Abstract
PurposeTo investigate the carbohydrate metabolism, acid–base balance, and potassium kinetics in response to exercise in moderate hypoxia among endurance athletes.MethodsNine trained endurance athletes [maximal oxygen uptake (VO2max): 62.5 ± 1.2 mL/kg/min] completed two different trials on different days: either exercise in moderate hypoxia [fraction of inspired oxygen (FiO2) = 14.5%, HYPO] or exercise in normoxia (FiO2 = 20.9%, NOR). They performed a high-intensity interval-type endurance exercise consisting of 10 × 3 min runs at 90% of VO2max with 60 s of running (active rest) at 50% of VO2max between sets in hypoxia (HYPO) or normoxia (NOR). Venous blood samples were obtained before exercise and during the post-exercise. The subjects consumed 13C-labeled glucose immediately before exercise, and we collected expired gas samples during exercise to determine the 13C-excretion (calculated as 13CO2/12CO2).ResultsThe running velocities were significantly lower in HYPO (15.0 ± 0.2 km/h) than in NOR (16.4 ± 0.3 km/h, P < 0.0001). Despite the lower running velocity, we found a significantly greater exercise-induced blood lactate elevation in HYPO compared with in NOR (P = 0.002). The bicarbonate ion concentration (P = 0.002) and blood pH (P = 0.002) were significantly lower in HYPO than in NOR. There were no significant differences between the two trials regarding the exercise-induced blood potassium elevation (P = 0.87) or 13C-excretion (HYPO, 0.21 ± 0.02 mmol⋅39 min; NOR, 0.14 ± 0.03 mmol⋅39 min; P = 0.10).ConclusionEndurance exercise in moderate hypoxia elicited a decline in blood pH. However, it did not augment the exercise-induced blood K+ elevation or exogenous glucose oxidation (13C-excretion) compared with the equivalent exercise in normoxia among endurance athletes. The findings suggest that endurance exercise in moderate hypoxia causes greater metabolic stress and similar exercise-induced elevation of blood K+ and exogenous glucose oxidation compared with the same exercise in normoxia, despite lower mechanical stress (i.e., lower running velocity).
Highlights
Carbohydrate metabolism during endurance exercise in hypoxia has been evaluated using several parameters, including blood glucose, lactate response, and the respiratory exchange ratio (RER) (Friedmann et al, 2004; Katayama et al, 2010; Morishima et al, 2014)
In our previous study (Sumi et al, 2018b), we evaluated the effect of endurance exercise in hypoxia on acid-base balance and K+ responses among middle-long distance runners
Because the training adaptations arise from repetition of the acute physiological responses in each training session, determination of the exercise-induced acid–base balance and K+ responses would greatly improve our understanding of the mechanism underlying the enhanced endurance exercise capacity after several weeks of endurance training in hypoxia (Dufour et al, 2006; Czuba et al, 2011, 2013, 2017)
Summary
Carbohydrate metabolism during endurance exercise in hypoxia has been evaluated using several parameters, including blood glucose, lactate response, and the respiratory exchange ratio (RER) (Friedmann et al, 2004; Katayama et al, 2010; Morishima et al, 2014). Lactate and hydrogen ions (H+) are produced in working muscle via the augmented energy supply from the glycolytic system and are subsequently released into the blood circulation by Na+/H+ exchanger isoform 1 and monocarboxylate transporters (Juel, 1997, 2006), which elicits metabolic acidosis (lower muscle pH). Sprint endurance training (30 s runs), with greater disturbance of muscle ion homeostasis (higher blood lactate and K+ concentrations) during the training sessions, caused greater adaptation of Na+/H+ exchanger isoform 1 and the Na+/K+-ATPase α1 isoform. These adaptations led to lower venous H+ and K+ concentrations during intensive running exercise and further improved exercise performance compared with a normal endurance training group. Because the training adaptations arise from repetition of the acute physiological responses in each training session, determination of the exercise-induced acid–base balance and K+ responses would greatly improve our understanding of the mechanism underlying the enhanced endurance exercise capacity after several weeks of endurance training in hypoxia (Dufour et al, 2006; Czuba et al, 2011, 2013, 2017)
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