The Effects of Endurance Exercise in Hypoxia on Acid-Base Balance, Potassium Kinetics, and Exogenous Glucose Oxidation

Abstract

Purpose To investigate the carbohydrate metabolism, acid–base balance, and potassium kinetics in response to exercise in moderate hypoxia among endurance athletes. Methods Nine trained endurance athletes [maximal oxygen uptake (VO 2max ): 62.5 ± 1.2 mL/kg/min] completed two different trials on different days: either exercise in moderate hypoxia [fraction of inspired oxygen (FiO 2 ) = 14.5%, HYPO] or exercise in normoxia (FiO 2 = 20.9%, NOR). They performed a high-intensity interval-type endurance exercise consisting of 10 × 3 min runs at 90% of VO 2max with 60 s of running (active rest) at 50% of VO 2max between sets in hypoxia (HYPO) or normoxia (NOR). Venous blood samples were obtained before exercise and during the post-exercise. The subjects consumed 13 C-labeled glucose immediately before exercise, and we collected expired gas samples during exercise to determine the 13 C-excretion (calculated as 13 CO 2 / 12 CO 2 ). Results The 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 13 C-excretion (HYPO, 0.21 ± 0.02 mmol⋅39 min; NOR, 0.14 ± 0.03 mmol⋅39 min; P = 0.10). Conclusion Endurance 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 ( 13 C-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).

Effects of endurance exercise under hypoxia on acid-base and ion balance in healthy males

“…However, our results did not show a significant difference in K + after exercise between SH and MH trials and the N trial. Although the exercise type and intensity differed, results reported by Sumi et al 10 and Sumi et al 24 regarding ion balance were similar to those of our study. Sumi et al 10 investigated the effects of acid-base and ion balance in response to high-intensity interval exercise under moderate hypoxia (14.5% F i O 2 ) and normoxia in endurance athletes.…”

“…9,10,24 The augmented metabolic stress stimulates the opening of ATP-sensitive K + channels in the muscle, subsequently increasing K + outflow to the extracellular fluid in the active muscle. 24,25 Additionally, proton production is further increased during exercise under hypoxia; protons are then released into the bloodstream, and the blood is buffered by the HCO 3 -buffer system. 14,15 Moreover, the acid-base response by the HCO 3 -buffer system is caused by an increase in ventilation during exercise.…”

“…Because lower S C O 2 and pH increases the opening of K ATP channels, we believed that K + would efflux from the working muscle into the bloodstream. 24,27 The increased accumulation of extracellular K + during exercise under hypoxia is manifested by the enhanced release of K + in the working muscle and decreased reuptake of K + during exercise. 24 Street et al 18 verified that extracellular K + accumulation and metabolic alkalosis were strongly correlated; their findings seem reasonable, considering the significant increase in K + and Ca 2+ induced by exercise in all trials (SH, MH, and N) in our study.…”

“…The difference between these previous studies is due to the difference in hypoxic conditions and exercise intensity. Additionally, Sumi et al 24 investigated the acid-base balance and K + kinetics in response to exercise (relative exercise intensity) under moderate hypoxia (14.5% F i O 2 ) among endurance athletes (age: 20.7 ± 0.9 years, height: 172.5 ± 2.2 cm, body mass: 61.6 ± 2.8 kg). They reported that endurance exercise under moderate hypoxia elicited a decline in venous pH; however, it did not induce an increase in blood K + levels compared with normoxia.…”

“…Hypoxia decreases the systemic oxygen-carrying capacity and peripheral oxygen-utilizing capacity, making it more dependent on glycolysis; these changes induce an increase in blood glucose levels, blood lactate levels, and respiratory exchange ratio during exercise [ 8 , 23 ]. Exposure to and exercise under hypoxia induce a decrease in oxygen saturation in the arterial blood, resulting in an augmented energy supply from the glycolytic system, increasing the blood lactate level and production of hydrogen ions (H+) [ 9 , 10 , 24 ]. The augmented metabolic stress stimulates the opening of ATP-sensitive K + channels in the muscle, subsequently increasing K + outflow to the extracellular fluid in the active muscle [ 24 , 25 ].…”