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.

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)

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?

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

Chronic Ablation of TRPV1 Sensitive Skeletal Muscle Afferents Attenuates the Muscle Metaboreflex

2021 ◽  
Author(s):  
Joseph Mannozzi ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
Alberto Alvarez ◽  
Danielle Senador ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Intrathecal Administration ◽  
Exercise Intolerance ◽  
Stroke Work ◽  
Muscle Metaboreflex

Exercise intolerance is a hallmark symptom of cardiovascular disease and likely occurs via enhanced activation of muscle metaboreflex- induced vasoconstriction of the heart and active skeletal muscle which, thereby limits cardiac output and peripheral blood flow. Muscle metaboreflex vasoconstrictor responses occur via activation of metabolite-sensitive afferent fibers located in ischemic active skeletal muscle, some of which express Transient Receptor Potential Vanilloid 1 (TRPV1) cation channels. Local cardiac and intrathecal administration of an ultra-potent noncompetitive, dominant negative agonist resiniferatoxin (RTX) can ablate these TRPV1 sensitive afferents. This technique has been used to attenuate cardiac sympathetic afferents and nociceptive pain. We investigated whether intrathecal administration (L4-L6) of RTX (2 μg/kg) could chronically attenuate subsequent muscle metaboreflex responses elicited by reductions in hindlimb blood flow during mild exercise (3.2 km/h) in chronically instrumented conscious canines. RTX significantly attenuated metaboreflex induced increases in mean arterial pressure (27 ± 5.0 mmHg vs. 6 ± 8.2 mmHg), cardiac output (1.40 ± 0.2 L/min vs. 0.28 ± 0.1 L/min) and stroke work (2.27 ± 0.2 L*mmHg vs. 1.01 ± 0.2 L*mmHg). Effects were maintained until 78 ± 14 days post RTX at which point the efficacy of RTX injection was tested by intra-arterial administration of capsaicin (20 μg/kg). A significant reduction in the mean arterial pressure response (+45.7 ± 6.5 mmHg pre RTX vs +19.7 ± 3.1mmHg post RTX) was observed. We conclude that intrathecal administration of RTX can chronically attenuate the muscle metaboreflex and could potentially alleviate enhanced sympatho-activation observed in cardiovascular disease states.

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.

Regional circulatory contributions to increased systemic vascular conductance of pregnancy

1991 ◽  
Vol 261 (6) ◽  
pp. H1842-H1847 ◽  
Author(s):  
D. Curran-Everett ◽  
K. G. Morris ◽  
L. G. Moore
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Late Gestation ◽  
Whole Body ◽  
Ang Ii ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Regional Blood Flows ◽  
In Pregnancy

In pregnancy, maternal systemic vascular conductance increases, a new vascular circuit grows, and the maternal systemic circulation develops a diminished pressor response to angiotensin II (ANG II). However, the quantitative contributions of the latter two circulatory changes to the increased systemic vascular conductance of pregnancy have not been explored. In this experiment, we examined regional circulatory contributions to the increased systemic vascular conductance in conscious, late-gestation guinea pigs. Systemic arterial pressure, cardiac output (dye dilution), and regional blood flows (radiolabeled microspheres) were measured during baseline conditions and progressive ANG II infusion. Systemic and regional conductances were calculated from arterial pressure and cardiac output or regional blood flows. In pregnancy, maternal systemic vascular conductance increased from 3.2 to 5.0 ml.min-1.mmHg-1 (P less than 0.001); increased nonuteroplacental conductance contributed 71% to the increase in whole body conductance. Pregnancy tended to decrease the nonuteroplacental conductance response (P = 0.072), but did not change the uteroplacental conductance response (P greater than or equal to 0.29), to ANG II. The increased uteroplacental blood flow of pregnancy was preserved during ANG II-induced vasoconstriction. We conclude that maternal systemic vascular conductance increased primarily because nonuteroplacental vascular conductance increased.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Resistance training increases basal limb blood flow and vascular conductance in aging humans

2006 ◽  
Vol 101 (5) ◽  
pp. 1351-1355 ◽  
Author(s):  
Maria M. Anton ◽  
Miriam Y. Cortez-Cooper ◽  
Allison E. DeVan ◽  
Daria B. Neidre ◽  
Jill N. Cook ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Strength Training ◽  
Whole Body ◽  
Control Group ◽  
Limb Blood Flow ◽  
Vascular Conductance ◽  
Femoral Blood Flow ◽  
Femoral Blood

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 ± 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 ± 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested ( P < 0.05). Whole body lean body mass increased ( P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55–60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.

scholarly journals Whole-Body Circulatory Autoregulation and Hypertension

1971 ◽  
Vol 28 (5_suppl_2) ◽  
Author(s):  
THOMAS G. COLEMAN ◽  
HARRIS J. GRANGER ◽  
ARTHUR C. GUYTON
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fluid Retention ◽  
Whole Body ◽  
Hemodynamic Pattern ◽  
Elevated Arterial Pressure ◽  
Anephric Patients ◽  
Goldblatt Hypertension

A possible cause of elevated arterial pressure involves the interrelationship between autoregulation of blood flow and control of arterial blood pressure. An autoregulatory response could theoretically result in an elevated arterial pressure and an elevated peripheral resistance with normal or nearly normal cardiac output. Several experimental studies support this theory. Autoregulation of blood flow has been observed in a number of the body's tissues, and the summated effect, whole-body autoregulation, has been demonstrated in areflex dogs. An increase in cardiac output precedes an increase in total peripheral resistance, and a decrease in cardiac output precedes a decrease in total peripheral resistance. The gain of the system was calculated to be slightly greater than three. This same hemodynamic pattern, that is, an increase in cardiac output preceding an increase in resistance, has been observed at the onset of hypertension. We have observed increases in cardiac output at the beginning of salt-induced hypertension in dogs and at the beginning of hypertension secondary to fluid volume expansion in anephric patients, while other investigators have observed this hemodynamic pattern in a number of instances, including labile hypertension, perinephritis hypertension, and Goldblatt hypertension. The increased cardiac output can be caused by several factors, although in many instances the cause appears to be fluid retention. A hemodynamic response suggesting the involvement of whole-body autoregulation, that is, a decrease in cardiac output precedes a decrease in peripheral resistance, has been observed in the reversal of hypertension. Dehydrating overhydrated (and hypertensive) anephric patients and unclipping the renal artery in Goldblatt hypertension elicits this pattern, as well as administration of diuretics or several other antihypertensive drugs to hypertensives. Theoretically, the role of the kidney in hypertension is either to initiate the autoregulatory response by causing fluid retention or to allow the autoregulatory response to occur by preventing the loss of fluid in the face of an elevated arterial pressure.

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.

Is active skeletal muscle functionally vasoconstricted during dynamic exercise in conscious dogs?

1997 ◽  
Vol 272 (1) ◽  
pp. R386-R391 ◽  
Author(s):  
D. S. O'Leary ◽  
E. D. Robinson ◽  
J. L. Butler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Dynamic Exercise ◽  
Conscious Dogs ◽  
Aortic Blood Flow ◽  
Vascular Conductance ◽  
Adrenergic Antagonist ◽  
Sympathetic Nervous

We investigated whether the increase in hindlimb blood flow and vascular conductance in conscious dogs during graded dynamic exercise is functionally restrained by the sympathetic nervous system. Dogs were chronically instrumented to monitor terminal aortic blood flow (TAQ) as an index of hindlimb skeletal muscle blood flow and mean arterial pressure (MAP). The extent of functional sympathetic tone was assessed by measuring the increase in TAQ and terminal aortic vascular conductance (TAC, calculated as TAQ/MAP) in response to intra-arterial infusion of the alpha-adrenergic antagonist prazosin (PZ; 50 micrograms/kg) into the hind-limbs at rest and during steady-state dynamic (treadmill) exercise ranging from mild (3.2 km/h, 0% grade to moderately heavy (8 km/h, 15% grade) workloads. This dose of PZ completely abolished the large hindlimb vasoconstrictor response to phenylephrine (1 microgram/kg ia). At rest, PZ increased TAQ by 0.10 +/- 0.02 l/min and TAC by 1.85 +/- 0.53 ml.min-1.mmHg-1. During exercise, as workload increased and the control levels of TAQ and TAC rose progressively delta TAQ and delta TAC with PZ infusion also increased. At the highest workload, PZ increased TAQ by 0.41 +/- 0.07 l/min and TAC by 4.81 +/- 0.38 ml.min-1.mmHg-1. The increase in TAQ and TAC with PZ were linearly related to the control level of TAQ, indicating that as workload increases progressively greater restraint of muscle vasodilation by the sympathetic nervous system occurs. We conclude that during dynamic exercise in conscious dogs the sympathetic nervous system progressively restrains the normal vasodilation in active skeletal muscle, thereby limiting skeletal muscle perfusion.

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