Effects of hyperoxia on leg blood flow and metabolism during exercise

Abstract

These experiments were designed to investigate the effects of O2 breathing on limb blood flow and metabolism during exercise. Six subjects took part in the study. Four subjects breathed air or 100% O2 while pedaling a Krogh bicycle at 150 W (55-70% of maximal aerobic capacity). Two subjects breathed either 60% or 100% O2 while working at a power output at or slightly in excess of their maximal aerobic capacities. The major findings of the study were 1) leg blood flow is reduced during exercise when comparing hyperoxia with normoxia; 2) VO2 of the exercising limb is not different during hyperoxia; 3) O2 delivery to the leg (the product of blood flow and arteriovenous O2 difference) is not significantly different in the two conditions; and 4) blood pressure is not markedly affected in the experiments at 150 W. Since BP was not different during hyperoxia, at a time when flow was reduced by 11%, this suggests an increased resistance to flow in the exercising limb. In general, these findings are consistent with those reported for the in situ dog muscle but are at variance with results of experiments with humans, especially the reports indicating substantial increases in O2 uptake during hypertoxic conditions.

Reduced muscle oxidative capacity is independent of O2 availability in elderly people

“…This increase in the PO 2 gradient is induced by a greater arterial O 2 saturation and O 2 delivery, provided that muscle blood flow is unchanged. However, it has been suggested that hyperoxia can reduce muscle blood flow during exercise thereby reducing O 2 delivery to the muscle to a level similar to normoxic conditions (Welch et al 1977;Pedersen et al 1999). For instance, Pedersen et al (1999) reported diminished leg blood flow and a trend for a lower maximal O 2 consumption during one-leg knee extension exercise in hyperoxia compared to normoxia (Pedersen et al 1999).…”

Stimulation of ventilation by normobaric hyperoxia in exercising dogs

“…It appears, indeed, that hyperoxia may impede not only tissue COµ removal but also the muscle blood flow response to exercise (Welch et al 1977;Wilson & Stainsby, 1978). Therefore, in keeping with a vascular mediation of the effects of muscle COµ accumulation during exercise, hyperoxia by impeding the normal circulatory response in the muscles (Bredle et al 1988) should, per se, depress the normal response of muscle afferent fibres to the contractions and the ensuing ýE response, as, for example, in patients with peripheral vascular disease (Haouzi et al 1997), or in dogs with impeded arterial supply ).…”

“…Experimental Physiology (2000) 85.6, 829-838. et al 1958) during the steady state of moderate intensity exercise and that of 'prolonged' Oµ exposure. Indeed Oµ produces various physiological effects during exercise such as a reduction in muscle blood flow (Welch et al 1977;Bredle et al 1988) and COµ output (Welch et al 1977;Wilson & Stainsby, 1978;Griffiths et al 1986), which may not be of importance at rest but could affect ventilatory control specifically during hyperoxic exercise (see Whipp & Ward, 1991 for review). The aim of this study was to describe more precisely the interactions between the mechanisms that depress ventilation during Oµ exposure in exercise and those stimulating ventilation.…”

Opposite effects of hyperoxia on mitochondrial and contractile efficiency in human quadriceps muscles

“…However, conflicting results have been reported regarding the interaction between O 2 availability and muscle efficiency in humans. For instance, other studies have reported constant O 2 cost during cycling exercise with FI O 2 ϭ 0.12-1.0 (3,34,37,63,66) and even a decreased exercise efficiency during cycling exercise in hypoxia (54).The major caveat to most of the above-mentioned studies is the exclusive assessment of aerobic energy production using gas exchange measurements, from the lung or the systemic circulation, to assess muscle efficiency, thereby ignoring potential changes in anaerobic energy contribution [glycolysis and phosphocreatine (PCr)] to meet muscle ATP demand. Yet changes in these pathways have been largely acknowledged to occur when O 2 availability is altered (14,15,18,19,42) and, therefore, influence estimation of the total energy expenditure.…”

“…However, conflicting results have been reported regarding the interaction between O 2 availability and muscle efficiency in humans. For instance, other studies have reported constant O 2 cost during cycling exercise with FI O 2 ϭ 0.12-1.0 (3,34,37,63,66) and even a decreased exercise efficiency during cycling exercise in hypoxia (54).…”