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Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia

Timothy D. Noakes1,*, Juha E. Peltonen2 and Heikki K. Rusko3

1 Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town, Sports Science Institute of South Africa, PO Box 115, Newlands 7725, South Africa,
2 Unit for Sports and Exercise Medicine, Institute of Clinical Medicine, University of Helsinki, FIN-00250 Helsinki, Finland and
3 KIHU-Research Institute of Olympic Sports, FIN-40760 Jyväskylä, Finland



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  		Fig. 1. Changes in blood oxygen concentration reduce the arterial oxygen supply to both the skeletal muscles and the heart. If the heart is the slave to the muscles, as predicted by the classical theory, then the output of the heart must increase during hypoxia to ensure that oxygen delivery to the skeletal muscles is maintained. In contrast, the central governor theory predicts that cardiac output will fall during hypoxia in proportion to the reduction in oxygen delivery to the heart, specifically to prevent hypoxic damage to the heart or other vital organs including, perhaps, the brain and respiratory muscles.

 


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  		Fig. 2. The central governor theory proposes that afferent sensory information from the heart, but also perhaps from the brain and respiratory muscles, informs the brain of any threat that hypoxia or ischaemia may develop in those organs. In response, the central governor acts via the motor cortex to reduce the efferent neural activation of the exercising muscles, thereby reducing the mass of muscle that can be recruited and, hence, reducing the exercise intensity that can be sustained. The existence of peripheral governors in skeletal muscle and heart is proved by the rapidly deleterious effects of ischaemia on contractile function of both the heart and skeletal muscles and the existence of the condition of myocardial hibernation (Noakes, 2001).

 

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