Abstract

The aim of this study was to evaluate the effects of sodium phosphate (SP) supplementation on aerobic capacity in hypoxia. Twenty-four trained male cyclists received SP (50 mg·kg−1 of FFM/day) or placebo for six days in a randomized, crossover study, with a three-week washout period between supplementation phases. Before and after each supplementation phase, the subjects performed an incremental exercise test to exhaustion in hypoxia (FiO2 = 16%). Additionally, the levels of 2,3-diphosphoglycerate (2,3-DPG), hypoxia-inducible factor 1 alpha (HIF-1α), inorganic phosphate (Pi), calcium (Ca), parathyroid hormone (PTH) and acid-base balance were determined. The results showed that phosphate loading significantly increased the Pi level by 9.0%, whereas 2,3-DPG levels, hemoglobin oxygen affinity, buffering capacity and myocardial efficiency remained unchanged. The aerobic capacity in hypoxia was not improved following SP. Additionally, our data revealed high inter-individual variability in response to SP. Therefore, the participants were grouped as Responders and Non-Responders. In the Responders, a significant increase in aerobic performance in the range of 3–5% was observed. In conclusion, SP supplementation is not an ergogenic aid for aerobic capacity in hypoxia. However, in certain individuals, some benefits can be expected, but mainly in athletes with less training-induced central and/or peripheral adaptation.

Highlights

  • Publisher’s Note: MDPI stays neutralAcute exposure to hypoxia leads to a reduction in maximal oxygen uptake (VO2max )and endurance exercise performance in athletes [1–4]

  • Similar changes were not observed after placebo ingestion

  • There were no significant changes in WRmax, VO2max, HRmax, SVmax, Qmax, VEmax or VO2 /HRmax following sodium phosphate (SP) supplementation (Table 1)

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Summary

Introduction

Acute exposure to hypoxia leads to a reduction in maximal oxygen uptake (VO2max ). The decrease in VO2max in hypoxia is a consequence of a drop in blood oxygen partial pressure and blood oxygen saturation (SpO2 ), which results in a reduction in oxygen supply to tissues [3,5]. At an altitude of ~2000 m, a decrease in endurance performance by 8–10% may be expected [4,7–9]. Since the magnitude of the decrease in aerobic performance shows considerable individual variation [10], in more vulnerable athletes, a decrease may occur at altitudes even below 1000 m [11,12]. Despite many years of research on human adaptation to altitude, the current research issue is the search for methods of limiting the decline in exercise capacity due to acute hypoxic exposure. Adaptation to altitude requires a with regard to jurisdictional claims in published maps and institutional affiliations

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