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This Article Full Text Full Text (PDF) All Versions of this Article: 548/3/666    most recent 2003.040535v2 2003.040535v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kaufman, M. P. Search for Related Content PubMed PubMed Citation Articles by Kaufman, M. P. Related Collections Perspectives

Has the phoenix risen?

Marc P. Kaufman

Both static and dynamic exercise increase the activity of postganglionic sympathetic fibres innervating the vasculature of limb muscles. This increase in sympathetic activity is believed to serve two purposes. The first is to increase perfusion pressure in the vessels supplying exercising muscles, and the second is to counter excessive vasodilatation in muscles where metabolism is greatly increased over resting levels. Two neural mechanisms have been investigated as the cause of the exercise-induced increase in muscle sympathetic nerve activity (MSNA). The first is the exercise pressor reflex (Mitchell et al. 1983), which arises from both mechanical and metabolic stimuli in the contracting muscles. The second is central command, which is defined as the parallel activation of motor, autonomic and ventilatory neuronal circuits in the brainstem. Central command does not depend on sensory input from exercising muscles (Eldridge et al. 1985).

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