Abstract

Background: Hyperoxia (HYPER) increases O2 carrying capacity resulting in a higher O2 delivery to the working muscles during exercise. Several lines of evidence indicate that lactate metabolism, power output, and endurance are improved by HYPER compared to normoxia (NORM). Since HYPER enables a higher exercise power output compared to NORM and considering the O2 delivery limitation at exercise intensities near to maximum, we hypothesized that hyperoxic-supplemented high-intensity interval training (HIIT) would upregulate muscle mitochondrial oxidative capacity and enhance endurance cycling performance compared to training in normoxia.Methods: 23 trained cyclists, age 35.3 ± 6.4 years, body mass 75.2 ± 9.6 kg, height 179.8 ± 7.9 m, and VO2max 4.5 ± 0.7 L min−1 performed 6 weeks polarized and periodized endurance training on a cycle ergometer consisting of supervised HIIT sessions 3 days/week and additional low-intensity training 2 days/week. Participants were randomly assigned to either HYPER (FIO2 0.30; n = 12) or NORM (FIO2 0.21; n = 11) breathing condition during HIIT. Mitochondrial respiration in permeabilized fibers and isolated mitochondria together with maximal and submaximal VO2, hematological parameters, and self-paced endurance cycling performance were tested pre- and posttraining intervention.Results: Hyperoxic training led to a small, non-significant change in performance compared to normoxic training (HYPER 6.0 ± 3.7%, NORM 2.4 ± 5.0%; p = 0.073, ES = 0.32). This small, beneficial effect on the self-paced endurance cycling performance was not explained by the change in VO2max (HYPER 1.1 ± 3.8%, NORM 0.0 ± 3.7%; p = 0.55, ES = 0.08), blood volume and hemoglobin mass, mitochondrial oxidative phosphorylation capacity (permeabilized fibers: HYPER 27.3 ± 46.0%, NORM 16.5 ± 49.1%; p = 0.37, ES = 3.24 and in isolated mitochondria: HYPER 26.1 ± 80.1%, NORM 15.9 ± 73.3%; p = 0.66, ES = 0.51), or markers of mitochondrial content which were similar between groups post intervention.Conclusions: This study showed that 6 weeks hyperoxic-supplemented HIIT led to marginal gain in cycle performance in already trained cyclists without change in VO2max, blood volume, hemoglobin mass, mitochondrial oxidative phosphorylation capacity, or exercise efficiency. The underlying mechanisms for the potentially meaningful performance effects of hyperoxia training remain unexplained and may raise ethical questions for elite sport.

Highlights

  • It is still under the debate whether strategies such as hyperoxia supplementation enabling acute improvement of exercise performance leads to superior training adaptations and greater performance enhancement (Ploutz-Snyder et al, 1996; Hamalainen et al, 2000; Morris et al, 2000; Perry et al, 2005, 2007; Kilding et al, 2012; Przyklenk et al, 2017)

  • Considering the O2 delivery limitation at near maximal exercise intensities (Saltin and Calbet, 2006) and that the mitochondria possess an excess capacity above the O2 delivery (Boushel et al, 2011), we postulated that hyperoxic-supplemented exercise training allowing a higher training load leads to a greater training stimulus at the muscle level and greater performance enhancement compared to the same training regimen breathing normoxia

  • The training intervention consisted of 15 supervised high-intensity interval training (HIIT) bouts breathing either HYPER or NORM and 10 non-supervised low-intensity exercise sessions distributed within a 6-week period

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Summary

Introduction

It is still under the debate whether strategies such as hyperoxia supplementation enabling acute improvement of exercise performance leads to superior training adaptations and greater performance enhancement (Ploutz-Snyder et al, 1996; Hamalainen et al, 2000; Morris et al, 2000; Perry et al, 2005, 2007; Kilding et al, 2012; Przyklenk et al, 2017). Considering the O2 delivery limitation at near maximal exercise intensities (Saltin and Calbet, 2006) and that the mitochondria possess an excess capacity above the O2 delivery (Boushel et al, 2011), we postulated that hyperoxic-supplemented exercise training allowing a higher training load leads to a greater training stimulus at the muscle level and greater performance enhancement compared to the same training regimen breathing normoxia. This hypothesis is supported by the finding that exercise training with recombinant human erythropoietin treatment enhanced skeletal muscle mitochondrial capacity compared to controls (Plenge et al, 2012). Since HYPER enables a higher exercise power output compared to NORM and considering the O2 delivery limitation at exercise intensities near to maximum, we hypothesized that hyperoxic-supplemented high-intensity interval training (HIIT) would upregulate muscle mitochondrial oxidative capacity and enhance endurance cycling performance compared to training in normoxia

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