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J Appl Physiol (1985). 2018 May 1;124(5):1264-1273. doi: 10.1152/japplphysiol.00988.2017. Epub 2018 Feb 1.

Greater fluid loss does not fully explain the divergent hemodynamic balance mediating postexercise hypotension in endurance-trained men.

Author information

1
Human and Environmental Physiology Research Unit, University of Ottawa , Ottawa , Canada.
2
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center , Dallas, Texas.
3
Cardiovascular Prevention and Rehabilitation Centre, Montreal Heart Institute , Montréal, Quebec , Canada.
4
Département de Pharmacologie et Physiologie, Faculté de Médecine, Université de Montréal , Montréal, Quebec , Canada.
5
Clinical Epidemiology Program, Ottawa Hospital Research Institute , Ottawa, Ontario , Canada.

Abstract

Following exercise, mean arterial pressure (MAP) is reduced ~5-10 mmHg from preexercise baseline. In nonendurance-trained males, postexercise hypotension results from peripheral vasodilation not offset by increased cardiac output (CO). By contrast, postexercise hypotension occurs through a reduction in CO from preexercise baseline in endurance-trained males. The reason(s) explaining these divergent responses remain unknown. Exercise at fixed percentage of peak oxygen consumption (V̇o2peak) is associated with a greater rate of metabolic heat production in trained individuals and therefore elevated sweat rates, both when compared with untrained individuals. We hypothesized that greater fluid loss would explain the postexercise reduction in CO of endurance-trained males. Twelve endurance-trained males (Trained: V̇o2peak, 64 ± 5 ml O2·kg-1·min-1) cycled for 60 min at 60% V̇o2peak (Trained60%). On separate days, 12 nonendurance trained males (Untrained: V̇o2peak, 49 ± 3 ml O2·kg-1·min-1) cycled at 1) 60% V̇o2peak (Untrained60%), and 2) a rate of heat production equivalent to that achieved by the Trained group (UntrainedMatched). Fluid loss was similar between Trained60% (-1.32 ± 0.20 kg) and UntrainedMatched (-1.32 ± 0.23 kg; P = 0.99) but was greater in these conditions relative to Untrained60% (-0.95 ± 0.11 kg; both P < 0.01). During the final 30 min of postexercise supine recovery, MAP was similarly reduced by 5 ± 2 mmHg in all three conditions ( P = 0.91). The reduction in MAP was mediated by a 0.5 ± 0.3 l/min reduction in CO from baseline in Trained60% ( P = 0.01). In contrast, CO returned to baseline following exercise during UntrainedMatched and Untrained60% (both P ≥ 0.30). These data demonstrate that greater fluid loss does not fully explain the divergent postexercise hemodynamic responses observed in trained relative to untrained males. NEW & NOTEWORTHY Even when matched for exercise-induced fluid loss, cardiac output was decreased in trained males but returned to baseline following exercise in their untrained counterparts. However, as per our hypothesis, reductions in stroke volume were similar between groups. This suggests that exercise-induced fluid loss is an important determinant of the stroke volume response during recovery but factors affecting heart rate such as exercise intensity and/or heat stress are also important determinants of postexercise hemodynamics.

KEYWORDS:

cardiovascular; heat loss; recovery

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