Ergogenic value of oxygen supplementation in chronic obstructive pulmonary disease

Abstract

Patients with COPD exhibit limited exercise endurance time compared to healthy age-matched individuals. Oxygen supplementation is often applied to improve endurance time during pulmonary rehabilitation in patients with COPD and thus a comprehensive understanding of the mechanisms leading to improved endurance is desirable. This review analyses data from two studies by our research group investigating the effect of oxygen supplementation on cerebrovascular, systemic, respiratory and locomotor muscle oxygen availability on the same cohort of individuals with advanced COPD, and the mechanisms associated with improved endurance time in hyperoxia, which was essentially doubled (at the same power output). In hyperoxia at isotime (the time at which patients became exhausted in normoxia) exercise was associated with greater respiratory and locomotor muscle (but not frontal cortex) oxygen delivery (despite lower cardiac output), lower lactate concentration and less tachypnoea. Frontal cortex oxygen saturation was higher, and respiratory drive lower. Hence, improved endurance in hyperoxia appears to be facilitated by several factors: increased oxygen availability to the respiratory and locomotor muscles, less metabolic acidosis, and lower respiratory drive. At exhaustion in both normoxia and hyperoxia, only cardiac output and breathing pattern were not different between conditions. However, minute ventilation in hyperoxia exceeded the critical level of ventilatory constraints (VE/MVV > 75–80%). Lactate remained lower and respiratory and locomotor muscle oxygen delivery greater in hyperoxia, suggesting greater muscle oxygen availability improving muscle function. Taken together, these findings suggest that central haemodynamic and ventilatory limitations and not contracting muscle conditions dictate endurance time in COPD during exercise in hyperoxia.

Hyperoxia improves exercise capacity in cardiopulmonary disease: a series of randomised controlled trials

“…A possible explanation for the improvements with hyperoxia could be a change of energy metabolism while breathing supplemental oxygen, shifting the anaerobic threshold to more sustained aerobic metabolism with longer aerobic steady-state periods in CWRET [ 3 ]. We found significantly reduced levels of blood lactate in CWRET at end-exercise which are in line with another study that observed similar findings at end-exercise and isotimes in patients with COPD [ 24 ]. The higher blood oxygenation at end-exercise ( S pO 2 : IET +4%, CWRET +6%; S aO 2 : IET +7%, CWRET +9.6%) could additionally lead to an inhibition of hypoxia-stimulated chemoreceptors which decrease V ′ E and HR, resulting in more efficient breathing patterns.…”

“…In line with our results, a recent review [24] reported the physiological mechanisms underlying the beneficial ergogenic effect of FiO 2 1.0 compared to ambient air on CWRET at the endexercise and at isotime in patients with COPD. Authors synthesised data from two different trials undertaken by their group.…”

“…This could be interpreted as an indicator of longer endurance with cardiac reserves. These findings are supported by another study which observed a reduction of cardiac output by 10% at isotime while breathing hyperoxia during exercise in patients with COPD [ 24 ]. Reduction of HR could also be attributed to the oxygen-induced peripheral vasoconstriction activating arterial baroreceptor reflex, resulting in vagal activation and sympathetic depression [ 27 ].…”

“…Additionally, the study reports changes in locomotor and respiratory muscle and cerebral frontal cortex blood flow and oxygen delivery. Authors concluded that several factors contribute to the improved exercise tolerance during hyperoxia including greater oxygen delivery to the locomotor and respiratory muscles, while cardiac and breathing reserves were higher during isotime in hyperoxia compared to normoxia leading to decreased symptoms [ 24 ].…”

Pulmonary rehabilitation and physical interventions

“…Oxygen supplements reduce ventilatory requirements and hence dynamic hyperinflation during exercise in patients with COPD – even in patients that maintain saturation during exercise [ 53 ]. In patients with more pronounced desaturation during exercise [ 54 , 55 ], but not those with mild hypoxia [ 56 ], oxygen supplements also lead to reduced lactate levels during exercise. Hence both chemoreceptor inhibition as well as lower lactate may cause lower ventilatory needs during exercise in patients with COPD.…”