Effects of hydration state and resistance exercise on markers of muscle damage

It is well established that resistance exercise can damage muscle tissue, but the combined effects of hypohydration and resistance exercise on muscle damage are unclear. Two common circulating markers of muscle damage, myoglobin (Mb) and creatine kinase (CK) may be attenuated by fluid ingestion post-exercise. The purpose of this study was to examine the combined effect of resistance exercise and hydration state on muscle damage. Seven healthy resistance-trained males (age = 23 +/- 4 years; body mass = 87.8 +/- 6.8 kg; body fat = 11.5 +/- 5.2%) completed 3 identical resistance exercise bouts (6 sets of up to 10 repetitions of the back squat) in different hydration states: euhydrated (HY0), hypohydrated approximately 2.5% body mass (HY2.5), and hypohydrated approximately 5.0% body mass (HY5). Subjects achieved desired hydration states via controlled water deprivation, exercise-heat stress, and fluid intake. Both Mb and CK were measured during euhydrated rest (PRE). Mb was also measured immediately post-exercise, 1 hour (+1H) and 2 hours (+2H) post-exercise; CK was measured at 24 and 48 hours post-exercise. Body mass decreased 0.2 +/- 0.4%, 2.4 +/- 0.4%, and 4.8 +/- 0.4% during HY0, HY2.5, and HY5, respectively. Mb concentrations increased significantly (effect size >or=1, p < 0.05) from PRE (2.6 +/- 1.1, 3.5 +/- 2.8, and 3.2 +/- 1.6 nmol x L(-1)) to +1H (5.3 +/- 3.4, 6.8 +/- 3.2, and 7.6 +/- 2.8 nmol x L(-1)), and +2H (5.5 +/- 3.8, 6.2 +/- 3.0, and 7.2 +/- 3.0 nmol x L(-1)) for HY0, HY2.5, and HY5, respectively, but were not significantly different between trials. CK concentrations remained within the normal resting range at all time points. Thus, hypohydration did not enhance muscle damage following the resistance exercise challenge. Despite these results, athletes are encouraged to commence exercise in a euhydrated state to maximize endogenous hormonal, mechanical, and metabolic benefits.     

Hypohydration adversely affects lactate threshold in endurance athletes

The purpose of this investigation was to observe the effect of hypohydration (-4% body mass) on lactate threshold (LAT) in 14 collegiate athletes (8 men and 6 women; age, 20.9 +/- 0.5 years; height, 171.1 +/- 2.4 cm; weight, 64.8 +/- 2.3 kg; V(O)2 max, 62.8 +/- 1.9 ml x kg(-1) x min(-1); percentage of fat, 11.4 +/- 1.5%). Subjects performed 2 randomized, discontinuous treadmill bouts at a dry bulb temperature (T(db)) of 22 degrees C to volitional exhaustion in 2 states of hydration, euhydrated and hypohydrated. The hypohydrated condition was achieved in a thermally neutral environment (T(db), 22 degrees C; humidity, 45%), with exercise conducted at a moderate intensity as defined by rating of perceived exertion (RPE, approximately 12) 12-16 hours before testing. On average, subjects decreased 3.9% of their body mass before the hypohydration test. Blood lactate, hematocrit, V(O)2, minute ventilation (VE), R value, heart rate (HR), and RPE were measured during each 4-minute stage of testing. In the hypohydrated condition, LAT occurred significantly earlier during exercise and at a lower absolute V(O)2, VE, respiratory exchange ratio, RPE, and blood lactate concentration. Also, the blood lactate concentration was significantly lower in the hypohydrated condition (6.7 +/- 0.8 mmol) compared with the euhydrated condition (10.2 +/- 0.9 mmol) at peak exercise. There were no differences in HR or percentage of maximum HR at LAT nor did plots of V(CO2):V(O)2 reveal differences in bicarbonate buffering during exercise between the 2 conditions. From these results, we speculate that hypohydration did not significantly alter cardiovascular function or buffering capacity but did cause LAT to occur at a lower absolute exercise intensity.     

Hydration and vascular fluid shifts during exercise in the heat

This study examined the effects of hypohydration on plasma volume and red cell volume during rest in a comfortable (20 degrees C, 40% relative humidity) and exercise in a hot-dry (49 degrees C, 20% relative humidity) environment. A group of six male and six female volunteers [matched for maximal O2 uptake (VO2 max)] completed two test sessions following a 10-day heat acclimation program. One test session was completed when subjects were euhydrated and the other when subjects were hypohydrated (-5% from base-line body wt). The test sessions consisted of rest for 30 min in a 20 degrees C antechamber, followed by two 25-min bouts of treadmill walking (approximately 30% of VO2 max) in the heat, interspersed by 10 min of rest. No significant differences were found between the genders for the examined variables. At rest, hypohydration elicited a 5% decrease in plasma volume with less than 1% change in red cell volume. During exercise, plasma volume increased by 4% when subjects were euhydrated and decreased by 4% when subjects were hypohydrated. These percent changes in plasma volume values were significantly (P less than 0.01) different between the euhydration and hypohydration tests. Although red cell volume remained fairly constant during the euhydration test, these values were significantly (P less than 0.01) lower when hypohydrated during exercise. We conclude that hydration level alters vascular fluid shifts during exercise in a hot environment; hemodilution occurs when euhydrated and hemoconcentration when hypohydrated during light intensity exercise for this group of fit men and women.     

Hypohydration and exercise: effects of heat acclimation, gender, and environment

This study examined the effects of heat acclimation and subject gender on treadmill exercise in comfortable (20 degrees C, 40% rh), hot-dry (49 degrees C, 20% rh), and hot-wet (35 degrees C, 79% rh) environments while subjects were hypo- or euhydrated. Six male and six female subjects, matched for maximal aerobic power and percent body fat, completed two exercise tests in each environment both before and after a 10-day heat acclimation program. One exercise test was completed during euhydration and one during hypohydration (-5.0% from baseline body weight). In general, no significant (P greater than 0.05) differences were noted between men and women at the completion of exercise for rectal temperature (Tre), mean skin temperature (Tsk), or heat rate (HR) during any of the experimental conditions. Hypohydration generally increased Tre and HR values and decreased sweat rate values while not altering Tsk values. In the hypohydration experiments, heat acclimation significantly reduced Tre (0.19 degrees C) and HR (13 beats X min-1) values in the comfortable environment, but only HR values were reduced in hot-dry (21 beats X min-1) and hot-wet (21 beats X min-1) environments. The present findings indicated that men and women respond in a physiologically similar manner to hypohydration during exercise. They also indicated that for hypohydrated subjects heat acclimation decreased thermoregulatory and cardiovascular strain in a comfortable environment, but only cardiovascular strain decreased in hot environments.     

Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise

The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient water was ingested during the upper body exercise and heat exposure to maintain euhydration (EU). In both trials, 400 g of carbohydrate were ingested at the completion of exercise and followed by 15 h of rest while the desired hydration level was maintained. Muscle biopsy samples were obtained from the vastus lateralis immediately after intermittent cycle exercise (T1) and after 15 h of rest (T2). During the HY trial, the muscle water content was lower (P less than 0.05) at T1 and T2 (288 +/- 9 and 265 +/- 5 ml/100 g dry wt, respectively; NS) than during EU (313 +/- 8 and 301 +/- 4 ml/100 g dry wt, respectively; NS). Muscle glycogen concentration was not significantly different during EU and HY at T1 (200 +/- 35 vs. 251 +/- 50 mumol/g dry wt) or T2 (452 +/- 34 vs. 491 +/- 35 mumol/g dry wt). These data indicate that, despite reduced water content during the first 15 h after heavy exercise, skeletal muscle glycogen resynthesis is not impaired.     

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.     

Heat acclimation and hypohydration in aged rats: The involvement of adrenergic pathways in thermal-induced vasomotor responses in the portal circulation

1. 1. The beneficial effects of heat acclimation on thermal induced vasomotor responses of hypohydrated aged rats were assessed by measuring the isometric tension of aortic and portal rings of old and young rats under heat acclimation and hypohydration in response to -adrenergic (-AR) and β-adrenergic (β-AR) stimulation (phenylephrine 10⁻⁹–10⁻² mM and isoprenaline 10⁻⁹–10⁻⁴ respectively). In parallel, portal blood flow (PBF), which drains the splanchnic vasculature, was measured in conscious rats, before and during heat stress (42°C).

2. 2. In the aorta, heat acclimation augmented phenylephrine (-AR) induced tension, to a great extent in the older rats. Hypohydration increased -AR sensitivity in all experimental groups. Acclimation and aging brought about decreased responsiveness in isoprenaline induced relaxation (β-AR) in both the aorta and the portal vein. Hypohydration increased β-AR responsiveness in the portal vein of OR, acclimated and acclimated-hypohydrated rats.

3. 3. Normothermic euhydrated resting PBF was similar for young and old rats. Hypohydration decreased resting PBF. Upon heat stress, thermal induced vasoconstriction in hypohydrated YR and OR occurred earlier than in the euhydrated groups and was more pronounced. The latter responses were attenuated in the old rats.

4. 4. Taken together, these results imply that chronic environmental stressors such as heat acclimation and hypohydration produce selective alterations in AR responsiveness of the vasculature in both young and old rats. Consequently, thermoregulatory vasomotor mediated mechanisms, as exhibited in this study in PBF, may differ in their responsiveness in these two age groups.

     

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.     

The influence of hydration status on heart rate variability after exercise heat stress

While exercise heat stress and hydration status are known to independently influence heart rate variability (HRV), the combined effect of these physiological stressors is unknown. Thus, heat-acclimated subjects (n=5) performed exercise heat trials (40 °C, 20% relative humidity) in the euhydrated and hypohydrated state (3.9±0.7% body weight loss). During each trial, cardiac cycle R–R interval data were collected for 45 min at rest (pre-) and after (post-) completing 90 min of cycle ergometer exercise. Pre- and post-exercise RRI data were analyzed by Fast Fourier Power Spectral analysis to determine the high-frequency (HF), low-frequency (LF), very low-frequency (VLF), and total power (TP) components of HRV. Overall HRV was decreased by both hypohydration and exercise heat stress. Hypohydration reduced TP, LF, VLF, and LF:HF ratio $(P<0.05)$ while HF was significantly higher. The change in both LF and HF power (pre- vs. post-exercise) were blunted during hypohydration compared to euhydration. These data suggest that dehydration alone positively influences the parasympathetic (HF) control of HRV, but the reduction in overall HRV and the blunted oscillations in LF and HF power following exercise heat stress support an overall deleterious effect of dehydration on autonomic cardiac stability.     

Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake

Armstrong, Lawrence E., Carl M. Maresh, Catherine V. Gabaree, Jay R. Hoffman, Stavros A. Kavouras, Robert W. Kenefick, JohnW. Castellani, and Lynn E. Ahlquist. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, andwater intake. J. Appl. Physiol. 82(6):2028-2035, 1997.This investigation examined the distinct andinteractive effects of initial hydration state, exercise-induceddehydration, and water rehydration in a hot environment. On fouroccasions, 10 men performed a 90-min heat stress test (treadmillwalking at 5.6 km/h, 5% grade, 33°C, 56% relative humidity).These heat stress tests differed in pretest hydration [2euhydrated (EU) and 2 hypohydrated (HY) trials] and water intakeduring exercise [2 water ad libitum (W) and 2 no water (NW)trials]. HY + NW indicated greater physiological strain than allother trials (P < 0.05-0.001)in heart rate, plasma osmolality(P_osm), sweat sensitivity(g / °C · min), and rectal temperature.Unexpectedly, final HY + W and EU + W responses for rectal temperature,heart rate, and P_osm were similar,despite the initial 3.9 ± 0.2% hypohydration in HY + W. Weconcluded that differences in pretestP_osm (295 ± 7 and 287 ± 5 mosmol/kg for HY + W and EU + W, respectively) resulted in greaterwater consumption (1.65 and 0.31 liter for HY + W and EU + W,respectively), no voluntary dehydration (0.9% body mass increase), andattenuated thermal and circulatory strain during HY + W.

     

Gastric emptying during exercise: effects of heat stress and hypohydration

To determine the effects of acute heat stress, heat acclimation and hypohydration on the gastric emptying rate of water (W) during treadmill exercise, ten physically fit men ingested 400 ml of W before each of three 15 min bouts of exercise (treadmill, approximately 50% VO2max) on five separate occasions. Stomach contents were aspirated after each exercise bout. Before heat acclimation (ACC), experiments were performed in a neutral (18 degrees C), hot (49 degrees C) and warm (35 degrees C) environment. Subjects were euhydrated for all experiments before ACC. After ACC, the subjects completed two more experiments in the warm (35 degrees C) environment; one while euhydrated and a final one while hypohydrated (-5% of body weight). The volume of ingested water emptied into the intestines at the completion of each exercise bout was inversely correlated (P less than 0.01) with the rectal temperature (r = -0.76). The following new observations were made: 1) exercise in a hot (49 degrees C) environment impairs gastric emptying rate as compared with a neutral (18 degrees C) environment, 2) exercise in a warm (35 degrees C) environment does not significantly reduce gastric emptying before or after heat acclimation, but 3) exercise in a warm environment (35 degrees C) when hypohydrated reduces gastric emptying rate and stomach secretions. Reductions in gastric emptying appear to be related to the severity of the thermal strain induced by an exercise/heat stress.     

Thermoregulatory and blood responses during exercise at graded hypohydration levels

We studied the effects of graded hypohydration levels on thermoregulatory and blood responses during exercise in the heat. Eight heat-acclimated male subjects attempted four heat-stress tests (HSTs). One HST was attempted during euhydration, and three HSTs were attempted while the subjects were hypohydrated by 3, 5, and 7% of their body weight. Hypohydration was achieved by an exercise-heat regimen on the day prior to each HST. After 30 min of rest in a 20 degrees C antechamber the HST consisted of a 140-min exposure (4 repeats of 10 min rest and 25 min treadmill walking) in a hot-dry (49 degrees C, 20% relative humidity) environment. The following observations were made: 1) a low-to-moderate hypohydration level primarily reduced plasma volume with little effect on plasma osmolality, whereas a more severe hypohydration level resulted in no further plasma volume reduction but a large increment in plasma osmolality; 2) core temperature and heart rate responses increased with severity of hypohydration; 3) sweating rate responses for a given rectal temperature were systematically decreased with severity of hypohydration; and 4) the reduction in sweating rate was more strongly associated with plasma hyperosmolality than hypovolemia. In conclusion, an individual's thermal strain increases linearly with the severity of hypohydration during exercise in the heat, and plasma hyperosmolality influences the reduction in sweating more profoundly than hypovolemia.     

Reduced exercise-associated response of the GH-IGF-I axis and catecholamines in obese children and adolescents.

Obesity blunts catecholamine and growth hormone (GH) responses to exercise in adults, but the effect of obesity on these exercise-associated hormonal responses in children is unclear. Therefore, the aim of the present study was to asses the effect of childhood obesity on the counterregulatory hormonal response to acute exercise. Twenty-five obese children (Ob; body mass index > 95%), and 25 age, gender, and maturity-matched normal-weight controls (NW) participated in the study. Exercise consisted of ten 2-min bouts of constant-cycle ergometry above the anaerobic threshold, with 1-min rest intervals between each bout. Pre-, post-, and 120-min postexercise blood samples were collected for circulating components of the GH-IGF-I axis and catecholamines. There were no differences in peak exercise heart rate, serum lactate, and peak O2 uptake normalized to lean body mass between the groups. Obesity attenuated the GH response to exercise (8.9 +/- 1.1 vs. 3.4 +/- 0.7 ng/ml in NW and Ob participants, respectively; P < 0.02). No significant differences in the response to exercise were found for other components of the GH-IGF-I axis. Obesity attenuated the catecholamine response to exercise (epinephrine: 52.5 +/- 12.7 vs. 18.7 +/- 3.7 pg/ml, P < 0.02; norepinephrine: 479.5 +/- 109.9 vs. 218.0 +/- 26.0 pg/ml, P < 0.04; dopamine: 17.2 +/- 2.9 vs. 3.5 +/- 1.9 pg/ml, P < 0.006 in NW and Ob, respectively). Insulin levels were significantly higher in the obese children and dropped significantly after exercise in both groups. Despite the elevated insulin levels and the blunted counterregulatory response, none of the participants developed hypoglycemia. Childhood obesity was associated with attenuated GH and catecholamine response to acute exercise. These abnormalities were compensated for, so that exercise was not associated with hypoglycemia, despite increased insulin levels in obese children.     

Changes in plasma volume during hypohydration and rehydration in subjects from the tropics

Plasma volume (PV) at different levels of hypohydration was determined using radio-iodinated serum albumin-125 in 28 heat acclimated male volunteers in hot dry condition in a climatic chamber. The heat acclimated subjects were hypohydrated to varying degrees i.e. 1%, 2%, 3% and 4% body mass deficit by moderate work in hot conditions in a climatic chamber maintained at 45 degrees C dry bulb temperature and 30% relative humidity. A rehydration study was carried out in only those subjects who were hypohydrated to 3% and 4% body mass and they were brought back to a 2% level of hypohydration by giving a calculated amount of water. A significant decrease in PV was observed at 3% and 4% hypohydration only. The magnitude of the decrease was the same in both the groups and not related to the level of hypohydration. With partial rehydration in the 3% hypohydrated group PV was restored fully, while in the 4% hypohydrated group restoration was incomplete, indicating that at this hypohydration level some of the replenished water that entered in plasma may have moved to the intracellular compartment which may have contributed more at 4% hypohydration. It is suggested that with higher levels of thermal hypohydration significant reduction in the intracellular compartment may result in accentuated physiological strain during work in the heat.     

Human tolerance to heat strain during exercise: influence of hydration.

This study determined whether 1) exhaustion from heat strain occurs at the same body temperatures during exercise in the heat when subjects are euhydrated as when they are hypohydrated, 2) aerobic fitness influences the body temperature at which exhaustion from heat strain occurs, and 3) curves could be developed to estimate exhaustion rates at a given level of physiological strain. Seventeen heat-acclimated men [maximal oxygen uptake (VO2max) from 45 to 65 ml.kg-1.min-1] attempted two heat stress tests (HSTs): one when euhydrated and one when hypohydrated by 8% of total body water. The HSTs consisted of 180 min of rest and treadmill walking (45% VO2max) in a hot-dry (ambient temperature 49 degrees C, relative humidity 20%) environment. The required evaporative cooling (Ereq) exceeded the maximal evaporative cooling capacity of the environment (Emax); thus thermal equilibrium could not be achieved and 27 of 34 HSTs ended by exhaustion from heat strain. Our findings concerning exhaustion from heat strain are 1) hypohydration reduced the core temperature that could be tolerated; 2) aerobic fitness, per se, did not influence the magnitude of heat strain that could be tolerated; 3) curves can be developed to estimate exhaustion rates for a given level of physiological strain; and 4) exhaustion was rarely associated with a core temperature up to 38 degrees C, and it always occurred before a temperature of 40 degrees C was achieved. These findings are applicable to heat-acclimated individuals performing moderate-intensity exercise under conditions where Ereq approximates or exceeds Emax and who have high skin temperatures.     

Effect of Hypohydration on Peripheral and Corticospinal Excitability and Voluntary Activation

We investigated whether altered peripheral and/or corticospinal excitatory output and voluntary activation are implicated in hypohydration-induced reductions in muscle isometric and isokinetic (90°.s⁻¹) strength. Nine male athletes completed two trials (hypohydrated, euhydrated) comprising 90 min cycling at 40°C, with body weight losses replaced in euhydrated trial. Peripheral nerve and transcranial magnetic stimulations were applied during voluntary contractions pre- and 40 min post-exercise to quantify voluntary activation and peripheral (M-wave) and corticospinal (motor evoked potential) evoked responses in m. vastus medialis. Both maximum isometric (−15.3±3.1 vs −5.4±3.5%) and isokinetic eccentric (−24.8±4.6 vs −7.3±7.2%) torque decreased to a greater extent in hypohydrated than euhydrated trials (p<0.05). Half relaxation time of the twitch evoked by peripheral nerve stimulation during maximal contractions increased after exercise in the hypohydrated (21.8±9.3%) but stayed constant in the euhydrated (1.6±10.7%; p = 0.017) condition. M-wave amplitude during maximum voluntary contraction increased after exercise in the heat in hypohydrated (10.7±18.0%) but decreased in euhydrated condition (−17.4±16.9%; p = 0.067). Neither peripheral nor cortical voluntary activation were significantly different between conditions. Motor evoked potential amplitude increased similarly in both conditions (hypohydrated: 25.7±28.5%; euhydrated: 52.9±33.5%) and was accompanied by lengthening of the cortical silent period in euhydrated but not hypohydrated condition (p = 0.019). Different neural strategies seem to be adopted to regulate neural drive in the two conditions, with increases in inhibitory input of either intracortical or corticospinal origin during the euhydrated trial. Such changes were absent in the hypohydrated condition, yet voluntary activation was similar to the euhydrated condition, perhaps due to smaller increases in excitatory drive rather than increased inhibition. Despite this maximal isometric and eccentric strength were impaired in the hypohydrated condition. The increase in peripheral muscle excitability evident in the hypohydrated condition was not sufficient to preserve performance in the face of reduced muscle contractility or impaired excitation-contraction coupling.     

Comparison of measured and predicted residual lung volume in determining body composition of collegiate wrestlers

This investigation compared percent fat obtained via underwater weighing using measured and predicted residual lung volume (RLV) in euhydrated and hypohydrated collegiate wrestlers (N = 67). RLV was measured using O(2) rebreathing or O(2) dilution and predicted using 3 equations-Equation 1: (0.019 x height [cm]) + (0.0115 x age [years]) - 2.24; Equation 2: (0.017 x age [years]) + (0.06858 x height [in.]) - 3.477; and Equation 3: (0.0275 age [years]) + (0.0189 height [cm]) - 2.6139. Percent fat determined using RLV Equation 2 did not differ from the value obtained using measured RLV in the euhydrated (10.9 +/- 5.1 vs. 11.5 +/- 5.6% fat) or hypohydrated (10.8 +/- 5.1 vs. 12.3 +/- 5.6% fat) trials. All other percent fat values differed (p < 0.05) from the value obtained using measured RLV in euhydrated subjects. The use of RLV Equation 2 may be a practical alternative to measured RLV in determining percent fat in euhydrated and hypohydrated collegiate wrestlers.     

Effects of hyperglycemia on the cerebrovascular response to rhythmic handgrip exercise

Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity (V(mean)) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU (P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA V(mean) increased (P < 0.05), whereas brain catecholamine uptake and arterial Pco(2) did not change significantly. HY did not affect the normalized low-frequency gain between mean arterial pressure and MCA V(mean) or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 +/- 7% vs. 9 +/- 7%; P < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 +/- 4% vs. 14 +/- 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA V(mean). These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise.     

Effect of acute postexercise ethanol intoxication on the neuroendocrine response to resistance exercise.

This investigation was conducted to determine the effect of postexercise ethanol intoxication (21.97 +/- 1.09 mmol/l blood) on the response of selected aspects of the neuroendocrine system to a resistance exercise (Ex) session. Nine resistance-trained men (25.0 +/- 1.4 yr, 179.4 +/- 3.4 cm, 79.7 +/- 3.3 kg) were used to compare three 3-day treatments: control, Ex, and ethanol after exercise (ExEt). Blood was collected serially from an antecubital vein before exercise, immediately after exercise, and for pooled analysis at 20-40 (2 samples), 60-120 (4 samples), and 140-300 (9 samples) min after exercise on day 1 and in the morning (2 samples each) on days 2 and 3. Ethanol did not increase circulating epinephrine, norepinephrine, or cortisol concentration (Cort) above Ex elevations. At 60-120 min, only ExEt Cort was greater than control Cort. Concentrations of testosterone, luteinizing hormone, and corticotropin were not affected by either treatment. It is concluded that, although this blood ethanol concentration is insufficient to acutely increase Cort above that caused by Ex alone, it appears that ethanol may have a prolonged effect beyond the Ex response. This blood ethanol concentration does not further stimulate the sympathoadrenal system during the postexercise response.     

The effect of prior exercise and caffeine ingestion on metabolic rate and hormones in young adult males

The purposes of this study were to examine (a) the effects of acute exercise on metabolic rate 24 and 48 h postexercise and (b) the interaction of acute exercise and the thermic effect of caffeine on metabolic rate and hormonal changes during the late postexercise recovery period. In six young males, who were regular consumers of caffeine, resting energy expenditure was measured before and after caffeine (5 mg.kg-1) and placebo ingestion under the following conditions: (i) control (e.g., no prior exercise), (ii) 24 h postexercise, and (iii) 48 h postexercise. Blood samples were drawn for plasma glucose, insulin, glycerol, free fatty acids, catecholamines, and thyroid hormones (triiodothyronine, thyroxine, and free thyroxine). Results showed that acute exercise did not exert a detectable effect on resting metabolic rate in the late postexercise recovery period, that is, resting metabolic rate was similar among the conditions of control (1.17 +/- 0.12 kcal.min-1), 24 h postexercise (1.16 +/- 0.12), and 48 h postexercise (1.16 +/- 0.11). Caffeine ingestion increased metabolic rate (approximately 7%), but the thermic effect was not different among the experimental conditions. Plasma insulin and norepinephrine were lower after caffeine ingestion, whereas an increase in plasma free fatty acids was noted. Other hormones and substrates did not change significantly in response to caffeine ingestion. Furthermore, the hormonal and substrate milieu was not significantly different 24 and 48 h postexercise when compared with the control condition. Our results support the view that acute exercise does not alter the resting metabolic rate in the late postexercise recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)