Personalized hydration strategies play a key role in optimizing the performance and safety of athletes during sporting activities. Clinicians should be aware of the many physiological, behavioral, logistical and psychological issues that determine both the athlete’s fluid needs during sport and his/her opportunity to address them; these are often specific to the environment, the event and the individual athlete. In this paper we address the major considerations for assessing hydration status in athletes and practical solutions to overcome obstacles of a given sport. Based on these solutions, practitioners can better advise athletes to develop practices that optimize hydration for their sports.

Whole‐body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress‐induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 ± 10 years: mean ±s.d.), orthostatic tolerance was assessed using graded lower‐body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole‐body heating, and whole‐body heating + acute volume expansion. For the whole‐body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre‐heat stress values. Whole‐body heat stress alone reduced orthostatic tolerance by ∼80% compared to normothermia (938 ± 152 versus 182 ± 57 CSI; mean ±s.e.m., P < 0.001). Acute volume expansion during whole‐body heating completely ameliorated the heat stress‐induced reduction in orthostatic tolerance (1110 ± 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat‐stressed human.

Introduction: Greater cardiovascular (CV) drift occurs during cycling compared to running in temperate conditions. CV drift also corresponds to proportional reductions in maximal oxygen uptake (V˙O_2max) during heat stress. Whether exercise mode differentially affects CV drift—and accompanying declines in V˙O_2max—during heat stress is uncertain. The purpose of this study was to test the hypothesis that a greater magnitude of CV drift, accompanied by a greater decrement in V˙O_2max, occurs during cycling compared to running in hot conditions. Methods: 7 active men (mean ± SD; age = 25 ± 6 yr, percent body fat = 11.9% ± 2.4%) completed a control graded exercise test (GXT) on a cycle ergometer and treadmill. Then on separate, counterbalanced occasions they completed 15 or 45 min of cycling or running at 60% V˙O_2max in 35°C, immediately followed by a GXT to measure V˙O_2max (4 trials total). The separate 15- and 45-min trials were designed to measure CV drift and V˙O_2max over the same time interval. Results: Heart rate increased 19% and 17% and stroke volume decreased 20% and 15% between 15 and 45 min during running and cycling, respectively, but modes were not different (all P > 0.05). Despite a 1.8°C larger core-to-skin thermal gradient during running, decrements in V˙O_2peak were not different between exercise modes (95% CI for difference in change scores between 15 and 45 min: −0.2, 0.3). Conclusions: CV strain (indexed as CV drift) during prolonged exercise in the heat corresponds to reduced V˙O_2max, irrespective of exercise mode or the thermal gradient. As such, the upward drift in heart rate associated with CV drift reflects increased relative metabolic intensity (%V˙O_2max) during prolonged cycling or running in the heat.

Cardiovascular drift—a progressive increase in heart rate (HR) and decrease in stroke volume (SV) during prolonged exercise—is exacerbated by heat stress and thermal strain, and often accompanied by a decrease in work capacity (indexed as maximal oxygen uptake [$\stackrel{.}{\mathrm{V}}$O_2max]). To attenuate physiological strain during work in the heat, use of work:rest ratios is recommended by the National Institute for Occupational Safety and Health. The purpose of this study was to test the hypothesis that during moderate work in hot conditions, utilizing the recommended 45:15 min work:rest ratio would result in cardiovascular drift ‘accumulating’ over consecutive work:rest cycles and accompanying decrements in $\stackrel{.}{\mathrm{V}}$O_2max. Eight people (5 women; (mean ± SD) age = 25 ± 5 y; body mass = 74.8 ± 11.6 kg; $\stackrel{.}{\mathrm{V}}$O_2max = 42.9 ± 5.6 mL·kg⁻¹·min⁻¹) performed 120 min of simulated moderate work (201–300 kcal·h⁻¹) in hot conditions (indoor wet-bulb globe temperature = 29.0 ± 0.6 °C). Participants completed two 45:15 min work:rest cycles. Cardiovascular drift was evaluated at 15 and 45 min of each work bout; $\stackrel{.}{\mathrm{V}}$O_2max was measured after 120 min. On a separate day, $\stackrel{.}{\mathrm{V}}$O_2max was measured after 15 min under identical conditions for comparison before and after cardiovascular drift occurred. HR increased 16.7% (18 ± 9 beats·min⁻¹, p = 0.004) and SV decreased 16.9% (−12.3 ± 5.9 mL, p = 0.003) between 15 and 105 min, but $\stackrel{.}{\mathrm{V}}$O_2max was unaffected after 120 min (p = 0.14). Core body temperature increased 0.5 ± 0.2 °C (p = 0.006) over 2 h. Recommended work:rest ratios preserved work capacity but did not prevent the accumulation of cardiovascular and thermal strain.

Cardiovascular (CV) drift, the progressive increase in heart rate (HR) and decrease in stroke volume (SV) during constant rate, moderate intensity exercise, is related to reduced maximal oxygen uptake (V̇O_2max) during heat stress. Once it has already occurred, it is unknown whether the detrimental effects of CV drift on V̇O_2max can be reversed. This study tested the hypothesis that fan cooling after CV drift has occurred attenuates decrements in V̇O_2max associated with CV drift. Eight men completed a control graded exercise test (GXT) in 22°C to measure V̇O_2max. Then on separate, counterbalanced occasions, they completed one 15-min (15MIN) and two 45-min bouts (45NF and 45FAN) of cycling in 35°C, 40% RH at 60% V̇O_2max, each immediately followed by a GXT to measure V̇O_2max. For one of the 45-min trials (45FAN), fan airflow (4.5 m/s) was directed at participants beginning ~5 min before the GXT and continuing throughout the remainder of exercise. The purpose of the separate 15- and 45-min trials was to measure V̇O_2max during the same time interval that CV drift occurred. HR increased (13.8% and 11.4%) and SV decreased (14.4% and 14.1%) for 45NF and 45FAN, respectively; trials were not different (all P > 0.05). Despite a decrease in mean skin temperature of ~1°C with fan use, V̇O_2max decreased similarly between conditions (17% vs. 15% for 45NF and 45FAN, P = 0.54). Fan cooling after CV drift was insufficient to reverse the negative consequences of CV drift on V̇O_2max after prolonged exercise in a hot environment. Abbreviations: 15MIN: 15-min trial; 45FAN: 45-min, fan trial; 45NF: 45-min, no fan trial; ANOVA: Analysis of variance; CV: Cardiovascular; GXT: Graded exercise test; HR: Heart rate; SV: Stroke volume; T̅_b: Mean body temperature; T_re: Rectal temperature; T̅_sk: Mean skin temperature; V̇O_2max: Maximal oxygen uptake