Neuromuscular fatigue during hypoxia is mediated by the hypoxic ventilatory response

Neurons of the corticospinal tract are inherently sensitive to oxygen availability and, in response to hypoxia, reduce their metabolic requirements and activity [1]. Consequently, hypoxia is associated with neuromuscular fatigue, attributed in part to central (i.e., CNS) mechanisms [2]. Although changes in cerebral blood flow (CBF), mediated by the ratio of hypoxia induced vasodilation to hypoxic ventilatory response (HVR) induced hypocapnia (i.e., PETCO2) [3], may be implicated in the development of central fatigue, the contribution from the chemoreflex control of HVR and CBF vs. reductions in CBF per se has yet to be isolated.