Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

<jats:p> The drive to breathe in exercise is thought to result from a combination of neural and humoral factors, but the exact nature of the controlling signals is controversial. This review examines evidence suggesting that potassium could be a signal that drives ventilation (VE) in exercise. Potassium is lost from working muscle, which results in a marked hyperkalemia in the arterial plasma. The rise in potassium is directly proportional to the increase in carbon dioxide production during exercise and is also well correlated with VE in normal subjects and in subjects who do not produce acid (McArdle's syndrome). In the anesthetized and decerebrate cat, physiological levels of hyperkalemia stimulate VE by direct excitation of the peripheral arterial chemoreceptors, because surgical and chemical denervation of the chemoreceptors abolishes the increase in VE caused by potassium. The effect of hyperkalemia on chemoreceptor activity is further enhanced by hypoxia, but an abrupt switch to hyperoxia removes this effect. From these studies, it is suggested that potassium fulfills many of the criteria of being the special substance or “work factor” that was postulated over a century ago to stimulate VE in exercise. Although there is no direct proof that potassium causes an increase in breathing during exercise, circumstantial evidence strongly supports the idea that it should be considered as a stimulus to exercise hyperpnea. </jats:p>

Original publication




Journal article


Journal of Applied Physiology


American Physiological Society

Publication Date





811 - 820