Role of speed vs. grade in relation to muscle pump function at locomotion onset

2001 ◽  
Vol 91 (1) ◽  
pp. 269-276 ◽  
Author(s):  
Don D. Sheriff ◽  
Amy L. Hakeman
Keyword(s):  
Blood Flow ◽  
High Speed ◽  
Time Course ◽  
Muscle Blood Flow ◽  
Male Rats ◽  
Low Grade ◽  
Total Work ◽  
Vascular Conductance ◽  
Contraction Frequency ◽  
Muscle Pump

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.

Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump?

1993 ◽  
Vol 265 (4) ◽  
pp. H1227-H1234 ◽  
Author(s):  
D. D. Sheriff ◽  
L. B. Rowell ◽  
A. M. Scher
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Venous Pressure ◽  
Work Rate ◽  
Dynamic Exercise ◽  
Aortic Flow ◽  
Vascular Conductance ◽  
Muscle Pump ◽  
Autonomic Blockade ◽  
Metabolic Vasodilation

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)

Skeletal muscle blood flow capacity: role of muscle pump in exercise hyperemia

1987 ◽  
Vol 253 (5) ◽  
pp. H993-H1004 ◽  
Author(s):  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Muscle Pump ◽  
Blood Flows ◽  
Flow Capacity

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.

Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes

1990 ◽  
Vol 69 (2) ◽  
pp. 407-418 ◽  
Author(s):  
L. B. Rowell ◽  
D. S. O'Leary
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Nervous Activity ◽  
Isometric Exercise ◽  
Muscle Afferents ◽  
Operating Point ◽  
Central Command ◽  
Vascular Conductance ◽  
Muscle Chemoreflex ◽  
Vagal Withdrawal

The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.

Effects of prior heavy-intensity exercise during single-leg knee extension on v̇o2 kinetics and limb blood flow

2005 ◽  
Vol 99 (4) ◽  
pp. 1462-1470 ◽  
Author(s):  
Nicole D. Paterson ◽  
John M. Kowalchuk ◽  
Donald H. Paterson
Keyword(s):  
Blood Flow ◽  
Phase Ii ◽  
Time Course ◽  
Muscle Blood Flow ◽  
Knee Extension ◽  
Phase Iii ◽  
Limb Blood Flow ◽  
Heavy Exercise ◽  
Pulsed Wave Doppler ◽  
Young Subjects

The effects of prior heavy-intensity exercise on O2 uptake (V̇o2) kinetics of a second heavy exercise may be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. This study examined the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with V̇o2 kinetics. Five young subjects completed five to eight repeats of two 6-min bouts of heavy-intensity one-legged, knee-extension exercise separated by 6 min of loadless exercise. V̇o2 was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. V̇o2 and blood flow velocity data were fit using a monoexponential model to identify phase II and phase III time periods and estimate the response amplitudes and time constants (τ). Phase II V̇o2 kinetics was speeded on the second heavy-intensity exercise [mean τ (SD), 29 ( 10 ) s to 24 ( 10 ) s, P < 0.05] with no change in the phase II (or phase III) amplitude. Qleg was elevated before the second exercise [1.55 (0.34) l/min to 1.90 (0.25) l/min, P < 0.05], but the amplitude and time course [τ, 25 ( 13 ) s to 35 ( 13 ) s] were not changed, such that throughout the transient the Qleg (and ΔQleg/ΔV̇o2) did not differ from the prior heavy exercise. Thus V̇o2 kinetics were accelerated on the second exercise, but the faster kinetics were not associated with changes in Qleg. Thus limb blood flow appears not to limit V̇o2 kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered V̇o2 response after heavy-intensity prior exercise.

A method for using microspheres to measure muscle blood flow in exercising rats

1982 ◽  
Vol 52 (6) ◽  
pp. 1629-1635 ◽  
Author(s):  
M. H. Laughlin ◽  
R. B. Armstrong ◽  
J. White ◽  
K. Rouk
Keyword(s):  
Blood Flow ◽  
High Speed ◽  
Muscle Blood Flow ◽  
Reference Sample ◽  
Left Ventricular ◽  
Ascending Aorta ◽  
Treadmill Running ◽  
Tissue Samples ◽  
Skeletal Muscle Blood Flow ◽  
Catheter Implantation

A catheter-implantation procedure allowing use of the radiolabeled microsphere (MS) technique for measuring skeletal muscle blood flow (BF) in rats during high-speed treadmill running was desired. Attempts to use existing procedures were unsuccessful. We found that Silastic catheters (0.02 in. ID X 0.037 in. OD) placed in the ascending aorta (for MS infusions) and the renal artery (for reference sample withdrawal) minimized these exercise performance problems. It was then necessary to establish that aortic MS infusions result in good MS-blood mixing. We tested the method with the following: 1) the radioactivities found in reference withdrawal samples taken from two locations in the aorta were compared after left ventricular (LV) infusion and after aortic infusion; 2) BFs to bilaterally paired tissues were compared in anesthetized and conscious rats with LV and aortic infusions; 3) the distribution of MSs in the muscles was studied histologically; and 4) BFs in bilaterally paired tissues were compared in rats with aortic MS infusions during treadmill running. The results indicate that 1) the percent difference between the radioactivities found in the proximal and distal reference withdraw samples was the same for LV and aortic MS infusions; 2) BF to bilaterally paired tissue samples was the same with both LV or aortic MS infusions; 3) the MSs were distributed uniformly within muscles, and MS aggregation was not a significant problem; and 4) BFs to bilaterally paired tissue samples were the same in exercising rats. We conclude that this technique can be used to measure muscle BF in rats running on a treadmill.

Skeletal muscle blood flow and vascular conductance are enhanced in humans with high‐affinity hemoglobin during handgrip exercise in severe hypoxia

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Chad C. Wiggins ◽  
Paolo B. Dominelli ◽  
Jonathon W. Senefeld ◽  
John R.A. Shepherd ◽  
Sarah E. Baker ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Severe Hypoxia ◽  
Handgrip Exercise ◽  
Vascular Conductance ◽  
Skeletal Muscle Blood Flow ◽  
High Affinity

Do vasoregulatory mechanisms in exercising human muscle compensate for changes in arterial perfusion pressure?

2007 ◽  
Vol 293 (5) ◽  
pp. H2928-H2936 ◽  
Author(s):  
Kathryn L. Walker ◽  
Natasha R. Saunders ◽  
Dennis Jensen ◽  
Jennifer L. Kuk ◽  
Suzi-Lai Wong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Human Muscle ◽  
Isometric Handgrip ◽  
Vascular Conductance ◽  
Arterial Perfusion ◽  
Arterial Blood ◽  
Myogenic Regulation

We tested the hypothesis that vasoregulatory mechanisms completely counteract the effects of sudden changes in arterial perfusion pressure on exercising muscle blood flow. Twelve healthy young subjects (7 female, 5 male) lay supine and performed rhythmic isometric handgrip contractions (2 s contraction/ 2 s relaxation 30% maximal voluntary contraction). Forearm blood flow (FBF; echo and Doppler ultrasound), mean arterial blood pressure (arterial tonometry), and heart rate (ECG) were measured. Moving the arm between above the heart (AH) and below the heart (BH) level during contraction in steady-state exercise achieved sudden ∼30 mmHg changes in forearm arterial perfusion pressure (FAPP). We analyzed cardiac cycles during relaxation (FBFrelax). In an AH-to-BH transition, FBFrelax increased immediately, in excess of the increase in FAPP (∼69% vs. ∼41%). This was accounted for by pressure-related distension of forearm resistance vasculature [forearm vascular conductance (FVCrelax) increased by ∼19%]. FVCrelax was restored by the second relaxation. Continued slow decreases in FVCrelax stabilized by 2 min without restoring FBFrelax. In a BH-to-AH transition, FBFrelax decreased immediately, in excess of the decrease in FAPP (∼37% vs. ∼29%). FVCrelax decreased by ∼14%, suggesting pressure-related passive recoil of resistance vessels. The pattern of FVCrelax was similar to that in the AH-to-BH transition, and FBFrelax was not restored. These data support rapid myogenic regulation of vascular conductance in exercising human muscle but incomplete flow restoration via slower-acting mechanisms. Local arterial perfusion pressure is an important determinant of steady-state blood flow in the exercising human forearm.

Ideas about control of skeletal and cardiac muscle blood flow (1876–2003): cycles of revision and new vision

2004 ◽  
Vol 97 (1) ◽  
pp. 384-392 ◽  
Author(s):  
Loring B. Rowell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Muscle ◽  
Neural Control ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Site Of Action ◽  
New Vision ◽  
Muscle Chemoreflex

This perspective examines origins of some key ideas central to major issues to be addressed in five subsequent mini-reviews related to Skeletal and Cardiac Muscle Blood Flow. The questions discussed are as follows. 1) What causes vasodilation in skeletal and cardiac muscle and 2) might the mechanisms be the same in both? 3) How important is muscle's mechanical contribution (via muscle pumping) to muscle blood flow, including its effect on cardiac output? 4) Is neural (vasoconstrictor) control of muscle vascular conductance and muscle blood flow significantly blunted in exercise by muscle metabolites and what might be a dominant site of action? 5) What reflexes initiate neural control of muscle vascular conductance so as to maintain arterial pressure at its baroreflex operating point during dynamic exercise, or is muscle blood flow regulated so as to prevent accumulation of metabolites and an ensuing muscle chemoreflex or both?

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