Comment on Point:Counterpoint “The muscle pump is/is not an important determinant of muscle blood flow during exercise”

2005 ◽  
Vol 99 (6) ◽  
pp. 2451-2451
Author(s):  
Jurgen W.G.E. Vanteeffelen ◽  
Steven S. Segal
2005 ◽  
Vol 99 (2) ◽  
pp. 778-778 ◽  
Author(s):  
Vladimir S Panchev ◽  
Adelina V Suvandjieva ◽  
Marieta V Pancheva

2018 ◽  
Vol 124 (2) ◽  
pp. 302-311 ◽  
Author(s):  
K. A. Zuj ◽  
C. N. Prince ◽  
R. L. Hughson ◽  
S. D. Peterson

This study tested the hypothesis that intermittent compression of the lower limb would increase blood flow during exercise and postexercise recovery. Data were collected from 12 healthy individuals (8 men) who performed 3 min of standing plantar flexion exercise. The following three conditions were tested: no applied compression (NoComp), compression during the exercise period only (ExComp), and compression during 2 min of standing postexercise recovery. Doppler ultrasound was used to determine superficial femoral artery (SFA) blood flow responses. Mean arterial pressure (MAP) and cardiac stroke volume (SV) were assessed using finger photoplethysmography, with vascular conductance (VC) calculated as VC = SFA flow/MAP. Compared with the NoComp condition, compression resulted in increased MAP during exercise [+3.5 ± 4.1 mmHg (mean ± SD)] but not during postexercise recovery (+1.6 ± 5.9 mmHg). SV increased with compression during both exercise (+4.8 ± 5.1 ml) and recovery (+8.0 ± 6.6 ml) compared with NoComp. There was a greater increase in SFA flow with compression during exercise (+52.1 ± 57.2 ml/min) and during recovery (+58.6 ± 56.7 ml/min). VC immediately following exercise was also significantly greater in the ExComp condition compared with the NoComp condition (+0.57 ± 0.42 ml·min−1·mmHg−1), suggesting the observed increase in blood flow during exercise was in part because of changes in VC. Results from this study support the hypothesis that intermittent compression applied during exercise and recovery from exercise results in increased limb blood flow, potentially contributing to changes in exercise performance and recovery. NEW & NOTEWORTHY Blood flow to working skeletal muscle is achieved in part through the rhythmic actions of the skeletal muscle pump. This study demonstrated that the application of intermittent pneumatic compression during the diastolic phase of the cardiac cycle, to mimic the mechanical actions of the muscle pump, accentuates muscle blood flow during exercise and elevates blood flow during the postexercise recovery period. Intermittent compression during and after exercise might have implications for exercise performance and recovery.


1996 ◽  
Vol 28 (Supplement) ◽  
pp. 175
Author(s):  
M. E. Tschakovsky ◽  
B. Thornburn ◽  
J. K. Shoemaker ◽  
M. T.E. Hopman ◽  
R. L. Hughson

2001 ◽  
Vol 91 (1) ◽  
pp. 269-276 ◽  
Author(s):  
Don D. Sheriff ◽  
Amy L. Hakeman

We sought to clarify the roles of contraction frequency (speed) and contraction force (grade) in the rise in muscle blood flow at the onset of locomotion. Shoemaker et al. ( Can J Physiol Pharmacol 76: 418–427, 1998) explored this relationship in human handgrip exercise and found that the time course of the rise in muscle vascular conductance was similar when a light weight was lifted in a fast cadence and a heavy weight was lifted in a slow cadence (total work constant). This indicates that muscle pumping (contraction frequency) was of limited importance in governing the time course. Rather, vasodilator substances released in proportion to the total work performed appeared to determine the pattern and extent of the rise in conductance. We hypothesized that conductance would rise faster during locomotion at a high speed (frequency) and low grade (force) than at a low speed and high grade, despite similar total increases in conductance, owing to more effective muscle pumping at faster contraction rates. Seven male rats performed nine 1-min bouts of treadmill locomotion across a combination of three speeds (5, 10, and 20 m/min) and three grades (−10, 0, and +15°) in random order. Locomotion at 10 m/min and 0° grade and 20 m/min and −10° grade led to an equal rise in terminal aortic vascular conductance. However, the equal rise was achieved more quickly at the higher running speed, suggestive of more effective muscle pumping. Across the nine combinations of exercise, speed began to exert a statistically significant influence on conductance by the 3rd s of locomotion. Grade did not begin to exert an influence until the 12th s of locomotion (similar to the delays reported for arteriolar dilation to muscle contraction). Additional experiments in dogs provided similar results. Thus the muscle pump appears to initiate the increase in blood flow in proportion to contraction frequency at locomotion onset.


2005 ◽  
Vol 98 (4) ◽  
pp. 1575-1583 ◽  
Author(s):  
Barbara J. Lutjemeier ◽  
Akira Miura ◽  
Barry W. Scheuermann ◽  
Shunsaku Koga ◽  
Dana K. Townsend ◽  
...  

To test for evidence of a muscle pump effect during steady-state upright submaximal knee extension exercise, seven male subjects performed seven discontinuous, incremental exercise stages (3 min/stage) at 40 contractions/min, at work rates ranging to 60–75% peak aerobic work rate. Cardiac cycle-averaged muscle blood flow (MBF) responses and contraction-averaged blood flow responses were calculated from continuous Doppler sonography of the femoral artery. Net contribution of the muscle pump was estimated by the difference between mean exercise blood flow (MBFM) and early recovery blood flow (MBFR). MBFM rose in proportion with increases in power output with no significant difference between the two methods of calculating MBF. For stages 1 and 5, MBFM was greater than MBFR; for all others, MBFM was similar to MBFR. For the lighter work rates ( stages 1–4), there was no significant difference between exercise and early recovery mean arterial pressure (MAP). During stages 5–7, MAP was significantly higher during exercise and fell significantly early in recovery. From these results we conclude that 1) at the lightest work rate, the muscle pump had a net positive effect on MBFM, 2) during steady-state moderate exercise ( stages 2–4) the net effect of rhythmic muscle contraction was neutral (i.e., the impedance due to muscle contraction was exactly offset by the potential enhancement during relaxation), and 3) at the three higher work rates tested ( stages 5–7), any enhancement to flow during relaxation was insufficient to fully compensate for the contraction-induced impedance to muscle perfusion. This necessitated a higher MAP to achieve the MBFM.


2003 ◽  
Vol 284 (6) ◽  
pp. H2185-H2191 ◽  
Author(s):  
Don D. Sheriff

We imposed opposing oscillations in treadmill speed and grade on nine rats to test for direct mechanical coupling between stride frequency and hindlimb blood flow. Resting hindlimb blood flow was 15.5 ± 1.7 ml/min. For 90 s at 7.5 m/min, rats alternated walking at −10° for 10 s and +10° for 10 s. This elicited oscillations in hindlimb blood flow having an amplitude of 4.1 ± 0.5 ml/min (18% of mean flow) with a delay presumably due to metabolic vasodilation. Similar oscillations in speed (5.5–9.5 m/min) elicited oscillations in hindlimb blood flow (amplitude 3.4 ± 0.5 ml/min, 15% of mean flow) with less of a delay, possibly due to changes in vasodilation and muscle pump function. We then simultaneously imposed these speed and grade oscillations out of phase (slow uphill, fast downhill). The rationale was that the oscillations in vasodilation evoked by the opposing oscillations in speed and grade would cancel each other, thereby testing the degree to which stride frequency affects hindlimb blood flow directly (i.e., muscle pumping). Opposing oscillations in speed and grade evoked oscillations in hindlimb blood flow having an amplitude of 3.3 ± 0.6 ml/min (16% of mean flow) with no delay and directly in phase with the changes in speed and stride frequency. The finding that hindlimb blood flow changes directly with speed (when vasodilation caused by changes in speed and grade oppose each other) indicates that there is a direct coupling of stride frequency and hindlimb blood flow (i.e., muscle pumping).


1993 ◽  
Vol 265 (4) ◽  
pp. H1227-H1234 ◽  
Author(s):  
D. D. Sheriff ◽  
L. B. Rowell ◽  
A. M. Scher

We tested the hypothesis that rapid increases in muscle blood flow and vascular conductance (C) at onset of dynamic exercise are caused by the muscle pump. We measured arterial (AP) and central venous pressure (CVP) in nine awake dogs, eight with atrioventricular block, pacemakers, and ascending aortic flow probes for control of cardiac output (CO) (2 also had terminal aortic flow probes). One dog had only an iliac artery probe. At exercise onset (0 and 10% grade, 4 mph) C and CVP rose to early plateaus, and AP reached a nadir, all in 2-5 s. At 20% grade and 4 mph, C increased continuously after its initial sudden rise. Timing and magnitude of initial change in conductance (delta C) were independent of CO, AP, work rate (change in grade at constant speed), or autonomic function (blocked by hexamethonium). Speed of initial delta C and its independence from work rate and blood flow ruled out metabolic vasodilation as its cause; insensitivity to AP and autonomic blockade ruled out myogenic relaxation and sympathetic vasodilation as causes of sudden delta C. Sensitivity to contraction frequency (not work per se) implicates the muscle pump. When reflexes were blocked, a large secondary rise in C, presumably caused by metabolic vasodilation, began after 10 s of mild exercise. When reflexes were intact in mild exercise, C was lowered below its initial plateau by sympathetic vasoconstriction, which partially raised AP from its nadir toward its preexercise level. Our conclusion is that dynamic exercise has a large rapid effect on C that is not explained by known neural, metabolic, myogenic, or hydrostatic influences.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 253 (5) ◽  
pp. H993-H1004 ◽  
Author(s):  
M. H. Laughlin

An appreciation for the potential of skeletal muscle vascular beds for blood flow (blood flow capacity) is required if one is to understand the limits of the cardiorespiratory system in exercise. To assess this potential, an index of blood flow capacity that can be objectively measured is required. One obvious index would be to measure maximal muscle blood flow (MBF). However, a unique value for maximal MBF cannot be measured, since once maximal vasodilation is attained MBF is a function of perfusion pressure. Another approach would be to measure maximal or peak vascular conductance. However, peak vascular conductance is different among skeletal muscles composed of different fiber types and is a function of perfusion pressure during peak vasodilation within muscle composed of a given fiber type. Also, muscle contraction can increase or decrease blood flow and/or the apparent peak vascular conductance depending on the experimental preparation and the type of muscle contraction. Blood flows and calculated values of conductance appear to be greater during rhythmic contractions (with the appropriate frequency and duration) than observed in resting muscle during what is called "maximal" vasodilation. Moreover, dynamic exercise in conscious subjects produces the greatest skeletal muscle blood flows. The purpose of this review is to consider the interaction of the determinants of muscle blood flow during locomotory exercise. Emphasis is directed toward the hypothesis that the "muscle pump" is an important determinant of perfusion of active skeletal muscle. It is concluded that, during normal dynamic exercise, MBF is determined by skeletal muscle vascular conductance, the perfusion pressure gradient, and the efficacy of the muscle pump.


Sign in / Sign up

Export Citation Format

Share Document