Dehydration increases the magnitude of selective brain cooling independently of core temperature in sheep

By cooling the hypothalamus during hyperthermia, selective brain cooling reduces the drive on evaporative heat loss effectors, in so doing saving body water. To investigate whether selective brain cooling was increased in dehydrated sheep, we measured brain and carotid arterial blood temperatures at 5-min intervals in nine female Dorper sheep (41 +/- 3 kg, means +/- SD). The animals, housed in a climatic chamber at 23 degrees C, were exposed for nine days to a cyclic protocol with daytime heat (40 degrees C for 6 h). Drinking water was removed on the 3rd day and returned 5 days later. After 4 days of water deprivation, sheep had lost 16 +/- 4% of body mass, and plasma osmolality had increased from 290 +/- 8 to 323 +/- 9 mmol/kg (P < 0.0001). Although carotid blood temperature increased during heat exposure to similar levels during euhydration and dehydration, selective brain cooling was significantly greater in dehydration (0.38 +/- 0.18 degrees C) than in euhydration (-0.05 +/- 0.14 degrees C, P = 0.0008). The threshold temperature for selective brain cooling was not significantly different during euhydration (39.27 degrees C) and dehydration (39.14 degrees C, P = 0.62). However, the mean slope of lines of regression of brain temperature on carotid blood temperature above the threshold was significantly lower in dehydrated animals (0.40 +/- 0.31) than in euhydrated animals (0.87 +/- 0.11, P = 0.003). Return of drinking water at 39 degrees C led to rapid cessation of selective brain cooling, and brain temperature exceeded carotid blood temperature throughout heat exposure on the following day. We conclude that for any given carotid blood temperature, dehydrated sheep exposed to heat exhibit selective brain cooling up to threefold greater than that when euhydrated.     

Effects of marked hyperthermia with and without dehydration on VO(2) kinetics during intense exercise.

This study determined whether marked hyperthermia alone or in combination with dehydration reduces the initial rate of rise in O(2) consumption (VO(2) on-kinetics) and the maximal rate of O(2) uptake (VO(2 max)) during intense cycling exercise. Six endurance-trained male cyclists completed four maximal cycle ergometer exercise tests (402 +/- 4 W) when euhydrated or dehydrated (4% body wt) with normal (starting esophageal temperature, 37.5 +/- 0.2 degrees C; mean skin temperature, approximately 31 degrees C) or elevated (+1 and +6 degrees C, respectively) thermal strain. In the euhydrated and normal condition, subjects reached VO(2 max) (4.7 +/- 0.2 l/min) in 228 +/- 34 s, with a mean response time of 42 +/- 2 s, and fatigued after 353 +/- 39 s. Hyperthermia alone or in combination with dehydration reduced mean response time (17-23%), VO(2 max) (16%), and performance time (51-53%) (all P < 0.01) but did not alter the absolute response time (i.e., the time to reach 63% response in the control trial, 3.2 +/- 0.1 l/min, 42 s). Reduction in VO(2 max) was accompanied by proportional decline in O(2) pulse and significantly elevated maximal heart rate (195 vs. 190 beats/min for hyperthermia vs. normal). Preventing hyperthermia in dehydrated subjects restored VO(2 max) and performance time by 65 and 50%, respectively. These results demonstrate that impaired high-intensity exercise performance with marked skin and internal body hyperthermia alone or in combination with dehydration is not associated with a diminished rate of rise in VO(2) but decreased VO(2 max).     

Stroke volume during exercise: interaction of environment and hydration

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O(2) consumption (VO(2 max)) 4.5 +/- 0.1 l/min; means +/- SE] cycled for 30 min (72% VO(2 max)) in the heat (H; 35 degrees C) or the cold (C; 8 degrees C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T(es) 38. 2-38.3 degrees C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 +/- 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 +/- 1.3 ml (4.8%) in H and 3.4 +/- 0.4 ml (2.5%) in C, whereas T(es) increased 0.21 +/- 0.02 and 0. 10 +/- 0.02 degrees C in H and C, respectively (P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H (R = 0.96; P < 0.01) and C (R = 0. 85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.     

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 acute mild dehydration on cognitive-motor performance in golf

ABSTRACT: Smith, MF, Newell, AJ, and Baker, MA. Effect of acute mild dehydration on cognitive-motor performance in golf. J Strength Cond Res 26(11): 3075-3080, 2012-Whether mild dehydration (-1 to 3% body mass change [ΔBM]) impairs neurophysiological function during sport-specific cognitive-motor performance has yet to be fully elucidated. To investigate this within a golfing context, 7 low-handicap players (age: 21 ± 1.1 years; mass: 76.1 ± 11.8 kg; stature: 1.77 ± 0.07 m; handicap: 3.0 ± 1.2) completed a golf-specific motor and cognitive performance task in a euhydrated condition (EC) and dehydrated condition (DC) (randomized counterbalanced design; 7-day interval). Dehydration was controlled using a previously effective 12-hour fluid restriction, monitored through ΔBM and urine color assessment (UCOL). Mild dehydration reduced the mean BM by 1.5 ± 0.5% (p = 0.01), with UCOL increasing from 2 (EC) to 4 (DC) (p = 0.02). Mild dehydration significantly impaired motor performance, expressed as shot distance (114.6 vs. 128.6 m; p < 0.001) and off-target accuracy (7.9 vs. 4.1 m; p = 0.001). Cognitive performance, expressed as the mean error in distance judgment to target increased from 4.1 ± 3.0 m (EC) to 8.8 ± 4.7 m (DC) (p < 0.001). The findings support those of previous research that indicates mild dehydration (-1 to 2% ΔBM) significantly impairs cognitive-motor task performance. This study is the first to show that mild dehydration can impair distance, accuracy, and distance judgment during golf performance.     

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.     

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.     

Dehydration anorexia is attenuated in oxytocin-deficient mice

Evidence in rats suggests that central oxytocin (OT) signaling pathways contribute to suppression of food intake during dehydration (i.e., dehydration anorexia). The present study examined water deprivation-induced dehydration anorexia in wild-type and OT -/- mice. Mice were deprived of food alone (fasted, euhydrated) or were deprived of both food and water (fasted, dehydrated) for 18 h overnight. Fasted wild-type mice consumed significantly less chow during a 60-min refeeding period when dehydrated compared with their intake when euhydrated. Conversely, fasting-induced food intake was slightly but not significantly suppressed by dehydration in OT -/- mice, evidence for attenuated dehydration anorexia. In a separate experiment, mice were deprived of water (but not food) overnight for 18 h; then they were anesthetized and perfused with fixative for immunocytochemical analysis of central Fos expression. Fos was elevated similarly in osmo- and volume-sensitive regions of the basal forebrain and hypothalamus in wild-type and OT -/- mice after water deprivation. OT-positive neurons expressed Fos in dehydrated wild-type mice, and vasopressin-positive neurons were activated to a similar extent in wild-type and OT -/- mice. Conversely, significantly fewer neurons within the hindbrain dorsal vagal complex were activated in OT -/- mice after water deprivation compared with activation in wild-type mice. These findings support the view that OT-containing projections from the hypothalamus to the hindbrain are necessary for the full expression of compensatory behavioral and physiological responses to dehydration.     

Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism.

Hypohydration (decreased total body water) exacerbates the catabolic hormonal response to endurance exercise with unclear effects on anabolic hormones. Limited research exists that evaluates the effect of hypohydration on endocrine responses to resistance exercise; this work merits attention as the acute postexercise hormonal environment potently modulates resistance training adaptations. The purpose of this study was to examine the effect of hydration state on the endocrine and metabolic responses to resistance exercise. Seven healthy resistance-trained men (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three identical resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via controlled water deprivation and exercise-heat stress. Cortisol, epinephrine, norepinephrine, testosterone, growth hormone, insulin-like growth factor-I, insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding resistance exercise, immediately postexercise, and during 60 min of recovery. Body mass decreased 0.2 +/- 0.4, 2.4 +/- 0.4, and 4.8 +/- 0.4% during EU, HY25, and HY50, respectively, supported by humoral and urinary changes that clearly indicated subjects achieved three distinct hydration states. Hypohydration significantly 1) increased circulating concentrations of cortisol and norepinephrine, 2) attenuated the testosterone response to exercise, and 3) altered carbohydrate and lipid metabolism. These results suggest that hypohydration can modify the hormonal and metabolic response to resistance exercise, influencing the postexercise circulatory milieu.     

Atrial natriuretic factor inhibits vasopressin secretion in conscious sheep

To test the hypothesis that atrial natriuretic factor (ANF) has a centrally mediated action on body fluid homeostasis, the effects of intracerebroventricularly (ICV) infused ANF on plasma vasopressin (AVP) concentration and urinary water and electrolyte excretion were investigated in euhydrated and water-deprived conscious sheep. ICV ANF decreased plasma AVP concentration and increased urinary free water excretion in euhydrated sheep, with excretion of Na and K unaltered. However, ICV ANF did not affect urinary volume, free water clearance, or excretion of Na and K in dehydrated animals, although plasma AVP concentration was significantly decreased. The relationship between urine volume and plasma AVP concentration was fitted by a power curve: urine volume = 0.79 X [AVP]-0.71; urine volume changes very little as a function of AVP concentration at the higher ranges. Intravenous infusion of the same amount of ANF was without effect on plasma AVP concentration or urinary excretion in both euhydrated and dehydrated animals. Mean arterial pressure was unchanged throughout all experiments. These results are consistent with the hypothesis that central ANF inhibits AVP secretion.     

Continuous measurement of Na concentration in CSF during gastric water infusion in dehydrated rats.

To assess the differential stimulus to central and intravascular osmoreceptors during recovery from thermal dehydration, we measured Na concentrations in cerebrospinal fluid ([Na]CSF) and plasma ([Na]p) continuously and compared these during simulated drinking by gastric water infusion (INF) in euhydrated and thermally dehydrated rats under anesthesia. Continuous measurement of [Na]CSF was obtained with a double-barreled Na electrode placed in the lateral ventricle. Continuous measurement of [Na]p was obtained from a flow cell Na electrode in an extracorporeal shunt. Measurements were made during 10 min of INF (2.5 ml/100 g body wt) into the stomach and during 20 min of recovery. Changes in [Na]CSF always lagged behind those in [Na]p and were quantitatively smaller after INF. The decrease in [Na]CSF occurred sooner in dehydrated than in euhydrated rats in response to the decrease in [Na]p (P < 0.01). These results suggest that water and/or Na movement between blood and CSF is accelerated during restitution from thermal dehydration, acting to prevent overhydration during the early phase of rehydration.     

The neurohypophyseal vasopressin content under conditions of inhibited synthesis of prostaglandins in euhydrated and dehydrated rats

Rats euhydrated or dehydrated up to eight days were given intraperitoneally indomethacin (IM) twice daily in a dose of 0.2 mg/100 g of initial body weight. A single dose of IM injected to euhydrated animals did not affect the neurohypophyseal vasopressor activity; however, when administered repeatedly during four or eight days, IM increased significantly the neurohypophyseal vasopressor activity. Under conditions of severe dehydration (eight days of water deprivation) the known depletion of neurohypophyseal vasopressin store was not significantly affected by indomethacin. It is, therefore, suggested that impulses of osmoreceptor origin are of distinct importance in determining the function of vasopressinergic neurons under conditions of inhibited prostaglandin synthesis.     

The validity of multifrequency bioelectrical impedance measures to detect changes in the hydration status of wrestlers during acute dehydration and rehydration

The objective of this study was to examine the validity of multifrequency direct segmental bioelectrical impedance analysis (DSM-BIA) measures to detect changes in the hydration status of wrestlers after they underwent 3% acute dehydration and a 2-hour rehydration period. Fifty-six National Collegiate Athletic Association wrestlers: (mean ± SEM); age 19.5 ± 0.2 years, height 1.73 ± 0.01 m, and body mass (BM) 82.5 ± 2.3 kg were tested in euhydrated, dehydrated (-3.5%), and 2-hour rehydration conditions using DSM-BIA to detect the changes in hydration status. The hydration status was quantified by measuring the changes in plasma osmolality (P(osm)), urine osmolality (Uosm), urine specific gravity (U(sg)), BM, and weighted segmental impedance at frequencies of 5, 20, 50, 100, and 500 kHz. Weighted segmental impedance significantly increased after a 3.5% reduction in the body weight for all the 5 frequencies evaluated, but it did not return to baseline at 2-hour rehydration. P(osm) (303 ± 0.6 mOsm·L(-1)), Uosm (617 ± 47 mOsm·L(-1)), and U(sg) (1.017 ± 0.001) all significantly increased at postdehydration and returned to baseline at 2-hour rehydration. Estimations of extracellular water were significantly different throughout the trial, but there were no significant changes in the estimations of the total body water or intracellular water. The results of this study demonstrate the potential use of DSM-BIA as a field measure to assess the hydration status of wrestlers for the purpose of minimal weight certification before the competitive season. When employing DSM-BIA to assess the hydration status, the results indicated that the changes in weighted segmental impedance at the frequencies evaluated (5, 20, 50, 100, and 500 kHz) are sensitive to acute changes in dehydration but lag behind changes in the standard physiological (plasma and urinary) markers of hydration status after a 2-hour rehydration period.     

Mechanically braked elliptical Wingate test: modification considerations, load optimization, and reliability

The 30-second, all-out Wingate test evaluates anaerobic performance using an upper or lower body cycle ergometer (cycle Wingate test). A recent study showed that using a modified electromagnetically braked elliptical trainer for Wingate testing (EWT) leads to greater power outcomes because of larger muscle group recruitment. The main purpose of this study was to modify an elliptical trainer using an easily understandable mechanical brake system instead of an electromagnetically braked modification. Our secondary aim was to determine a proper test load for the EWT to reveal the most efficient anaerobic test outcomes such as peak power (PP), average power (AP), minimum power (MP), power drop (PD), and fatigue index ratio (FI%) and to evaluate the retest reliability of the selected test load. Delta lactate responses (ΔLa) were also analyzed to confirm all the anaerobic performance of the athletes. Thirty healthy and well-trained male university athletes were selected to participate in the study. By analysis of variance, an 18% body mass workload yielded significantly greater test outcomes (PP = 19.5 ± 2.4 W·kg, AP = 13.7 ± 1.7 W·kg, PD = 27.9 ± 5 W·s, FI% = 58.4 ± 3.3%, and ΔLa = 15.4 ± 1.7 mM) than the other (12-24% body mass) tested loads (p < 0.05). Test and retest results for relative PP, AP, MP, PD, FI%, and ΔLa were highly correlated (r = 0.97, 0.98, 0.94, 0.91, 0.81, and 0.95, respectively). In conclusion, it was found that the mechanically braked modification of an elliptical trainer successfully estimated anaerobic power and capacity. A workload of 18% body mass was optimal for measuring maximal and reliable anaerobic power outcomes. Anaerobic testing using an EWT may be more useful to athletes and coaches than traditional cycle ergometers because a greater proportion of muscle groups are worked during exercise on an elliptical trainer.     

Precooling leg muscle improves intermittent sprint exercise performance in hot, humid conditions.

We used three techniques of precooling to test the hypothesis that heat strain would be alleviated, muscle temperature (Tmu) would be reduced, and as a result there would be delayed decrements in peak power output (PPO) during exercise in hot, humid conditions. Twelve male team-sport players completed four cycling intermittent sprint protocols (CISP). Each CISP consisted of twenty 2-min periods, each including 10 s of passive rest, 5 s of maximal sprint against a resistance of 7.5% body mass, and 105 s of active recovery. The CISP, preceded by 20 min of no cooling (Control), precooling via an ice vest (Vest), cold water immersion (Water), and ice packs covering the upper legs (Packs), was performed in hot, humid conditions (mean +/- SE; 33.7 +/- 0.3 degrees C, 51.6 +/- 2.2% relative humidity) in a randomized order. The rate of heat strain increase during the CISP was faster in Control than Water and Packs (P < 0.01), but it was similar to Vest. Packs and Water blunted the rise of Tmu until minute 16 and for the duration of the CISP (40 min), respectively (P < 0.01). Reductions in PPO occurred from minute 32 onward in Control, and an increase in PPO by approximately 4% due to Packs was observed (main effect; P < 0.05). The method of precooling determined the extent to which heat strain was reduced during intermittent sprint cycling, with leg precooling offering the greater ergogenic effect on PPO than either upper body or whole body cooling.     

Growth hormone treatment in growth hormone-deficient adults. II. Effects on exercise performance

Growth hormone (GH) treatment in adults with GH deficiency increases lean body mass and thigh muscle cross-sectional area. The functional significance of this was examined by incremental cycle ergometry in 24 GH-deficient adults treated in a double-blind placebo-controlled trial with recombinant DNA human GH (rhGH) for 6 mo (0.07 U/kg body wt daily). Compared with placebo, the rhGH group increased mean maximal O2 uptake (VO2max) (+406 +/- 71 vs. +133 +/- 84 ml/min; P = 0.016) and maximal power output (+24.6 +/- 4.3 vs. +9.7 +/- 4.8 W; P = 0.047), without differences in maximal heart rate or ventilation. Forced expiratory volume in 1 s, vital capacity, and corrected CO gas transfer were within normal limits and did not change with treatment. Mean predicted VO2max, based on height and age, increased from 78.9 to 96.0% in the rhGH group (compared with 78.5 and 85.0% for placebo; P = 0.036). The anaerobic ventilatory threshold increased in the rhGH group (+159 +/- 39 vs. +1 +/- 51 ml/min; P = 0.02). The improvement in VO2max was noted when expressed per kilogram body weight but not lean body mass or thigh muscle area. We conclude that rhGH treatment in adults with GH deficiency improves and normalizes maximal exercise performance and improves submaximal exercise performance and that these changes are related to increases in lean body mass and muscle mass. Improved cardiac output may also contribute to the effect of rhGH on exercise performance.     

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise

González-Alonso, José, RicardoMora-Rodríguez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function inhyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229-1236, 1997.Weidentified the cardiovascular stress encountered by superimposingdehydration on hyperthermia during exercise in the heat and themechanisms contributing to the dehydration-mediated stroke volume (SV)reduction. Fifteen endurance-trained cyclists [maximalO₂ consumption(O_{2 max}) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinkingfluids. Measurements were made after they continued exercise at 71%O_{2 max} for 30 minwhile 1) euhydrated with anesophageal temperature (T_es) of38.1-38.3°C (control); 2)euhydrated and hyperthermic (39.3°C);3) dehydrated and hyperthermic withskin temperature (T_sk) of34°C; 4) dehydrated withT_es of 38.1°C and T_sk of 21°C; and5) condition4 followed by restored blood volume. Compared withcontrol, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separatelylowered SV 7-8% (11 ± 3 ml/beat;P < 0.05) and increased heart ratesufficiently to prevent significant declines in cardiac output.However, when dehydration was superimposed on hyperthermia, thereductions in SV were significantly (P < 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterialpressure declined 5 ± 2%, and systemic vascular resistanceincreased 10 ± 3% (both P < 0.05). When hyperthermia wasprevented, all of the decline in SV with dehydration was due to reducedblood volume (~200 ml). These results demonstrate that thesuperimposition of dehydration on hyperthermia during exercise in theheat causes an inability to maintain cardiac output and blood pressurethat makes the dehydrated athlete less able to cope with hyperthermia.

     

Whole body and abdominal lipolytic sensitivity to epinephrine is suppressed in upper body obese women

We measured whole body and regional lipolytic and adipose tissue blood flow (ATBF) sensitivity to epinephrine in 8 lean [body mass index (BMI): 21 +/- 1 kg/m(2)] and 10 upper body obese (UBO) women (BMI: 38 +/- 1 kg/m(2); waist circumference >100 cm). All subjects underwent a four-stage epinephrine infusion (0.00125, 0.005, 0.0125, and 0.025 microgram. kg fat-free mass(-1). min(-1)) plus pancreatic hormonal clamp. Whole body free fatty acid (FFA) and glycerol rates of appearance (R(a)) in plasma were determined by stable isotope tracer methodology. Abdominal and femoral subcutaneous adipose tissue lipolytic activity was determined by microdialysis and (133)Xe clearance methods. Basal whole body FFA R(a) and glycerol R(a) were both greater (P < 0.05) in obese (449 +/- 31 and 220 +/- 12 micromol/min, respectively) compared with lean subjects (323 +/- 44 and 167 +/- 21 micromol/min, respectively). Epinephrine infusion significantly increased FFA R(a) and glycerol R(a) in lean (71 +/- 21 and 122 +/- 52%, respectively; P < 0.05) but not obese subjects (7 +/- 6 and 39 +/- 10%, respectively; P = not significant). In addition, lipolytic and ATBF sensitivity to epinephrine was blunted in abdominal but not femoral subcutaneous adipose tissue of obese compared with lean subjects. We conclude that whole body lipolytic sensitivity to epinephrine is blunted in women with UBO because of decreased sensitivity in upper body but not lower body subcutaneous adipose tissue.     

The effects of protein and amino acid supplementation on performance and training adaptations during ten weeks of resistance training

The purpose of this study was to examine the effects of whey protein supplementation on body composition, muscular strength, muscular endurance, and anaerobic capacity during 10 weeks of resistance training. Thirty-six resistance-trained males (31.0 +/- 8.0 years, 179.1 +/- 8.0 cm, 84.0 +/- 12.9 kg, 17.8 +/- 6.6%) followed a 4 days-per-week split body part resistance training program for 10 weeks. Three groups of supplements were randomly assigned, prior to the beginning of the exercise program, in a double-blind manner to all subjects: 48 g per day (g.d(-1)) carbohydrate placebo (P), 40 g.d(-1) of whey protein + 8 g.d(-1) of casein (WC), or 40 g.d(-1) of whey protein + 3 g.d(-1) branched-chain amino acids + 5 g.d(-1) L-glutamine (WBG). At 0, 5, and 10 weeks, subjects were tested for fasting blood samples, body mass, body composition using dual-energy x-ray absorptiometry (DEXA), 1 repetition maximum (1RM) bench and leg press, 80% 1RM maximal repetitions to fatigue for bench press and leg press, and 30-second Wingate anaerobic capacity tests. No changes (p > 0.05) were noted in all groups for energy intake, training volume, blood parameters, and anaerobic capacity. WC experienced the greatest increases in DEXA lean mass (P = 0.0 +/- 0.9; WC = 1.9 +/- 0.6; WBG = -0.1 +/- 0.3 kg, p < 0.05) and DEXA fat-free mass (P = 0.1 +/- 1.0; WC = 1.8 +/- 0.6; WBG = -0.1 +/- 0.2 kg, p < 0.05). Significant increases in 1RM bench press and leg press were observed in all groups after 10 weeks. In this study, the combination of whey and casein protein promoted the greatest increases in fat-free mass after 10 weeks of heavy resistance training. Athletes, coaches, and nutritionists can use these findings to increase fat-free mass and to improve body composition during resistance training.