Abstract
Static skeletal muscle contraction increases arterial blood pressure, heart rate, myocardial contractility, and sympathetic nerve activity. These changes occur when humans or conscious cats perform static exercise, and can also be produced by evoking static contractions using anesthetized animals (14). Two potential mechanisms for these cardiovascular changes have been proposed: 1) a reflex arising from the contracting muscles, and 2) a descending input from higher brain centers. The first theory, termed the “exercise pressor reflex,” proposes that the cardiovascular changes are produced reflexly by a contraction induced activation of muscle afferents (1,12,15). The second theory proposes that the cardiovascular changes are elicited by signals arising from central areas that recruit motor units and also activate cardiovascular neurons located in the medulla and/or spinal cord (central command) (6,11,27). Currently,both mechanisms are thought to be important in mediating the cardiovascular responses during exercise. However, the relative contributions of these mechanisms to the cardiovascular changes produced by skeletal muscle contraction and how they are integrated needs further study.
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Wilson, L.B., Mitchell, J.H. (1995). Exercise Pressor Reflex. In: Kappagoda, C.T., Kaufman, M.P. (eds) Control of the Cardiovascular and Respiratory Systems in Health and Disease. Advances in Experimental Medicine and Biology, vol 381. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1895-2_17
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