The Effect of Hyperoxia on Central and Peripheral Factors of Arm Flexor Muscles Fatigue Following Maximal Ergometer Rowing in Men.

Stefanos Volianitis,Nicolas C Petersen,Niels H Secher,Peter Rasmussen

doi:10.3389/fphys.2022.829097

Stefanos Volianitis, Nicolas C Petersen + Show 2 more

Open Access

https://doi.org/10.3389/fphys.2022.829097

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Abstract

PurposeThis study evaluates the effect of hyperoxia on cerebral oxygenation and neuromuscular fatigue mechanisms of the elbow flexor muscles following ergometer rowing.MethodsIn 11 competitive male rowers (age, 30 ± 4 years), we measured near-infrared spectroscopy determined frontal lobe oxygenation (ScO2) and transcranial Doppler ultrasound determined middle cerebral artery mean flow velocity (MCA Vmean) combined with maximal voluntary force (MVC), peak resting twitch force (Ptw) and cortical voluntary activation (VATMS) of the elbow flexor muscles using electrical motor point and magnetic motor cortex stimulation, respectively, before, during, and immediately after 2,000 m all-out effort on rowing ergometer with normoxia and hyperoxia (30% O2).ResultsArterial hemoglobin O2 saturation was reduced to 92.5 ± 0.2% during exercise with normoxia but maintained at 98.9 ± 0.2% with hyperoxia. The MCA Vmean increased by 38% (p < 0.05) with hyperoxia, while only marginally increased with normoxia. Similarly, ScO2 was not affected with hyperoxia but decreased by 7.0 ± 4.8% from rest (p = 0.04) with normoxia. The MVC and Ptw were reduced (7 ± 3% and 31 ± 9%, respectively, p = 0.014), while VATMS was not affected by the rowing effort in normoxia. With hyperoxia, the deficit in MVC and Ptw was attenuated, while VATMS was unchanged.ConclusionThese data indicate that even though hyperoxia restores frontal lobe oxygenation the resultant attenuation of arm muscle fatigue following maximal rowing is peripherally rather than centrally mediated.

Highlights

Maximal rowing provokes disturbance to systemic and intramuscular homeostasis (Volianitis and Secher, 2009; Volianitis et al, 2018) that exacerbates pulmonary diffusion limitations and reduces arterial hemoglobin oxygen saturation (SaO2) to below 88% (Nielsen et al, 1998)
When cerebral oxygenation is enhanced with oxygen supplementation rowing performance is improved (Nielsen et al, 1999), suggesting that the performance improvement may be attributed to attenuation of “central fatigue” (Gandevia, 2001), that is, enhanced volitional motor output to locomotor muscles (Nybo and Rasmussen, 2007)
The contribution of central and peripheral mechanisms to neuromuscular fatigue depends on the tested muscle group (Enoka et al, 2011) as shown for the upper and lower limbs (Vernillo et al, 2018), for example, 2 min Maximal voluntary contraction (MVC) result in central fatigue of the lower limbs, but not of the upper limbs indicating that fatigue mechanisms may be regulated differently and limb specific

Summary

Introduction

Maximal rowing provokes disturbance to systemic and intramuscular homeostasis (Volianitis and Secher, 2009; Volianitis et al, 2018) that exacerbates pulmonary diffusion limitations and reduces arterial hemoglobin oxygen saturation (SaO2) to below 88% (Nielsen et al, 1998). Oxygen supplementation attenuates the rate of development of peripheral fatigue provoked both by high intensity whole body exercise (Amann et al, 2006b; Romer et al, 2006; Dominelli et al, 2017) and isolated muscle exercise (Katayama et al, 2007), indicating that the effect is independent of possible attenuation of fatiguing metabolites, secondary to a hyperoxiainduced increase in maximal exercise capacity and, changes in relative work intensity The contribution of both central and peripheral fatigue mechanisms is considered when attempting to explain performance fatigability, albeit implications for performance should be approached with caution, as the translation of fatigue mechanisms to human whole body performance is not straightforward (Enoka and Duchateau, 2016). The functional significance of such differential contribution of central activation to the force production of different muscle groups can be appreciated with the leg “strength paradox,” that is, the strength deficit of a bilateral leg effort, typically 15–20%, compared to the strength expected from the sum of the separate unilateral leg efforts, as observed in rowers (Secher, 1975)

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