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

An enduring hypothesis in exercise physiology holds that a limiting cardior espiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called per ipheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London b etween 1923 and 1925. According to their classical model, peripheral fatigu e occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the ske letal muscle, that is at risk of anaerobiosis or ischaemia during maximal e xercise. To prevent myocardial damage during maximal exercise, Hill propose d the existence of a 'governor' in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function durin g maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor a nd its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maxi mum delivery of oxygen to the active muscle. In contrast, if the function o f the heart or some other oxygen-sensitive organ is to be protected, then p eak cardiovascular function will be higher during hyperoxia and reduced dur ing hypoxia compared with normoxia. This paper reviews the evidence that pe ak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocar dial function. Since peak skeletal muscle electromyographic activity is als o reduced during hypoxia, these data support a model in which a central, ne ural governor constrains the cardiac output by regulating the mass of skele tal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.