Effect of beta-adrenoceptor blockade on thermoregulation during prolonged exercise

The effect of clinically used equipotent doses of nonselective (beta 1/beta 2; propranolol) and selective (beta 1; atenolol) beta-adrenoceptor blockers on thermoregulation was studied during prolonged exercise in the heat. Oral propranolol (160 mg/day), atenolol (100 mg/day) or matching placebo were taken for 6 days each by 11 healthy young adult caucasian males. Subjects participated in 2 h of block-stepping at a work rate of 54 W in an environmental chamber with a temperature of 33.2 +/- 0.3 degree C dry bulb and 31.7 /+- 0.3 degree C wet bulb, 2 h after ingestion of the final dose of each drug. Both active agents produced similar marked (P less than 0.001) increases in subjective perception of effort, the mechanism of which was not immediately evident from changes in serum electrolytes, blood glucose, blood lactate, or ventilatory parameters. Propranolol did, however, cause a greater rise in serum K+ than placebo (P less than 0.02) and atenolol (P = NS) after exercise. Although rectal and mean skin temperatures were insignificantly altered by beta-adrenoceptor blockade, an increased total sweat production was noted with propranolol (P less than 0.01 vs. placebo) and to a lesser degree atenolol (P = NS vs. placebo) therapy. Analysis of the time course of sweat production showed the propranolol-mediated enhancement of sweating to ensue largely during the initial hour of block-stepping and to be transient in nature. The scientific and clinical implications of this observation will be dependent upon the precise underlying mechanism, a factor not identified by the present study.     

Exercise endurance 1, 3, and 6 h after caffeine ingestion in caffeine users and nonusers.

The purpose of the present study was to examine the duration of caffeine's ergogenic effect and whether it differs between users and nonusers of the drug. Twenty-one subjects (13 caffeine users and 8 nonusers) completed six randomized exercise rides to exhaustion at 80% of maximal oxygen consumption after ingesting either a placebo or 5 mg/kg of caffeine. Exercise to exhaustion was completed once per week at either 1, 3, or 6 h after placebo or drug ingestion. Exercise time to exhaustion differed between users and nonusers with the ergogenic effect being greater and lasting longer in nonusers. For the nonusers, exercise times 1, 3, and 6 h after caffeine ingestion were 32.7 +/- 8.4, 32.1 +/- 8.6, and 31.7 +/- 12.0 min, respectively, and these values were each significantly greater than the corresponding placebo values of 24.2 +/- 6.4, 25.8 +/- 9.0, and 23.2 +/- 7.1 min. For caffeine users, exercise times 1, 3, and 6 h after caffeine ingestion were 27.4 +/- 7.2, 28.1 +/- 7.8, and 24.5 +/- 7.6 min, respectively. Only exercise times 1 and 3 h after drug ingestion were significantly greater than the respective placebo trials of 23.3 +/- 6.5, 23.2 +/- 7.1, and 23.5 +/- 5.7 min. In conclusion, both the duration and magnitude of the ergogenic effect that followed a 5 mg/kg dose of caffeine were greater in the nonusers compared with the users.     

Water and carbohydrate ingestion during prolonged exercise increase maximal neuromuscular power.

This study investigated the individual and combined effects of water and carbohydrate ingestion during prolonged cycling on maximal neuromuscular power (P(max)), thermoregulation, cardiovascular function, and metabolism. Eight endurance-trained cyclists exercised for 122 min at 62% maximal oxygen uptake in a 35 degrees C environment (50% relative humidity, 2 m/s fan speed). P(max) was measured in triplicate during 6-min periods beginning at 26, 56, 86, and 116 min. On four different occasions, immediately before and during exercise, subjects ingested 1) 3.28 +/- 0.21 liters of water with no carbohydrate (W); 2) 3.39 +/- 0.23 liters of a solution containing 204 +/- 14 g of carbohydrate (W+C); 3) 204 +/- 14 g of carbohydrate in only 0.49 +/- 0.03 liter of solution (C); and 4) 0. 37 +/- 0.02 liter of water with no carbohydrate (placebo; Pl). These treatments were randomized, disguised, and presented double blind. At 26 min of exercise, P(max) was similar in all trials. From 26 to 116 min, P(max) declined 15.2 +/- 3.3 and 14.5 +/- 2.1% during C and Pl, respectively; 10.4 +/- 1.9% during W (W > C, W > Pl; P < 0.05); and 7.4 +/- 2.2% during W+C (W+C > W, W+C > C, and W+C > Pl; P < 0. 05). As an interesting secondary findings, we also observed that carbohydrate ingestion increased heat production, final core temperature, and whole body sweating rate. We conclude that, during prolonged moderate-intensity exercise in a warm environment, ingestion of W attenuates the decline in P(max). Furthermore, ingestion of W+C attenuates the decline in maximal power more than does W alone, and ingestion of C alone does not attenuate the decline in P(max) compared with Pl.     

Predictors of sweat loss in man during prolonged exercise

Nineteen healthy male subjects, differing in training status and Vo2max (52 +/- 1 ml.min-1.kg-1, mean +/- SEM; 43-64 ml.min-1.kg-1, range), exercised for 1 h at an absolute workload of 192 +/- 8 W (140-265 W); this was equivalent to 70 +/- 1% Vo2max (66-74%). Each exercise test was performed on an electrically braked cycle ergometer at a constant ambient temperature (22.5 +/- 0.0 degrees C) and relative humidity (85 +/- 0%). Nude body weight was recorded prior to and after each exercise test. Absolute sweat loss (body weight loss corrected for respiratory weight loss) during each test was 910 +/- 82 g (426-1665 g); this was equivalent to 1.3 +/- 0.1% (0.7-2.2%) of pre-exercise body weight (relative sweat loss). Weighted mean skin temperature and rectal temperature increased after 5 min of exercise from 30.5 +/- 0.3 degrees C and 37.2 +/- 0.1 degrees C respectively to 32.5 +/- 0.2 degrees C and 38.8 +/- 0.1 degrees C respectively, recorded immediately prior to the end of exercise. Bivariate linear regression and Pearson's correlation demonstrated absolute sweat loss was related to Vo2max (r = 0.72, p less than 0.001), absolute exercise workload (r = 0.66, p less than 0.01), body surface area (r = 0.62, p less than 0.01), weight (r = 0.60, p less than 0.01) and height (r = 0.53, p less than 0.05). Relative sweat loss was related to VO2max (r = 0.77, P less than 0.001) and absolute exercise workload (R = 0.59, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of cold, exercise, and caffeine on catecholamines and metabolism in men

Recently we found that caffeine ingestion did not enhance either thermal or fat metabolic responses to resting in cold air, despite an increase in plasma epinephrine and free fatty acids. Theophylline, another methylxanthine, has been shown to be effective during exercise but not at rest during cold stress. Therefore we hypothesized that caffeine ingestion before exercise in cold air would have a thermal-metabolic impact by increasing fat metabolism and increasing oxygen consumption. Young adult men (n = 6) who did not normally have caffeine in their diet performed four double-blind trials. Thirty minutes after ingesting placebo (dextrose, 5 mg/kg) or caffeine (5 mg/kg) they either exercised (60 W) or rested for 2 h in 5 degrees C air. Cold increased (P less than 0.05) plasma norepinephrine while both caffeine and exercise increased (P less than 0.05) epinephrine. Serum free fatty acids and glycerol were increased, but there were no differences between rest and exercise or placebo and caffeine. Caffeine had no influence on either respiratory exchange ratio or oxygen consumption either at rest or during exercise. The exercise trials did not significantly warm the body, and they resulted in higher plasma norepinephrine concentrations and lower mean skin temperatures for the first 30 min. The data suggest that skin temperature stimulates plasma norepinephrine while caffeine has little effect. In contrast, caffeine and exercise stimulate plasma epinephrine while cold has minimal effect. Within the limits of this study caffeine gave no thermal or metabolic advantage during a cold stress.     

Equine sweating responses to submaximal exercise during 21 days of heat acclimation.

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32-34 degrees C, 80-85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6 degrees incline) at a speed eliciting 50% of maximal O(2) uptake until a pulmonary artery temperature of 41.5 degrees C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na(+), K(+), and Cl(-)) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5 degrees C (range 19.09 +/- 1.41 min on day 0 to 20.92 +/- 1.98 min on day 3). Peak SR during exercise (ml. m(-2). min(-1)) increased on day 7 (57.5 +/- 5. 0) but was not different on day 21 (48.0 +/- 4.7) compared with day 0 (52.0 +/- 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na(+) concentration for a given SR during exercise and recovery; this contributed to an approximately 26% decrease in calculated total sweat ion losses (3,112 +/- 114 mmol on day 0 vs. 2,295 +/- 107 mmol on day 21). By day 21, there was a decrease in sweating threshold ( approximately 1 degrees C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na(+) concentration and SR during recovery.     

Comparison of the effects of pre-exercise feeding of glucose, glycerol and placebo on endurance and fuel homeostasis in man

Six men were studied during exercise to exhaustion on a cycle ergometer at 73% of VO2max following ingestion of glycerol, glucose or placebo. Five of the subjects exercised for longer on the glucose trial compared to the placebo trial (p less than 0.1; 108.8 vs 95.9 min). Exercise time to exhaustion on the glucose trial was longer (p less than 0.01) than on the glycerol trial (86.0 min). No difference in performance was found between the glycerol and placebo trials. The ingestion of glucose (lg X kg-1 body weight) 45 min before exercise produced a 50% rise in blood glucose and a 3-fold rise in plasma insulin at zero min of exercise. Total carbohydrate oxidation was increased by 26% compared to placebo and none of the subjects exhibited a fall in blood glucose below 4 mmol X 1-1 during the exercise. The ingestion of glycerol (lg X kg-1 body weight) 45 min before exercise produced a 340-fold increase in blood glycerol concentration at zero min of exercise, but did not affect resting blood glucose or plasma insulin levels; blood glucose levels were up to 14% higher (p less than 0.05) in the later stages of exercise and at exhaustion compared to the placebo or glucose trials. Both glycerol and glucose feedings lowered the magnitude of the rise in plasma FFA during exercise compared to placebo. Levels of blood lactate and alanine during exercise were not different on the 3 dietary treatments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pre-exercise hyperhydration delays dehydration and improves endurance capacity during 2 h of cycling in a temperate climate

Whether the use of pre-exercise hyperhydration could improve the performance of athletes who do not hydrate sufficiently during prolonged exercise is still unknown. We therefore compared the effects of pre-exercise hyperhydration and pre-exercise euhydration on endurance capacity, peak power output and selected components of the cardiovascular and thermoregulatory systems during prolonged cycling. Using a randomized, crossover experimental design, 6 endurance-trained subjects underwent a pre-exercise hyperhydration (26 ml of water x kg body mass(-1) with 1.2 g glycerol x kg body mass(-1)) or pre-exercise euhydration period of 80 min, followed by 2 h of cycling at 65% maximal oxygen consumption (VO(.)2max) (26-27 degrees C) that were interspersed by 5, 2-min intervals performed at 80% V(.)O2max. Following the 2 h cycling exercise, subjects underwent an incremental cycling test to exhaustion. Pre-exercise hyperhydration increased body water by 16.1+/-2.2 ml.kg body mass(-1). During exercise, subjects received 12.5 ml of sports drink x kg body mass(-1). With pre-exercise hyperhydration and pre-exercise euhydration, respectively, fluid ingestion during exercise replaced 31.0+/-2.9% and 37.1+/-6.8% of sweat losses (p>0.05). Body mass loss at the end of exercise reached 1.7+/-0.3% with pre-exercise hyperhydration and 3.3+/-0.4% with pre-exercise euhydration (p<0.05). During the 2 h of cycling, pre-exercise hyperhydration significantly decreased heart rate and perceived thirst, but rectal temperature, sweat rate, perceived exertion and perceived heat-stress did not differ between conditions. Pre-exercise hyperhydration significantly increased time to exhaustion and peak power output, compared with pre-exercise euhydration. We conclude that pre-exercise hyperhydration improves endurance capacity and peak power output and decreases heart rate and thirst sensation, but does not reduce rectal temperature during 2 h of moderate to intense cycling in a moderate environment when fluid consumption is 33% of sweat losses.     

Sweat ammonia excretion during submaximal cycling exercise

This study was undertaken to investigate whether part of the ammonia formed during muscular exercise was excreted with the sweat. Male medical students volunteered for the experiment. They exercised 30 min on a bicycle ergometer at 80 and 40% of the predetermined maximal O2 uptake (VO2max). Exercise at 80% VO2max was performed twice, at room temperature (20 degrees C) and in a cold room (0 degrees C), whereas exercise at 40% was performed only at room temperature (20 degrees C). Blood was collected from the antecubital vein immediately before and after exercise. Sweat was collected from the hypogastric region by use of gauze pads. It was shown that the plasma ammonia level was elevated after exercise at 80% VO2max and remained stable after exercise at 40% VO2max. The volume of sweat produced during exercise at 80% VO2max at 20 degrees C was 428 +/- 138 ml and at 0 degrees C 245 +/- 86 ml and during exercise at 40% VO2max was 183 +/- 69 ml. The ammonia concentration in the sweat after exercise at 80% VO2max at 20 degrees C was 7,140 mumol/l and at 0 degrees C 11,816 mumol/l. After exercise at 40% VO2max, it was 2,076 mumol/l. The total ammonia lost through the sweat during exercise at 80% VO2max was similar at both temperatures, despite the difference in the sweat volume (at 20 degrees C, 3,360 +/- 2,080 mumol; at 0 degrees C, 3,310 +/- 1,250 mumol). During exercise at 40% VO2max, it was 350 +/- 230 mumol. These results show that part of ammonia formed during exercise is lost with sweat. The amount lost increases with increased work rate and the plasma ammonia concentration.     

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.     

Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (Tes) = 35.9 +/- 0.2, 37.4 +/- 0. 1, or 38.2 +/- 0.1 (SE) degrees C induced by 30 min of water immersion], seven cyclists (maximal O2 uptake = 5.1 +/- 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O2 uptake) in the heat (40 degrees C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05 degrees C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with Tes of 37.0 degrees C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (Tes = 40. 1-40.2 degrees C, muscle temperature = 40.7-40.9 degrees C, skin temperature = 37.0-37.2 degrees C) and cardiovascular strain (heart rate = 196-198 beats/min, cardiac output = 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 +/- 3, 46 +/- 3, and 28 +/- 2 min with initial Tes of approximately 36, 37, and 38 degrees C, respectively (all P < 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar Tes and muscle temperature (40.1-40.3 and 40. 7-40.9 degrees C, respectively), but with significantly different skin temperature (38.4 +/- 0.4 vs. 35.6 +/- 0.2 degrees C during high vs. low rate of heat storage, respectively, P < 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 +/- 4 vs. 56 +/- 11 min, respectively, P < 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40 degrees C), with skin blood flow plateauing at Tes of approximately 38 degrees C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage.     

Possible biphasic sweating response during short-term heat acclimation protocol for tropical natives

The aim of the present study was to evaluate the sweat loss response during short-term heat acclimation in tropical natives. Six healthy young male subjects, inhabitants of a tropical region, were heat acclimated by means of nine days of one-hour heat-exercise treatments (40+/-0 degrees C and 32+/-1% relative humidity; 50% (.)VO(2peak) on a cycle ergometer). On days 1 to 9 of heat acclimation whole-body sweat loss was calculated by body weight variation corrected for body surface area. On days 1 and 9 rectal temperature (T(re)) and heart rate (HR) were measured continuously, and rating of perceived exertion (RPE) every 4 minutes. Heat acclimation was confirmed by reduced HR (day 1 rest: 77+/-5 b.min(-1); day 9 rest: 68+/-3 b.min(-1); day 1 final exercise: 161+/-15 b.min(-1); day 9 final exercise: 145+/-11 b.min(-1), p<0.05), RPE (13 vs. 11, p<0.05) and T(re) (day 1 rest: 37.2+/-0.2 degrees C; day 9 rest: 37.0+/-0.2 degrees C; day 1 final exercise: 38.2+/-0.2 degrees C; day 9 final exercise: 37.9+/-0.1 degrees C, p<0.05). The main finding was that whole-body sweat loss increased in days 5 and 7 (9.49+/-1.84 and 9.56+/-1.86 g.m(-2).min(-1), respectively) compared to day 1 (8.31+/-1.31 g.m(-2).min(-1), p<0.05) and was not different in day 9 (8.48+/-1.02 g.m(-2).min(-1)) compared to day 1 (p>0.05) of the protocol. These findings are consistent with the heat acclimation induced adaptations and suggest a biphasic sweat response (an increase in the sweat rate in the middle of the protocol followed by return to initial values by the end of it) during short-term heat acclimation in tropical natives.     

Exercise training and 3-day head down bed rest deconditioning: exercise thermoregulation.

Bed rest (BR) deconditioning causes excessive increase of exercise core body tempera-ture, while aerobic training improves exercise thermoregulation. The study was designed to determine whether 3 days of 6 degrees head-down bed rest (HDBR) affects body temperature and sweating dynamics during exercise and, if so, whether endurance training before HDBR modifies these responses. Twelve healthy men (20.7+/-0.9 yrs, VO2max: 46+/-4 ml x kg(-1) x min(-1) ) underwent HDBR twice: before and after 6 weeks of endurance training. Before and after HDBR, the subjects performed 45 min sitting cycle exercise at the same workload equal to 60% of VO2max determined before training. During exercise the VO2, HR, tympanic (Ttymp) and skin (Tsk) temperatures were recorded; sweating dynamics was assayed from a ventilated capsule on chest. Training increased VO2max by 12.1% (p<0.001). Resting Ttymp increased only after first HDBR (by 0.22 +/- 0.08 degrees C, p<0.05), while exercise equilibrium levels of Ttymp were increased (p<0.05) by 0.21 +/- 0.07 and 0.26 +/- 0.08 degrees C after first and second HDBR, respectively. Exercise mean Tsk tended to be lower after both HDBR periods. Total sweat loss and time-course of sweating responses were similar in all exercise tests. The sweating threshold related to Ttymp was elevated (p<0.05) only after first HDBR. In conclusion: six-week training regimen prevents HDBR-induced elevation of core temperature (Ttymp) at rest but not during ex-ercise. The post-HDBR increases of Ttymp without changes in sweating rate and the tendency for lower Tsk suggest an early (<3d) influence of BR on skin blood flow.     

Rehydration after exercise with fresh young coconut water,carbohydrate-electrolyte beverage and plain water

This is to cross-over study to assess the effectiveness of fresh young coconut water (CW), and carbohydrate-electrolyte beverage (CEB) compared with plain water (PW) for whole body rehydration and blood volume (BV) restoration during a 2 h rehydration period following exercise-induced dehydration. Eight healthy male volunteers (mean age and VO2max of 22.4 +/- 3.3 years and 45.8 +/- 1.5 ml min kg-1 respectively) exercised at 60% of VO2max in the heat (31.1 +/- 0.03 degrees C, 51.4 +/- 0.1% rh) until 2.78 +/- 0.06% (1.6 +/- 0.1 kg) of their body weight (BW) was lost. After exercise, the subjects sat for 2 h in a thermoneutral environment (22.5 +/- 0.1 degrees C; 67.0 +/- 1.0% rh) and drank a volume of PW, CW and CEB on different occasions representing 120% of the fluid loss. A blood and urine sample, and the body weight of each subject was taken before and after exercise and at 30 min intervals throughout a rehydration period. Each subject remained fasted throughout rehydration. Each fluid was consumed in three portions in separate trials representing 50% (781 +/- 47 ml), 40% (625 +/- 33 ml) and 30% (469 +/- 28 ml) of the 120% fluid loss at 0, 30 and 60 min of the 2 h rehydration period, respectively. The drinks given were randomised. In all the trials the subjects were somewhat hypohydrated (range 0.08-0.18 kg BW below euhydrated BW; p > 0.05) after a 2 h rehydration period since additional water and BW were lost as a result of urine formation, respiration, sweat and metabolism. The percent of body weight loss that was regained (used as index of percent rehydration) during CW, PW, and CEB trials was 75 +/- 5%, 73 +/- 5% and 80 +/- 4% respectively, but was not statistically different between trials. The rehydration index, which provided an indication of how much of what was actually ingested was used for body weight restoration, was again not different statistically between trials (1.56 +/- 0.14, 1.36 +/- 0.13 and 1.71 +/- 0.21 for CW, CEB and PW respectively). Although BV restoration was better with CW, it was not statistically different from CEB and PW. Cumulative urine output was similar in all trials. There were no difference at any time in serum Na+ and Cl-, serum osmolality, and net fluid balance between the three trials. Urine osmolality decreased after 1 h during the rehydration period and it was lowest in the PW trial. Plasma glucose concentrations were significantly higher compared with PW ingestion when CW and CEB were ingested during the rehydration period. CW was significantly sweeter, caused less nausea, fullness and no stomach upset and was also easier to consume in a larger amount compared with CEB and PW ingestion. In conclusion, ingestion of fresh young coconut water, a natural refreshing beverage, could be used for whole body rehydration after exercise.     

Function of human eccrine sweat glands during dynamic exercise and passive heat stress.

The purpose of this study was to identify the pattern of change in the density of activated sweat glands (ASG) and sweat output per gland (SGO) during dynamic constant-workload exercise and passive heat stress. Eight male subjects (22.8 +/- 0.9 yr) exercised at a constant workload (117.5 +/- 4.8 W) and were also passively heated by lower-leg immersion into hot water of 42 degrees C under an ambient temperature of 25 degrees C and relative humidity of 50%. Esophageal temperature, mean skin temperature, sweating rate (SR), and heart rate were measured continuously during both trials. The number of ASG was determined every 4 min after the onset of sweating, whereas SGO was calculated by dividing SR by ASG. During both exercise and passive heating, SR increased abruptly during the first 8 min after onset of sweating, followed by a slower increase. Similarly for both protocols, the number of ASG increased rapidly during the first 8 min after the onset of sweating and then ceased to increase further (P > 0.05). Conversely, SGO increased linearly throughout both perturbations. Our results suggest that changes in forearm sweating rate rely on both ASG and SGO during the initial period of exercise and passive heating, whereas further increases in SR are dependent on increases in SGO.     

Low doses of melatonin and diurnal effects on thermoregulation and tolerance to uncompensable heat stress.

This study examined whether the reported hypothermic effect of melatonin ingestion increased tolerance to exercise at 40 degrees C, for trials conducted either in the morning or afternoon, while subjects were wearing protective clothing. Nine men performed four randomly ordered trials; two each in the morning (0930) and afternoon (1330) after the double-blind ingestion of either two placebo capsules or two 1-mg capsules of melatonin. Despite significant elevations in plasma melatonin to over 1,000 ng/ml 1 h after the ingestion of the first 1-mg dose, rectal temperature (T(re)) was unchanged before or during the heat-stress exposure. Also, all other indexes of temperature regulation and the heart rate response during the uncompensable heat stress were unaffected by the ingestion of melatonin. Initial T(re) was increased during the afternoon (37.1 +/- 0.2 degrees C), compared with the morning (36.8 +/- 0.2 degrees C) exposures, and these differences remained throughout the uncompensable heat stress, such that final T(re) was also increased for the afternoon (39.2 +/- 0.2 degrees C) vs. the morning (39.0 +/- 0.3 degrees C) trials. Tolerance times and heat storage were not different among the exposures at approximately 110 min and 16 kJ/kg, respectively. It was concluded that this low dose of melatonin had no impact on tolerance to uncompensable heat stress and that trials conducted in the early afternoon were associated with an increased T(re) tolerated at exhaustion that offset the circadian influence on resting T(re) and thus maintained tolerance times similar to those of trials conducted in the morning.     

Mean body temperature does not modulate eccrine sweat rate during upright tilt.

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9.internal temperature + 0.1.mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30 degrees head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 +/- 0.1 to 38.0 +/- 0.1 degrees C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt (r = 0.07; P = 0.62), sweating within the innervated area (r = 0.06; P = 0.56), sweating at the neostigmine treated site (r = 0.04; P = 0.69), or sweating at the control site (r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 +/- 0.11 and 0.68 +/- 0.11 mg.cm(-2).min(-1) within the innervated area; 1.04 +/- 0.16 and 1.06 +/- 0.16 mg.cm(-2).min(-1) at the neostigmine-treated site; and 0.85 +/- 0.15 and 0.85 +/- 0.15 mg.cm(-2).min(-1) at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30 degrees head-up tilt.     

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255-413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.     

Performance and metabolic responses to a high caffeine dose during prolonged exercise.

The present study examined whether a high caffeine dose improved running and cycling performance and altered substrate metabolism in well-trained runners. Seven trained competitive runners [maximal O2 uptake (VO2max) 72.6 +/- 1.5 ml.kg-1.min-1] completed four randomized and double-blind exercise trials at approximately 85% VO2max; two trials running to exhaustion and two trials cycling to exhaustion. Subjects ingested either placebo (PL, 9 mg/kg dextrose) or caffeine (CAF, 9 mg/kg) 1 h before exercise. Endurance times were increased (P less than 0.05) after CAF ingestion during running (PL 49.2 +/- 7.2 min, CAF 71.0 +/- 11.0 min) and cycling (PL 39.2 +/- 6.5 min, CAF 59.3 +/- 9.9 min). Plasma epinephrine concentration [EPI] was increased (P less than 0.05) with CAF before running (0.22 +/- 0.02 vs. 0.44 +/- 0.08 nM) and cycling (0.31 +/- 0.06 vs. 0.45 +/- 0.06 nM). CAF ingestion also increased [EPI] (P less than 0.05) during exercise; PL and CAF values at 15 min were 1.23 +/- 0.13 and 2.51 +/- 0.33 nM for running and 1.24 +/- 0.24 and 2.53 +/- 0.32 nM for cycling. Similar results were obtained at exhaustion. Plasma norepinephrine was unaffected by CAF at rest and during exercise. CAF ingestion also had no effect on respiratory exchange ratio or plasma free fatty acid data at rest or during exercise. Plasma glycerol was elevated (P less than 0.05) by CAF before exercise and at 15 min and exhaustion during running but only at exhaustion during cycling. Urinary [CAF] increased to 8.7 +/- 1.2 and 10.0 +/- 0.8 micrograms/ml after the running and cycling trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

Protein coingestion stimulates muscle protein synthesis during resistance-type exercise

In contrast to the effect of nutritional intervention on postexercise muscle protein synthesis, little is known about the potential to modulate protein synthesis during exercise. This study investigates the effect of protein coingestion with carbohydrate on muscle protein synthesis during resistance-type exercise. Ten healthy males were studied in the evening after they consumed a standardized diet throughout the day. Subjects participated in two experiments in which they ingested either carbohydrate or carbohydrate with protein during a 2-h resistance exercise session. Subjects received a bolus of test drink before and every 15 min during exercise, providing 0.15 g x kg(-1) x h(-1) carbohydrate with (CHO + PRO) or without (CHO) 0.15 g x kg(-1) x h(-1) protein hydrolysate. Continuous intravenous infusions with l-[ring-(13)C(6)]phenylalanine and l-[ring-(2)H(2)]tyrosine were applied, and blood and muscle biopsies were collected to assess whole body and muscle protein synthesis rates during exercise. Protein coingestion lowered whole body protein breakdown rates by 8.4 +/- 3.6% (P = 0.066), compared with the ingestion of carbohydrate only, and augmented protein oxidation and synthesis rates by 77 +/- 17 and 33 +/- 3%, respectively (P < 0.01). As a consequence, whole body net protein balance was negative in CHO, whereas a positive net balance was achieved after the CHO + PRO treatment (-4.4 +/- 0.3 vs. 16.3 +/- 0.4 micromol phenylalanine x kg(-1) x h(-1), respectively; P < 0.01). In accordance, mixed muscle protein fractional synthetic rate was 49 +/- 22% higher after protein coingestion (0.088 +/- 0.012 and 0.060 +/- 0.004%/h in CHO + PRO vs. CHO treatment, respectively; P < 0.05). We conclude that, even in a fed state, protein coingestion stimulates whole body and muscle protein synthesis rates during resistance-type exercise.