Hyperhydration: tolerance and cardiovascular effects during uncompensable exercise-heat stress

This study examined the efficacy of glycerol andwater hyperhydration (1 h before exercise) on tolerance andcardiovascular strain during uncompensable exercise-heat stress. Theapproach was to determine whether 1-h preexercise hyperhydration (29.1 ml H₂O/kg lean body mass with orwithout 1.2 g/kg lean body mass of glycerol) provided a physiologicaladvantage over euhydration. Eight heat-acclimated men completed threetrials (control euhydration before exercise, and glycerol and waterhyperhydrations) consisting of treadmill exercise-heat stress (ratio ofevaporative heat loss required to maximal capacity of climate = 416).During exercise (~55% maximalO₂ uptake), there was nodifference between glycerol and water hyperhydration methods forincreasing (P < 0.05) total bodywater. Glycerol hyperhydration endurance time (33.8 ± 3.0 min) waslonger (P < 0.05) than for control(29.5 ± 3.5 min), but was not different(P > 0.05) from that of waterhyperhydration (31.3 ± 3.1 min). Hyperhydration didnot alter (P > 0.05) core temperature, whole body sweating rate, cardiac output, blood pressure, total peripheral resistance, or core temperature tolerance. Exhaustion from heat strain occurred at similar core and skin temperatures andheart rates in each trial. Symptoms at exhaustion included syncope andataxia, fatigue, dyspnea, and muscle cramps(n = 11, 10, 2, and 1 cases,respectively). We conclude that 1-h preexercise glycerolhyperhydration provides no meaningful physiological advantage overwater hyperhydration and that hyperhydration per se only provides theadvantage (over euhydration) of delaying hypohydration duringuncompensble exercise-heat stress.

     

Pre-exercise stretching does not impact upon running economy

Pre-exercise stretching has been widely reported to reduce performance in tasks requiring maximal or near-maximal force or torque. The purpose of this study was to compare the effects of 3 different pre-exercise stretching routines on running economy. Seven competitive male middle and long-distance runners (mean +/- SD) age: 32.5 +/- 7.7 years; height: 175.0 +/- 8.8 cm; mass: 67.8 +/- 8.6 kg; V(.-)O2max: 66.8 +/- 7.0 ml x kg(-1) x min(-1)) volunteered to participate in this study. Each participant completed 4 different pre-exercise conditions: (a) a control condition, (b) static stretching, (c) progressive static stretching, and (d) dynamic stretching. Each stretching routine consisted of 2 x 30-second stretches for each of 5 exercises. Dependent variables measured were sit and reach test before and after each pre-exercise routine, running economy (ml x kg(-1) x km(-1)), and steady-state oxygen uptake (ml x kg(-1) x min(-1)), which were measured during the final 3 minutes of a 10-minute run below lactate threshold. All 3 stretching routines resulted in an increase in the range of movement (p = 0.008). There was no change in either running economy (p = 0.915) or steady-state V(.-)O2 (p = 0.943). The lack of change in running economy was most likely because it was assessed after a period of submaximal running, which may have masked any effects from the stretching protocols. Previously reported reductions in performance have been attributed to reduced motor unit activation, presumably IIX. In this study, these motor units were likely not to have been recruited; this may explain the unimpaired performance. This study suggests that pre-exercise stretching has no impact upon running economy or submaximal exercise oxygen cost.     

Hyperhydration: thermoregulatory effects during compensable exercise-heat stress

Latzka, William A., Michael N. Sawka, Scott J. Montain, GaryS. Skrinar, Roger A. Fielding, Ralph P. Matott, and Kent B. Pandolf.Hyperhydration: thermoregulatory effects during compensable exercise-heat stress. J. Appl.Physiol. 83(3): 860-866, 1997.This studyexamined the effects of hyperhydration on thermoregulatory responsesduring compensable exercise-heat stress. The general approach was todetermine whether 1-h preexercise hyperhydration [29.1 ml/kg leanbody mass; with or without glycerol (1.2 g/kg lean body mass)]would improve sweating responses and reduce core temperature duringexercise. During these experiments, the evaporative heat loss required(E_req = 293 W/m²) to maintain steady-statecore temperature was less than the maximal capacity(E_max = 462 W/m²) of the climate forevaporative heat loss(E_req/E_max = 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and withoutrehydration (replace sweat loss during exercise). During exercise inthe heat (35°C, 45% relative humidity), there was no differencebetween hyperhydration methods for increasing total body water (~1.5liters). Compared with euhydration, hyperhydration did not alter coretemperature, skin temperature, whole body sweating rate, local sweatingrate, sweating threshold temperature, sweating sensitivity, or heartrate responses. Similarly, no difference was found between water andglycerol hyperhydration for these physiological responses. These datademonstrate that hyperhydration provides no thermoregulatory advantageover the maintenance of euhydration during compensable exercise-heatstress.

     

Thermoregulation in hyperhydrated men during physical exercise

The influence of hyperhydration on thermoregulatory function was tested in 8 male volunteers. The subjects performed cycle exercise in the upright position at 52% Vo2max for 45 min in a thermoneutral (Ta = 23 degrees C) environment. The day after the control exercise the subjects were hyperhydrated with tap water (35 ml X kg-1 of body weight) and then performed the same physical exercise as before. Total body weight loss was lower after hyperhydration (329 +/- 85 g) than during the control exercise (442 +/- 132 g), p less than 0.05. The decrease in weight loss after hyperhydration was probably due to a decrease in dripped sweat (58 +/- 64 and 157 +/- 101 g, p less than 0.05). With hyperhydration delay in onset of sweating was reduced from 5.8 +/- 3.2 to 3.7 +/- 2.0 min (p less than 0.05), and rectal temperature increased less (0.80 +/- 0.20 and 0.60 +/- 0.10 degrees C, p less than 0.01). The efficiency of sweating was higher in hyperhydrated (81.4%) than in euhydrated subjects (57.1%), p less than 0.01. It is concluded that hyperhydration influences thermoregulatory function in exercising men by shortening the delay in onset of sweating and by decreasing the quantity of dripped sweat. As a result, the increases in body temperature in hyperhydrated exercising men are lower than in normally hydrated individuals.     

Effect of hydration status on thirst, drinking, and related hormonal responses during low-intensity exercise in the heat.

During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 +/- 1 yr, 57 +/- 1 ml x kg(-1) x min(-1) maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33 degrees C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to -3.8 +/- 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (P(osm)), plasma vasopressin (P(AVP)), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 +/- 0.65) and drank more during Hy+W (1.65 +/- 0.18 liters) than Eu+W (1.59 +/- 0.41 and 0.31 +/- 0.11 liters, respectively). Postexercise measures of P(osm) and P(AVP) were significantly greater during Hy+NW and plasma volume lower [Hy+NW = -5.5 +/- 1.4% vs. Hy+W = +1.0 +/- 2.5% (P = 0.059), Eu+NW = -0.7 +/- 0.6% (P < 0.05), Eu+W = +0.5 +/- 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.     

Effect of creatine supplementation on cycle ergometer exercise in a hyperthermic environment

In order to examine thermoregulatory response to creatine (CR) supplementation, competitive male cyclists and triathletes (n = 7, VO2max = 50.6 +/- 0.8 ml x kg(-1) x min(-1)) completed three 1-hour hyperthermic (ambient temperature = 38.7 +/- 1.0 degrees C, relative humidity = 33 +/- 4%) exercise sessions at 181 +/- 12 W (50% of Wmax, approximately 66% of VO2max). Subjects completed a baseline (BL) session, then 2 sessions following 5 days of CR (20 g x d(-1)) and placebo (PL, 20 g x d(-1)) administered in a double-blind counterbalanced crossover manner with > or = 28-day washout. Pre-exercise BL, CR, and PL body mass were unchanged, with similar decreases in postexercise mass among the three conditions. Tympanic temperature, heart rate, systolic blood pressure, perceived exertion, and lactate, cortisol, and aldosterone concentrations increased similarly during BL, CR, and PL exercise. A greater (p = 0.013) estimated decrease in plasma volume occurred following BL (-16.5 +/- 2.0%) and PL (-17.6 +/- 1.7%) exercise compared to CR (-13.5 +/- 2.1%). Creatine supplementation reduces plasma volume loss during 1 hour of hyperthermic exercise but does not appear to otherwise change thermoregulatory response to hyperthermic exercise.     

Carbohydrate loading failed to improve 100-km cycling performance in a placebo-controlled trial.

We evaluated the effect of carbohydrate (CHO) loading on cycling performance that was designed to be similar to the demands of competitive road racing. Seven well-trained cyclists performed two 100-km time trials (TTs) on separate occasions, 3 days after either a CHO-loading (9 g CHO. kg body mass(-1). day(-1)) or placebo-controlled moderate-CHO diet (6 g CHO. kg body mass(-1). day(-1)). A CHO breakfast (2 g CHO/kg body mass) was consumed 2 h before each TT, and a CHO drink (1 g CHO. kg(.)body mass(-1). h(-1)) was consumed during the TTs to optimize CHO availability. The 100-km TT was interspersed with four 4-km and five 1-km sprints. CHO loading significantly increased muscle glycogen concentrations (572 +/- 107 vs. 485 +/- 128 mmol/kg dry wt for CHO loading and placebo, respectively; P < 0.05). Total muscle glycogen utilization did not differ between trials, nor did time to complete the TTs (147.5 +/- 10.0 and 149.1 +/- 11.0 min; P = 0.4) or the mean power output during the TTs (259 +/- 40 and 253 +/- 40 W, P = 0.4). This placebo-controlled study shows that CHO loading did not improve performance of a 100-km cycling TT during which CHO was consumed. By preventing any fall in blood glucose concentration, CHO ingestion during exercise may offset any detrimental effects on performance of lower preexercise muscle and liver glycogen concentrations. Alternatively, part of the reported benefit of CHO loading on subsequent athletic performance could have resulted from a placebo effect.     

Metabolic and performance effects of raisins versus sports gel as pre-exercise feedings in cyclists

Research suggests that pre-exercise sources of dietary carbohydrate with varying glycemic indexes may differentially affect metabolism and endurance. This study was designed to examine potential differences in metabolism and cycling performance after consumption of moderate glycemic raisins vs. a high glycemic commercial sports gel. Eight endurance-trained male (n = 4) and female (n = 4) cyclists 30 +/- 5 years of age completed 2 trials in random order. Subjects were fed 1 g carbohydrate per kilogram body weight from either raisins or sports gel 45 minutes prior to exercise on a cycle ergometer at 70% V(.-)O2max. After 45 minutes of submaximal exercise, subjects completed a 15-minute performance trial. Blood was collected prior to the exercise bout, as well as after the 45th minute of exercise, to determine serum concentrations of glucose, insulin, lactate, free fatty acids (FFAs), triglycerides, and beta-hydroxybutyrate. Performance was not different (p > 0.05) between the raisin (189.5 +/- 69.9 kJ) and gel (188.0 +/- 64.8 kJ) trials. Prior to exercise, serum concentrations of glucose and other fuel substrates did not differ between trials; however, insulin was higher (p < 0.05) for the gel (110.0 +/- 70.4 microU x ml(-1)) vs. raisin trial (61.4 +/- 37.4 microU x ml(-1)). After 45 minutes of exercise, insulin decreased to 14.2 +/- 6.2 microU x ml(-1) and 13.3 +/- 18.9 microU x ml(-1) for gel and raisin trials, respectively. The FFA concentration increased (+0.2 +/- 0.1 mmol x L(-1)) significantly (p < 0.05) during the raisin trial. Overall, minor differences in metabolism and no difference in performance were detected between the trials. Raisins appear to be a cost-effective source of carbohydrate for pre-exercise feeding in comparison to sports gel for short-term exercise bouts.     

Effect of morning exercise on counterregulatory responses to subsequent, afternoon exercise.

The aim of this study was to determine whether a bout of morning exercise (EXE(1)) can alter neuroendocrine and metabolic responses to subsequent afternoon exercise (EXE(2)) and whether these changes follow a gender-specific pattern. Sixteen healthy volunteers (8 men and 8 women, age 27 +/- 1 yr, body mass index 23 +/- 1 kg/m(2), maximal O(2) uptake 31 +/- 2 ml x kg(-1) x min(-1)) were studied after an overnight fast. EXE(1) and EXE(2) each consisted of 90 min of cycling on a stationary bike at 48 +/- 2% of maximal O(2) uptake separated by 3 h. To avoid the confounding effects of hypoglycemia and glycogen depletion, carbohydrate (1.5 g/kg body wt po) was given after EXE(1), and plasma glucose was maintained at euglycemia during both episodes of exercise by a modification of the glucose-clamp technique. Basal insulin levels (7 +/- 1 microU/ml) and exercise-induced insulin decreases (-3 microU/ml) were similar during EXE(1) and EXE(2). Plasma glucose was 5.2 +/- 0.1 and 5.2 +/- 0.1 mmol/l during EXE(1) and EXE(2), respectively. The glucose infusion rate needed to maintain euglycemia during the last 30 min of exercise was increased during EXE(2) compared with EXE(1) (32 +/- 4 vs. 7 +/- 2 micromol x kg(-1) x min(-1)). Although this increased need for exogenous glucose was similar in men and women, gender differences in counterregulatory responses were significant. Compared with EXE(1), epinephrine, norepinephrine, growth hormone, pancreatic polypeptide, and cortisol responses were blunted during EXE(2) in men, but neuroendocrine responses were preserved or increased in women. In summary, morning exercise significantly impaired the body's ability to maintain euglycemia during later exercise of similar intensity and duration. We conclude that antecedent exercise can significantly modify, in a gender-specific fashion, metabolic and neuroendocrine responses to subsequent exercise.     

Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Fluid ingestion during exercise increases skin blood flow independent of increases in blood volume.

The purpose of this experiment was to determine whether fluid ingestion attenuates the hyperthermia and cardiovascular drift that occurs during exercise dehydration due to increases in blood volume. In addition, forearm blood flow, which is indicative of skin blood flow, was measured to determine whether the attenuation of hyperthermia and cardiovascular drift during exercise with fluid ingestion is due to higher skin blood flow. On three different occasions, seven trained cyclists [mean age, body weight, and maximum oxygen uptake: 23 +/- 3 yr, 73.9 +/- 10.5 kg, and 4.75 +/- 0.34 (SD) l/min, respectively] cycled at a power output equal to 62-67% maximum oxygen uptake for 2 h in a warm environment (33 degrees C, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or a volume of a carbohydrate-electrolyte fluid replacement solution (FR) sufficient to replace 80 +/- 2% of sweat loss or were intravenously infused with 5.3 ml/kg of a blood volume expander (BVX; 6% dextran in saline). The infusion of 398 +/- 23 ml of BVX maintained blood volume at levels similar to that when 2,404 +/- 103 ml of fluid were ingested during FR and greater than that when no fluid was ingested during the 2nd h of exercise (P less than 0.05). However, BVX and NF resulted in similar esophageal and rectal temperatures, forearm blood flow, and elevations in serum osmolality and sodium concentration during 2 h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (Tdb = 33.4 degrees C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% VO2max, with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml.kg BW-1 of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol.l-1 Na+, 3.2 mmol.l-1 K+). Beverages were administered in double blind, counterbalanced order. Mean (+/- SE) times for the 1200 cycling task differed significantly: WP = 13.62 +/- 0.33 min, *6% = 13.03 +/- 0.24 min, 8% = 13.30 +/- 0.25 min, 10% = 13.57 +/- 0.22 min (* = different from WP and 10%, P less than 0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P less than 0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Pre-exercise hypervolemia and cycle ergometer endurance in men

Time to exhaustion at 87-91% of peak VO2 was measured in 5 untrained men (age: 31 +/- 8 years, body mass: 74.20 +/- 16.50 kg, body surface area: 1.90 +/- 0.24 m2, peak VO2: 2.87 +/- 0.40 l min-1, plasma volume: 3.21 +/- 0.88 l; means +/-SD) after consuming nothing (N) or two fluid formulations (10 ml kg-1, 743 +/- 161 ml): Performance 1 (P1), a multi-ionic carbohydrate drink, containing 55 mEq l-1 Na+, 4.16 g l-1 citrate, 20.49 g l-1 glucose, and 365 mOsm kg-1 H2O, and AstroAde (AA), a sodium chloride-sodium citrate hyperhydration drink, containing 164 mEq l-1 Na+, 8.54 g l-1 citrate, <5 mg l-1 glucose, and 253 mOsm kg-1 H2O. Mean (+/-SE) endurance for N, P1 and AA was 24.68 +/- 1.50, 24.55 +/- 1.09, and 30.50 +/- 3.44 min respectively. Percent changes in plasma volume (PV) from -105 min of rest to zero min before exercise were -1.5 +/- 3.2% (N), 0.2 +/- 2.2% (P1), and 4.8 +/- 3.0% (AA; P < 0.05). The attenuated endurance for N and P1 could not be attributed to differences in exercise metabolism (VE, RE, VO2) from the carbohydrate or citrate, terminal heart rate, levels of perceived exertion, forehead or thigh skin blood flow velocity, changes or absolute termination levels of rectal temperature. Thus, the higher level of resting PV for AA just before exercise, as well as greater acid buffering and possible increased energy substrate from citrate, may have contributed to the greater endurance.     

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema.

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (Vo2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 +/- 7.4 and 100.7 +/- 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 +/- 9.5% Vo2 max) and 55.5 +/- 9.8 and 104.3 +/- 9.1 min following 60 min cycling exercise in H (intensity = 65.4 +/- 7.1% hypoxic Vo2 max), where Vo2 max = 65.0 +/- 7.5 ml x kg(-1) x min(-1) (N) and 54.1 +/- 7.0 ml x kg(-1) x min(-1) (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 +/- 1.1%) as measured noninvasively during the Vo2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 +/- 0.019, 0.181 +/- 0.019, and 0.173 +/- 0.019 g/ml (N) and 0.178 +/- 0.021, 0.174 +/- 0.022, and 0.176 +/- 0.019 g/ml (H), respectively. No significant differences (P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.     

Effect of different cycling frequencies during incremental exercise on the venous plasma potassium concentration in humans

The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min(-1) on the [K+]v in humans. Twenty-one healthy young men aged 22.5+/-2.2 years, body mass 72.7+/-6.4 kg, VO2 max 3.720+/-0.426 l. min(-1), performed an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800 S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min(-1) (test A) and a few days later at a frequency of 120 rev. min(-1) (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]p were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24+/-0.36 mmol.l(-1) in test A, and 4.37+/-0.45 mmol.l(-1) in test B. However, the [K+]p during cycling at 120 rev. min(-1) was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min(-1). The maximal power output reached 293+/-31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223+/-40 W. The VO2max values in both tests reached 3.720+/-0.426 l. min(-1) vs 3.777+/-0.514 l. min(-1). These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min(-1). The [K+]v measured at the VO2max level in tests A and B amounted to 6.00+/-0.47 mmol.l-1 vs 6.04+/-0.41 mmol.l-1, respectively. This difference was not significant. It may thus be concluded that: a) generation of the same external mechanical power output during cycling at a pedalling rate of 120 rev.min(-1) causes significantly higher [K+]v changes than when cycling at 60 rev.min(-1), b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. 475: 359-368, 1994), c) there is a tendency towards upward up shift in the [K+]v and % VO2max relation during cycling at 120 rev.min(-1) when compared to cycling at 60 rev.min(-1).     

Hypohydration impairs endurance exercise performance in temperate but not cold air.

This study compared the effects of hypohydration (HYP) on endurance exercise performance in temperate and cold air environments. On four occasions, six men and two women (age = 24 +/- 6 yr, height = 170 +/- 6 cm, weight = 72.9 +/- 11.1 kg, peak O2 consumption = 48 +/- 9 ml.kg(-1).min(-1)) were exposed to 3 h of passive heat stress (45 degrees C) in the early morning with [euhydration (EUH)] or without (HYP; 3% body mass) fluid replacement. Later in the day, subjects sat in a cold (2 degrees C) or temperate (20 degrees C) environment with minimal clothing for 1 h before performing 30 min of cycle ergometry at 50% peak O2 consumption followed immediately by a 30-min performance time trial. Rectal and mean skin temperatures, heart rate, and ratings of perceived exertion measurements were made at regular intervals. Performance was assessed by the total amount of work (kJ) completed in the 30-min time trial. Skin temperature was significantly lower in the cold compared with the temperate trial, but there was no independent effect of hydration. Rectal temperature in both HYP trials was higher than EUH after 60 min of exercise, but the difference was only significant within the temperate trials (P < 0.05). Heart rate was significantly higher at 30 min within the temperate trial (HYP > EUH) and at 60 min within the cold trial (HYP > EUH) (P < 0.05). Ratings of perceived exertion increased over time with no differences among trials. Total work performed during the 30-min time trial was not influenced by environment but was less (P < 0.05) for HYP than EUH in the temperate trials. The corresponding change in performance (EUH-HYP) was greater for temperate (-8%) than for cold (-3%) (P < 0.05). These data demonstrate that 1) HYP impairs endurance exercise performance in temperate but not cold air but 2) cold stress per se does not.     

The effects of dietary manipulation on blood acid-base status and the performance of high intensity exercise

The effect of a pattern of exercise and dietary modification, which is normally used to alter muscle glycogen content, upon the acid-base status of the blood and the ability to perform high intensity exercise was studied. Eleven healthy male subjects cycled to exhaustion on an electrically braked cycle ergometer at a workload equivalent to 100% of their maximal oxygen uptake (VO2max) on three separate occasions. The first exercise test took place after a normal diet (46.2 +/- 6.7% carbohydrate (CHO)), and was followed by prolonged exercise to exhaustion to deplete muscle glycogen stores. The second test was performed after three days of a low carbohydrate diet (10.1 +/- 6.8% CHO) and subsequently after three days of a high CHO diet (65.5 +/- 9.8% CHO) the final test took place. Acid-base status and selected metabolites were measured on arterialised venous blood at rest prior to exercise and during the post-exercise period. Exercise time to exhaustion was longer after the normal (p less than 0.05) and high (p less than 0.05). CHO dietary phases compared with the low CHO phase. Resting pre-exercise pH was higher after the high CHO diet (p less than 0.05) compared with the low CHO diet. Pre-exercise bicarbonate, PCO2 and base excess measurements were higher after the high CHO treatment compared with both the normal (p less than 0.01, p less than 0.05, p less than 0.01 respectively) and low CHO phases (p less than 0.001, p less than 0.01, p less than 0.001 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of caffeine supplementation on the extracellular heat shock protein 72 response to exercise.

The stimulus for the release of 72-kDa heat shock protein (HSP72) during exercise in humans is currently unclear. Recent evidence in an animal model is suggestive of an involvement of catecholamines. The present study, therefore, investigated the effect of caffeine supplementation, a known stimulator of sympathetic activity, on the extracellular (e)HSP72 response to prolonged exercise. Ten healthy male endurance-trained cyclists were recruited (age: 21 +/- 1 yr, maximum O(2) uptake 61.1 +/- 1.7 ml x kg(-1) x min(-1), mean +/- SE). Each subject was randomly assigned to ingest either 6 mg/kg body mass of caffeine (Caff) or placebo (Pla) 60 min before one of two 90-min bouts of cycling at 74 +/- 1% maximum O(2) uptake. Trials were performed at least 7 days apart in a counterbalanced design. Venous blood samples were collected by venepuncture at pretreatment, preexercise, postexercise, and 1 h postexercise. Serum caffeine and plasma catecholamines were determined using a spectrophotometric assay and high-performance liquid chromatography, respectively. Plasma HSP72 and cortisol were determined by ELISA. Serum caffeine concentrations were significantly increased throughout Caff, while no increases were detected in Pla. Caffeine supplementation and exercise was associated with a greater eHSP72 response than exercise alone (postexercise Caff 8.6 +/- 1.3 ng/ml; Pla 5.9 +/- 0.9 ng/ml). This greater eHSP72 response was associated with a greater epinephrine response to exercise in Caff. There was a significant increase in norepinephrine and cortisol, with no intertrial differences. The present data suggest that, in humans, catecholamines may be an important mediator of the exercise-induced increase in eHSP72 concentration.     

Physiological and metabolic responses to work in heat with graded hypohydration in tropical subjects

Studies were conducted on 25 healthy male volunteers aged 20-25 years drawn randomly from the tropical regions of India. The subjects initially underwent an 8 day heat acclimatization schedule with 2 hours moderate work in a climatic chamber at 45 degrees C DB and 30% RH. These heat acclimatized subjects were then hypohydrated to varying levels of body weight deficits, i.e. 1.3 +/- 0.03, 2.3 +/- 0.04 and 3.3 +/- 0.04%, by a combination of water restriction and moderate exercise inside the hot chamber. After 2 hours rest in a thermoneutral room (25 +/- 1 degree C) the hypohydrated subjects were tested on a bicycle ergometer at a fixed submaximal work rate (40 W, 40 min) in a hot dry condition (45 degrees C DB, 30% RH, 34 degrees C WBGT). Significant increases in exercise heart rate and oral temperature were observed in hypohydrated subjects as compared to euhydration. Sweat rate increased with 1% and 2% hypohydration as compared to euhydration, but a significant decrease was observed with 3% hypohydration. Na+ & K+ concentrations in arm sweat increased with increase in the level of hypohydration. Oxygen consumption increased significantly only when hypohydration was about 2% or more. It appears that the increased physiological strain observed in tropical subjects working in heat with graded hypohydration is not solely due to reduced sweat rates.