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It is well appreciated that a loss of body water (dehydration) can impair endurance performance and that the effect is magnified by environmental heat stress. A majority of professional sports medicine and nutrition organizations recommend drinking during exercise to replace sweat losses and prevent dehydration, while also avoiding frank over-hydration. Knowledge of sweating rate, which is highest in the heat for any given metabolic rate, is therefore considered key to developing a sound drinking strategy. Exercise duration and the provision of liquid fuel interacts with required drink volumes in important ways that are infrequently discussed but are of utmost practical concern. This review details some challenges related to the optimized coupling of fluid and fuel needs during prolonged exercise in the heat and the need for personalization., (Copyright © 2021. Published by Elsevier Ltd.)

Acetazolamide (AZ) is a medication commonly used to prevent acute mountain sickness (AMS) during rapid ascent to high altitude. However, it is unclear whether AZ use impairs exercise performance; previous literature regarding this topic is equivocal. The purpose of this study was to evaluate the impact of AZ on time-trial (TT) performance during a 30-h exposure to hypobaric hypoxia equivalent to 3,500-m altitude. Ten men [sea-level peak oxygen consumption (VO 2 peak): 50.8 ± 6.5 mL·kg -1 ·min -1 ; body fat %: 20.6 ± 5.2%] completed 2 30-h exposures at 3,500 m. In a crossover study design, subjects were given 500 mg/day of either AZ or a placebo. Exercise testing was completed 2 h and 24 h after ascent and consisted of 15-min steady-state treadmill walking at 40%-45% sea-level VO 2 peak, followed by a 2-mile self-paced treadmill TT. AMS was assessed after ~12 h and 22 h at 3,500 m. The incidence of AMS decreased from 40% with placebo to 0% with AZ. Oxygen saturation was higher ( P < 0.05) in AZ versus placebo trials at the end of the TT after 2 h (85 ± 3% vs. 79 ± 3%) and 24 h (86 ± 3% vs. 81 ± 4%). There was no difference in time to complete 2 miles between AZ and PL after 2 h (20.7 ± 3.2 vs. 22.7 ± 5.0 min, P > 0.05) or 24 h (21.5 ± 3.4 vs. 21.1 ± 2.9 min, P > 0.05) of exposure to altitude. Our results suggest that AZ (500 mg/day) does not negatively impact endurance exercise performance at 3,500 m. NEW & NOTEWORTHY To our knowledge, this is the first study to examine the impact of acetazolamide (500 mg/day) versus placebo on self-paced, peak-effort exercise performance using a short-duration exercise test in a hypobaric hypoxic environment with a repeated-measures design. In the present study, acetazolamide did not impact exercise performance after 2-h or 24-h exposure to 3,500-m simulated altitude.

Purpose: To determine the efficacy residing for 2 d at various altitudes while sedentary (S) or active (A; ~90 min hiking 2 d) on exercise performance at 4300 m., Methods: Sea-level (SL) resident men (n = 45) and women (n = 21) (mean ± SD; 23 ± 5 yr; 173 ± 9 cm; 73 ± 12 kg; V˙O2peak = 49 ± 7 mL·kg·min) were randomly assigned to a residence group and, S or A within each group: 2500 m (n = 11S, 8A), 3000 m (n = 6S, 12A), 3500 m (n = 6S, 8A), or 4300 m (n = 7S, 8A). Exercise assessments occurred at SL and 4300 m after 2-d residence and consisted of 20 min of steady-state (SS) treadmill walking (45% ± 3% SL V˙O2peak) and a 5-mile, self-paced running time trial (TT). Arterial oxygen saturation (SpO2) and HR were recorded throughout exercise. Resting SpO2 was recorded at SL, at 4 and 46 h of residence, and at 4300 m before exercise assessment. To determine if 2-d altitude residence improved 4300 m TT performance, results were compared with estimated performances using a validated prediction model., Results: For all groups, resting SpO2 was reduced (P < 0.01) after 4 h of residence relative to SL inversely to the elevation and did not improve after 46 h. Resting SpO2 (~83%) did not differ among groups at 4300 m. Although SL and 4300 m SS exercise SpO2 (97% ± 2% to 74% ± 4%), HR (123 ± 10 bpm to 140 ± 12 bpm) and TT duration (51 ± 9 to 73 ± 16 min) were different (P < 0.01), responses at 4300 m were similar among all groups, as was actual and predicted 4300 m TT performances (74 ± 12 min)., Conclusions: Residing for 2 d at 2500 to 4300 m, with or without daily activity, did not improve resting SpO2, SS exercise responses, or TT performance at 4300 m.

Background: How hypohydration impacts non-bodyweight (BW)-dependent muscle performance and vertical jumping ability remains to be determined using meta-analytic procedures., Objectives: Our objective was to determine the impact of hypohydration on muscle endurance, strength, anaerobic power and capacity and vertical jumping ability using a meta-analytic approach., Data Sources: Studies were located using database searches and cross-referencing., Synthesis Methods: Effect summaries were obtained using random-effects models; method of moments mixed-effects analysis-of-variance-like procedures were used to determine differences between groups; and restricted maximum likelihood random-effects meta-regressions were performed to determine relationships between variables, impact of confounders, and interaction effects., Results: A total of 28 manuscripts met the inclusion criteria, producing six (upper body muscle endurance), ten (lower body muscle endurance), 14 (upper body muscle strength), 25 (lower body muscle strength), nine (muscle anaerobic power), nine (muscle anaerobic capacity), and 12 (vertical jumping ability) effect estimates. Hypohydration impaired overall muscle endurance by 8.3 ± 2.3% (P < 0.05), with no significant difference between upper body (-8.4 ± 3.3%) and lower body (-8.2 ± 3.2%). As a whole, muscle strength fell by 5.5 ± 1.0% (P < 0.05) with hypohydration; the difference between lower (-3.7 ± 1.8%) and upper (-6.2 ± 1.1%) body was non-significant. Anaerobic power (-5.8 ± 2.3%) was significantly altered with hypohydration, but anaerobic capacity (-3.5 ± 2.3%) and vertical jumping ability (0.9 ± 0.7%) were not. No significant correlations were observed between the changes in any of the muscle performance variables or vertical jumping ability and the changes in hypohydration level. Using an active procedure to dehydrate participants decreased muscle performance by an additional 5.4 ± 1.9% (2.76-fold) (P = 0.02) compared with using a passive dehydration procedure. Trained individuals demonstrated a 3.3 ± 1.7% (1.76-fold) (P = 0.06) lesser decrease in muscle performance with hypohydration than did untrained individuals., Conclusion: Hypohydration, or factors associated with dehydration, are likely to be associated with practically important decrements in muscle endurance, strength, and anaerobic power and capacity. However, their impact on non-BW-dependent muscle performance is substantially mitigated in trained individuals or when hypohydration is induced passively. Conversely, it is possible that body water loss (~3% BW) may improve performance in BW-dependent tasks such as vertical jumping ability.

This article provides a comprehensive review of dehydration assessment and presents a unique evaluation of the dehydration and performance literature. The importance of osmolality and volume are emphasized when discussing the physiology, assessment, and performance effects of dehydration. The underappreciated physiologic distinction between a loss of hypo-osmotic body water (intracellular dehydration) and an iso-osmotic loss of body water (extracellular dehydration) is presented and argued as the single most essential aspect of dehydration assessment. The importance of diagnostic and biological variation analyses to dehydration assessment methods is reviewed and their use in gauging the true potential of any dehydration assessment method highlighted. The necessity for establishing proper baselines is discussed, as is the magnitude of dehydration required to elicit reliable and detectable osmotic or volume-mediated compensatory physiologic responses. The discussion of physiologic responses further helps inform and explain our analysis of the literature suggesting a ≥ 2% dehydration threshold for impaired endurance exercise performance mediated by volume loss. In contrast, no clear threshold or plausible mechanism(s) support the marginal, but potentially important, impairment in strength, and power observed with dehydration. Similarly, the potential for dehydration to impair cognition appears small and related primarily to distraction or discomfort. The impact of dehydration on any particular sport skill or task is therefore likely dependent upon the makeup of the task itself (e.g., endurance, strength, cognitive, and motor skill)., (© 2014 American Physiological Society.)

Evidence suggests that core temperatures of approximately 40 degrees 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 (T(re)) is >40 degrees 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 approximately 13 degrees C; n = 6), warm (WBGT approximately 27 degrees C; n = 4), or both (n = 7) conditions. T(re), chest skin temperature, and heart rate were logged continuously; elapsed time was recorded every 200 m. Running velocity for T(re) >40 degrees C was compared with that for T(re) <40 degrees C for each runner. Changes in running velocity over the last 600 m were compared between runners with T(re) >40 degrees C and <40 degrees C. Twelve runners achieved T(re) >40.0 degrees C with >or=600 m remaining (range 600-3,400 m). Average running velocity for T(re) <40 degrees C (282 +/- 27 m/min) was not different from that for T(re) >40 degrees C (279 +/- 28 m/min; P = 0.82). There were no differences in running velocity during the final 600 m between runners with final T(re) >40 degrees C or <40 degrees C (P = 0.16). Chest skin temperature ranged from 30 to 34 degrees C, and heart rate was >95% of age-predicted maximum. Our observation that runners were able to sustain running velocity despite T(re) >40 degrees C is evidence against 40 degrees C representing a "critical" core temperature limit to performance.

Nutritional adenosine receptor antagonists can enhance endurance exercise performance in temperate environments, but their efficacy during heat stress is not well understood. This double-blinded, placebo-controlled study compared the effects of an acute dose of caffeine or quercetin on endurance exercise performance during compensable heat stress (40 degrees C, 20-30% rh). On each of three occasions, 10 healthy men each performed 30-min of cycle ergometry at 50% Vo2peak followed by a 15-min performance time trial after receiving either placebo (Group P), caffeine (Group C; 9 mg/kg), or quercetin (Group Q; 2,000 mg). Serial blood samples, physiological (heart rate, rectal, and mean skin body temperatures), perceptual (ratings of perceived exertion, pain, thermal comfort, motivation), and exercise performance measures (total work and pacing strategy) were made. Supplementation with caffeine and quercetin increased preexercise blood concentrations of caffeine (55.62 +/- 4.77 microM) and quercetin (4.76 +/- 2.56 microM) above their in vitro inhibition constants for adenosine receptors. No treatment effects were observed for any physiological or perceptual measures, with the exception of elevated rectal body temperatures (0.20-0.30 degrees C; P < 0.05) for Group C vs. Groups Q and P. Supplementation did not affect total work performed (Groups P: 153.5 +/- 28.3, C: 157.3 +/- 28.9, and Q: 151.1 +/- 31.6 kJ; P > 0.05) or the self-selected pacing strategy employed. These findings indicate that the nutritional adenosine receptor antagonists caffeine and quercetin do not enhance endurance exercise performance during compensable heat stress.

This investigation sought to study changes in leukocyte subsets after an acute bout of resistance exercise (ARE) and to determine whether ingestion of carbohydrate (CHO) could attenuate those immune responses. Nine male track-and-field athletes (21.1 +/- 1.4 yr, 177.2 +/- 5.5 cm, 80.9 +/- 9.7 kg, 8.7% +/- 3.8% fat) and 10 male ice hockey athletes (21.0 +/- 2.2 yr, 174.3 +/- 6.2 cm, 79.6 +/-11.1 kg, 13.9% +/- 3.73% fat) participated in 2 different ARE protocols. Both experiments employed a counterbalanced double-blind research design, wherein participants consumed either a CHO (1 g/kg body weight) or placebo beverage before, during, and after a weight-lifting session. Serum cortisol decreased (p < .05) at 90 min into recovery compared with immediately postexercise. Plasma lactate, total leukocyte, neutrophil, and monocyte concentrations increased (p < .05) from baseline to immediately postexercise. Lymphocytes decreased significantly (p < .05) from baseline to 90 min postexercise. Lymphocytes were lower (p < .05) for the CHO condition than for placebo. The findings of this study indicate the following: ARE appears to evoke changes in immune cells similar to those previously reported during endurance exercise, and CHO ingestion attenuates lymphocytosis after ARE.

The purpose of this study was to determine the optimal 1.63-km (1-mile) pacing strategy for 5-km running performance in moderately trained women distance runners. Eleven women distance runners (20.7 +/- 0.8 years, 163.8 +/- 2.0 cm, 57.0 +/- 2.2 kg, 51.7 +/- 1.0 ml.kg(-1).min(-1), 18.9 +/- 0.8% fat, 78.1 +/- 1.4% VO(2)max at lactate threshold) performed 2 preliminary 5-km time trials on a treadmill to establish baseline 5-km times. The average 1.63-km split pace of the fastest preliminary trial was manipulated for the first 1.63 km of the experimental trials and run either equal to (EVEN), 3% faster than (3%), or 6% faster than (6%) the current baseline average 1.63-km pace for each subject. Ventilation (V(E)), oxygen consumption VO(2)max )), respiratory exchange ratio, and heart rate were measured continuously. Overall 5-km times were not different (p > 0.05) for the EVEN, 3% and 6% trials finishing in 21:11 (minutes/seconds) +/- 29 seconds, 20:52 +/- 36 seconds and 20:39 +/- 29 seconds, respectively. The fastest time for 8 subjects resulted from the 6% trial and the other 3 subjects' fastest times resulted from the 3% trial. The overall exercise intensity (%VO(2)max , %VO(2)max above lactate threshold, V(E), and respiratory exchange ratio) of the first 1.63-km split was not different between the 3 and 6% trials, despite the 6% trial being 13 seconds faster than the 3% trial. Based on these findings, initial 1.63-km starting paces of a 5-km race can be 3 to 6% greater than current average race pace without negatively impacting performance. In order to optimize 5-km performance, runners should start the initial 1.63 km of a 5-km race at paces 3-6% greater than their current average race pace.

Background: The importance of lactate threshold (LT) as a determinant of performance in endurance sports has been established. In addition, it has been shown that during running and selected other endurance competitions, athletes perform at a velocity and VO2 slightly above LT for the duration of the event. Prior work indicates however, that this may not be true during a cycling time-trial (TT). This investigation sought to compare physiological variables during a 20-k TT with those corresponding to the athlete's LT., Methods: Thirteen male cyclists (22.7+/-0.8 yrs; 180.6+/-8.0 cm; 77.1+/-10.0 kg; 8.3+/-2.5% fat; 4.9+/-2.2 l x min(-1), VO2max) participated in the study. Subjects performed a graded protocol starting at 150 Watts (W) to determine LT (2 mmol x L(-1) above baseline) which consisted of 20 W increases every 4-min. Following an 8 min-recovery, subjects cycled at the wattage corresponding to LT-20 W for 1 min and then workload increased 20 W every minute until volitional exhaustion to determine VO2max x On a separate occasion a self-paced, 20-k TT was completed., Results: Mean values of blood lactate, HR and % HRmax, VO2 and % VO2max, and power output throughout the 20-k TT were greater (p<0.01) than those at LT. During the TT these cyclists performed at an intensity well above LT (blood lactate=252.0+/-0.1%, HR=9.4+/-0.03%, %HRmax=9.2+/-0.15%, VO2=26.5+/-0.7%, %VO2max=17.2+/-0.08% and power out-put=14.8+/-0.14% above LT) for over 30 min., Conclusions: Therefore, while LT may be highly correlated to performance, it may not be representative of race pace for a cycling TT, and may be questionable as a benchmark used to prescribe training intensity for competitive TT-cycling.

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.

Purpose: Previous laboratory testing has identified the importance of upper-body aerobic and anaerobic power to cross-country skiing performance. The purpose of this investigation was to extend laboratory research into a field setting to identify predictors of performance through ski-specific testing., Methods: Thirteen male collegiate skiers performed three field-testing sessions on roller skis to establish lactate threshold (LT) and ski economy (ECON) and maximal oxygen uptake (SK VO(2max)) and a 1-km double-pole time trial (UBTT) to determine peak upper-body oxygen uptake (UB VO(2)). As a measure of skiing performance, the subjects performed a 10-km skating time trial (TT) and were ranked according to competitive season performance (RANK)., Results: Significant correlations (P < 0.05) were found between SK VO(2max), LT VO(2), UB VO(2), and RANK (r = -0.66 to -0.84) and TT time (r = -0.74 to -0.79), as well as ECON to RANK (r = 0.57) and TT time (r = 0.68). Time to complete the UBTT (UB time) exhibited the strongest correlation to both RANK (r = 0.95) and TT time (r = 0.92). Multiple regression analyses revealed that UB time was the best predictor of RANK and TT time, as demonstrated by the significant beta values (0.77, P < 0.001, and 0.79, P < 0.001, respectively). The importance of the UB component was further seen in that UB time was still the best predictor of performance when the subjects were divided into two distinct groups of greater and lesser competitive ability., Conclusions: These findings identify the importance of the upper body component to cross-country skiing performance, suggesting a need to focus on upper-body conditioning within a well-rounded endurance training program. Additionally, the UBTT exhibits potential as a simple field test to predict cross-country skiing performance over more sophisticated and costly laboratory and field testing.