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

Low fractions of inspired oxygen ([Formula: see text]; i.e., hypoxia) affect aspects of skeletal muscle contractility in humans, but it remains unclear if postactivation potentiation (PAP) and the torque-frequency (T-F) relationship are altered. We investigated the effects of 2 (H2) and 4 (H4) h of normobaric hypoxia ([Formula: see text] = 0.11 ± 0.47) on the magnitude of PAP of the knee extensors and the T-F relationship of the dorsiflexors in 13 and 12 healthy participants, respectively. To assess PAP, a resting twitch was evoked via femoral nerve stimulation before and 2-300 s after 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 and 100 Hz. During hypoxia, peripheral oxygen saturation decreased by ∼18% from 98.0 ± 0.8% at baseline ( < 0.001). MVC force and voluntary activation (VA) of the knee extensors were lower than baseline throughout hypoxia (e.g., ∼8% and ∼5%, respectively, at H2; ≤ 0.027); however, the magnitude of PAP was not altered by hypoxia ( ≥ 0.711). Surprisingly, PAP did increase with time across the control day ( ≤ 0.012). MVC torque and VA of the dorsiflexors were unaffected by hypoxia ( ≥ 0.127), but the estimated frequency required to evoke 50% of 100 Hz torque increased by ∼1.2 Hz at H2 ( ≤ 0.021). These results imply that 2 h of normobaric hypoxia were sufficient to ) impair neural drive to the knee extensors but not the mechanism(s) responsible for PAP and ) lead to a rightward shift of the T-F relationship for the dorsiflexors. Postactivation potentiation of the knee extensors was unaffected by 4 h of normobaric hypoxia exposure but may be confounded by hypoxia-related impairments to the conditioning contraction. In the dorsiflexors, contractile rates increased in hypoxia, which led to a rightward shift of the torque-frequency relationship, such that a higher frequency was required to obtain 50% of maximal torque. These results expand our understanding of the acute effects of hypoxia on skeletal muscle function.