Exercise attenuates α-adrenergic-receptor responsiveness in skeletal muscle vasculature

2001 ◽  
Vol 90 (1) ◽  
pp. 172-178 ◽  
Author(s):  
John B. Buckwalter ◽  
Jay S. Naik ◽  
Zoran Valic ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Femoral Artery ◽  
Adrenergic Receptor ◽  
Systemic Blood Pressure ◽  
Heavy Exercise ◽  
Adrenergic Agonist ◽  
Vascular Conductance ◽  
Iliac Arteries ◽  
Sympathetic Vasoconstriction ◽  
Selective Agonists

Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. A potential mechanism is a reduction in α-adrenergic-receptor responsiveness. The purpose of this study was to examine α1- and α2-adrenergic-receptor-mediated vasoconstriction in resting and exercising skeletal muscle using intra-arterial infusions of selective agonists. Thirteen mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective α1-adrenergic agonist (phenylephrine) or the selective α2-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of 76 ± 4, 71 ± 5, and 31 ± 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by 81 ± 5, 49 ± 4, and 14 ± 2%, respectively. The response to intra-arterial infusion of clonidine was unaffected by surgical sympathetic denervation. Agonist infusion did not affect either systemic blood pressure, heart rate, or blood flow in the contralateral iliac artery. α1-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, α2-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. These results suggest that the mechanism of exercise sympatholysis may involve reductions in postsynaptic α-adrenergic-receptor responsiveness.

Role of Nitric Oxide and α-Adrenergic Receptor Responsiveness in Exercising Skeletal Muscle

2005 ◽  
Vol 98 (4) ◽  
pp. 1584-1585
Author(s):  
Adriaan M. Kamper ◽  
Anton J. M. de Craen
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Femoral Artery ◽  
Adrenergic Receptor ◽  
Heavy Exercise ◽  
Adrenergic Agonist ◽  
Vascular Conductance ◽  
Exercise Induced ◽  
Oxide Synthase

The production of nitric oxide is the putative mechanism for the attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during exercise. We hypothesized that nitric oxide synthase blockade would eliminate the reduction in α-adrenergic-receptor responsiveness in exercising skeletal muscle. Ten mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective α1-adrenergic agonist (phenylephrine) or the selective α2-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Before nitric oxide synthase inhibition with NG-nitro-l-arginine methyl ester l-NAME), intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of −91 ± 3, −80 ± 5, and −75 ± 6% (means ± SE) at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by −65 ± 6, −39 ± 4, and −30 ± 3%. After l-NAME, intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of −85 ± 5, −85 ± 5, and −84 ± 5%, whereas clonidine reduced vascular conductance by −67 ± 5, −45 ± 3, and −35 ± 3%, at rest, 3 miles/h, and 6 miles/h and 10% grade. α1-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, α2-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. Whereas the inhibition of nitric oxide production eliminated the exercise-induced attenuation of α1-adrenergic-receptor responsiveness, the attenuation of α2-adrenergic-receptor responsiveness was unaffected. These results suggest that the mechanism of exercise sympatholysis is not entirely mediated by the production of nitric oxide.

Role of nitric oxide in exercise sympatholysis

2004 ◽  
Vol 97 (1) ◽  
pp. 417-423 ◽  
Author(s):  
John B. Buckwalter ◽  
Jessica C. Taylor ◽  
Jason J. Hamann ◽  
Philip S. Clifford
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Femoral Artery ◽  
Adrenergic Receptor ◽  
Heavy Exercise ◽  
Adrenergic Agonist ◽  
Vascular Conductance ◽  
Sympathetic Vasoconstriction ◽  
Exercise Induced ◽  
Oxide Synthase

The production of nitric oxide is the putative mechanism for the attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during exercise. We hypothesized that nitric oxide synthase blockade would eliminate the reduction in α-adrenergic-receptor responsiveness in exercising skeletal muscle. Ten mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective α1-adrenergic agonist (phenylephrine) or the selective α2-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Before nitric oxide synthase inhibition with NG-nitro-l-arginine methyl ester (l-NAME), intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of −91 ± 3, −80 ± 5, and −75 ± 6% (means ± SE) at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by −65 ± 6, −39 ± 4, and −30 ± 3%. After l-NAME, intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of −85 ± 5, −85 ± 5, and −84 ± 5%, whereas clonidine reduced vascular conductance by −67 ± 5, −45 ± 3, and −35 ± 3%, at rest, 3 miles/h, and 6 miles/h and 10% grade. α1-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, α2-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. Whereas the inhibition of nitric oxide production eliminated the exercise-induced attenuation of α1-adrenergic-receptor responsiveness, the attenuation of α2-adrenergic-receptor responsiveness was unaffected. These results suggest that the mechanism of exercise sympatholysis is not entirely mediated by the production of nitric oxide.

α1-Adrenergic-receptor responsiveness in skeletal muscle during dynamic exercise

1998 ◽  
Vol 85 (6) ◽  
pp. 2277-2283 ◽  
Author(s):  
John B. Buckwalter ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Femoral Artery ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Systemic Blood Pressure ◽  
Dynamic Exercise ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Selective Agonist ◽  
Sympathetic Vasoconstriction ◽  
Adrenergic Receptor Agonist

Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. One potential mechanism is a reduction in α1-adrenergic-receptor responsiveness. The purpose of this study was to examine α1-adrenergic-receptor-mediated vasoconstriction in resting and working skeletal muscles by using intra-arterial infusions of a selective agonist. Seven mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. A selective α1-adrenergic-receptor agonist (phenylephrine) was infused as a bolus into the femoral artery catheter at rest and during exercise. All dogs ran on a motorized treadmill at two exercise intensities (3 and 6 miles/h). Intra-arterial infusions of the same effective concentration of phenylephrine elicited reductions in vascular conductance of 76 ± 4, 76 ± 6, and 67 ± 5% ( P > 0.05) at rest, 3 miles/h, and 6 miles/h, respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by phenylephrine. These results do not demonstrate an attenuation of vasoconstriction to a selective α1-agonist during exercise and do not support the concept of sympatholysis.

scholarly journals Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise

1997 ◽  
Vol 83 (5) ◽  
pp. 1575-1580 ◽  
Author(s):  
John B. Buckwalter ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Femoral Artery ◽  
Skeletal Muscles ◽  
Systemic Blood Pressure ◽  
Dynamic Exercise ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Adrenergic Antagonist ◽  
Sympathetic Vasoconstriction ◽  
Adrenergic Antagonists ◽  
Arterial Blockade

Buckwalter, John B., Patrick J. Mueller, and Philip S. Clifford. Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise. J. Appl. Physiol. 83(5): 1575–1580, 1997.—Studies utilizing systemic administration of α-adrenergic antagonists have failed to demonstrate sympathetic vasoconstriction in working muscles during dynamic exercise. The purpose of this study was to examine the existence of active sympathetic vasoconstriction in working skeletal muscles by using selective intra-arterial blockade. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and with a catheter in one femoral artery. All dogs ran on a motorized treadmill at three intensities on separate days. After 2 min, the selective α1-adrenergic antagonist prazosin (0.1 mg) was infused as a bolus into the femoral artery catheter. At mild, moderate, and heavy workloads, there were immediate increases in iliac conductance of 76 ± 7, 54 ± 11, and 22 ± 6% (mean ± SE), respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected. These results demonstrate that there is sympathetic vasoconstriction in active skeletal muscles even at high exercise intensities.

α-Adrenergic vasoconstriction in active skeletal muscles during dynamic exercise

1999 ◽  
Vol 277 (1) ◽  
pp. H33-H39 ◽  
Author(s):  
John B. Buckwalter ◽  
Philip S. Clifford
Keyword(s):  
Blood Flow ◽  
Exercise Intensity ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Systemic Blood Pressure ◽  
Dynamic Exercise ◽  
Iliac Arteries ◽  
Adrenergic Antagonist ◽  
Sympathetic Vasoconstriction ◽  
Adrenergic Antagonists

Sympathetic vasoconstriction in working muscles during dynamic exercise has been demonstrated by intra-arterial administration of α1-adrenergic antagonists. The purpose of this study was to examine the existence of α1- and α2-adrenergic receptor-mediated vasoconstriction in active skeletal muscles during exercise. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs, and a catheter was inserted in one femoral artery. All dogs ran on a motorized treadmill at three exercise intensities (3 miles/h, 6 miles/h, and 6 miles/h at 10% grade) on separate days. After 5 min of exercise, a selective α1- (prazosin) or a selective α2-adrenergic antagonist (rauwolscine) was infused as a bolus into the femoral arterial catheter (only one drug per day). The doses of the antagonists were adjusted to maintain the same effective concentration at each exercise intensity. At the mild, moderate, and heavy workloads prazosin infusion produced immediate increases in iliac conductance of 65 ± 9, 35 ± 6, and 18 ± 4% (means ± SE), respectively, and increases in blood flow of 290 ± 24, 216 ± 23, and 172 ± 18 ml/min, respectively. Rauwolscine infusion produced increases in conductance of 52 ± 5%, 36 ± 5%, and 26 ± 3%, respectively, and blood flow increases of 250 ± 34, 244 ± 39, and 259 ± 35 ml/min at the three workloads. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by any of the antagonist infusions. These results demonstrate that there is ongoing α1- and α2-adrenergic receptor-mediated vasoconstriction in exercising skeletal muscles even at heavy workloads and that the magnitude of vasoconstriction decreases as exercise intensity increases.

Vasoconstriction in exercising skeletal muscles: a potential role for neuropeptide Y?

2004 ◽  
Vol 287 (1) ◽  
pp. H144-H149 ◽  
Author(s):  
John B. Buckwalter ◽  
Jason J. Hamann ◽  
Heidi A. Kluess ◽  
Philip S. Clifford
Keyword(s):  
Skeletal Muscle ◽  
Neuropeptide Y ◽  
Femoral Artery ◽  
Potential Role ◽  
Sympathetic Nerves ◽  
No Production ◽  
Vascular Conductance ◽  
Receptor Stimulation ◽  
Iliac Arteries ◽  
Vasoconstrictor Response

There is evidence that neuropeptide Y (NPY) acts as a neurotransmitter in vascular smooth muscle and is released with norepinephrine from sympathetic nerves. We hypothesized that NPY Y1 receptor stimulation would produce vasoconstriction in resting and exercising skeletal muscle. Nine mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective NPY Y1 receptor agonist [Leu31,Pro34]NPY was infused as a bolus into the femoral artery catheter at rest and during mild, moderate, and heavy exercise. Intra-arterial infusions of [Leu31,Pro34]NPY elicited reductions ( P < 0.05) in vascular conductance of 38 ± 3, 25 ± 2, 17 ± 1, and 11 ± 1% at rest, 3 miles/h, 6 miles/h, and 6 miles/h and 10% grade, respectively. The agonist infusions did not affect ( P > 0.05) blood flow in the contralateral iliac artery. To examine whether nitric oxide (NO) is responsible for the attenuated vasoconstrictor response during exercise to NPY Y1 receptor stimulation, the infusions were repeated after NO synthase blockade. These infusions yielded reductions ( P < 0.05) in vascular conductance of 47 ± 3, 23 ± 2, 19 ± 3, and 12 ± 2% at rest, 3 miles/h, 6 miles/h, and 6 miles/h and 10% grade, respectively. NPY Y1 receptor responsiveness was attenuated ( P < 0.05) during exercise compared with rest. Blockade of NO production did not affect ( P > 0.05) the attenuation of NPY Y1 receptor responsiveness during exercise. These data support the hypothesis that NPY Y1 receptors can produce vasoconstriction in exercising skeletal muscle.

Vasoconstriction in active skeletal muscles: a potential role for P2X purinergic receptors?

2003 ◽  
Vol 95 (3) ◽  
pp. 953-959 ◽  
Author(s):  
John B. Buckwalter ◽  
Jason J. Hamann ◽  
Philip S. Clifford
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Femoral Artery ◽  
Purinergic Receptors ◽  
Sympathetic Nerves ◽  
P2x Receptor ◽  
Vascular Conductance ◽  
Iliac Arteries ◽  
Vasoconstrictor Response ◽  
Oxide Synthase

There is evidence that ATP acts as a neurotransmitter in vascular smooth muscle and is coreleased with norepinephrine from sympathetic nerves. We hypothesized that P2X-receptor stimulation with the selective P2X-receptor agonist α,β-methylene ATP would produce vasoconstriction in resting and exercising skeletal muscle. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective P2X agonist α,β-methylene ATP was infused as a bolus into the femoral artery catheter at rest and during mild, moderate, and heavy exercise. Intra-arterial infusions of α,β-methylene ATP elicited reductions in vascular conductance of 54 ± 5, 49 ± 8, 39 ± 8, and 30 ± 6% at rest, 3 miles/h, 6 miles/h, and 6 miles/h at a 10% grade, respectively. The agonist infusions did not affect blood flow in the contralateral iliac artery. To examine whether nitric oxide is responsible for the attenuated vasoconstrictor response to P2X stimulation, the infusions were repeated in the presence of NG-nitro-l-arginine methyl ester. After nitric oxide synthase blockade, intra-arterial infusions of α,β-methylene ATP elicited reductions in vascular conductance of 56 ± 7, 61 ± 8, 52 ± 9, and 40 ± 7% at rest, 3 miles/h, 6 miles/h, and 6 miles/h at a 10% grade, respectively. P2X-receptor responsiveness was attenuated during exercise compared with rest. Blockade of nitric oxide production did not affect the attenuation of P2X-receptor responsiveness during exercise. These data support the hypothesis that P2X purinergic receptors can produce vasoconstriction in exercising skeletal muscle.

scholarly journals Mechanisms of sympathetic restraint in human skeletal muscle during exercise: role of α-adrenergic and nonadrenergic mechanisms

2020 ◽  
Vol 319 (1) ◽  
pp. H192-H202
Author(s):  
Alexander B. Hansen ◽  
Gilbert Moralez ◽  
Steven A. Romero ◽  
Christopher Gasho ◽  
Michael M. Tymko ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptors ◽  
Whole Body ◽  
Cycle Exercise ◽  
Vascular Conductance ◽  
Hand Grip ◽  
Vasodilatory Response ◽  
Sympathetic Vasoconstriction ◽  
Exercise Induced

Sympathetic restraint of vascular conductance to inactive skeletal muscle is critical to maintain blood pressure during moderate- to high-intensity whole body exercise. This investigation shows that cycle exercise-induced restraint of inactive skeletal muscle vascular conductance occurs primarily because of activation of α-adrenergic receptors. Furthermore, exercise-induced vasoconstriction restrains the subsequent vasodilatory response to hand-grip exercise; however, the restraint of active skeletal muscle vasodilation was in part due to nonadrenergic mechanisms. We conclude that α-adrenergic receptors are the primary but not exclusive mechanism by which sympathetic vasoconstriction restrains blood flow in humans during whole body exercise and that metabolic activity modulates the contribution of α-adrenergic receptors.

Skeletal muscle vasodilation at the onset of exercise

1998 ◽  
Vol 85 (5) ◽  
pp. 1649-1654 ◽  
Author(s):  
John B. Buckwalter ◽  
Stephen B. Ruble ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscarinic Receptors ◽  
Treadmill Exercise ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Iliac Arteries ◽  
Blood Flows ◽  
Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

No effect of NOS inhibition on skeletal muscle glucose uptake during in situ hindlimb contraction in healthy and diabetic Sprague-Dawley rats

2015 ◽  
Vol 308 (10) ◽  
pp. R862-R871 ◽  
Author(s):  
Yet Hoi Hong ◽  
Andrew C. Betik ◽  
Dino Premilovac ◽  
Renee M. Dwyer ◽  
Michelle A. Keske ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Femoral Artery ◽  
Systemic Blood Pressure ◽  
Sprague Dawley ◽  
Capillary Recruitment ◽  
Sprague Dawley Rats ◽  
Skeletal Muscle Glucose Uptake

Nitric oxide (NO) has been shown to be involved in skeletal muscle glucose uptake during contraction/exercise, especially in individuals with Type 2 diabetes (T2D). To examine the potential mechanisms, we examined the effect of local NO synthase (NOS) inhibition on muscle glucose uptake and muscle capillary blood flow during contraction in healthy and T2D rats. T2D was induced in Sprague-Dawley rats using a combined high-fat diet (23% fat wt/wt for 4 wk) and low-dose streptozotocin injections (35 mg/kg). Anesthetized animals had one hindlimb stimulated to contract in situ for 30 min (2 Hz, 0.1 ms, 35 V) with the contralateral hindlimb rested. After 10 min, the NOS inhibitor, NG-nitro-l-arginine methyl ester (l-NAME; 5 μM) or saline was continuously infused into the femoral artery of the contracting hindlimb until the end of contraction. Surprisingly, there was no increase in skeletal muscle NOS activity during contraction in either group. Local NOS inhibition had no effect on systemic blood pressure or muscle contraction force, but it did cause a significant attenuation of the increase in femoral artery blood flow in control and T2D rats. However, NOS inhibition did not attenuate the increase in muscle capillary recruitment during contraction in these rats. Muscle glucose uptake during contraction was significantly higher in T2D rats compared with controls but, unlike our previous findings in hooded Wistar rats, NOS inhibition had no effect on glucose uptake during contraction. In conclusion, NOS inhibition did not affect muscle glucose uptake during contraction in control or T2D Sprague-Dawley rats, and this may have been because there was no increase in NOS activity during contraction.

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