SlowV˙O2kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia

Abstract

We examined whether slower pulmonary O uptake (V˙O) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of step-changes in cycle ergometer power output from 20W to 80% lactate threshold in the following conditions: i) normoxia (CON; room air); ii) hypoxia (HX, inspired O = 12%; lowered end-tidal O pressure [PO] and end-tidal CO pressure [PCO]); iii) hyperventilation (HV; increased PO and lowered PCO); and iv) normocapnic hypoxia (NC-HX; lowered PO and PCO matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions. During each condition VO˙ was measured and phase II V˙O kinetics were modeled with a mono-exponential function. The V˙O time constant was different (p < 0.05) amongst all conditions: CON, 26 ± 11s; HV, 36 ± 14s; HX, 46 ± 14s; and NC-HX, 52 ± 13s. Hypocapnia may prevent further slowing of V˙O kinetics in hypoxic exercise.

The effects of exercise intensity and duration on the relationship between the slow component of V̇O2 and peripheral fatigue

“…[23][24][25] It is noteworthy that exercise intensity was normalized by a target metabolic response (ie, MLSS) amongst participants and conditions, rather than using estimations based on the percentage of peak power output. 2,5,16,18,27 Based on this approach, we established a homogenous exercise-induced metabolic response, and thus allowed a better understanding of the above-mentioned mechanisms inducing the development of peripheral fatigue and the VȮ 2SC . [28][29][30] Alternatively, a loss in muscle contraction efficiency, thus increased O 2 consumption for a given fixed workload, might also be caused by greater recruitment of more type II muscle fibres 31 and/or a shift in the bioenergetic system, such as a change from glycolytic resources to βoxidation.…”

“…3 Although the precise mechanisms contributing to the development of the VȮ 2SC remain to be fully elucidated, it is believed that a large portion (~85%) of the VȮ 2SC is because of the changes within the active muscles. 4 VȮ 2SC has been mostly related to impairments in contractile function and the development of neuromuscular fatigue (NMF), 5 despite a possible contribution in muscle substrate utilization shift from glycolysis to βoxidation during the submaximal exercise. [6][7][8] This has important physiological and applied connotations, as the development of both the VȮ 2SC and NMF has been linked with exercise tolerance.…”

Voluntary hypocapnic hyperventilation lasting 5 min and 20 min similarly reduce aerobic metabolism without affecting power outputs during Wingate anaerobic test

“…Previous studies have consistently shown that voluntary hypocapnic hyperventilation increases the anaerobic metabolic rate, as evidenced by a reduction in the aerobic energy supply (Chin, Heigenhauser, Paterson, & Kowalchuk, 2010, 2013; Chin et al, 2007; Keir et al, 2018; LeBlanc, Parolin, Jones, & Heigenhauser, 2002) and an increase in phosphocreatine break down (Forbes, Kowalchuk, Thompson, & Marsh, 2007) with unchanged total workload during moderate intensity exercise. This suggests voluntary hyperventilation accompanied by reduced arterial CO 2 partial pressure (hypocapnia) may be an effective approach to stressing the anaerobic energy system.…”