Acute normobaric hypoxia causes a rightward shift in the torque-frequency relationship, but has no effect on post-activation potentiation.

Low fractions of inspired oxygen (FI_O2; i.e., hypoxia) affect aspects of skeletal muscle contractility in humans, but it remains unclear if post-activation potentiation (PAP) and the torque-frequency (T-F) relationship are altered. We investigated the effects of two (H2) and four hours (H4) of normobaric hypoxia (FI_O2=0.11±0.47) on the magnitude of PAP of the knee extensors (KE) and the T-F relationship of the dorsiflexors (DF) in 13 and 12 healthy participants, respectively. To assess PAP, a resting twitch was evoked via femoral nerve stimulation before, and 2-300 s following a 10-s maximal voluntary contraction (MVC). A T-F relationship was obtained by stimulating the common fibular nerve with a single pulse and 1-s trains between 5-100 Hz. During hypoxia, peripheral oxygen saturation decreased by ~18% from 98.0±0.8% at baseline (P<0.001). MVC force and voluntary activation (VA) of the KE were lower than baseline throughout hypoxia (e.g., ~8 and ~5%, respectively at H2; P≤0.027); however, the magnitude of PAP was not altered by hypoxia (P≥0.711). Surprisingly, PAP did increase with time across the control day (P≤0.012). MVC torque and VA of the DF were unaffected by hypoxia (P≥0.127), but the estimated frequency required to evoke 50 % of 100-Hz torque increased by ~1.2 Hz at H2 (P≤0.021). These results imply that two hours of normobaric hypoxia were sufficient to: i) impair neural drive to the KE but not the mechanism(s) responsible for PAP, and ii) lead to a rightward shift of the T-F relationship for the DF.