Abstract
PURPOSEThe main objective of this study was to investigate the physiological effects of single and repetitive diving‐induced hyperoxic conditions on neuromuscular performance at 1.35 atmospheres absolute (ATA). We hypothesized that following five days of consecutive, resting, long‐duration hyperoxic water immersion (WI)s, neuromuscular performance would be reduced with a longer recovery period in comparison to normoxic WIs at 1.35 ATA.METHODSThroughout a dive week (DW), twenty‐eight healthy, active male divers [30±1 (24–43)years; mean ± SEM] completed five consecutive 6‐hour resting WIs with 18‐hour surface intervals while breathing compressed atmospheric air (Air: n=15) or 100% oxygen(O2:n=13) at 1.35 ATA. Skeletal neuromuscular performance was assessed immediately before and after each WI, and 24 and 72 hours after the final WI. Assessments included knee extension and elbow flexion maximum voluntary isometric contractions (MVIC) and maximal isokinetic (IK) contractions, as well as measurement of maximum handgrip strength (MHG). Simultaneously, surface electromyography (sEMG) amplitude of the vastus lateralis, rectus femoris, vastus medialis, biceps brachii, and brachioradialis was measured.RESULTSSignificant decreases were seen in maximal strength performance on WI 3 (MVIC knee extension: 3.4%, p<0.001; O2: 4.3%, p=0.016; MVIC elbow flexion: 3.5%, p=0.002, combined group result) with recovery occurring by WI5. The O2 group knee extensor neuromuscular activation decreased by 10% throughout the DW and remained reduced by 14% through the 72‐hr post‐WI. The Air group neuromuscular activation increased throughout the DW but returned to baseline by 72‐hr post‐dive. Combined group maximal IK elbow flexion and MHG strength performance decreased by 4% and 5%, respectively, throughout the DW (WI1> WI3 and WI5, p<0.001).CONCLUSIONConsecutive, resting, long‐duration normoxic WIs cause noticeable decrements in muscular strength performance after three days of WIs with recovery seen by 24‐hr post‐WI. Hyperoxic WIs caused significant reductions to neuromuscular activation. Future research should examine the causes of hyperoxia‐induced decreased neuromuscular activity.Support or Funding InformationOffice of Naval Research (ONR) Award Number N000141612112 and NAVSEA DSBDP N0002416WX02277This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Published Version
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