HYPOXIA ALTERS THE TIMING, NOT THE MAGNITUDE, OF NEUROMUSCULAR FATIGUE: A PREDOMINANTLY NEURAL EFFECT OF OXYGEN DESATURATION

Author(s): FIORASO, E., CUNIBERTI, G.C., GIURIATO, G., CALLOVINI, A., PEDRINOLLA, A., Institution: UNIVERSITY OF VERONA, Country: ITALY, Abstract-ID: 2465

INTRODUCTION:
Although neuromuscular fatigue during exercise in normoxia has been extensively characterized, the mechanisms contributing to fatigue in extreme environmental conditions, such as hypoxia remain incompletely understood. Interpretation of existing evidence is complicated by variability in hypoxic severity and by methodological differences in the assessments of neuromuscular fatigue. Therefore, it remains unclear whether hypoxia increases the magnitude of fatigue or accelerates its development, and whether oxygen desaturation preferentially impairs neural rather than contractile function.
METHODS:
14 high-altitude experienced mountaineers were recruited. Maximal voluntary isometric contraction (MViC), voluntary activation (VMA%, central component), and potentiated twitch force (Qtw.pot, peripheral component) were assessed using the interpolated twitch (IT) technique in the lower limb, in normoxia (N:FiO2%=20.9) and hypoxia (H:FiO2%=11.6). Torque for MViC and Qtw.pot was calculated and normalized to the thigh muscle mass. The maximal Rate of Torque Development (RTDMAX), early RTD (RTD0-100) and late RTD (RTD100-200) were measured for each MViC. MViC+IT protocol was repeated at rest and within 30 seconds after a time-to-exhaustion (TTE) cycling task performed at 80% of the maximal exercise capacity Total time to exhaustion was recorded for each participant. During the TTE, surface electromyography (EMG) was recorded; root mean square (RMS) and median frequency (MDF), as well as oxygen saturation (SpO2%) were recorded throughout the TTE.
RESULTS:
A paired t-test results show differences between conditions for time TTE (N:604±261s; H:362±107s; p=0.007) and SpO2% (N:-4.9±3.0%; H:-8.9±5.3%; p=0.01). A linear mixed-effect model was developed to control for CONDITION and STATUS, with SpO2% included as covariate. The results showed a significant effect of STATUS on MViC (p<0.001, Δ=-27%), Qtw.pot. (p<0.001, Δ=-39.2%), RFD0-100 (p<0.001, Δ=-87.7%) and VMA% (p=0.002, Δ=-10.9%10.99). A significant CONDITION effect was found for RFD0-100 (p=0.021), partly explained by SpO2%. No significant results were observed for RFDMAX and RFD100-200. RMS values were significantly higher in hypoxia compared to normoxia (p = 0.011), whereas MDF values were significantly lower in hypoxia (p< 0.001).
CONCLUSION:
This study reveals that similar levels of neuromuscular fatigue are attained in both normoxia and hypoxia. However, fatigue occurs significantly earlier under hypoxic conditions. This accelerated development of fatigue appears to be largely driven by exercise-induced reductions in SpO2 and primarily affects neural drive rather than the muscle’s contractile capacity, as further supported by the altered trajectory of EMG median frequency (MDF) observed in hypoxia. Consequently, force expression is constrained under hypoxic conditions, reflecting an early limitation in neural drive.