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Environmental heat stress can challenge the limits of human cardiovascular and temperature regulation, body fluid balance, and thus aerobic performance. This minireview proposes that the cardiovascular adjustments accompanying high skin temperatures (Tsk), alone or in combination with high core body temperatures (Tc), provide a primary explanation for impaired aerobic exercise performance in warm-hot environments. The independent (Tsk) and combined (Tsk + Tc) effects of hyperthermia reduce maximal oxygen uptake (V̇o2max), which leads to higher relative exercise intensity and an exponential decline in aerobic performance at any given exercise workload. Greater relative exercise intensity increases cardiovascular strain, which is a prominent mediator of rated perceived exertion. As a consequence, incremental or constant-rate exercise is more difficult to sustain (earlier fatigue) or requires a slowing of self-paced exercise to achieve a similar sensation of effort. It is proposed that high Tsk and Tc impair aerobic performance in tandem primarily through elevated cardiovascular strain, rather than a deterioration in central nervous system (CNS) function or skeletal muscle metabolism. Evaporative sweating is the principal means of heat loss in warm-hot environments where sweat losses frequently exceed fluid intakes. When dehydration exceeds 3% of total body water (2% of body mass) then aerobic performance is consistently impaired independent and additive to heat stress. Dehydration augments hyperthermia and plasma volume reductions, which combine to accentuate cardiovascular strain and reduce V̇o2max. Importantly, the negative performance consequences of dehydration worsen as Tsk increases.

Evidence suggests that core temperatures of ∼40°C can induce fatigue, although this may be confounded by coincident elevations in skin temperatures and maximal cardiovascular strain. In an observational field study to examine core temperature threshold for fatigue, we investigated whether running performance is impaired when rectal temperature (Tre) is >40°C and skin temperature remains modest. Seventeen competitive runners (7/10 women/men: 8 km best 1,759 ± 78/1,531 ± 60 s) completed 8-km track time trials in cool (WBGT ∼13°C; n = 6), warm (WBGT ∼27°C; n = 4), or both ( n = 7) conditions. Tre, chest skin temperature, and heart rate were logged continuously; elapsed time was recorded every 200 m. Running velocity for Tre>40°C was compared with that for Trere>40°C and re>40.0°C with ≥600 m remaining (range 600–3,400 m). Average running velocity for Trere>40°C (279 ± 28 m/min; P = 0.82). There were no differences in running velocity during the final 600 m between runners with final Tre>40°C or 95% of age-predicted maximum. Our observation that runners were able to sustain running velocity despite Tre>40°C is evidence against 40°C representing a “critical” core temperature limit to performance.

Sweating threshold temperature and sweating sensitivity responses are measured to evaluate thermoregulatory control. However, analytic approaches vary, and no standardized methodology has been validated. This study validated a simple and standardized method, segmented linear regression (SReg), for determination of sweating threshold temperature and sensitivity. Archived data were extracted for analysis from studies in which local arm sweat rate (ṁsw; ventilated dew-point temperature sensor) and esophageal temperature (Tes) were measured under a variety of conditions. The relationship ṁsw/Tes from 16 experiments was analyzed by seven experienced raters (Rater), using a variety of empirical methods, and compared against SReg for the determination of sweating threshold temperature and sweating sensitivity values. Individual interrater differences ( n = 324 comparisons) and differences between Rater and SReg ( n = 110 comparisons) were evaluated within the context of biologically important limits of magnitude (LOM) via a modified Bland-Altman approach. The average Rater and SReg outputs for threshold temperature and sensitivity were compared ( n = 16) using inferential statistics. Rater employed a very diverse set of criteria to determine the sweating threshold temperature and sweating sensitivity for the 16 data sets, but interrater differences were within the LOM for 95% (threshold) and 73% (sensitivity) of observations, respectively. Differences between mean Rater and SReg were within the LOM 90% (threshold) and 83% (sensitivity) of the time, respectively. Rater and SReg were not different by conventional t-test ( P > 0.05). SReg provides a simple, valid, and standardized way to determine sweating threshold temperature and sweating sensitivity values for thermoregulatory studies.

Insulin-like growth factor (IGF)-I is a biomarker that may have greater utility than other conventional nutritional biomarkers in assessing nutritional, health, and fitness status. We hypothesized that the IGF-I system would directionally track a short-term energy deficit and would be more related to changes in body composition than other nutritional biomarkers. Thirty-five healthy men (24 ± 0.3 yr) underwent 8 days of exercise and energy imbalance. Total and free IGF-I, IGF binding proteins-1, -2, and -3, the acid labile subunit, transferrin, ferritin, retinol binding protein, prealbumin, testosterone, triiodothyronine, thyroxine, and leptin responses were measured. Dual-energy X-ray absorptiometry assessed changes in body mass and composition. Repeated-measures ANOVA, correlation analysis, and receiver operator characteristic curves were used for statistical analyses ( P ≤ 0.05). Body mass (−3.8%), fat-free mass (−2.2%), and fat mass (−12.9%) all decreased. Total and free IGF-I, IGF binding protein-3, and the acid labile subunit and prealbumin, but not transferrin, retinol-binding protein, and ferritin, directionally tracked the energy deficit and losses in body composition. The correlation ( r = 0.43) between changes in free IGF-I and body and fat-free mass was the only significant association observed. Receiver operator characteristic curve analysis revealed that a baseline value < 1.67 for the molar volume ratio of IGF-I to acid labile subunit had an area under the curve of 0.745 and was a significant discriminator for those subjects losing >5% body mass. The IGF-I system is an important adjunct in the overall assessment of adaptation to stress imposed by high levels of physical activity superimposed on energy and sleep restriction and is more closely associated with losses in body mass and fat-free mass than other conventional nutritional biomarkers.

Recent human isolated muscle fiber studies suggest that phosphocreatine (PCr) and creatine (Cr) concentrations play a role in the regulation of mitochondrial respiration rate. To determine whether similar regulatory mechanisms are present in vivo, this study examined the relationship between skeletal muscle mitochondrial respiration rate and end-exercise PCr, Cr, PCr-to-Cr ratio (PCr/Cr), ADP, and pH by using 31P-magnetic resonance spectroscopy in 16 men and women (36.9 ± 4.6 yr). The initial PCr resynthesis rate and time constant (Tc) were used as indicators of mitochondrial respiration after brief (10–12 s) and exhaustive (1–4 min) dynamic knee extension exercise performed in placebo and creatine-supplemented conditions. The results show that the initial PCr resynthesis rate has a strong relationship with end-exercise PCr, Cr, and PCr/Cr ( r > 0.80, P < 0.001), a moderate relationship with end-exercise ADP ( r = 0.77, P < 0.001), and no relationship with end-exercise pH ( r = -0.14, P = 0.34). The PCr Tc was not as strongly related to PCr, Cr, PCr/Cr, and ADP ( r < 0.77, P < 0.001–0.18) and was significantly influenced by end-exercise pH ( r = -0.43, P < 0.01). These findings suggest that end-exercise PCr and Cr should be taken into consideration when PCr recovery kinetics is used as an indicator of mitochondrial respiration and that the initial PCr resynthesis rate is a more reliable indicator of mitochondrial respiration compared with the PCr Tc.

Insulin-like growth factor (IGF) I and IGF binding proteins (IGFBPs) modulate metabolic activity and tissue repair and are influenced by nutritional status. IGF-I circulates in free, ternary [IGF-I + IGFBP-3 + acid labile subunit (ALS)], and binary (IGF-I + IGFBP) molecular complexes, and the relative proportions regulate IGF-I extravascular shifting and bioavailability. This study examined the hypothesis that sustained physical activity and sleep deprivation superimposed on a short-term energy deficit would alter the IGFBP concentrations and alter the proportions of IGF-I circulating in ternary vs. binary molecular complexes. Components of the IGF-I system (total and free IGF-I; IGFBP-1, -3, and ALS; nonternary IGF-I and IGFBP-3), biomarkers of metabolic and nutritional status (transferrin, ferritin, prealbumin, glucose, free fatty acids, glycerol, beta-hydroxybutyrate), and body composition were measured in 12 men (22 +/- 3 yr, 87 +/- 8 kg, 183 +/- 7 cm, 20 +/- 5% body fat) on days 1, 3, and 4 during a control and experimental (Exp) period. During Exp, subjects performed prolonged work (energy expenditure of approximately 4500 kcal/day) with caloric (1600 kcal/day) and sleep (6.2 h total) restriction. IGF-I and IGFBP-3 were measured by immunoassay before and after immunoaffinity depletion of ALS-based complexes (i.e., ternary complex removal). Exp produced losses in body mass (-3.0%), lowered total IGF-I (-24%), free IGF-I (-42%), IGFBP-3 (-6%), nonternary IGF-I (-27%), and IGFBP-3 (-16%), and increased IGFBP-1 (256%). No Exp effects were observed for ALS. No changes were observed in the proportion of IGF-I circulating in free ( approximately 1.2%), ternary ( approximately 87.4%), or nonternary ( approximately 11.4%) molecular complexes. During Exp, glucose concentrations were lower on day 3, but days 1 and 4 were statistically similar. In conclusion, during a short-term energy deficit in young, healthy men, 1). IGF-I system components differentially respond (both in direction and magnitude) to a given metabolic perturbation and 2). the relative proportion of IGF-I sequestered in ternary vs. nonternary molecular complexes appears to be well maintained.

The vasomotor response to cold may compromise the capacity for microclimate cooling (MCC) to reduce thermoregulatory strain. This study examined the hypothesis that intermittent, regional MCC (IRC) would abate this response and improve heat loss when compared with constant MCC (CC) during exercise heat stress. In addition, the relative effectiveness of four different IRC regimens was compared. Five heat-acclimated men attempted six experimental trials of treadmill walking (∼225 W/m2) in a warm climate (dry bulb temperature = 30°C, dewpoint temperature = 11°C) while wearing chemical protective clothing (insulation = 2.1; moisture permeability = 0.32) with a water-perfused (21°C) cooling undergarment. The six trials conducted were CC (continuous perfusion) of 72% body surface area (BSA), two IRC regimens cooling 36% BSA by using 2:2 (IRC1) or 4:4 (IRC2) min on-off perfusion ratios, two IRC regimens cooling 18% BSA by using 1:3 (IRC3) or 2:6 (IRC4) min on-off perfusion ratios, and a no cooling (NC) control. Compared with NC, CC significantly reduced changes in rectal temperature (∼1.2°C) and heart rate (∼60 beats/min) ( P < 0.05). The four IRC regimens all provided a similar reduction in exercise heat strain and were 164–215% more efficient than CC because of greater heat flux over a smaller BSA. These findings indicate that the IRC approach to MCC is a more efficient means of cooling when compared with CC paradigms and can improve MCC capacity by reducing power requirements.

This study examined the efficacy of glycerol and water hyperhydration (1 h before exercise) on tolerance and cardiovascular strain during uncompensable exercise-heat stress. The approach was to determine whether 1-h preexercise hyperhydration (29.1 ml H2O/kg lean body mass with or without 1.2 g/kg lean body mass of glycerol) provided a physiological advantage over euhydration. Eight heat-acclimated men completed three trials (control euhydration before exercise, and glycerol and water hyperhydrations) consisting of treadmill exercise-heat stress (ratio of evaporative heat loss required to maximal capacity of climate = 416). During exercise (∼55% maximal O2 uptake), there was no difference between glycerol and water hyperhydration methods for increasing ( P < 0.05) total body water. Glycerol hyperhydration endurance time (33.8 ± 3.0 min) was longer ( P < 0.05) than for control (29.5 ± 3.5 min), but was not different ( P > 0.05) from that of water hyperhydration (31.3 ± 3.1 min). Hyperhydration did not 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 and heart rates in each trial. Symptoms at exhaustion included syncope and ataxia, fatigue, dyspnea, and muscle cramps ( n = 11, 10, 2, and 1 cases, respectively). We conclude that 1-h preexercise glycerol hyperhydration provides no meaningful physiological advantage over water hyperhydration and that hyperhydration per se only provides the advantage (over euhydration) of delaying hypohydration during uncompensble exercise-heat stress.

The purpose of this study was to determine whether hypohydration reduces skeletal muscle endurance and whether increased H+ and Pi might contribute to performance degradation. Ten physically active volunteers (age 21–40 yr) performed supine single-leg, knee-extension exercise to exhaustion in a 1.5-T whole body magnetic resonance spectroscopy (MRS) system when euhydrated and when hypohydrated (4% body wt).31P spectra were collected at a rate of one per second at rest, exercise, and recovery, and were grouped and averaged to represent 10-s intervals. The desired hydration level was achieved by having the subjects perform 2–3 h of exercise in a warm room (40°C dry bulb, 20% relative humidity) with or without fluid replacement 3–8 h before the experiment. Time to fatigue was reduced ( P < 0.05) by 15% when the subjects were hypohydrated [213 ± 12 vs. 251 ± 15 (SE) s]. Muscle strength was generally not affected by hypohydration. Muscle pH and Pi/β-ATP ratio were similar during exercise and at exhaustion, regardless of hydration state. The time constants for phosphocreatine recovery were also similar between trials. In summary, moderate hypohydration reduces muscle endurance, and neither H+ nor Pi concentration appears to be related to these reductions.

The purpose of this study was to examine the thermoregulatory sweating control parameters of threshold temperature and sensitivity to determine whether 1) these variables were altered by hypohydration level and exercise intensity and 2) these alterations, if present, were additive and independent. Nine heat-acclimated men completed a matrix of nine trials: three exercise intensities of 25, 45, and 65% maximal O2 uptake and three hydration levels, i.e., euhydration and hypohydration (Hy) at 3 and 5% of body weight. During each trial, subjects attempted 50 min of treadmill exercise in a warm room (30 degrees C dry bulb, 50% relative humidity) while esophageal temperature and upper arm sweating rate were continuously measured. Hypohydration was achieved by exercise and fluid restriction the day preceding the trials. The following new findings were made: 1) threshold temperature increased in graded manner with hypohydration level (approximately 0.06 degree C/% Hy); 2) sensitivity decreased in a graded manner with hypohydration level (approximately 0.06 units/%Hy); 3) threshold temperature was not altered by exercise intensity; and 4) sensitivity increased from low- to moderate- and high-intensity exercise. We conclude that both hypohydration level and exercise intensity produce independent effects on control of thermoregulatory sweating.