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?

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.

Plasma lactate concentration and muscle blood flow during dynamic exercise with negative-pressure breathing

2000 ◽  
Vol 89 (6) ◽  
pp. 2196-2205 ◽  
Author(s):  
Y. Kamijo ◽  
Y. Takeno ◽  
A. Sakai ◽  
M. Inaki ◽  
T. Okumoto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Negative Pressure ◽  
Muscle Blood Flow ◽  
Lactate Concentration ◽  
Dynamic Exercise ◽  
Plasma Lactate ◽  
Vascular Conductance ◽  
Graded Exercise ◽  
Plasma Lactate Concentration ◽  
Negative Pressure Breathing

This study assessed the hypothesis that increasing cardiac filling pressure (CFP) would enhance contracting muscle blood flow (MBF) by stretching cardiopulmonary baroreceptors and attenuate the increase in plasma lactate concentration ([Lac−]p) during dynamic exercise. Continuous negative-pressure breathing (CNPB) (−15 cmH2O) was used to increase the CFP by accelerating the venous return to the heart. In the first series of experiments, 10 men performed a graded exercise seated on a cycle ergometer with (N1) and without CNPB (C1). The increase in [Lac−]p for N1 was attenuated at 60%, 90%, and 100% of maximal exercise intensity compared with that in C1 ( P < 0.001). Also, the increases in mean arterial pressure (MAP) and plasma catecholamine concentrations were attenuated in N1 compared with those in C1 throughout the graded exercise ( P < 0.05). However, heart rate and pulse pressure were not significantly influenced by CNPB. Second, we studied the impact of CNPB on forearm MBF during a rhythmic handgrip exercise in 5 of the 10 subjects. Forearm MBF was measured immediately after cessation of the exercise by venous occlusion plethysmography at rest, 30%, 50%, and 70% of maximal work load (WLmax) with (N2) and without CNPB (C2). Forearm MBF and vascular conductance for both trials increased with the increase in intensity, but forearm skin blood flow measured by laser-Doppler flowmetry remained unchanged. MBF and vascular conductance in N2, however, increased more than in C2 at every intensity ( P < 0.01) except for MBF at 70% WLmax, whereas the increase in MAP for N2 was attenuated compared with that in C2 ( P < 0.05). Thus augmented active muscle vasodilation occurred in N2 with a lower increase in MAP compared with that in C2. These findings suggest that the stretch of intrathoracic baroreceptors, such as cardiopulmonary mechanoreceptors, by CNPB increased MBF by suppressing sympathetic nerve activity. The attenuation of the increase in [Lac−]p might be caused, at least partially, by the increased MBF.

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.

Baroreflex participation in redistribution of cardiac output at onset of exercise

1988 ◽  
Vol 64 (2) ◽  
pp. 627-634 ◽  
Author(s):  
J. R. Hales ◽  
J. Ludbrook
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Muscle ◽  
Treadmill Exercise ◽  
Arteriovenous Anastomoses ◽  
Vascular Conductance ◽  
Conscious Animal ◽  
Vascular Beds ◽  
Increased Blood Flow ◽  
Distribution Of Cardiac Output

The distribution of cardiac output and systemic vascular conductance was measured in five rabbits. Cardiac output was measured by ascending aortic flowmetry and was partitioned according to the distribution of 15-micron radiolabeled microspheres injected into the left atrium. The rabbits were studied under four conditions: at rest and after 20 s of treadmill exercise, both before and approximately 5 min after acute barodenervation of the conscious animal. During exercise in the baroinnervated state, approximately 40% of the increased blood flow to skeletal and cardiac muscle was contributed by diversion from the splanchnic organs, kidneys, systemic arteriovenous anastomoses, and skin. This diversion of blood flow during exercise was absent after arterial barodenervation. We conclude that at the onset of exercise in rabbits the mismatch between cardiac output and the metabolic demands of skeletal and cardiac muscle is accommodated by vasoconstriction in other vascular beds. We suggest that the vasoconstriction in the splanchnic organs and skin may be caused by transient suppression of the reflex effects of arterial baroreceptor input at the onset of exercise.

Integrative control of the skeletal muscle microcirculation in the maintenance of arterial pressure during exercise

2004 ◽  
Vol 97 (3) ◽  
pp. 1112-1118 ◽  
Author(s):  
Michael D. Delp ◽  
Donal S. O'Leary
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Dynamic Exercise ◽  
Whole Body ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Vascular Conductance ◽  
Body Dynamic

Skeletal muscle blood flow and vascular conductance are influenced by numerous factors that can be divided into two general categories: central cardiovascular control mechanisms and local vascular control mechanisms. Central cardiovascular control mechanisms are thought to be designed primarily for the maintenance of arterial pressure and central cardiovascular homeostasis, whereas local vascular control mechanisms are thought to be designed primarily for the maintenance of muscle homeostasis. To support the high metabolic rates that can be generated during muscle contraction, skeletal muscle has a tremendous capacity to vasodilate and increase oxygen and nutrient delivery. During whole body dynamic exercise at maximal oxygen consumption (V̇o2 max), the skeletal muscle receives 85–90% of cardiac output. Yet despite receiving such a large fraction of cardiac output during high-intensity exercise, a vasodilator reserve remains with the potential to produce further elevations in skeletal muscle vascular conductance and blood flow. However, because maximal cardiac output is reached during exercise at V̇o2 max, further elevations in muscle vascular conductance would produce a fall in arterial pressure. Therefore, limits on muscle perfusion must be imposed during whole body exercise to prevent such drops in pressure. Effective arterial pressure control in response to a potentially hypotensive challenge during high-intensity exercise occurs primarily through reflex-mediated increases in sympathetic nerve activity, which are capable of modulating vasomotor tone of the skeletal muscle resistance vasculature. Thus skeletal muscle vascular conductance and perfusion are primarily mediated by local factors at rest and during exercise, but other centrally mediated control systems are superimposed on the dominant local control mechanisms to provide an integrated regulation of both arterial pressure and skeletal muscle vascular conductance and perfusion during whole body dynamic exercise.

Influence of cardiac output distribution on cardiac filling pressure during rest and dynamic exercise in dogs

1994 ◽  
Vol 267 (6) ◽  
pp. H2378-H2382 ◽  
Author(s):  
D. D. Sheriff ◽  
X. Zhou
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Right Atrial ◽  
Cardiac Filling ◽  
The Relationship ◽  
Distribution Of Cardiac Output ◽  
Total Muscle ◽  
Rest And Exercise

The distribution of cardiac output (CO) between compliant and noncompliant organs is an important determinant of the slope of the relationship predicted between CO and right atrial pressure (RAP). However, curves relating CO to RAP at rest are shifted rightward (higher CO) and upward (higher RAP) by exercise with no change in slope, despite a large rise in the fraction of CO directed to noncompliant muscle vasculature, which is predicted to decrease the slope. We sought to test whether reductions in CO imposed during rest and exercise are accompanied by changes in its distribution that would favor constant slopes. Six dogs had atrioventricular block produced surgically and had blood flow transducers implanted on the ascending aorta and the terminal aorta. Total muscle blood flow (MBF) was estimated from terminal aortic flow by assuming that all of the increase in CO in mild dynamic exercise is directed to muscle. CO was reduced by lowering ventricular pacing rate at rest and during graded treadmill exercise (2 and 4 miles/h at 0% grade). Exercise increased the fraction of CO directed to muscle (MBF/CO) (P < 0.001). The effect of changes in CO on MBF/CO depended on exercise intensity (P < 0.01). At rest, MBF/CO fell from 0.53 to 0.45 when CO was reduced; this is expected to reduce the slope of the measured relationship between CO and RAP. During exercise at 2 miles/h, MBF/CO changed little when CO was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Leg vasoconstriction during dynamic exercise with reduced cardiac output

1992 ◽  
Vol 73 (5) ◽  
pp. 1838-1846 ◽  
Author(s):  
J. A. Pawelczyk ◽  
B. Hanel ◽  
R. A. Pawelczyk ◽  
J. Warberg ◽  
N. H. Secher
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Dynamic Exercise ◽  
Adrenergic Blockade ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Norepinephrine Spillover

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document