![]() Therefore, a synthesis of key facts and concepts is needed to frame the overall discussion of exercise hyperemia. Our rationale for this top down approach is that in an era of reductionism, many scientists and trainees are less familiar with fundamental concepts related to whole body oxygen consumption, cardiac output, and blood flow distribution. We then discuss the magnitude of the cardiac output required to deliver this oxygen to the contracting muscles, and how blood flow is distributed to the microcirculation to meet the demand for oxygen by the active muscles. To explore our first physiological need, we describe the range of oxygen consumption observed in humans and focus on the large increases in oxygen consumption that can occur during large muscle mass rhythmic exercise. With our high level perspective as a background, we will work our way down from ideas related to oxygen consumption, cardiac output, skeletal muscle blood flow, and blood pressure regulation. These three points reflect an integrative perspective that we and others have been developing over the last 15 or so years ( 68, 392). We also make the case that during heavy exercise sympathetic modulation of the peripheral circulation (including contracting skeletal muscle) operates in a way that 1) maintains arterial blood pressure at a minimal “acceptable” level of ∼100 mmHg, 2) facilitates the perfusion of a large mass of active muscle, and 3) increases oxygen extraction across the contracting skeletal muscles. In this review we consider the many factors that contribute to the homeostatic and regulatory mechanisms operating to meet the two main physiological needs emphasized above. However, there were hints that this was an issue as early as the 1960s ( 301). The potential competition between vasodilation and blood pressure regulation outlined above has emerged as a major new idea in integrative physiology over the last 30 or so years ( 392). This raises the possibility that vasodilation in the contracting muscles might outstrip cardiac output and threaten blood pressure regulation ( 68, 301, 392, 393). The idea that these two important physiological needs “compete” arises when the mass and vasodilator capacity of skeletal muscle are considered in the context of the maximum values for cardiac output seen during exercise. Second, regulation of blood pressure is also needed to ensure there is adequate perfusion pressure to all organs. First, because the metabolic costs of muscle contraction can be high and prolonged, skeletal muscle blood flow needs to be matched to the metabolic demands of the contracting muscles. The major theme of this review is that during large muscle mass exercise like running or cycling there are two potentially competing physiological needs. Additionally, complex interactions between the sympathetic nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise in humans. At this time, no one dominant dilator mechanism accounts for exercise hyperemia. Finally, the competition between demand for blood flow by contracting muscles and maximum systemic cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large muscle mass or whole body exercise in humans. ![]() ![]() We also discuss the vasodilating factors in the contracting muscles responsible for these very high flows. We highlight the very high muscle blood flow responses to exercise discovered in the 1980s. In this context, we take a top down approach and review the basics of oxygen consumption at rest and during exercise in humans, how these values change with training, and the systemic hemodynamic adaptations that support them. The idea is that blood flow to the contracting muscles links oxygen in the atmosphere with the contracting muscles where it is consumed. ![]() This review focuses on how blood flow to contracting skeletal muscles is regulated during exercise in humans. ![]()
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