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Systemic immune function is impaired by sleep restriction. However, the impact of sleep restriction on local immune responses and to what extent any impairment can be mitigated by nutritional supplementation is unknown. We assessed the effect of 72-h sleep restriction (2-h nightly sleep) on local immune function and skin barrier restoration of an experimental wound, and determined the influence of habitual protein intake (1.5 g·kg−1·day−1) supplemented with arginine, glutamine, zinc sulfate, vitamin C, vitamin D3, and omega-3 fatty acids compared with lower protein intake (0.8 g·kg−1·day−1) without supplemental nutrients on these outcomes. Wounds were created in healthy adults by removing the top layer of less than or equal to eight forearm blisters induced via suction, after adequate sleep (AS) or 48 h of a 72-h sleep restriction period (SR; 2-h nightly sleep). A subset of participants undergoing sleep restriction received supplemental nutrients during and after sleep restriction (SR+). Wound fluid was serially sampled 48 h postblistering to assess local cytokine responses. The IL-8 response of wound fluid was higher for AS compared with SR [area-under-the-curve (log10), 5.1 ± 0.2 and 4.9 ± 0.2 pg/ml, respectively; P = 0.03]; and both IL-6 and IL-8 concentrations were higher for SR+ compared with SR ( P < 0.0001), suggestive of a potentially enhanced early wound healing response. Skin barrier recovery was shorter for AS (4.2 ± 0.9 days) compared with SR (5.0 ± 0.9 days) ( P = 0.02) but did not differ between SR and SR+ ( P = 0.18). Relatively modest sleep disruption delays wound healing. Supplemental nutrition may mitigate some decrements in local immune responses, without detectable effects on wound healing rate. NEW & NOTEWORTHY The data herein characterizes immune function in response to sleep restriction in healthy volunteers with and without nutrition supplementation. We used a unique skin wound model to show that sleep restriction delays skin barrier recovery, and nutrition supplementation attenuates decrements in local immune responses produced by sleep restriction. These findings support the beneficial effects of adequate sleep on immune function. Additional studies are necessary to characterize practical implications for populations where sleep restriction is unavoidable.

DON'T FORGET THE GUT—IT IS AN IMPORTANT ATHLETIC ORGAN! {#article-title-2} to the editor: It was with great interest that we read the Journal of Applied Physiology Viewpoint on the 2-h marathon barrier ([3][1]). We would argue that, alongside having a superlative Vo2max, lactate threshold

The Institute of Medicine expressed a need for improved sweating rate (ṁsw) prediction models that calculate hourly and daily water needs based on metabolic rate, clothing, and environment. More than 25 years ago, the original Shapiro prediction equation (OSE) was formulated as ṁsw (g·m−2·h−1) = 27.9· Ereq·( Emax)−0.455, where Ereq is required evaporative heat loss and Emax is maximum evaporative power of the environment; OSE was developed for a limited set of environments, exposures times, and clothing systems. Recent evidence shows that OSE often overpredicts fluid needs. Our study developed a corrected OSE and a new ṁsw prediction equation by using independent data sets from a wide range of environmental conditions, metabolic rates (rest to ≤450 W/m2), and variable exercise durations. Whole body sweat losses were carefully measured in 101 volunteers (80 males and 21 females; >500 observations) by using a variety of metabolic rates over a range of environmental conditions (ambient temperature, 15–46°C; water vapor pressure, 0.27–4.45 kPa; wind speed, 0.4–2.5 m/s), clothing, and equipment combinations and durations (2–8 h). Data are expressed as grams per square meter per hour and were analyzed using fuzzy piecewise regression. OSE overpredicted sweating rates ( P < 0.003) compared with observed ṁsw. Both the correction equation (OSEC), ṁsw = 147·exp (0.0012·OSE), and a new piecewise (PW) equation, ṁsw = 147 + 1.527· Ereq − 0.87· Emax were derived, compared with OSE, and then cross-validated against independent data (21 males and 9 females; >200 observations). OSEC and PW were more accurate predictors of sweating rate (58 and 65% more accurate, P < 0.01) and produced minimal error (standard error estimate < 100 g·m−2·h−1) for conditions both within and outside the original OSE domain of validity. The new equations provide for more accurate sweat predictions over a broader range of conditions with applications to public health, military, occupational, and sports medicine settings.

Energy restriction coupled with high energy expenditure from arduous work is associated with an altered insulin-like growth factor-I (IGF-I) system and androgens that are coincident with losses of fat-free mass. The aim of this study was to determine the effects of two levels of dietary protein content and its effects on IGF-I, androgens, and losses of fat-free mass accompanying energy deficit. We hypothesized that higher dietary protein content would attenuate the decline of anabolic hormones and, thus, prevent losses of fat-free mass. Thirty-four men [24 (SD 0.3) yr, 180.1 (SD 1.1) cm, and 83.0 (SD 1.4) kg] participated in an 8-day military exercise characterized by high energy expenditure (16.5 MJ/day), low energy intake (6.5 MJ/day), and sleep deprivation (4 h/24 h) and were randomly divided into two dietary groups: 0.9 and 0.5 g/kg dietary protein intake. IGF-I system analytes, androgens, and body composition were assessed before and on days 4 and 8 of the intervention. Total, free, and nonternary IGF-I and testosterone declined 50%, 64%, 55%, and 45%, respectively, with similar reductions in both groups. There was, however, a diet × time interaction on day 8 for total IGF-I and sex hormone-binding globulin. Decreases in body mass (3.2 kg), fat-free mass (1.2 kg), fat mass (2.0 kg), and percent body fat (1.5%) were similar in both groups ( P = 0.01). Dietary protein content of 0.5 and 0.9 g/kg minimally attenuated the decline of IGF-I, the androgenic system, and fat-free mass during 8 days of negative energy balance associated with high energy expenditure and low energy intake.

The induction of cellular acquired thermal tolerance (ATT) during heat acclimation (HA) in humans is not well described. This study determined whether exercise-HA modifies the human heat shock protein (HSP)72 and HSP90 responses and whether changes are correlated with physiological adaptations to HA. Using a 10-day HA protocol comprising daily exercise (treadmill walking) in a hot environment ( Ta = 49°C, 20% RH), we analyzed baseline and ex vivo heat-induced expression of HSP72 and HSP90 in peripheral blood mononuclear cells (PBMCs) isolated prior to exercise from eight subjects on day 1 and 10 of the HA protocol. Classical physiological responses to HA were observed, including significantly reduced heart rate and core body temperature, and significantly increased sweating rate. Baseline levels of HSP72 and HSP90 were significantly increased following acclimation by 17.7 ± 6.1% and 21.1 ± 6.5%, respectively. Ex vivo induction of HSP72 in PBMCs exposed to heat shock (43°C) was blunted on day 10 compared with day 1. A correlation was identified ( r2 = 0.89) between changes in core temperature elevation and ex vivo HSP90 responses to heat shock between days 1 and 10, indicating that volunteers demonstrating the greatest physiological HA tended to exhibit the greatest blunting of ex vivo HSP induction in response to heat shock. In summary, 1) exercise-HA resulted in increased baseline levels of HSP72 and HSP90, 2) ex vivo heat inducibility of HSP72 was blunted after HA, and 3) volunteers demonstrating the greatest physiological HA tended to exhibit the greatest blunting of ex vivo HSP induction in response to heat shock. These data demonstrate that physiological adaptations in humans undergoing HA are accompanied by both increases in baseline levels and changes in regulation of cytoprotective HSPs.

The pulsatile release of growth hormone (GH) and luteinizing hormone (LH) from the anterior pituitary gland is integral for signaling secretion of insulin-like growth factor (IGF)-I and testosterone, respectively. This study examined the hypothesis that 84 h of sustained physical exertion with caloric and sleep restriction alters the secretion of GH and LH. Ten male soldiers [22 yr (SD 3), 183 cm (SD 7), 87 kg (SD 8)] had blood drawn overnight from 1800 to 0600 every 20 min for GH, LH, and leptin and every 2 h for IGF-I (total and free), IGF binding proteins-1 and -3, testosterone (total and free), glucose, and free fatty acids during a control week and after 84 h of military operational stress. Time-series cluster and deconvolution analyses assessed the secretion parameters of GH and LH. Significant results (Por = 0.05) were as follows: body mass (-3%), fat-free mass (-2.3%), and fat mass (-7.3%) declined after military operational stress. GH and LH secretion burst amplitude (approximately 50%) and overnight pulsatile secretion (approximately 50%), IGF binding protein-1 (+67%), and free fatty acids (+33%) increased, whereas leptin (-47%), total (-27%) and free IGF-I (-32%), total (-24%) and free testosterone (-30%), and IGF binding protein-3 (-6%) decreased. GH and LH pulse number were unaffected. Because GH and LH positively regulate IGF-I and testosterone, these data imply that the physiological strain induced a certain degree of peripheral resistance. During periods of energy deficiency, amplitude modulation of GH and LH pulses may precede alterations in pulse numbers.

This study was conducted to determine whether hypohydration (Hy) alters blood flow, skin temperature, or cold-induced vasodilation (CIVD) during peripheral cooling. Fourteen subjects sat in a thermoneutral environment (27°C) during 15-min warm-water (42°C) and 30-min cold-water (4°C) finger immersion (FI) while euhydrated (Eu) and, again, during Hy. Hy (−4% body weight) was induced before FI by exercise-heat exposure (38°C, 30% relative humidity) with no fluid replacement, whereas during Eu, fluid intake maintained body weight. Finger pad blood flow [as measured by laser-Doppler flux (LDF)] and nail bed (Tnb), pad (Tpad), and core (Tc) temperatures were measured. LDF decreased similarly during Eu and Hy (32 ± 10 and 33 ± 13% of peak during warm-water immersion). Mean Tnb and Tpad were similar between Eu (7.1 ± 1.0 and 11.5 ± 1.6°C) and Hy (7.4 ± 1.3 and 12.6 ± 2.1°C). CIVD parameters (e.g., nadir, onset time, apex) were similar between trials, except Tpad nadir was higher during Hy (10.4 ± 3.8°C) than during Eu (7.9 ± 1.6°C), which was attributed to higher Tc in six subjects during Hy (37.5 ± 0.2°C), compared with during Eu (37.1 ± 0.1°C). The results of this study provide no evidence that Hy alters finger blood flow, skin temperature, or CIVD during peripheral cooling.

This study examined whether muscle injury and the accompanying inflammatory responses alter thermoregulation during subsequent exercise-heat stress. Sixteen subjects performed 50 min of treadmill exercise (45–50% maximal O2 consumption) in a hot room (40°C, 20% relative humidity) before and at select times after eccentric upper body (UBE) and/or eccentric lower body (LBE) exercise. In experiment 1, eight subjects performed treadmill exercise before and 6, 25, and 30 h after UBE and then 6, 25, and 30 h after LBE. In experiment 2, eight subjects performed treadmill exercise before and 2, 7, and 26 h after LBE only. UBE and LBE produced marked soreness and significantly elevated creatine kinase levels ( P < 0.05), but only LBE increased ( P < 0.05) interleukin-6 levels. In experiment 1, core temperatures before and during exercise-heat stress were similar for control and after UBE, but some evidence for higher core temperatures was found after LBE. In experiment 2, core temperatures during exercise-heat stress were 0.2–0.3°C ( P < 0.05) above control values at 2 and 7 h after LBE. The added thermal strain after LBE ( P < 0.05) was associated with higher metabolic rate ( r = 0.70 and 0.68 at 2 and 6–7 h, respectively) but was not related ( P > 0.05) to muscle soreness ( r = 0.47 at 6–7 h), plasma interleukin-6 ( r = 0.35 at 6–7 h), or peak creatine kinase levels ( r = 0.22). Local sweating responses (threshold core temperature and slope) were not altered by UBE or LBE. The results suggest that profuse muscle injury can increase body core temperature during exercise-heat stress and that the added heat storage cannot be attributed solely to increased heat production.

Five women and 3 men (29.8 ± 1.4 yr) performed dynamic knee-extension exercise inside a magnetic resonance system (means ± SE). Two trials were performed 7–14 days apart, consisting of a 4- to 5-min exhaustive exercise bout. To determine quadriceps cost of contraction, brief static and dynamic contractions were performed pre- and postexercise.31P spectra were used to determine pH and relative concentrations of Pi, phosphocreatine (PCr), and βATP. Subjects consumed 0.3 g ⋅ kg−1 ⋅ day−1of a placebo ( trial 1) or creatine ( trial 2) for 5 days before each trial. After creatine supplementation, resting ΔPCr increased from 40.7 ± 1.8 to 46.6 ± 1.1 mmol/kg ( P = 0.04) and PCr during exercise declined from −29.6 ± 2.4 to −34.1 ± 2.8 mmol/kg ( P = 0.02). Muscle static (ΔATP/N) and dynamic (ΔATP/J) costs of contraction were unaffected by creatine supplementation as well as were ATP, Pi, pH, PCr resynthesis rate, and muscle strength and endurance. ΔATP/J and ΔATP/N were greatest at the onset of the exercise protocol ( P< 0.01). In summary, creatine supplementation increased muscle PCr concentration, which did not affect muscle ATP cost of contraction.

Young [ n = 5, 30 ± 5 (SD) yr] and middle-aged ( n = 4, 58 ± 4 yr) men and women performed single-leg knee-extension exercise inside a whole body magnetic resonance system. Two trials were performed 7 days apart and consisted of two 2-min bouts and a third bout continued to exhaustion, all separated by 3 min of recovery.31P spectra were used to determine pH and relative concentrations of Pi, phosphocreatine (PCr), and β-ATP every 10 s. The subjects consumed 0.3 g ⋅ kg−1 ⋅ day−1of a placebo ( trial 1) or creatine ( trial 2) for 5 days before each trial. During the placebo trial, the middle-aged group had a lower resting PCr compared with the young group (35.0 ± 5.2 vs. 39.5 ± 5.1 mmol/kg, P < 0.05) and a lower mean initial PCr resynthesis rate (18.1 ± 3.5 vs. 23.2 ± 6.0 mmol ⋅ kg−1 ⋅ min−1, P < 0.05). After creatine supplementation, resting PCr increased 15% ( P < 0.05) in the young group and 30% ( P < 0.05) in the middle-aged group to 45.7 ± 7.5 vs. 45.7 ± 5.5 mmol/kg, respectively. Mean initial PCr resynthesis rate also increased in the middle-aged group ( P < 0.05) to a level not different from the young group (24.3 ± 3.8 vs. 24.2 ± 3.2 mmol ⋅ kg−1 ⋅ min−1). Time to exhaustion was increased in both groups combined after creatine supplementation (118 ± 34 vs. 154 ± 70 s, P < 0.05). In conclusion, creatine supplementation has a greater effect on PCr availability and resynthesis rate in middle-aged compared with younger persons.

A physiological strain index (PSI), based on rectal temperature (Tre) and heart rate (HR), was recently suggested for evaluating heat stress. The purpose of this study was to evaluate the PSI for different combinations of hydration level and exercise intensity. This index was applied to two databases. The first database was obtained from eight endurance-trained men dehydrated to four different levels (1.1, 2.3, 3.4, and 4.2% of body wt) during 120 min of cycling at a power output of 62–67% maximum O2 consumption (V˙o 2 max) in the heat [33°C and 50% relative humidity (RH)]. The second database was obtained from nine men performing exercise in the heat (30°C and 50% RH) for 50 min. These subjects completed a matrix of nine trials of exercise on a treadmill at three exercise intensities (25, 45, and 65%V˙o 2 max) and three hydration levels (euhydration and hypohydration at 3 and 5% of body wt). Tre, HR, esophageal temperature (Tes), and local sweating rate were measured. PSI (obtained from either Tre or Tes) significantly ( P < 0.05) differentiated among all exposures in both databases categorized by exercise intensity and hydration level, and we assessed the strain on a scale ranging from 0 to 10. Therefore, PSI applicability was extended for heat strain associated with hypohydration and continues to provide the potential to be universally accepted.

Latzka, William A., Michael N. Sawka, Scott J. Montain, Gary S. 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 study examined the effects of hyperhydration on thermoregulatory responses during compensable exercise-heat stress. The general approach was to determine whether 1-h preexercise hyperhydration [29.1 ml/kg lean body mass; with or without glycerol (1.2 g/kg lean body mass)] would improve sweating responses and reduce core temperature during exercise. During these experiments, the evaporative heat loss required (Ereq = 293 W/m2) to maintain steady-state core temperature was less than the maximal capacity (Emax = 462 W/m2) of the climate for evaporative heat loss (Ereq/Emax= 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and without rehydration (replace sweat loss during exercise). During exercise in the heat (35°C, 45% relative humidity), there was no difference between hyperhydration methods for increasing total body water (∼1.5 liters). Compared with euhydration, hyperhydration did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responses. Similarly, no difference was found between water and glycerol hyperhydration for these physiological responses. These data demonstrate that hyperhydration provides no thermoregulatory advantage over the maintenance of euhydration during compensable exercise-heat stress.

Glycerol ingestion has been shown to mediate hyperhydration; however, the mechanism(s) responsible for this improved fluid retention is not well understood. This study examined the hormonal, renal, and vascular fluid responses to glycerol hyperhydration in 11 resting male volunteers who ingested one of two experimental solutions and then a water bolus. The volume of fluid ingested was determined from the subjects' measured total body water (TBW; total volume = 37 ml/l TBW, 1,765 +/- 162 ml). Experimental solutions (5.0 ml/l TBW) were matched for color and taste and differed only in that one contained 1.5 g glycerol/l TBW (total osmolar load = 777 +/- 24 mosmol). Nine of the 11 subjects also completed a control trial during which no fluid was ingested. Glycerol ingestion (GI) resulted in greater fluid retention than the ingestion of water alone (WI; 60 vs. 32% 3-h posthyperhydration, P < 0.01). This improved fluid retention with GI resulted from lower urine flow rates (peak 6.2 vs. 10.5 ml/min, P < 0.01) associated with lower free water clearance rates (peak = 1.2 vs. 8.2 ml/min, P < 0.01). Hyperhydration had no effect on plasma atrial natriuretic peptide concentrations. Changes in plasma aldosterone were unrelated to differences in fluid retention. Antidiuretic hormone concentrations (ADH) were significantly reduced from prehyperhydration levels during both hyperhydration trials but tended (P = 0.07) to rise during GI compared with WI at the very time urine flow and free water clearance differences were also evident. This suggests that ADH may, in part, be responsible for glycerol's effectiveness, although differences in ADH concentrations were small and near the assay's sensitivity limits. Alternatively, glycerol's effectiveness may result from its directly increasing the kidneys' medullary concentration gradient and, hence, water reabsorption.