Abstract
An increase in blood pressure occurs during exercise and has been suggested to be due, in part, via direct afferent signalling within the active skeletal muscle. Initial observations from Alam & Smirk (1937) indicated that elevations in blood pressure during exercise may arise from accumulation of metabolites within skeletal muscle, and suggested that this reflex may be designed so that the central nervous system (CNS) could aid in regulating the supply of blood to the active muscle. In this respect, blood flow to the active muscle could be increased via an augmented perfusion pressure. Recent evidence confirms the presence of metabolically sensitive (Type IV) afferent fibres in skeletal muscle tissue as well as mechanically sensitive (Type III) afferents that are suggested to be activated during muscle contraction and initiate this exercise pressor reflex (EPR) (Kaufman et al. 1983).
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