Aerobic exercise capacity, best quantified by maximal oxygen uptake (VO2max), varies between individuals and is dependent on cardiac output (CO) and oxygen uptake in the periphery (a-vO2 diff). Environmental stressors like hypoxia, microgravity, and heat negatively impact these parameters, thereby reducing aerobic exercise capacity. However, in response to acute and chronic exposures to these environments, compensatory processes serve to counteract reductions in VO2max. In hypoxic environments, reduced oxygen partial pressure (PO2) leads to hypoxic pulmonary vasoconstriction (HPV) and a diffusion limitation at the level of the lungs and skeletal muscle, resulting in a reduction in VO2max. Microgravity environments reduce VO2max through cardiac and skeletal muscle deconditioning, as well as reductions in plasma volume (PV), resulting in an increase in sympathetic nerve activity through baroreceptor-mediated pathways. In heat stress environments, increases in skin perfusion upon acute exposure hinder exercise performance, whereas compensatory PV expansion mitigates further decreases in VO2max. As humans are increasingly exposed to austere environments and environmental extremes, it is critical to understand how these environments impact cardiovascular exercise physiology so that effective strategies and protocols ensuring proper aerobic functioning may be implemented.
Dumais et al. (Fri,) studied this question.