Abstract
Permissive dehydration during exercise heat acclimation (HA) may enhance hematological and cardiovascular adaptations and thus acute responses to prolonged exercise. However, the independent role of permissive dehydration on vascular and cardiac volumes, ventricular-arterial (VA) coupling and systemic hemodynamics has not been systematically investigated. Seven males completed two 10-day exercise HA interventions with controlled heart rate (HR) where euhydration was maintained or permissive dehydration (-2.9 ± 0.5% body mass) occurred. Two experimental trials were conducted before and after each HA intervention where euhydration was maintained (-0.5 ± 0.4%) or dehydration was induced (-3.6 ± 0.6%) via prescribed fluid intakes. Rectal (Tre) and skin temperatures, HR, blood (BV) and left ventricular (LV) volumes, and systemic hemodynamics were measured at rest and during bouts of semi-recumbent cycling (55% V̇O2peak) in 33°C at 20, 100, and 180 min. Throughout HA sweat rate (12 ± 9%) and power output (18 ± 7 W) increased (P < 0.05), whereas Tre was 38.4 ± 0.2°C during the 75 min of HR controlled exercise (P = 1.00). Neither HA intervention altered resting and euhydrated exercising Tre, BV, LV diastolic and systolic volumes, systemic hemodynamics, and VA coupling (P > 0.05). Furthermore, the thermal and cardiovascular strain during exercise with acute dehydration post-HA was not influenced by HA hydration strategy. Instead, elevations in Tre and HR and reductions in BV and cardiac output matched pre-HA levels (P > 0.05). These findings indicate that permissive dehydration during exercise HA with controlled HR and maintained thermal stimulus does not affect hematological or cardiovascular responses during acute endurance exercise under moderate heat stress with maintained euhydration or moderate dehydration.
Highlights
Heat acclimation (HA) increases the rate and sensitivity of sweating and skin blood flow, and attenuates the rise in whole body temperature and heart rate (HR) during submaximal exercise in the heat (Fox et al, 1963; Rowell et al, 1967; Nadel et al, 1974; Roberts et al, 1977)
Similar to controlled hyperthermia heat acclimation (HA), where the workload to maintain a Tre of 38.5◦C in a given environment may be lower when fluid intake is restricted (Garrett et al, 2014), exercising HR was maintained by substantially larger reductions in workload during HA with dehydration (∼30 W or 17% of initial workload, compared to ∼17 W or 9% for euhydrated HA)
Dextran infusion to maintain blood volume (BV) during exercise with fluid restriction attenuates the decline in stroke volume (SV) and the increase in HR such that Qis maintained (Montain and Coyle, 1992). These findings indicate that elevations in HR and reductions in BV with acute dehydration independently contribute to reductions in preload of the left ventricular (LV) during exercise in the heat (Watanabe et al, 2020), and that these thermal and cardiovascular perturbations persist following HA with varying fluid intake strategies
Summary
Heat acclimation (HA) increases the rate and sensitivity of sweating and skin blood flow, and attenuates the rise in whole body temperature and heart rate (HR) during submaximal exercise in the heat (Fox et al, 1963; Rowell et al, 1967; Nadel et al, 1974; Roberts et al, 1977). Permissive dehydration via fluid restriction during controlled hyperthermia HA has been demonstrated to result in greater attenuations in exercising HR, increases in post-exercise aldosterone, and elevations in resting PV when nine trained individuals restricted fluid during a 5-day intervention, compared to when the same individuals maintained pre-exercise euhydration daily (Garrett et al, 2014) This hypervolemic state can purportedly be maintained throughout protocols lasting up to 28 days (Patterson et al, 2004b, 2014) when fluid regulatory responses are consistently stimulated via dehydration and a constant thermal impulse for adaptation is provided (i.e., controlled hyperthermia HA) (Taylor, 2014). Whether restricting fluid intake during exercise HA provides a greater stimulus for hematological and cardiovascular adaptations that enhance vascular, cardiac, or hemodynamic stability during exercise in the heat remains unclear
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