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Skeletal and Cardiac Muscle Blood Flow

Joyner, Michael J.

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Exercise and Sport Sciences Reviews: January 2005 - Volume 33 - Issue 1 - p 1-2
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In several recent editions of the Journal of Applied Physiology, some outstanding short reviews concerning regulation of cardiac and skeletal muscle blood flow during exercise were published. The goal of the series was to provide a brief overview of the factors that govern blood flow to these vital organs, and to discuss new ideas about how blood flow is regulated to these tissues during exercise. This topic is especially important because a variety of new ideas and concepts have recently emerged related to exercise hyperemia, and, more importantly, some older ideas have been reinvigorated. This series was especially timely because of the recent explosion of information about how substances from the vascular endothelium might influence exercise hyperemia in cardiac and skeletal muscle, because of new insight into how vasoconstricting sympathetic nerves and metabolic vasodilation might interact, and because of a variety of ideas related to how skeletal and cardiac muscle blood flow are regulated as part of the overall cardiovascular response to exercise.

Central to these reviews was a powerful historical perspective written by Loring Rowell (4). Professor Rowell has been interested in related topics for more than 40 years, and he has a number of editorials, review articles, book chapters, and texts that have generally been seen as landmarks in integrating our understanding of how the cardiovascular system responds to exercise, gravitational, and thermal stress. In this review he lucidly summarizes where ideas about exercise hyperemia have come from, how they have been modified over time, and how various concepts have shifted in and out of focus. Clearly, ideas about the muscle pump, metabolic vasodilation, the interaction between nerves and blood vessels, and the possible role of substances carried in the blood as regulators of skeletal muscle blood flow during exercise have been around for a long time. In this context, Professor Rowell’s recent review is a “must” read for those seeking a broader historical perspective on regulation of skeletal and cardiac muscle blood flow.

In other articles in this series, Tschakovsky and Sheriff review their long running debate about the contribution of the muscle pump versus rapid vasodilation at the onset of exercise (6). The argument is that a single brief contraction can cause an almost immediate rise in skeletal muscle blood flow. This rise in flow may happen too fast to be explained by vasodilation, thus mechanical factors such as the muscle pump are postulated to play a major role in this rapid response. However, there are serious questions about just how much flow the muscle pump might be able to generate. There are also a host of experimental problems that make current resolution of this stimulating debate difficult. The authors succeed in their goal of clearly laying out the parameters of the debate, the current state of knowledge, and the limitations to the various arguments. Continued understanding of how mechanical and metabolic factors interact to regulate skeletal muscle blood flow will be important as this field moves forward.

In another paper in this series, Clifford and Hellston review the role of various vasodilating substances, their source, and their mechanisms of action in blood vessels that perfuse contracting skeletal muscle (1). This review highlights the continued failure to find “the” metabolic vasodilator, and even several key dilators might explain the majority of exercise hyperemia. The concept of redundant control mechanisms is emphasized. This topic is especially interesting because there is a long, creative, and colorful history associated with the discussion of vasodilation in active skeletal muscles.

In another review in this series, Gail Thomas and Steve Segal discuss the role of nerves in either initiating and/or modulating the vasodilation in the active muscles (5). Although ideas about the contribution of nerves to exercise hyperemia date back to at least the 1870s, new experimental approaches by many investigators, especially Drs. Thomas and Segal, have led to important new progress on a variety of concepts. Additionally, these investigators have performed carefully conducted animal studies that have raised important and also testable hypotheses for studies in conscious humans and whole animals. These authors succeeded in their goal of discussing neural control of blood flow to exercising muscle in the context of helping other investigators develop a clear set of specific aims for future research.

One of the main questions when considering exercise hyperemia has always been whether the mechanisms that govern the rise in coronary blood flow through the heart during exercise are the same or different than those that govern the rise in skeletal muscle blood flow. In the JAP series Tune, Gorman, and Feigl review their recent work and the work of others (7). This paper is nicely integrated with the skeletal muscle blood flow papers, and makes a variety of important points. First (as is the case with skeletal muscles), no clear single dilator substance appears to be obligatory for the rise in coronary blood flow during exercise, and no clear combination of dilators appears responsible. Additionally, as is the case in skeletal muscle, the sympathetic nerves and adrenergic receptors play an important role in local modulation of the blood flow. The authors indicate that although much is known about how blood flow is regulated to areas involved in pathophysiological ischemia, what happens in the normal heart is less known. They brusquely conclude their review by indicating that “several potential mediators of local metabolic control to coronary circulation have been evaluated without success. More research is needed.” This frustrating comment might be applied equally well to the mechanisms that govern exercise hyperemia in contracting skeletal muscles.

Although most of this series focuses on issues related to the acute responses associated with exercise hyperemia in skeletal and cardiac muscle, Prior, Yang, and Terjung discuss how skeletal muscle blood vessels grow in response to exercise training (3). The remodeling of the muscle vasculature in response to the increased demands of chronic endurance exercise is a remarkable physiological adaptation. Many of the putative vasodilating substances discussed in the other reviews play a role in activating local angiogenisis via various vascular growth factors and their signaling pathways. Additionally, the mechanical effects of increased flow in conducting vessels also contribute to these responses. In this context, it is interesting to note the same general mechanical and metabolic factors involved in the acute hyperemic responses to exercise might also contribute ultimately to the remodeling of vessels involved in the hyperemia.

Finally, how is all of this “action” at the level of the skeletal muscle integrated from the microcirculation to arterial blood pressure? Delp and O’Leary address the fundamental problem of the tug-of-war between metabolic vasodilation in skeletal muscle, and the need (during large muscle mass exercise) to potentially restrain this vasodilation for the purposes of regulating whole body arterial pressure (2). They conclude that “thus skeletal muscle conductance and perfusion are primarily mediated by local factors, at rest and during exercise, but other centrally mediated control systems are superimposed on the dominant local control mechanisms to provide integrative regulation of both arterial pressure and skeletal muscle vascular conductance and perfusion during whole body dynamic exercise.” In this context, these authors have done an admirable job in piecing the current jigsaw puzzle together on this complex and challenging topic.


Regulation of skeletal and cardiac muscle blood flow during exercise is a continuing puzzle. This series effectively highlights the current state of knowledge on this broad topic. When viewed in the context of Professor Rowell’s historical review, one is struck simultaneously with thoughts of how much we know and how much is left to know.


1. Clifford, P.S., and Y. Hellsten. Vasodilatory mechanisms in contracting skeletal muscle. J. Appl. Physiol. 97:393–403, 2004.
2. Delp, M.D., and D.S. O’Leary. Integrative control of the skeletal muscle microcirculation in the maintenance of arterial pressure during exercise. J. Appl. Physiol. 97:1112–8, 2004.
3. Prior, B.M., H. T. Yang, and R.L. Terjung. What makes vessels grow with exercise training? J. Appl. Physiol. 97:1119–28, 2004.
4. Rowell, L.B. Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision. J. Appl. Physiol. 97:384–9, 2004.
5. Thomas, G.D., and S.S. Segal. Neural control of muscle blood flow during exercise. J. Appl. Physiol. 97:731–8, 2004.
6. Tschakovsky, M.E., and D.D. Sheriff. Immediate exercise hyperemia: contributions of the muscle pump vs. rapid vasodilation. J. Appl. Physiol. 97:739–47, 2004 Aug.
7. Tune, J.D., M.W. Gorman, and E.O. Feigl. Matching coronary blood flow to myocardial oxygen consumption. J. Appl. Physiol. 97:404–15, 2004.
©2005 The American College of Sports Medicine