Reduced ventilation during underwater fin-swimming in hyperoxia

INTRODUCTION: Normobaric hyperoxia reduces ventilation (V’E), heart rate (HR), and whole blood lactate [Lac-] during exercise depending on intensity and modality (1). The effect might be allocated to an elevated arterial oxygen partial pressure (PaO2), enhancing muscular diffusion and reducing local O2 deficits (2,3). In turn, anaerobic metabolism and respiratory acidosis might be delayed (4). These laboratory results become practically relevant in SCUBA-diving, where an increased ambient pressure creates hyperoxic conditions with normal air. 40% O2, equal to 56 kPa inspiratory oxygen pressure (PIO2) at 4m depth, reduces V’E during high-intensity fin-swimming compared to air (29 kPa, 4m) (5). However, higher PIO2 is common in SCUBA diving and we hypothesize deviating effects for transient exercise intervals (TI) and steady-state intervals (SSI) which have to be distinguished for applied scenarios. All effects on V’E are highly relevant for dives with limited gas supply. METHODS: 15 healthy (5 female; 28±6.2 age), physically fit participants performed an underwater incremental step test at 4m depth, determining resting and maximum values for HR and [Lac-] (6). Subsequently, 8 min each of low (LOW), moderate (MOD), and vigorous (VIG) exercise intensity were conducted on 3 separate days differing solely by the breathing gas (21%, 40%, 100% O2). V’E, HR, and velocity (v) were recorded continuously and [Lac-] sampled post-exercise. ANOVAs with repeated measures were performed on the factors gas and intensity for v, V’E for TI (min 2-3) and SSI (min 6-7), and max [Lac-]. RESULTS: Significant main effects were found for V’E at TI and SSI for gas, intensity, and a gas*intensity interaction (TI: all P≤0.003; η2P≥0.258; SSI: all P≤0.014; η2P≥0.274). V’E was significantly lower for 100% and 40% compared to air (TI: all P≤0.021; SSI: all P≤0.029). [Lac-] and v significantly differed between intensities but were unaffected by gas. CONCLUSION: A sufficient PaO2 supply to the working muscle with air is assumed during LOW, explaining no beneficial effect of increased PIO2. Significant reductions in V’E with PIO2 of 56 kPa and 140 kPa (100% O2, 4m) during TI and SSI for MOD and VIG compared to air might reduce V’E. However, missing reductions from 56 kPa to 140 kPa indicate that PIO2 >56 kPa might not benefit oxidative processes any further. Since [Lac-] and v were not influenced by gas, increased O2 capacity at muscle level might be compensated by an increased sport-specific movement in the attempt to swim faster, whereby water resistance can no longer be overcome after a certain point. Otherwise, it is to speculate whether this increased exercise attempt takes advantage of the increased O2 capacity resulting in similar V’E and [Lac-] values to 56 kPa PIO2 rather than increasing them. Any possible [Lac-] delay effect at TI was reversed with duration.