The roles of exercise, heat and dehydration in exercise-induced hypotension and hypervolaemia

Physiology 2015 (Cardiff, UK) (2015) Proc Physiol Soc 34, C59

Oral Communications: The roles of exercise, heat and dehydration in exercise-induced hypotension and hypervolaemia

A. Akerman1, S. J. Lucas1,2, J. D. Cotter1

1. University of Otago, Dunedin, Otago, New Zealand. 2. University of Birmingham, Birmingham, United Kingdom.

View other abstracts by:


Exercise and exogenous heat each stimulate multiple adaptations, but the role of the related stressor, dehydration, is unclear. While severe hypohydration potentially “silences” the long-term heat acclimated phenotype (in rats) [1], mild-to-moderate dehydration may stimulate cardiovascular adaptations [2, 3]. We tested the hypothesis that exogenous heat stress and dehydration can additively potentiate short-term haematological adaptations to exercise. Five male and five female volunteers (mean ± SD: 173 ± 11 cm; 72.1 ± 11.5 kg; 24 ± 3 y) completed three trials in randomised order, involving 90-min orthostatically-stressful callisthenics, in: i) temperate (~22˚C, 50% rh; Con); ii) exogenous heat (~40˚C, 60% rh) whilst euhydrated (Hot+Euhy), and iii) exogenous heat with dehydration (12 h prior fluid restriction then permissive dehydration; Hot+Dehy). Time of day, menstrual phase, and activity levels were standardised. Measures recorded during exercise and intermittently until 24 h thereafter were rectal temperature, heart rate, mean arterial pressure (MAP) and Δ plasma volume. Plasma erythropoietin conc. (EPO) was measured before exercise and at 0 and 2 h after exercise. Compared to Con, core temperature tended to rise more in Hot+Euhy (by 0.48˚C; 95% CI: -0.06 – 1.01˚C: Cohen’s d=2.1; p=0.07), and more so with dehydration (by 0.47˚C for Hot+Dehy vs. Heat+Euhy; 0.18 – 0.76˚C; d=3.8 p=0.007; from ANOVA). Heart rate did likewise: (mean ± SD) +32 ± 7, +80 ± 30 and +95 ± 27 b/min for Con, Hot+Euhy, and Hot+Dehy respectively (all p<0.05). Post-exercise hypotension at 24 h was larger with the addition of heat (by 3 mm Hg for Hot+Euhy vs. Con; 1 – 5 mm Hg; d=0.9; p=0.03), and more so with dehydration (by 2 mm Hg for Hot+Dehy vs. Hot+Euhy; 1 – 3 mm Hg; d=2.1; p=0.008). Similarly, the hypervolaemic response at 24 h was larger with heat (by 4% for Hot+Euhy vs. Con; 1.9 – 6.9%; d=0.7; p=0.01), and more so with dehydration (by 8.8% for Hot+Dehy vs. Heat+Euhy; 3.2 – 14.3%; d=0.9; p=0.006). EPO was unchanged from baseline in any trial: 0.5 ± 2.2; -2.0 – 1; and -1.0 ± 3.2; -3.2 – 1.3 mU/mL change in Con. from baseline to post, and 2 h respectively; -0.9 ± 2.1: -2.8 – 0.9; and -1.6 ± 1.2: -2.7 – 0.6 mU/mL change in Heat+Euhy from baseline to post, and 2 h respectively; and 0.7 ± 2.0: -0.6 – 2.1; and 0.2 ± 4.1: -2.6 – 3.1 mU/mL change in Heat+Dehy from baseline to post, and 2 h respectively. Trials were pooled for correlational analysis. The rise in core temperature was strongly and negatively related to the hypotension at 24 h (r = -0.7; p<0.0001), which was similarly related to the hypervolaemia at 24 h (r = -0.7) The rise core temperature was also strongly and positively related to this hypervolaemia (r = 0.7). In conclusion, transient dehydration appeared to potentiate haematological (hypervolaemic) and cardiovascular (hypotensive) responses following exercise.



Where applicable, experiments conform with Society ethical requirements.

Site search

Filter

Content Type