Immediate exercise hyperemia: contributions of the muscle pump vs. rapid vasodilation

Abstract

A striking characteristic of the blood flow adaptation at exercise onset is the immediate and substantial increase in the first few (0-5 s) seconds of exercise. The purpose of this mini-review is to put into context the present evidence regarding mechanisms responsible for this phase of exercise hyperemia. One potential mechanism that has received much attention is the mechanical effect of muscle contraction (the muscle pump). The rapid vasodilatory mechanism(s) is another possible mechanism that has recently been shown to exist. This review will provide the reader with 1) an understanding of the basic physics of blood flow and the theories of muscle pump function, 2) a critical examination of evidence both for and against the contribution of the muscle pump or rapid vasodilatory mechanisms, and 3) an awareness of the limitations and impact of experimental models and exercise modes on the contribution of each of these mechanisms to the immediate exercise hyperemia. The inability to measure microvenular pressure continues to limit investigators to indirect assessments of the muscle pump vs. vasodilatory mechanism contributions to immediate exercise hyperemia in vivo. Future research directions should include examination of muscle-contraction-induced resistance vessel distortion as a trigger for rapid smooth muscle relaxation and further investigation into the exercise mode dependency of muscle pump vs. rapid vasodilatory contributions to immediate exercise hyperemia.

Kinetics of O2uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain

“…Tschakovsky and colleagues observed a rapid vasodilation within the first relaxation cycle after a single forearm contraction (34,38,39), and while this immediate increase in VC was identical in rest-to-mild and mild-to-moderate intensity forearm exercise transitions, a blunted response was seen with the forearm below compared with above heart level (34). Also, while VC increased further with continued contractions in both arm positions, the VC response with the forearm below heart level was attenuated in the mild-to-moderate compared with the rest-to-mild intensity condition, but was similar in both transitions with the forearm above heart level (34).…”

“…the similarity between LBF and HR (and its effect on cardiac output) seen between each of the exercise transitions suggests some correspondence between the two variables, either directly through bulk flow delivery, or indirectly through effects on shear stress. It is unlikely that a single factor contributes to the increase in VC and its time course during the exercise transition, and it is possible that the relative roles and contributions of the various factors may change with exercise intensity and duration [as suggested by Tschakovsky and Sheriff (39)]. …”

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

“…In fact, even a single muscle contraction produces a prompt increase in blood flow (1,7,14,26,36,39). There has been a debate over the last few decades about whether this rapid hyperemia is due to the muscle pump mechanism or to rapid vasodilation (5,35).…”

Squatting maneuver - an easy and efficient method to evaluate postural effect on human arterial blood pressure regulation

“…Further by Rossberg and Penaz and Krediet and Wieling added that on standing and loss of compression of the legs, there would be an immediate reduction in leg vascular resistance due to already existing locally mediated vasodilatation. [26][27][28][29] Moreover, also supported by studies by Tschakovsky and Sheriff as the muscular effort involved in standing up from a squat position is considerable, it has been demonstrated that rapid vasodilatory mechanisms act in proportion to contraction intensity. [30] This would be expected to cause further vasodilatation.…”