatigue during prolonged exercise in humans.

The present study investigated the effects of hyperthermia on the contributions of central and peripheral factors to the development of neuromuscular fatigue. Fourteen men exercised at 60% maximal oxygen consumption on a cycle ergometer in hot (40 degrees C; hyperthermia) and thermoneutral (18 degrees C; control) environments. In hyperthermia, the core temperature increased throughout the exercise period and reached a peak value of 40.0 +/- 0.1 degrees C (mean +/- SE) at exhaustion after 50 +/- 3 min of exercise. In control, core temperature stabilized at approximately 38.0 +/- 0.1 degrees C, and exercise was maintained for 1 h without exhausting the subjects. Immediately after the cycle trials, subjects performed 2 min of sustained maximal voluntary contraction (MVC) either with the exercised legs (knee extension) or with a "nonexercised" muscle group (handgrip). The degree of voluntary activation during sustained maximal knee extensions was assessed by superimposing electrical stimulation (EL) to nervus femoralis. Voluntary knee extensor force was similar during the first 5 s of contraction in hyperthermia and control. Thereafter, force declined in both trials, but the reduction in maximal voluntary force was more pronounced in the hyperthermic trial, and, from 30 to 120 s, the force was significantly lower in hyperthermia compared with control. Calculation of the voluntary activation percentage (MVC/MVC + EL) revealed that the degree of central activation was significantly lower in hyperthermia (54 +/- 7%) compared with control (82 +/- 6%). In contrast, total force of the knee extensors (MVC + force from EL) was not different in the two trials. Force development during handgrip contraction followed the same pattern of response as was observed for the knee extensors. In conclusion, these data demonstrate that the ability to generate force during a prolonged MVC is attenuated with hyperthermia, and the impaired performance is associated with a reduction in the voluntary activation percentage.     

Cerebral metabolism during upper and lower body exercise.

When continuation of exercise calls for a "will," the cerebral metabolic ratio of O2 to (glucose + lactate) decreases, with the largest reduction (30-50%) at exhaustion. Because a larger effort is required to exercise with the arms than with the legs, we tested the hypothesis that the reduction in the cerebral metabolic ratio would become more pronounced during arm cranking than during leg exercise. The cerebral arterial-venous differences for blood-gas variables, glucose, and lactate were evaluated in two groups of eight subjects during exhaustive arm cranking and leg exercise. During leg exercise, exhaustion was elicited after 25 +/- 6 (SE) min, and the cerebral metabolic ratio was reduced from 5.6 +/- 0.2 to 3.5 +/- 0.2 after 10 min and to 3.3 +/- 0.3 at exhaustion (P < 0.05). Arm cranking lasted for 35 +/- 4 min and likewise decreased the cerebral metabolic ratio after 10 min (from 6.7 +/- 0.4 to 5.0 +/- 0.3), but the nadir at exhaustion was only 4.7 +/- 0.4, i.e., higher than during leg exercise (P < 0.05). The results demonstrate that exercise decreases the cerebral metabolic ratio when a conscious effort is required, irrespective of the muscle groups engaged. However, the comparatively small reduction in the cerebral metabolic ratio during arm cranking suggests that it is influenced by the exercise paradigm.     

THE EFFECT OF HYPERTHERMIA UPON OXYGEN CONSUMPTION AND UPON ORGANIC PHOSPHATES, GLYCOLYTIC METABOLITES, CITRIC ACID CYCLE INTERMEDIATES AND ASSOCIATED AMINO ACIDS IN RAT CEREBRAL CORTEX

The influence of hyperthermia on cerebral blood flow, cerebral metabolic rate for oxygen and cerebral metabolite levels was studied by increasing body temperature from 37° to 40°C and 42°C in rats under nitrous oxide anaesthesia maintained at constant arterial CO₂ tension. The metabolic rate for oxygen increased by 5-6% per degree centigrade. At 42°C the increase in cerebral blood Row was comparable to that in the metabolic rate. The increased temperatures were not accompanied by changes in organic phosphates (phosphocreatine, ATP, ADP or AMP) or in lactate/pyruvate ratio. There was an increase in the tissue to blood glucose concentration ratio. At steady state, there was an increase in glucose-6-phosphate but no other changes in glycolytic metabolites or citric acid cycle intermediates, and the only change in amino acids studied (glutamate, glutamine, aspartate, alanine and GABA) was an increase in glutamate concentration.     

Cerebral carbohydrate cost of physical exertion in humans

Above a certain level of cerebral activation the brain increases its uptake of glucose more than that of O(2), i.e., the cerebral metabolic ratio of O(2)/(glucose + 12 lactate) decreases. This study quantified such surplus brain uptake of carbohydrate relative to O(2) in eight healthy males who performed exhaustive exercise. The arterial-venous differences over the brain for O(2), glucose, and lactate were integrated to calculate the surplus cerebral uptake of glucose equivalents. To evaluate whether the amount of glucose equivalents depends on the time to exhaustion, exercise was also performed with beta(1)-adrenergic blockade by metoprolol. Exhaustive exercise (24.8 +/- 6.1 min; mean +/- SE) decreased the cerebral metabolic ratio from a resting value of 5.6 +/- 0.2 to 3.0 +/- 0.4 (P < 0.05) and led to a surplus uptake of glucose equivalents of 9 +/- 2 mmol. beta(1)-blockade reduced the time to exhaustion (15.8 +/- 1.7 min; P < 0.05), whereas the cerebral metabolic ratio decreased to an equally low level (3.2 +/- 0.3) and the surplus uptake of glucose equivalents was not significantly different (7 +/- 1 mmol; P = 0.08). A time-dependent cerebral surplus uptake of carbohydrate was not substantiated and, consequently, exhaustive exercise involves a brain surplus carbohydrate uptake of a magnitude comparable with its glycogen content.     

Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise.

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.     

Heat induced fatigue and changes of the EEG is not related to reduced perfusion of the brain during prolonged exercise in humans

(1) Exercise-induced hyperthermia is associated with a gradual slowing of the electroencephalogram (EEG), an increase in perceived exertion (RPE) and a lowering of the cerebral perfusion.

(2) During exercise EEG changes were linearly correlated to core temperature (r²=0.67; P<0.05) and RPE (r² =0.54, P<0.05), but manipulation of cerebral perfusion by voluntary breathing efforts and by CO₂ inhalation did not alter RPE or EEG.

(3) In conclusion EEG changes with hyperthermic exercise are not a simple effect of the reduced cerebral perfusion but may relate to the fatigue that arises concomitantly with the increases in core and brain temperatures.     

Effects of PDH activation by dichloroacetate in human skeletal muscle during exercise in hypoxia

During the onset of exercise in hypoxia, the increased lactate accumulation is associated with a delayed activation of pyruvate dehydrogenase (PDH; Parolin ML, Spreit LL, Hultman E, Hollidge-Horvat MG, Jones NL, and Heigenhauser GJF. Am J Physiol Endocrinol Metab 278: E522-E534, 2000). The present study investigated whether activation of PDH with dichloroacetate (DCA) before exercise would reduce lactate accumulation during exercise in acute hypoxia by increasing oxidative phosphorylation. Six subjects cycled on two occasions for 15 min at 55% of their normoxic maximal oxygen uptake after a saline (control) or DCA infusion while breathing 11% O(2). Muscle biopsies of the vastus lateralis were taken at rest and after 1 and 15 min of exercise. DCA increased PDH activity at rest and at 1 min of exercise, resulting in increased acetyl-CoA concentration and acetylcarnitine concentration at rest and at 1 min. In the first minute of exercise, there was a trend toward a lower phosphocreatine (PCr) breakdown with DCA compared with control. Glycogenolysis was lower with DCA, resulting in reduced lactate concentration ([lactate]), despite similar phosphorylase a mole fractions and posttransformational regulators. During the subsequent 14 min of exercise, PDH activity was similar, whereas PCr breakdown and muscle [lactate] were reduced with DCA. Glycogenolysis was lower with DCA, despite similar mole fractions of phosphorylase a, and was due to reduced posttransformational regulators. The results from the present study support the hypothesis that lactate production is due in part to metabolic inertia and cannot solely be explained by an oxygen limitation, even under conditions of acute hypoxia.     

Effect of lowered muscle temperature on the physiological response to exercise in men

The effect of low muscle temperature on the response to dynamic exercise was studied in six healthy men who performed 42 min of exercise on a cycle ergometer at an intensity of 70% of their maximal O2 uptake. Experiments were performed under control conditions, i.e. from rest at room temperature, and following 45 min standing with legs immersed in a water bath at 12 degrees C. The water bath reduced quadriceps muscle temperature (at 3 cm depth) from 36.4 (SD 0.5) degrees C to 30.5 (SD 1.7) degrees C. Following cooling, exercise heart rate was initially lower, the mean difference ranged from 13 (SD 4) beats.min-1 after 6 min of exercise, to 4 (SD 2) beats.min-1 after 24 min of exercise. Steady-state oxygen uptake was consistently higher (0.2 l.min-1). However, no difference could be discerned in the kinetics of oxygen uptake at the onset of exercise. During exercise after cooling a significantly higher peak value was found for the blood lactate concentration compared to that under control conditions. The peak values were both reached after approximately 9 min of exercise. After 42 min of exercise the blood lactate concentrations did not differ significantly, indicating a faster rate of removal during exercise after cooling. We interpreted these observations as reflecting a relatively higher level of muscle hypoxia at the onset of exercise as a consequence of a cold-induced vasoconstriction. The elevated steady-state oxygen uptake may in part have been accounted for by the energetic costs of removal of the extra lactate released into the blood consequent upon initial tissue hypoxia.     

Acute plasma volume expansion: effect on metabolism during submaximal exercise.

To examine the effect of acute plasma volume expansion (PVE) on substrate selection during exercise, seven untrained men cycled for 40 min at 72 +/- 2% peak oxygen uptake (VO(2 peak)) on two occasions. On one occasion, subjects had their plasma volume expanded by 12 +/- 2% via an intravenous infusion of the plasma substitute Haemaccel, whereas on the other occasion no such infusion took place. Muscle samples were obtained before and immediately after exercise. In addition, heart rate and pulmonary gas and venous blood samples were obtained throughout exercise. No differences in oxygen uptake or heart rate during exercise were observed between trials, whereas respiratory exchange ratio, blood glucose, and lactate were unaffected by PVE. Muscle glycogen and lactate concentrations were not different either before or after exercise. In addition, there was no difference in total carbohydrate oxidation between trials (control: 108 +/- 2 g; PVE group: 105 +/- 2 g). Plasma catecholamine levels were not affected by PVE. These data indicate that substrate metabolism during submaximal exercise in untrained men is unaltered by acute hypervolemia.     

Exercise performance of normothermic and hyperthermic rats: Effect of warm rearing

1. 1.|Hypothalamic and rectal temperatures were recorded in 8 warm-reared (wr) and 12 control rats. Rats ran to exhaustion at a constant speed of 1.5 km h⁻¹ but at a variable ambient temperature adjusted to stabilize their hypothalamic temperature at 38.0°C (normothermia) or 41.0°C (hyperthermia). Blood lactate concentrations were determined before and after exercise.

2. 2.|Exercise caused exhaustion in normothermic control rats after 62.08 ± 5.43 min and in wr rats after 29.64 ± 2.09 min.

3. 3.|Hyperthermia shortened to one half (to 12.24 ± 1.36 min) and to one fourth (to 16.15 ± 1.20 min) the endurance time in wr and control rats, respectively.

4. 4.|There were no correlations between lactate concentraion and hyperthermia or endurance time.

5. 5.|In conclusion, in rats and other animals which have safe refuges, hyperthermia interferes with the ability to continue exercising.

Exhaustive exercise does not affect the preferred temperature for recovery in juvenile rainbow trout (Oncorhynchus mykiss)

We tested the hypothesis that juvenile rainbow trout (Oncorhynchus mykiss) would select a temperature colder than their acclimation temperature (16 deg +/-1 deg C) to minimize postexhaustive exercise metabolic demands and enhance oxygen availability. After an initial 3-h exploratory period in a thermal gradient (6 degrees -25 degrees C), fish selected a temperature of approximately 14 degrees C and had a baseline exploratory swimming activity of approximately 60 cm min(-1). Subsequently, experimental (chased) fish were individually removed, exhaustively exercised for 1.5 min, and replaced. Both control (unchased) and experimental fish were allowed to explore the thermal gradient for another 2 h. Immediately after being chased, trout had a metabolic profile that was consistent with being exhausted; levels of plasma and muscle lactate were 4.38+/-0.25 mmol L(-1) and 28.0+/-2.0 mmol kg(-1), respectively, and levels of muscle glycogen, adenosine triphosphate, and phosphocreatine were 3.89+/-0.95, 4.23+/-0.62, and 3.07+/-0.73 mmol kg(-1), respectively. Although exploratory swimming activity of the chased fish was significantly lower (by 81%) as compared with control fish during the first 5 min postchase, differences in the mean, median, and mode values for selected temperatures during the next 2 h were neither large (<1 degrees C) nor significant (P>0.05). Contrary to our initial hypothesis, these findings suggest that juvenile rainbow trout do not select a colder temperature to decrease metabolic rate following exhaustive exercise. Instead, rainbow trout selected a temperature marginally cooler than their acclimation temperature (16 degrees C) regardless of whether they had been previously exhausted.     

Leg and arm lactate and substrate kinetics during exercise

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal O(2) uptake. A high lactate appearance rate (R(a), 184 +/- 17 micromol x kg(-1) x min(-1)) but a low arterial lactate concentration ( approximately 2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of approximately 2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was approximately 45% at rest and approximately 95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate R(a) during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.     

Effect of carbohydrate ingestion on glucose kinetics and muscle metabolism during intense endurance exercise.

There has been recent interest in the potential performance and metabolic effects of carbohydrate ingestion during exercise lasting approximately 1 h. In this study, 13 well-trained men ingested in randomized order either a 6% glucose solution (CHO trial) or a placebo (Con trial) during exercise to exhaustion at 83+/-1% peak oxygen uptake. In six subjects, vastus lateralis muscle was sampled at rest, at 32 min, and at exhaustion, and in six subjects, glucose kinetics was determined by infusion of [6,6-(2)H]glucose in both trials and ingestion of [6-(3)H]glucose in the CHO trial. Of the 84 g of glucose ingested during exercise in the CHO trial, only 22 g appeared in the peripheral circulation. This resulted in a small (12 g) but significant (P<0.05) increase in glucose uptake without influencing carbohydrate oxidation, muscle glycogen use, or time to exhaustion (CHO: 68.1+/-4.1 min; Con: 69.6+/-5.5 min). Decreases in muscle phosphocreatine content and increases in muscle inosine monophosphate and lactate content during exercise were similar in the two trials. Although endogenous glucose production during exercise was partially suppressed in the CHO trial, it remained significantly above preexercise levels throughout exercise. In conclusion, only 26% of the ingested glucose appeared in the peripheral circulation. Glucose ingestion increased glucose uptake and partially reduced endogenous glucose production but had no effect on carbohydrate oxidation, muscle metabolism, or time to exhaustion during exercise at 83% peak oxygen uptake.     

Cytoprotection of vitamin E on hyperthermia-induced damage in bovine mammary epithelial cells

The protective effects of vitamin E (VE) against hyperthermia-induced damage in bovine mammary epithelial cells (BMEC) were studied. The structure of BMEC membrane was damaged by hyperthermia treatment. The VE (25 nmol/ml) efficiently increased cell viability and attenuated morphological damages in hyperthermia-treated BMEC. Compared with the control, VE significantly reduced lactate dehydrogenase leakage and malondialdehyde formation in hyperthermia-treated BMEC. Meanwhile, superoxide dismutase activity was increased significantly in the presence of VE. It is inferred that VE displayed cytoprotective effects on hyperthermia-induced damage in BMEC through increasing intracellular antioxidant levels and decreasing lipid peroxidation.     

Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise.

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20-22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.     

Effect of saline infusion on body temperature and endurance during heavy exercise

We tested the hypothesis that volume infusion during strenuous exercise, by expanding blood volume, would allow better skin blood flow and better temperature homeostasis and thereby improve endurance time. Nine males exercised to exhaustion at 84.0 +/- 3.14% (SE) of maximum O2 consumption on a cycle ergometer in a double-blind randomized protocol with either no infusion (control) or an infusion of 0.9% NaCl (mean vol 1,280.3 +/- 107.3 ml). Blood samples and expired gases (breath-by-breath), as well as core and skin temperatures, were analyzed. Plasma volume decreased less during exercise with the infusion at 15 min (-13.7 +/- 1.4% control vs. -5.3 +/- 1.7% infusion, P less than 0.05) and at exhaustion (-13.6 +/- 1.2% vs. -1.3 +/- 2.2%, P less than 0.01). The improved fluid homeostasis was associated with a lower core temperature during exercise (39.0 +/- 0.2 degrees C for control and 38.5 +/- 0.2 degrees C for infusion at exhaustion, P less than 0.01) and lower heart rate (194.1 +/- 3.9 beats/min for control and 186.0 +/- 5.1 beats/min for infusion at exhaustion, P less than 0.05). However, endurance time did not differ between control and infusion (21.96 +/- 3.56 and 20.82 +/- 2.63 min, respectively), and neither did [H+], peak O2 uptake, and CO2 production, end-tidal partial pressure of CO2, blood lactate, or blood pressure. In conclusion, saline infusion increases heat dissipation and lowers core temperature during strenuous exercise but does not influence endurance time.     

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (T(es)). Initial T(es) was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). T(es) after the water immersion was significantly higher in the Preheating trial (37.5 ± 0.3°C) and lower in the Precooling trial (36.1 ± 0.3°C) than in the Control trial (36.9 ± 0.3°C). In the Precooling trial, minute ventilation (Ve) showed little change until T(es) reached 37.1 ± 0.4°C. Above this core temperature threshold, Ve increased linearly in proportion to increasing T(es). In the Control trial, Ve increased as T(es) increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, Ve increased from the initially elevated levels of T(es) (from 37.6 to 38.6°C) and Ve. The sensitivity of Ve to increasing T(es) above the threshold for hyperventilation (the slope of the T(es)-Ve relation) did not significantly vary across trials (Precooling trial = 10.6 ± 5.9, Control trial = 8.7 ± 5.1, and Preheating trial = 9.2 ± 6.9 L·min(-1)·°C(-1)). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.     

Effects of 4- and 8-h preexercise feedings on substrate use and performance

Seven well-trained male cyclists were studied during 105 min of cycling (65% of maximal oxygen uptake) and a 15-min "performance ride" to compare the effects of 4- and 8-h preexercise carbohydrate (CHO) feedings on substrate use and performance. A high CHO meal was given 1) 4-h preexercise (M-4), 2) 8-h preexercise (M-8), 3) 4-h preexercise with CHO feedings during exercise (M-4CHO), and 4) 8-h preexercise with CHO feedings during exercise (M-8CHO). Blood samples were obtained at 0, 15, 60, 105, and 120 min and analyzed for lactate, glucose, insulin, and glycerol. Total work output during the performance ride was similar for the M-4 (217,893 +/- 13,348 N/m) and M-8 trials (216,542 +/- 13,905) and was somewhat higher for the M-4CHO (223,994 +/- 14,387) and M-8CHO (224,702 +/- 15,709) trials (P = 0.059, NS). Glucose was significantly elevated throughout exercise, and insulin levels were significantly elevated at 15 and 60 min during M-4CHO and M-8CHO compared with M-4 and M-8 trials. Glycerol levels were significantly lower during the CHO feeding trials compared with placebo and were not significantly different during exercise when the subject had fasted an additional 4 h. The results of this study suggest that when preexercise meals are ingested 4 or 8 h before submaximal cycling exercise, substrate use and performance are similar.