Metabolic Control of Muscle Blood Flow During Exercise in Humans

2003 ◽  
Vol 28 (5) ◽  
pp. 754-773 ◽  
Author(s):  
Robert Boushel
Keyword(s):  
Blood Flow ◽  
Muscle Contraction ◽  
Muscle Blood Flow ◽  
Selective Inhibition ◽  
Metabolic Demand ◽  
Close Coupling ◽  
Muscle Oxygen ◽  
Exercise Induced ◽  
Metabolic Vasodilation ◽  
Exercise In Humans

During muscle contraction, several mechanisms regulate blood flow to ensure a close coupling between muscle oxygen delivery and metabolic demand. No single factor has been identified to constitute the primary metabolic regulator, yet there are signal transduction pathways between skeletal muscle and the vasculature that induce vasodilation. A link between muscle metabolic events and microvascular control of blood flow is illustrated by local dilation of terminal arterioles during contraction of muscle fibers and conduction of vasodilation upstream. Endothelial-derived vasodilator mechanisms are known to exert control of muscle vasodilation. Adenosine, nitric oxide (NO), prostacyclin (PGI2), and endothelial-derived hyperpolarization factor (EDHF) are possible mediators of muscle vasodilation during exercise. In humans, adenosine has been shown to contribute to functional hyperemia as blood flow is reduced under nonselective adenosine-receptor blockade. No clear role has been demonstrated for either NO or PGI2, based on studies employing selective inhibition of these substances individually, suggesting a redundancy of vasodilator mechanisms. This is supported by recent work demonstrating that combined blockade of NOS and PGI2, and NOS and cytochrome P450, both attenuate exercise-induced hyperemia in humans. Combined vasodilator blockade studies offer the potential to uncover important interactions and compensatory vasodilator responses. The signaling pathways that link metabolic events evoked by muscle contraction to vasodilatory signals in the local vascular bed remains an important area of study. Key words: metabolic vasodilation, endothelium

scholarly journals Mechanical effects of muscle contraction increase intravascular ATP draining quiescent and active skeletal muscle in humans

2013 ◽  
Vol 114 (8) ◽  
pp. 1085-1093 ◽  
Author(s):  
Anne R. Crecelius ◽  
Brett S. Kirby ◽  
Jennifer C. Richards ◽  
Frank A. Dinenno
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Contraction ◽  
Cuff Pressure ◽  
Muscle Blood Flow ◽  
Muscle Contractions ◽  
Luciferase Assay ◽  
Metabolic Demand ◽  
Mechanical Effects

Intravascular adenosine triphosphate (ATP) evokes vasodilation and is implicated in the regulation of skeletal muscle blood flow during exercise. Mechanical stresses to erythrocytes and endothelial cells stimulate ATP release in vitro. How mechanical effects of muscle contractions contribute to increased plasma ATP during exercise is largely unexplored. We tested the hypothesis that simulated mechanical effects of muscle contractions increase [ATP]venous and ATP effluent in vivo, independent of changes in tissue metabolic demand, and further increase plasma ATP when superimposed with mild-intensity exercise. In young healthy adults, we measured forearm blood flow (FBF) (Doppler ultrasound) and plasma [ATP]v (luciferin-luciferase assay), then calculated forearm ATP effluent (FBF×[ATP]v) during rhythmic forearm compressions (RFC) via a blood pressure cuff at three graded pressures (50, 100, and 200 mmHg; Protocol 1; n = 10) and during RFC at 100 mmHg, 5% maximal voluntary contraction rhythmic handgrip exercise (RHG), and combined RFC + RHG ( Protocol 2; n = 10). [ATP]v increased from rest with each cuff pressure (range 144–161 vs. 64 ± 13 nmol/l), and ATP effluent was graded with pressure. In Protocol 2, [ATP]v increased in each condition compared with rest (RFC: 123 ± 33; RHG: 51 ± 9; RFC + RHG: 96 ± 23 vs. Mean Rest: 42 ± 4 nmol/l; P < 0.05), and ATP effluent was greatest with RFC + RHG (RFC: 5.3 ± 1.4; RHG: 5.3 ± 1.1; RFC + RHG: 11.6 ± 2.7 vs. Mean Rest: 1.2 ± 0.1 nmol/min; P < 0.05). We conclude that the mechanical effects of muscle contraction can 1) independently elevate intravascular ATP draining quiescent skeletal muscle without changes in local metabolism and 2) further augment intravascular ATP during mild exercise associated with increases in metabolism and local deoxygenation; therefore, it is likely one stimulus for increasing intravascular ATP during exercise in humans.

Relation of blood flow to VO2, PO2, and PCO2 in dog gastrocnemius muscle

1988 ◽  
Vol 255 (5) ◽  
pp. H1004-H1010 ◽  
Author(s):  
D. E. Mohrman ◽  
R. R. Regal
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Gastrocnemius Muscle ◽  
Muscle Blood Flow ◽  
Carbon Dioxide Tension ◽  
Experimental Conditions ◽  
Muscle Oxygen ◽  
Muscle Oxygen Consumption ◽  
Relationship Of ◽  
The Relationship

We pump-perfused gastrocnemius-plantaris muscle preparations at constant pressure to study the relationship of muscle blood flow (Q) to muscle oxygen consumption (VO2), venous oxygen tension (PVO2), and venous carbon dioxide tension (PVCO2) during steady-state exercise at different rates. Tests were performed under four experimental conditions produced by altering the perfusate blood-gas status with a membrane lung. The consistency of the relationship of Q to other variables was evaluated by statistical analysis of fitted curves. Not one of the above listed variables had the same relationship with Q in all four of the experimental conditions we tested. However, we did find that a consistent relationship existed among Q, PVO2, and PVCO2 in our data. That relationship is well described by the equation (Q-23).[PVO2 - (0.5.PVCO2) - 3] = 105 (when Q is expressed in ml.100 g-1.min-1 and PVO2 and PVCO2 in mmHg). One interpretation of this result is that both PO2 and PCO2 are important variables in the control of blood flow in skeletal muscle the combined influence of which could account for nearly all of the hyperemia response to steady-state muscle exercise.

scholarly journals Exercise-induced hyperemia is associated with knee extensor fatigability in adults with type 2 diabetes

2019 ◽  
Vol 126 (3) ◽  
pp. 658-667 ◽  
Author(s):  
Jonathon W. Senefeld ◽  
Jacqueline K. Limberg ◽  
Kathleen M. Lukaszewicz ◽  
Sandra K. Hunter
Keyword(s):  
Type 2 Diabetes ◽  
Blood Flow ◽  
Lower Limb ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Knee Extensor ◽  
Dynamic Exercise ◽  
Extensor Muscles ◽  
Exercise Induced

The aim of this study was to compare fatigability, contractile function, and blood flow to the knee extensor muscles after dynamic exercise in patients with type 2 diabetes mellitus (T2DM) and controls. The hypotheses were that patients with T2DM would demonstrate greater fatigability than controls, and greater fatigability would be associated with a lower exercise-induced increase in blood flow and greater impairments in contractile function. Patients with T2DM ( n = 15; 8 men; 62.4 ± 9.0 yr; 30.4 ± 7.7 kg/m2; 7,144 ± 3,294 steps/day) and 15 healthy control subjects (8 men, 58.4 ± 6.9 yr; 28.4 ± 4.6 kg/m2; 7,893 ± 2,323 steps/day) were matched for age, sex, body mass index, and physical activity. Fatigability was quantified as the reduction in knee extensor power during a 6-min dynamic exercise. Before and after exercise, vascular ultrasonography and electrical stimulation were used to assess skeletal muscle blood flow and contractile properties, respectively. Patients with T2DM had greater fatigability (30.0 ± 20.1% vs. 14.6 ± 19.0%, P < 0.001) and lower exercise-induced hyperemia (177 ± 90% vs. 194 ± 79%, P = 0.04) than controls but similar reductions in the electrically evoked twitch amplitude (37.6 ± 24.8% vs. 31.6 ± 30.1%, P = 0.98). Greater fatigability of the knee extensor muscles was associated with postexercise reductions in twitch amplitude ( r = 0.64, P = 0.001) and lesser exercise-induced hyperemia ( r = −0.56, P = 0.009). Patients with T2DM had greater lower-limb fatigability during dynamic exercise, which was associated with reduced contractile function and lower skeletal muscle blood flow. Thus, treatments focused on enhancing perfusion and reversing impairments in contractile function in patients with T2DM may offset lower-limb fatigability and aid in increasing exercise capacity. NEW & NOTEWORTHY Although prior studies compare patients with type 2 diabetes mellitus (T2DM) with lean controls, our study includes controls matched for age, body mass, and physical activity to more closely assess the effects of T2DM. Patients with T2DM demonstrated no impairment in macrovascular endothelial function, evidenced by similar flow-mediated dilation to controls. However, patients with T2DM had greater fatigability and reduced exercise-induced increase in blood flow (hyperemia) after a lower-limb dynamic fatiguing exercise compared with controls.

Enhanced arteriolar α-adrenergic constriction impairs dilator responses and skeletal muscle perfusion in obese Zucker rats

2004 ◽  
Vol 97 (2) ◽  
pp. 764-772 ◽  
Author(s):  
Jefferson C. Frisbee
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Gastrocnemius Muscle ◽  
Muscle Blood Flow ◽  
Zucker Rats ◽  
Metabolic Demand ◽  
Obese Zucker Rats ◽  
Isometric Twitch ◽  
Gastrocnemius Muscles

The present study tested the hypothesis that enhanced vascular α-adrenergic constriction in obese Zucker rats (OZR) impairs arteriolar dilation and perfusion of skeletal muscle at rest and with increased metabolic demand. In lean Zucker rats (LZR) and OZR, isolated gracilis arterioles were viewed via television microscopy, and the contralateral cremaster muscle or gastrocnemius muscle was prepared for study in situ. Gracilis and cremasteric arterioles were challenged with dilator stimuli under control conditions and after blockade of α-adrenoreceptors with prazosin, phentolamine, or yohimbine. Gastrocnemius muscles performed isometric twitch contractions of increasing frequency, and perfusion was continuously monitored. In OZR, dilator responses of arterioles to hypoxia (gracilis), wall shear rate (cremaster), acetylcholine, and iloprost (both) were impaired vs. LZR. Treatment with prazosin and phentolamine (and in cremasteric arterioles only, yohimbine) improved arteriolar reactivity to these stimuli in OZR, although responses remained impaired vs. LZR. Gastrocnemius muscle blood flow was reduced at rest in OZR; this was corrected with intravenous infusion of phentolamine or prazosin. At all contraction frequencies, blood flow was reduced in OZR vs. LZR; this was improved by infusion of phentolamine or prazosin at low-moderate metabolic demand only (1 and 3 Hz). At 5 Hz, adrenoreceptor blockade did not alter blood flow in OZR from levels in untreated rats. These results suggest that enhanced α-adrenergic constriction of arterioles of OZR contributes to impaired dilator responses and reduced muscle blood flow at rest and with mild-moderate (although not with large) elevations in metabolic demand.

Blood flow and muscle metabolism in chronic fatigue syndrome

2003 ◽  
Vol 104 (6) ◽  
pp. 641-647 ◽  
Author(s):  
Kevin K. McCULLY ◽  
Sinclair SMITH ◽  
Sheeva RAJAEI ◽  
John S. LEIGH ◽  
Benjamin H. NATELSON
Keyword(s):  
Blood Flow ◽  
Chronic Fatigue Syndrome ◽  
Muscle Blood Flow ◽  
Muscle Metabolism ◽  
Chronic Fatigue ◽  
Medial Gastrocnemius ◽  
Resonance Spectroscopy ◽  
Muscle Oxygen ◽  
Fatigue Syndrome ◽  
Rate Of Recovery

The purpose of this study was to determine if chronic fatigue syndrome (CFS) is associated with reduced blood flow and oxidative delivery to skeletal muscle. Patients with CFS according to CDC (Center for Disease Control) criteria (n=19) were compared with normal sedentary subjects (n=11). Muscle blood flow was measured with Doppler ultrasound after cuff ischaemia and exercise. Muscle oxygen delivery was measured as the rate of post-exercise and post-ischaemic oxygen-haem resaturation. Oxygen-haem resaturation was measured in the medial gastrocnemius muscle using continuous wavelength near-IR spectroscopy. Muscle metabolism was measured using 31P magnetic resonance spectroscopy. CFS patients and controls were not different in the peak blood flow after cuff ischaemia, the rate of recovery of phosphocreatine after submaximal exercise, and the rate of recovery of oxygen saturation after cuff ischaemia. In conclusion, CFS patients showed no deficit in blood flow or oxidative metabolism. This suggests that CFS symptoms do not require abnormal peripheral function.

Muscle blood flow studies in muscle-contraction headaches

Neurology ◽  
1961 ◽  
Vol 11 (11) ◽  
pp. 935-935 ◽  
Author(s):  
Y. Onel ◽  
A. P. Friedman ◽  
J. Grossman
Keyword(s):  
Blood Flow ◽  
Muscle Contraction ◽  
Muscle Blood Flow

alpha-Stimulation protects exercise increment in skeletal muscle oxygen consumption

1980 ◽  
Vol 238 (3) ◽  
pp. H331-H339 ◽  
Author(s):  
S. H. Nellis ◽  
S. F. Flaim ◽  
K. M. McCauley ◽  
R. Zelis
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Adrenergic Receptor ◽  
Analysis Of Covariance ◽  
Beta Blockade ◽  
Active Muscle ◽  
Muscle Oxygen ◽  
Muscle Oxygen Consumption ◽  
Exercise Induced

Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest (Qc and VO2c), after 5 min of exercise (Qe and VO2e) and after 5 more min of exercise with either NE or MO (Qt and VO2t). Data were normalized and plotted as the VO2e-VO2t)/(VO2c-VO2e) vs. (Qe-Qt)/(Qc-Qe) and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P less than 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a beta-adrenergic-receptor-mediated of skeletal muscle metabolic processes, the experiments were repeated in the presence of beta-blockade with propranolol. In the presence of beta-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

Relative contribution of vasodilator prostanoids and NO to metabolic vasodilation in the human forearm

1999 ◽  
Vol 276 (2) ◽  
pp. H663-H670 ◽  
Author(s):  
Stephen J. Duffy ◽  
Gishel New ◽  
Binh T. Tran ◽  
Richard W. Harper ◽  
Ian T. Meredith
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Venous Occlusion ◽  
Healthy Humans ◽  
Relative Contribution ◽  
Prostanoid Production ◽  
Before And After ◽  
Forearm Exercise ◽  
Exercise Induced ◽  
Metabolic Vasodilation

Although many factors are thought to contribute to the regulation of metabolic vasodilation in skeletal muscle vasculature, recent interest has focused on the role of the endothelium. We examined the relative roles of nitric oxide (NO) and of vasodilator prostanoids in the control of metabolically induced functional hyperemia in the forearm of humans. In 43 healthy volunteers [24 ± 5 (SD) yr] we assessed resting and functional hyperemic blood flow (FHBF) in response to 2 min of isotonic forearm exercise before and after inhibition of NO and/or vasodilator prostanoid production with intra-arterial N G-monomethyl-l-arginine (l-NMMA, 2 mg/min) and aspirin (ASA, 3 mg/min), respectively. Blood flow was measured using venous occlusion plethysmography.l-NMMA and ASA decreased resting forearm blood flow by 42% ( P < 0.0001) and 23% ( P < 0.0001), respectively, whereas infusion of ASA followed byl-NMMA reduced flow by a further 24% ( P < 0.05).l-NMMA reduced peak FHBF by 18% [from 13.9 ± 1.0 to 11.4 ± 1.1 (SE) ml ⋅ 100 ml forearm−1 ⋅ min−1, P = 0.003] and the volume “repaid” after 1 and 5 min by 25% (8.9 ± 0.7 vs. 6.7 ± 0.7 ml/100 ml, P < 0.0001) and 37% (26.6 ± 1.8 vs. 16.8 ± 1.6 ml/100 ml, P < 0.0001). ASA similarly reduced peak FHBF by 19% (from 14.5 ± 1.1 to 11.8 ± 0.9 ⋅ 100 ml forearm−1 ⋅ min−1, P < 0.001) and the volume repaid after 1 and 5 min by 14% (7.5 ± 0.6 vs. 6.4 ± 0.6 ml/100 ml, P = 0.0001) and 20% (21.2 ± 1.5 vs. 16.9 ± 1.5 ml/100 ml, P < 0.0001), respectively. The coinfusion of ASA andl-NMMA did not decrease FHBF to a greater extent than either agent alone. These data suggest that endothelium-derived NO and vasodilator prostanoids contribute to resting blood flow and metabolic vasodilation in skeletal muscle vasculature in healthy humans. Although these vasodilator mechanisms operate in parallel in exercise-induced hyperemia, they appear not to be additive. Other mechanisms must also be operative in metabolic vasodilation.

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