Control of skeletal muscle perfusion at the onset of dynamic exercise. Med. Sci. Sports Exerc., Vol. 31, No. 7, pp. 1011-1018, 1999. At the onset of exercise there is a rapid increase in skeletal muscle vascular conductance and blood flow. Several mechanisms involved in the regulation of muscle perfusion have been proposed to initiate this hyperemic response, including neural, metabolic, endothelial, myogenic, and muscle pump mechanisms. Investigators utilizing pharmacological blockade of cholinergic muscarinic receptors and sympathectomy have concluded that neither sympathetic cholinergic nor adrenergic neural mechanisms are involved in the initial hyperemia. Studies have also shown that the time course for vasoactive metabolite release, diffusion, accumulation, and action is too long to account for the rapid increase in vascular conductance at the initiation of exercise. Furthermore, there is little or no evidence to support an endothelium or myogenic mechanism as the initiating factor in the muscle hyperemia. Thus, the rise in muscle blood flow does not appear to be explained by known neural, metabolic, endothelial, or myogenic influences. However, the initial hyperemia is consistent with the mechanical effects of the muscle pump to increase the arteriovenous pressure gradient across muscle. Because skeletal muscle blood flow is regulated by multiple and redundant mechanisms, it is likely that neural, metabolic, and possibly endothelial factors become important modulators of mechanically induced exercise hyperemia following the first 5-10 s of exercise.
Departments of Health and Kinesiology and of Medical Physiology, Texas A&M University, College Station, TX 77843
Submitted for publication October 1998.
Accepted for publication October 1998.
I am deeply indebted to Robert B. Armstrong and M. Harold Laughlin and the writings of Carl R. Honig for stimulating my interest in the mechanisms that initiate muscle hyperemia. Research in the author's laboratory is supported by National Aeronautics and Space Administration (NASA) grants NAGW-4842 and NAG5-3754 and a NASA-National Space and Biomedical Research Institute grant NCC-9-58.
Address for correspondence: M. D. Delp, Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843. E-mail: email@example.com.