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.

Muscle blood flow responses to dynamic exercise in young obese humans

2010 ◽  
Vol 108 (2) ◽  
pp. 349-355 ◽  
Author(s):  
Jacqueline K Limberg ◽  
Michael D. De Vita ◽  
Gregory M. Blain ◽  
William G. Schrage
Keyword(s):  
Skeletal Muscle ◽  
Body Mass Index ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Vascular Conductance ◽  
Leg Exercise ◽  
Obese Subjects ◽  
Forearm Exercise

Exercise is a common nonpharmacological way to combat obesity; however, no studies have systematically tested whether obese humans exhibit reduced skeletal muscle blood flow during dynamic exercise. We hypothesized that exercise-induced blood flow to skeletal muscle would be lower in young healthy obese subjects (body mass index of >30 kg/m2) compared with lean subjects (body mass index of <25 kg/m2). We measured blood flow (Doppler Ultrasound of the brachial and femoral arteries), blood pressure (auscultation, Finapress), and heart rate (ECG) during rest and two forms of single-limb, steady-state dynamic exercise: forearm exercise (20 contractions/min at 4, 8, and 12 kg) and leg exercise (40 kicks/min at 7 and 14 W). Forearm exercise increased forearm blood flow (FBF) similarly in both groups ( P > 0.05; obese subjects n = 9, lean subjects n = 9). When FBF was normalized for perfusion pressure, forearm vascular conductance was not different between groups at increasing workloads ( P > 0.05). Leg exercise increased leg blood flow (LBF) similarly in both groups ( P > 0.05; obese subjects n = 10, lean subjects n = 12). When LBF was normalized for perfusion pressure, leg vascular conductance was not different between groups at increasing workloads ( P > 0.05). These results were confirmed when relative blood flow was expressed at average relative workloads. In conclusion, our results show that obese subjects exhibited preserved FBF and LBF during dynamic exercise.

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)

Sympathetic restraint of muscle blood flow at the onset of dynamic exercise

2002 ◽  
Vol 92 (6) ◽  
pp. 2452-2456 ◽  
Author(s):  
Jason J. Hamann ◽  
John B. Buckwalter ◽  
Zoran Valic ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Saline Control ◽  
Adrenergic Blockade ◽  
Arterial Infusion ◽  
Blood Flows ◽  
Peak Blood ◽  
Sustained Increase

Little attention has focused on sympathetic influences on skeletal muscle blood flow at the onset of exercise. We hypothesized that 1) the sympathetic nervous system constrains muscle blood flow and 2) the decline from peak blood flow is mediated by increasing sympathetic vasoconstrictor tone. Mongrel dogs ( n = 7) ran on a treadmill after intra-arterial infusion of saline (control) or combined α1- and α2-adrenergic blockade (prazosin and rauwolscine). Immediate and rapid increases in hindlimb blood flow occurred at commencement of exercise with peak iliac blood flows averaging 933 ± 79 and 1,227 ± 90 ml/min during control and blockade conditions, respectively. At 1 min of exercise, hindlimb blood flow had decreased to 629 ± 54 and 1,057 ± 89 ml/min. In the absence of sympathetic vasoconstrictor tone, there was an enhanced peak blood flow at the onset of exercise. In addition, α-blockade attenuated the overshoot of hindlimb blood flow compared with the control condition. These data suggest that an immediate and sustained increase in sympathetic outflow restrains hindlimb blood flow at the onset of exercise and is responsible, at least in part, for an overshoot of blood flow to exercising skeletal muscle.

Role of nitric oxide in skeletal muscle blood flow at rest and during dynamic exercise in humans

1997 ◽  
Vol 273 (1) ◽  
pp. H405-H410 ◽  
Author(s):  
R. C. Hickner ◽  
J. S. Fisher ◽  
A. A. Ehsani ◽  
W. M. Kohrt
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
And Control

The role of nitric oxide at rest and in the active hyperemic response within skeletal muscle was investigated in eight physically active men. Three microdialysis probes were inserted into the vastus lateralis of the quadriceps femoris muscle group in each subject. Microdialysis probes were perfused with a Ringer solution containing 5.0 mM ethanol, 2.5 mM glucose, and either 10 mg/ml of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) monoacetate salt, 30 mg/ml of the nitric oxide precursor L-arginine, or no additional substance (control probe). Subjects performed one-legged cycling exercise at work rates ranging from 25 to 100 W. Dialysate and perfusate ethanol concentrations were presented as the ratio of [ethanol]dialysate to [ethanol]perfusate (ethanol outflow-to-inflow ratio), an indicator that is inversely related to blood flow. The ethanol outflow-to-inflow ratios at rest were 0.614 +/- 0.032, 0.523 +/- 0.023, and 0.578 +/- 0.039 in the L-NMMA, L-arginine, and control probes, respectively. Calculated resting blood flows were therefore 8.7 +/- 4.1, 20.5 +/- 4.6, and 14.0 +/- 4.7 ml.min-1.100 g-1 around the L-NMMA, L-arginine, and control probes, respectively. The ethanol outflow-to-inflow ratios were significantly higher at all exercise intensities in the L-NMMA probe than in the control and L-arginine probes, resulting in calculated blood flows of 195 +/- 55, 407 +/- 47, and 352 +/- 60 ml.min-1.100 g-1 at 25 W and 268 +/- 65, 602 +/- 129, and 519 +/- 113 ml.min-1.100 g-1 at 100 W around the L-NMMA, L-arginine, and control probes, respectively. Skeletal muscle blood flow was therefore reduced both at rest and during continuous, dynamic exercise by the action of L-NMMA, whereas blood flow was increased only at rest by L-arginine.

Muscle blood flow during exercise in sedentary and trained hypothyroid rats

1995 ◽  
Vol 269 (6) ◽  
pp. H1949-H1954 ◽  
Author(s):  
R. M. McAllister ◽  
M. D. Delp ◽  
K. A. Thayer ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Treadmill Running ◽  
Exercise Intolerance ◽  
Vastus Lateralis Muscle ◽  
Blood Flows ◽  
Vastus Intermedius

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

Conditions for dipyridamole potentiation of skeletal muscle active hyperemia

1986 ◽  
Vol 250 (1) ◽  
pp. H62-H67 ◽  
Author(s):  
R. E. Klabunde
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Recovery Time ◽  
Free Flow ◽  
Isometric Contractions ◽  
Vascular Conductance ◽  
Arterial Infusion ◽  
Maximal Tension

The effects of dipyridamole on active hyperemia were evaluated in dog gracilis muscles undergoing sustained isometric contractions. Muscles were stimulated to contract for 5, 15, 25, and 50 s at 20% maximal tension (20% Tmax) or for 10 s at 100% Tmax during intra-arterial infusion of either saline or dipyridamole (1 microM). In two separate groups of dogs, muscles were stimulated to contract under free-flow or restricted-flow (ischemic) conditions. In the later group, blood flow was reduced to 50% of precontraction level during the period of contraction. Dipyridamole increased resting vascular conductance by about 45%; however, it did not affect the change in vascular conductance resulting from muscle contraction. The recovery time for active hyperemia following free-flow contractions at 20% Tmax was not altered by dipyridamole. However, dipyridamole increased the recovery time following 50 s of restricted-flow contraction (20% Tmax) and 10 s of 100% Tmax contractions by 46 and 169%, respectively. These results suggest that adenosine contributes to active hyperemia following sustained ischemic contractions at 20% Tmax and contractions at 100% Tmax but not from contractions at 20% Tmax where blood flow is allowed to increase freely.

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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