Angela R. Hillman

Exercise-induced dehydration with and without environmental heat stress results in increased oxidative stress

While in vitro work has revealed that dehydration and hyperthermia can elicit increased cellular and oxidative stress, in vivo research linking dehydration, hyperthermia, and oxidative stress is limited. The purpose of this study was to investigate the effects of exercise-induced dehydration with and without hyperthermia on oxidative stress. Seven healthy male, trained cyclists (power output (W) at lactate threshold (LT): 199 ± 19 W) completed 90 min of cycling exercise at 95% LT followed by a 5-km time trial (TT) in 4 trials: (i) euhydration in a warm environment (EU-W, control), (ii) dehydration in a warm environment (DE-W), (iii) euhydration in a thermoneutral environment (EU-T), and (iv) dehydration in a thermoneutral environment (DE-T) (W: 33.9 ± 0.9 °C; T: 23.0 ± 1.0 °C). Oxidized glutathione (GSSG) increased significantly postexercise in dehydration trials only (DE-W: p < 0.01, DE-T: p = 0.03), and while not significant, total glutathione (TGSH) and thiobarbituric acid reactive substances (TBARS) tended to increase postexercise in dehydration trials (p = 0.08 for both). Monocyte heat shock protein 72 (HSP72) concentration was increased (p = 0.01) while lymphocyte HSP32 concentration was decreased for all trials (p = 0.02). Exercise-induced dehydration led to an increase in GSSG concentration while maintenance of euhydration attenuated these increases regardless of environmental condition. Additionally, we found evidence of increased cellular stress (measured via HSP) during all trials independent of hydration status and environment. Finally, both 90-min and 5-km TT performances were reduced during only the DE-W trial, likely a result of combined cellular stress, hyperthermia, and dehydration. These findings highlight the importance of fluid consumption during exercise to attenuate thermal and oxidative stress during prolonged exercise in the heat.

A Comparison of Hyperhydration Versus Ad Libitum Fluid Intake Strategies on Measures of Oxidative Stress, Thermoregulation, and Performance

Dehydration has been shown to augment cellular stress. Glycerol hyperhydration can delay dehydration, which may decrease the level of pre- and post-exercise oxidative stress. This study aimed to compare the effects of glycerol (G) or water (W) hyperhydration with no hyperhydration (C) on oxidative stress, thermoregulation, and cycle performance. Seven trained males consumed 1.2 g of glycerol·kg−1 body mass (BM) in 26 ml·kg−1 BM water or equal volume water to achieve hyperhydration followed by a 90 min time trial. Total glutathione increased post exercise (PE) in all trials (p < 0.01), while oxidized glutathione (p < 0.05) and protein carbonyl concentrations (p < 0.001) were increased PE for the C trial only. Mean body temperature and heart rate increased with exercise but were not different between interventions. Total distance covered and power outputs were not different between interventions. Fluid intake attenuated oxidative stress but did not enhance thermoregulation or performance.

Metabolic Alkalosis, Recovery and Sprint Performance

Pre-exercise alkalosis and an active recovery improve the physiological state of recovery through slightly different mechanisms (e. g. directly increasing extracellular bicarbonate (HCO3 (-)) vs. increasing blood flow), and combining the two conditions may provide even greater influence on blood acid-base recovery from high-intensity exercise. Nine subjects completed four trials (Placebo Active ( PLAC A), sodium bicarbonate (NaHCO3) Active ( BICARB A), Placebo Passive ( PLAC P) and NaHCO3 Passive ( BICARB P)), each consisting of three, 30-s maximal efforts with a three min recovery between each effort. Pre-exercisealkalosis was evident in both NaHCO3 conditions, as pH and HCO3 (-) were significantly higher than both Placebo conditions (pH: 7.46 ± 0.04 vs. 7.39 ± 0.02; HCO3 (-): 28.8 ± 1.9 vs. 23.2 ± 1.4  mmol·L (-1); p<0.001). In terms of performance, significant interactions were observed for average speed (p<0.05), with higher speeds evident in the BICARB A condition (3.9 ± 0.3 vs. 3.7 ± 0.4  m·s (-1)). Total distance covered was different (p=0.05), with post hoc differences evident between the BICARB A and PLAC P conditions (368 ± 33 vs. 364 ± 35 m). These data suggest that successive 30-s high intensity performance may be improved when coupled with NaHCO3 supplementation.

Exercising in the Fasted State Reduced 24-Hour Energy Intake in Active Male Adults

The effect of fasting prior to morning exercise on 24-hour energy intake was examined using a randomized, counterbalanced design. Participants (12 active, white males, 20.8 ± 3.0 years old, VO2max: 59.1 ± 5.7 mL/kg/min) fasted (NoBK) or received breakfast (BK) and then ran for 60 minutes at 60%  VO2max. All food was weighed and measured for 24 hours. Measures of blood glucose and hunger were collected at 5 time points. Respiratory quotient (RQ) was measured during exercise. Generalized linear mixed models and paired sample t-tests examined differences between the conditions. Total 24-hour (BK: 19172 ± 4542 kJ versus NoBK: 15312 ± 4513 kJ; p < 0.001) and evening (BK: 12265 ± 4278 kJ versus NoBK: 10833 ± 4065; p = 0.039) energy intake and RQ (BK: 0.90 ± 0.03 versus NoBK: 0.86 ± 0.03; p < 0.001) were significantly higher in BK than NoBK. Blood glucose was significantly higher in BK than NoBK before exercise (5.2 ± 0.7 versus 4.5 ± 0.6 mmol/L; p = 0.025). Hunger was significantly lower for BK than NoBK before exercise, after exercise, and before lunch. Blood glucose and hunger were not associated with energy intake. Fasting before morning exercise decreased 24-hour energy intake and increased fat oxidation during exercise. Completing exercise in the morning in the fasted state may have implications for weight management.