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Circulation to Skeletal Muscle

John T. Shepherd

10.1002/cphy.cp020311

Source: Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow

Originally published: 1983

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Basal Vascular Resistance and Autoregulation
2 Role of Myogenic Mechanism in Reactive Hyperemia
3 Role of Myogenic Mechanism in Exercise Hyperemia
4 Types of Skeletal Muscle Fibers
5 Muscle Blood Flow During Exercise
5.1 Oxygen Lack
5.2 Lactic Acid, pH, and CO2
5.3 Potassium
5.4 Inorganic Phosphate
5.5 Osmolarity
5.6 Prostaglandins
5.7 Adenosine and Adenine Nucleotides
5.8 Intrinsic Neurons and Exercise Dilatation
5.9 General Conclusions
6 Mechanical Hindrance to Blood Flow in Skeletal Muscle
7 Reactive Hyperemia
7.1 Are Exercise and Reactive Hyperemia Due to the Same Mechanism(s)?
8 Propagated Vasodilatation
9 Sympathetic Vasomotor Outflow
10 Noradrenergic Innervation of Resistance Vessels in Muscles
10.1 Neuroeffector Junction
10.2 α‐Adrenergic Activation
11 Factors that Modulate Transmitter Output From Sympathetic Nerve Endings
11.1 Metabolic Action
11.2 Neurohumoral Action
12 Reflex Regulation of Skeletal Muscle Resistance Vessels by Sympathetic Noradrenergic Nerves
12.1 Carotid and Aortic Baroreflex
12.2 Carotid and Aortic Chemoreflex
12.3 Reflexes From the Heart and Lungs
12.4 Diving Reflex
12.5 Reflex From Receptors in Skeletal Muscles
13 Rhythmic Exercise
14 Isometric Exercise
15 Influence of Sympathetic Noradrenergic Fibers on the Blood Flow to Active Muscles
16 β2‐Adrenergic Activation
17 Cholinergic Vasodilator Nerves
17.1 Role of Cholinergic Nerves in the Carotid Baroreflex
17.2 Cholinergic Vasodilatation in Humans
18 Histaminergic Vasodilatation
18.1 Role of Histamine in the Vasodilatation Resulting From Reflex Inhibition of Sympathetic Outflow
19 Conclusions
Figure 1. Figure 1.

Regulation of resistance vessels in skeletal muscle by local, nervous, and humoral factors. Metabolites produced in muscles enter interstitial space and cause relaxation of adjacent resistance vessels, thus adjusting blood flow to meet local metabolic needs. An increase in transmural pressure can cause vessels to constrict and vice versa, partly because of a local myogenic mechanism, which results in autoregulation of blood flow. Prostaglandins synthesized in vessel wall can contribute to vasodilatation. Vessel caliber adjusts in response to changes in sympathetic noradrenergic activity governed by arterial and cardiopulmonary mechanoreceptors, arterial chemoreceptors, and afferents from contracting muscles. Histamine release from cells near arterioles can cause vasodilatation; this release is governed by sympathetic nerve activity. Emotional stress dilates muscle vessels by activating cholinergic nerves and by increasing epinephrine output from the adrenal medulla. ACh, acetylcholine; α, α‐adrenergic receptor; β2, β‐adrenergic receptor; NE, norepinephrine.
Figure 2. Figure 2.

Effect of stretch on rhythmicity and amplitude of spontaneous contractions (isometric tension recording) in a dog's mesenteric vein strip. Preparation length increased by 1 mm at each arrow; experiment starts at zero tension.

From Shepherd and Vanhoutte 441
Figure 3. Figure 3.

Forearm blood flow recorded in a normal subject (A), a patient who had had a cervical sympathectomy for Raynaud's disease 3 mo previously (B), and a patient who sustained a traumatic rupture of the brachial plexus 1 yr previously (C). Dashed lines indicate 5‐min period during which collecting cuff was kept inflated to produce venous congestion in forearm.

From Patterson and Shepherd 385
Figure 4. Figure 4.

Autoregulation index plotted as a function of hindlimb O2 uptake (ml · min−1 · kg−1 body wt). •, Rest; x, muscle stimulation; ○, cold. Curve represents linear regression of log (autoregulation index) on log (O2 uptake): log y = −0.58 log x + 0.59, r = 0.9. Autoregulation index is a measure of slope of flow‐pressure curve in pressure range of 50–150 mmHg. Perfect autoregulation results in an index of zero. An index between zero and one occurs when flow changes relatively less than pressure and indicates compensation for both direct pressure‐ and distensibility‐induced alterations in flow. When autoregulatory response is just sufficient to compensate for distensibility, flow changes are proportional to pressure changes and the index is one. An autoregulatory response too weak to compensate for distensibility results in an index greater than one. Figure illustrates 1) degree of steady‐state autoregulation correlates closely with metabolic O2 consumption; 2) as muscle metabolic rate increases with increased activity, degree of autoregulation becomes more marked; and 3) metabolism depression by cooling impairs autoregulation.

From Goodman et al. 195, by permission of the American Heart Association, Inc
Figure 5. Figure 5.

Reactive hyperemia in the human forearm. Vertical dashed lines indicate period of circulatory arrest by pneumatic cuff around the arm. A: after 5 min of circulatory arrest forearm blood flow returns to resting values more rapidly than after 5 min of rhythmic exercise of forearm muscles. B: when transmural pressure in forearm vessels distal to the site of circulatory arrest is maintained at a higher level by trapping extra blood in the forearm during period of arrest (by exposure to −100 mmHg for 30 s prior to arrest), the subsequent hyperemia is less. This is due to a local action of intravascular pressure on the smooth muscle of the arterioles, resulting in a greater wall tension (myogenic response). C: inhibition of prostaglandin synthesis by indomethacin decreases reactive hyperemia. D: antihistamines diminish reactive hyperemia after 10 min or more of circulatory arrest.

From Shepherd 437
Figure 6. Figure 6.

Major changes in composition of interstitial fluid during contraction of muscle cells. When muscles are inactive (left), 1) arterioles are constricted, 2) concentration of metabolites and CO2 in interstitial fluid is low, and 3) little O2 is used. When muscles become active (right), 1) depolarization of the cell membrane (CM) increases [K+] in the extracellular space; 2) regeneration of adenosine triphosphate (ATP) by mitochondria (Mi) augments CO2 production, which diffuses to the extracellular space; 3) anaerobic production of ATP in the cytoplasm results in formation of lactic acid, which slowly diffuses out of the cell; 4) increased amounts of lactic acid and CO2 cause an increase in [H+] of the extracellular fluid and thus a decrease in pH; 5) breakdown of ATP to diphosphate (ADP) and monophosphate (AMP) and to adenosine, with liberation of inorganic phosphate (Pi), augments concentrations of adenosine and adenine nucleotides in the extracellular space; and 6) osmolality of the extracellular fluid increases. Each change can relax contracted smooth muscle cells.

From Shepherd and Vanhoutte 442. In: The Human Cardiovascular System: Facts and Concepts. Raven Press, New York, 1979
Figure 7. Figure 7.

Plethysmography records of blood flow through forearms before and after 0.3‐s contraction of right forearm muscles. At time of contraction an artifact due to muscle movement appears on the plethysmographic tracing. Numbers above each plethysmogram represent forearm blood flow (in ml · 100 m−1 · min−1).

From Corcondilas, Koroxenidis, and Shepherd 108
Figure 8. Figure 8.

Forearm blood flow before and after rhythmic exercise of forearm muscles carried out during interval indicated by first pair of dashed lines. Second pair of dashed lines indicates 2‐min interval. ○, Blood flow during infusion of isotonic saline into the brachial artery; •, blood flow during infusion of ATP.

From Patterson and Shepherd 386
Figure 9. Figure 9.

Increase in forearm blood flow immediately after a 0.3‐s contraction of forearm muscles in a normal subject and in a subject who had had bilateral cervical sympathectomy 3 yr previously. Increase in forearm flow was obtained by subtracting resting flow before each contraction from flow measured just after contraction. Dilatation was unchanged when subject breathed O2 instead of air. Oxygen capacity of radial artery blood was 19.4 ml/100 ml; O2 content was 19.0 ml/100 ml while breathing air and 20.8 ml/100 ml while breathing O2.

From Corcondilas, Koroxenidis, and Shepherd 108
Figure 10. Figure 10.

A: correlation between vasodilator response and tissue (venous) hyperosmolality in cat skeletal muscle during graded exercise. B: quantitative evaluation of role of tissue hyperosmolality for early exercise hyperemia response in the cat.

From Mellander and Lundvall 361
Figure 11. Figure 11.

Comparison of time courses of tissue adenosine content (filled circles, dashed line) and estimated vascular resistance (shaded band). Vertical bars, 1 SEM for adenosine content. Horizontal bars, 1 SEM for time of biopsy. Adenosine scale has been shifted (nonzero at origin).

From Belloni et al. 41, by permission of the American Heart Association, Inc
Figure 12. Figure 12.

Alternations in adenonsine relative specific activity and vascular resistance during exercise onset. Inf. ON, start of

8‐14C]adenosine infusion. From Tominaga et al. 473
Figure 13. Figure 13.

Adenosine, AMP, ADP, and ATP cause dose‐dependent relaxation in rings of canine femoral arteries made to contract with norepinephrine (left). Mechanical removal of endothelium abolishes relaxations induced by ADP and ATP without affecting those caused by adenosine and AMP (right).

From De Mey and Vanhoutte 123
Figure 14. Figure 14.

Reduction in reflex vasoconstrictor response (7 dogs) in limb perfused at constant flow with progressive distal section of communicating rami between spinal nerves and sympathetic paravertebral lumbar chain. Each animal indicated by a separate symbol.

From Donald and Ferguson 128, by permission of the American Heart Association, Inc
Figure 15. Figure 15.

Products of cellular activity cause dilatation of arterioles because of their direct inhibitory effect on smooth muscle cells and because they interrupt vasoconstrictor impulses of sympathetic nerves. Arteriolar wall is shown as one layer of smooth muscle cells with an adrenergic nerve and one of its varicosities containing adrenergic neurotransmitter norepinephrine (NE). AMP, adenosine monophosphate; ADP, adenosine diphosphate; ATP, adenosine triphosphate; CM, cell membrane; +, activation; − and ∧∧∧, inhibition; α, α‐adrenergic receptor.

From Shepherd and Vanhoutte 442. In: The Human Cardiovascular System: Facts and Concepts. Raven Press, New York, 1979
Figure 16. Figure 16.

Adenosine concentration (left) and increase in [K+] (middle) or in osmolality (right), which do not inhibit responses to norepinephrine, cause relaxation (upper) and significant depression of release of [3H]norepinephrine (lower) evoked by nerve stimulation in 3 groups of dog saphenous veins.

From McGrath and Vanhoutte 354
Figure 17. Figure 17.

Concentrations of acetylcholine (left), histamine (middle), and 5‐hydroxytryptamine (right), which do not cause changes in tension in unstimulated preparations or during contractions to exogenous norepinephrine, cause a pronounced relaxation during sympathetic nerve stimulation (upper); relaxation is due to a decrease in evoked release of adrenergic neurotransmitter (lower). Experiments performed on 3 saphenous vein strips previously incubated with [3H]norepinephrine; overflow of latter is a qualitative measurement of amount of transmitter liberated.

From McGrath and Vanhoutte 354
Figure 18. Figure 18.

Comparison in the anesthetized dog of increases in perfusion pressure in femoral vascular bed (perfused at constant flow with autologous blood) evoked by norepinephrine (noradrenaline) and lumbar sympathetic nerve stimulation (OS stimulatie) before and during continuous infusion of acetylcholine (upper) and isoproterenol (lower). Acetylcholine depresses vasoconstrictor response to sympathetic stimulation more than that to exogenous norepinephrine, demonstrating prejunctional inhibitory effect of cholinergic transmitter.

From Vanhoutte and Levy 488
Figure 19. Figure 19.

Effect on left hindlimb and kidney perfusion pressures of decrease in carotid sinus pressure combined with a capsaicin injection into right femoral artery in a vagotomized dog. Capsaicin was used to stimulate receptors in skeletal muscle. Left hindlimb and kidney were perfused at constant flow with autologous blood.

From Pelletier and Shepherd 393
Figure 20. Figure 20.

Effects of carotid sinus and aortic arch baroreflexes on resistance vessels of dog hindlimbs perfused at constant flow. Response in perfusion pressure expressed as percent of maximal change evoked by carotid distension (mean ± SE, n = 11). Aortic arch curve is displaced to the right; maximal slope and height are less for aortic arch curve than for carotid sinus curve.

From Donald and Edis 127
Figure 21. Figure 21.

Vascular responses in normal young men to changes in carotid sinus pressure. Left: when carotid sinus pressure is increased by application of subatmospheric pressure to the neck, arterial blood pressure, heart rate, and forearm vascular resistance decrease. Right: when carotid sinus pressure is reduced by manual compression of common carotid arteries, arterial blood pressure, heart rate, and calf blood flow increase. There is no evidence that constriction of the calf resistance vessels contributes to increased arterial pressure.

From Donald and Shepherd 130
Figure 22. Figure 22.

Changes in muscle and renal vascular resistance in cats in response to electrical stimulation of right cardiac nerve and to alterations in pressure within partially isolated carotid sinus. Data plotted as percent of maximal decrease in resistance at a carotid sinus pressure of 250 mmHg. Stimulus‐response curves to activity changes in cardiac nerves and carotid sinus nerves have been adjusted so that threshold and maximal responses of each coincide. As carotid sinus pressure is increased above 150 mmHg, resultant increase in activity of carotid baroreceptors reduces muscle resistance more than does increase in activity in cardiac C‐fiber vagal afferents; both are similar in their modulation of renal resistance. As carotid sinus pressure is increased from 50 to 120 mmHg, resultant increase in activity of carotid baroreceptors is less effective in decreasing renal resistance than is an increase in activity of cardiac C‐fiber vagal afferents; both are similar in their modulation of muscle resistance.

Redrawn from Little et al. 320; from Donald and Shepherd 130
Figure 23. Figure 23.

Effect of separate and combined withdrawal of inhibitory influence of carotid sinus and cardiopulmonary baroreceptors on muscle and kidney resistance vessels. Normo‐ and hypervolemic dogs with aortic nerves cut. Responses plotted as percent of change from maximal reflex inhibition (carotid sinus pressure 250 mmHg) to no inhibition (carotid sinus pressure 40 mmHg and bilateral cervical vagal cold block) of resistance vessels in each vascular bed. Note greater influence of carotid baroreceptors on muscle vascular resistance. Cardiopulmonary receptors influence renal resistance to an equal or greater (hypervolemia) degree than carotid baroreceptors.

From Donald and Shepherd 130
Figure 24. Figure 24.

Contribution of carotid sinus and cardiopulmonary baroreflexes to increase in vascular resistance in hindlimb (left) and intestine (right) during 10% hemorrhage in dogs with aortic nerves cut. Iliac and superior mesenteric artery perfused at constant flow.

From Donald and Shepherd 130
Figure 25. Figure 25.

Effect of hypercapnea on inhibition of hindlimb and renal vascular resistance by aortic and cardiopulmonary mechanoreceptors in anesthetized rabbits. Left: vagal and carotid sinus nerves cut prior to aortic nerve block by cooling. Right: carotid sinus and aortic nerves cut prior to cold block of cervical vagal nerves. Note greater augmentation by hypercapnea of inhibitory influence of both systems on renal but not on hindlimb vascular resistance.

From Donald and Shepherd 130
Figure 26. Figure 26.

Vascular responses to vagal cold block before and after removal of lungs. Dog on cardiopulmonary bypass, with arterial baroreceptors denervated, vagi cut at diaphragm, and heart removed. One hindlimb and kidney were perfused at constant pressure of 120 mmHg. Cooling the cervical vagi to 0°C with lungs artificially ventilated caused an increase in aortic blood pressure and a decrease in renal and hindlimb blood flow. Removal of lungs resulted in an increase in aortic pressure and a decrease in renal and hindlimb blood flow (RF, HL). There was no further change with vagal cooling.

From Shepherd 438, by permission of the American Heart Association, Inc
Figure 27. Figure 27.

Effect of passive raising of legs of a normal subject on circulation through forearm. With leg raising, forearm blood flow increases. This was due to increase in muscle blood flow, since the O2 content of the blood draining forearm muscles increased (deep vein) but not that of the blood draining forearm skin (superficial vein). Increased flow was due to reflex dilatation, because blocking sympathetic nerves to the forearm vessels with local anesthetic prevented flow increase. Dilatation was not affected by atropine, indicating that it was caused by decreased activity of noradrenergic fibers and not by activation of cholinergic fibers. Reflex dilatation was caused by displacement of blood from the legs, since it was prevented by inflation of thigh cuffs to suprasystolic pressure prior to leg raising. Because arterial mean and pulse pressures were unchanged and central venous pressure increased, muscle vasodilatation is attributed to receptor excitation somewhere in the heart and lungs.

From Donald and Shepherd 130
Figure 28. Figure 28.

Effect of leg exercise in aortic stenosis. Reflex vasoconstrictor response seen in normal subjects and in patients with mitral stenosis is replaced by a vasodilator response in aortic stenosis. Dots, responses in individual patients. Horizontal lines, means of responses in each group.

From Mark et al. 344
Figure 29. Figure 29.

Blood flow during supine leg exercise in a subject with a normal and a sympathectomized forearm.

From Bevegård and Shepherd 52
Figure 30. Figure 30.

Reproduction of tracings obtained during experiment with a dog hindlimb perfused at constant flow. Vasoconstrictive responses to lumbar trunk stimulation at 6 cycles/s were recorded at rest, at intervals during 65 min of exercise, and 16 min after termination of exercise. Perfusion flows at rest, exercise, and recovery were 84, 285, and 78 ml/min, respectively.

From Rowlands and Donald 420, by permission of the American Heart Association, Inc
Figure 31. Figure 31.

Effect of increased sympathetic outflow to forearm blood vessels on blood flow through forearm during and after rhythmic exercise of forearm muscles. Increased sympathetic outflow induced by application of subatmospheric pressure to lower body (continuous suction).

From Strandell and Shepherd 461
Figure 32. Figure 32.

Effect of increased sympathetic outflow to forearm blood vessels on O2 saturation in a deep forearm vein during rhythmic exercise of forearm muscle. Increased sympathetic outflow induced by application of subatmospheric pressure to lower body (lower‐body suction).

From Strandell and Shepherd 461
Figure 33. Figure 33.

Average response of forearm blood flow (4 expts) to infusion of norepinephrine (Nor, 0.75 μg/min) into left brachial artery. Left: before α‐blockade. Center: during α‐blockade with phentolamine (1,600 μg/min ia). Right: during combined α‐ and β‐blockade with phentolamine (1,600 μg/min ia) and propranolol (10.0 μg/min ia). •, Blood flow in left or experimental forearm; ○, blood flow in right or control forearm; ▪, mean arterial blood pressure.

From Brick et al. 71
Figure 34. Figure 34.

Effect of echo stress test on heart rate, mean arterial blood pressure, forearm and calf blood flow, and resistances. Average values in 6 normal supine subjects.

From Rusch, Shepherd, et al. 422, by permission of the American Heart Association, Inc
Figure 35. Figure 35.

Changes in forearm blood flow and heart rate during moderately severe leg exercise (1,200 kg · m−1 · min−1); average values for 8 studies in 3 normal trained subjects.

From Bevegård and Shepherd 52
Figure 36. Figure 36.

Longitudinal sections through hypothalamus and midbrain of the dog. A: sites at which electrical stimulation produced noncholinergic dilator responses restricted to vasculature of the leg above the paw. B: sites at which electrical stimulation produced noncholinergic dilator responses restricted to vasculature of the paw. Filled star, sites at which electrical stimulation elicited antihistamine‐sensitive vasodilatation. Filled circle, sites at which electrical stimulation elicited antihistamine‐resistant vasodilatation. MI, massa intermedia; P, pituitary stalk; S, substantia nigra. Although stimulation was done in planes 2–5 mm lateral to the midline, diagrams are shown as midline sections for convenience.

From Lang et al. 310, by permission of the American Heart Association, Inc
Figure 37. Figure 37.

Left: separate perfusion of right and left hindlimbs at constant flow (1 dog). Measurement of mean aortic and limb perfusion pressure. Decrease in left leg perfusion pressure in response to stimulation of isolated left anterior spinal nerve root at level of L6. Right: blood flow measurement in right (R) and left (L) hindlimbs perfused at constant aortic (A) pressure (1 dog). Increase in blood flow in right leg in response to stimulation of right anterior nerve root.

From Donald and Ferguson 128, by permission of the American Heart Association, Inc


Figure 1.

Regulation of resistance vessels in skeletal muscle by local, nervous, and humoral factors. Metabolites produced in muscles enter interstitial space and cause relaxation of adjacent resistance vessels, thus adjusting blood flow to meet local metabolic needs. An increase in transmural pressure can cause vessels to constrict and vice versa, partly because of a local myogenic mechanism, which results in autoregulation of blood flow. Prostaglandins synthesized in vessel wall can contribute to vasodilatation. Vessel caliber adjusts in response to changes in sympathetic noradrenergic activity governed by arterial and cardiopulmonary mechanoreceptors, arterial chemoreceptors, and afferents from contracting muscles. Histamine release from cells near arterioles can cause vasodilatation; this release is governed by sympathetic nerve activity. Emotional stress dilates muscle vessels by activating cholinergic nerves and by increasing epinephrine output from the adrenal medulla. ACh, acetylcholine; α, α‐adrenergic receptor; β2, β‐adrenergic receptor; NE, norepinephrine.



Figure 2.

Effect of stretch on rhythmicity and amplitude of spontaneous contractions (isometric tension recording) in a dog's mesenteric vein strip. Preparation length increased by 1 mm at each arrow; experiment starts at zero tension.

From Shepherd and Vanhoutte 441


Figure 3.

Forearm blood flow recorded in a normal subject (A), a patient who had had a cervical sympathectomy for Raynaud's disease 3 mo previously (B), and a patient who sustained a traumatic rupture of the brachial plexus 1 yr previously (C). Dashed lines indicate 5‐min period during which collecting cuff was kept inflated to produce venous congestion in forearm.

From Patterson and Shepherd 385


Figure 4.

Autoregulation index plotted as a function of hindlimb O2 uptake (ml · min−1 · kg−1 body wt). •, Rest; x, muscle stimulation; ○, cold. Curve represents linear regression of log (autoregulation index) on log (O2 uptake): log y = −0.58 log x + 0.59, r = 0.9. Autoregulation index is a measure of slope of flow‐pressure curve in pressure range of 50–150 mmHg. Perfect autoregulation results in an index of zero. An index between zero and one occurs when flow changes relatively less than pressure and indicates compensation for both direct pressure‐ and distensibility‐induced alterations in flow. When autoregulatory response is just sufficient to compensate for distensibility, flow changes are proportional to pressure changes and the index is one. An autoregulatory response too weak to compensate for distensibility results in an index greater than one. Figure illustrates 1) degree of steady‐state autoregulation correlates closely with metabolic O2 consumption; 2) as muscle metabolic rate increases with increased activity, degree of autoregulation becomes more marked; and 3) metabolism depression by cooling impairs autoregulation.

From Goodman et al. 195, by permission of the American Heart Association, Inc


Figure 5.

Reactive hyperemia in the human forearm. Vertical dashed lines indicate period of circulatory arrest by pneumatic cuff around the arm. A: after 5 min of circulatory arrest forearm blood flow returns to resting values more rapidly than after 5 min of rhythmic exercise of forearm muscles. B: when transmural pressure in forearm vessels distal to the site of circulatory arrest is maintained at a higher level by trapping extra blood in the forearm during period of arrest (by exposure to −100 mmHg for 30 s prior to arrest), the subsequent hyperemia is less. This is due to a local action of intravascular pressure on the smooth muscle of the arterioles, resulting in a greater wall tension (myogenic response). C: inhibition of prostaglandin synthesis by indomethacin decreases reactive hyperemia. D: antihistamines diminish reactive hyperemia after 10 min or more of circulatory arrest.

From Shepherd 437


Figure 6.

Major changes in composition of interstitial fluid during contraction of muscle cells. When muscles are inactive (left), 1) arterioles are constricted, 2) concentration of metabolites and CO2 in interstitial fluid is low, and 3) little O2 is used. When muscles become active (right), 1) depolarization of the cell membrane (CM) increases [K+] in the extracellular space; 2) regeneration of adenosine triphosphate (ATP) by mitochondria (Mi) augments CO2 production, which diffuses to the extracellular space; 3) anaerobic production of ATP in the cytoplasm results in formation of lactic acid, which slowly diffuses out of the cell; 4) increased amounts of lactic acid and CO2 cause an increase in [H+] of the extracellular fluid and thus a decrease in pH; 5) breakdown of ATP to diphosphate (ADP) and monophosphate (AMP) and to adenosine, with liberation of inorganic phosphate (Pi), augments concentrations of adenosine and adenine nucleotides in the extracellular space; and 6) osmolality of the extracellular fluid increases. Each change can relax contracted smooth muscle cells.

From Shepherd and Vanhoutte 442. In: The Human Cardiovascular System: Facts and Concepts. Raven Press, New York, 1979


Figure 7.

Plethysmography records of blood flow through forearms before and after 0.3‐s contraction of right forearm muscles. At time of contraction an artifact due to muscle movement appears on the plethysmographic tracing. Numbers above each plethysmogram represent forearm blood flow (in ml · 100 m−1 · min−1).

From Corcondilas, Koroxenidis, and Shepherd 108


Figure 8.

Forearm blood flow before and after rhythmic exercise of forearm muscles carried out during interval indicated by first pair of dashed lines. Second pair of dashed lines indicates 2‐min interval. ○, Blood flow during infusion of isotonic saline into the brachial artery; •, blood flow during infusion of ATP.

From Patterson and Shepherd 386


Figure 9.

Increase in forearm blood flow immediately after a 0.3‐s contraction of forearm muscles in a normal subject and in a subject who had had bilateral cervical sympathectomy 3 yr previously. Increase in forearm flow was obtained by subtracting resting flow before each contraction from flow measured just after contraction. Dilatation was unchanged when subject breathed O2 instead of air. Oxygen capacity of radial artery blood was 19.4 ml/100 ml; O2 content was 19.0 ml/100 ml while breathing air and 20.8 ml/100 ml while breathing O2.

From Corcondilas, Koroxenidis, and Shepherd 108


Figure 10.

A: correlation between vasodilator response and tissue (venous) hyperosmolality in cat skeletal muscle during graded exercise. B: quantitative evaluation of role of tissue hyperosmolality for early exercise hyperemia response in the cat.

From Mellander and Lundvall 361


Figure 11.

Comparison of time courses of tissue adenosine content (filled circles, dashed line) and estimated vascular resistance (shaded band). Vertical bars, 1 SEM for adenosine content. Horizontal bars, 1 SEM for time of biopsy. Adenosine scale has been shifted (nonzero at origin).

From Belloni et al. 41, by permission of the American Heart Association, Inc


Figure 12.

Alternations in adenonsine relative specific activity and vascular resistance during exercise onset. Inf. ON, start of

8‐14C]adenosine infusion. From Tominaga et al. 473


Figure 13.

Adenosine, AMP, ADP, and ATP cause dose‐dependent relaxation in rings of canine femoral arteries made to contract with norepinephrine (left). Mechanical removal of endothelium abolishes relaxations induced by ADP and ATP without affecting those caused by adenosine and AMP (right).

From De Mey and Vanhoutte 123


Figure 14.

Reduction in reflex vasoconstrictor response (7 dogs) in limb perfused at constant flow with progressive distal section of communicating rami between spinal nerves and sympathetic paravertebral lumbar chain. Each animal indicated by a separate symbol.

From Donald and Ferguson 128, by permission of the American Heart Association, Inc


Figure 15.

Products of cellular activity cause dilatation of arterioles because of their direct inhibitory effect on smooth muscle cells and because they interrupt vasoconstrictor impulses of sympathetic nerves. Arteriolar wall is shown as one layer of smooth muscle cells with an adrenergic nerve and one of its varicosities containing adrenergic neurotransmitter norepinephrine (NE). AMP, adenosine monophosphate; ADP, adenosine diphosphate; ATP, adenosine triphosphate; CM, cell membrane; +, activation; − and ∧∧∧, inhibition; α, α‐adrenergic receptor.

From Shepherd and Vanhoutte 442. In: The Human Cardiovascular System: Facts and Concepts. Raven Press, New York, 1979


Figure 16.

Adenosine concentration (left) and increase in [K+] (middle) or in osmolality (right), which do not inhibit responses to norepinephrine, cause relaxation (upper) and significant depression of release of [3H]norepinephrine (lower) evoked by nerve stimulation in 3 groups of dog saphenous veins.

From McGrath and Vanhoutte 354


Figure 17.

Concentrations of acetylcholine (left), histamine (middle), and 5‐hydroxytryptamine (right), which do not cause changes in tension in unstimulated preparations or during contractions to exogenous norepinephrine, cause a pronounced relaxation during sympathetic nerve stimulation (upper); relaxation is due to a decrease in evoked release of adrenergic neurotransmitter (lower). Experiments performed on 3 saphenous vein strips previously incubated with [3H]norepinephrine; overflow of latter is a qualitative measurement of amount of transmitter liberated.

From McGrath and Vanhoutte 354


Figure 18.

Comparison in the anesthetized dog of increases in perfusion pressure in femoral vascular bed (perfused at constant flow with autologous blood) evoked by norepinephrine (noradrenaline) and lumbar sympathetic nerve stimulation (OS stimulatie) before and during continuous infusion of acetylcholine (upper) and isoproterenol (lower). Acetylcholine depresses vasoconstrictor response to sympathetic stimulation more than that to exogenous norepinephrine, demonstrating prejunctional inhibitory effect of cholinergic transmitter.

From Vanhoutte and Levy 488


Figure 19.

Effect on left hindlimb and kidney perfusion pressures of decrease in carotid sinus pressure combined with a capsaicin injection into right femoral artery in a vagotomized dog. Capsaicin was used to stimulate receptors in skeletal muscle. Left hindlimb and kidney were perfused at constant flow with autologous blood.

From Pelletier and Shepherd 393


Figure 20.

Effects of carotid sinus and aortic arch baroreflexes on resistance vessels of dog hindlimbs perfused at constant flow. Response in perfusion pressure expressed as percent of maximal change evoked by carotid distension (mean ± SE, n = 11). Aortic arch curve is displaced to the right; maximal slope and height are less for aortic arch curve than for carotid sinus curve.

From Donald and Edis 127


Figure 21.

Vascular responses in normal young men to changes in carotid sinus pressure. Left: when carotid sinus pressure is increased by application of subatmospheric pressure to the neck, arterial blood pressure, heart rate, and forearm vascular resistance decrease. Right: when carotid sinus pressure is reduced by manual compression of common carotid arteries, arterial blood pressure, heart rate, and calf blood flow increase. There is no evidence that constriction of the calf resistance vessels contributes to increased arterial pressure.

From Donald and Shepherd 130


Figure 22.

Changes in muscle and renal vascular resistance in cats in response to electrical stimulation of right cardiac nerve and to alterations in pressure within partially isolated carotid sinus. Data plotted as percent of maximal decrease in resistance at a carotid sinus pressure of 250 mmHg. Stimulus‐response curves to activity changes in cardiac nerves and carotid sinus nerves have been adjusted so that threshold and maximal responses of each coincide. As carotid sinus pressure is increased above 150 mmHg, resultant increase in activity of carotid baroreceptors reduces muscle resistance more than does increase in activity in cardiac C‐fiber vagal afferents; both are similar in their modulation of renal resistance. As carotid sinus pressure is increased from 50 to 120 mmHg, resultant increase in activity of carotid baroreceptors is less effective in decreasing renal resistance than is an increase in activity of cardiac C‐fiber vagal afferents; both are similar in their modulation of muscle resistance.

Redrawn from Little et al. 320; from Donald and Shepherd 130


Figure 23.

Effect of separate and combined withdrawal of inhibitory influence of carotid sinus and cardiopulmonary baroreceptors on muscle and kidney resistance vessels. Normo‐ and hypervolemic dogs with aortic nerves cut. Responses plotted as percent of change from maximal reflex inhibition (carotid sinus pressure 250 mmHg) to no inhibition (carotid sinus pressure 40 mmHg and bilateral cervical vagal cold block) of resistance vessels in each vascular bed. Note greater influence of carotid baroreceptors on muscle vascular resistance. Cardiopulmonary receptors influence renal resistance to an equal or greater (hypervolemia) degree than carotid baroreceptors.

From Donald and Shepherd 130


Figure 24.

Contribution of carotid sinus and cardiopulmonary baroreflexes to increase in vascular resistance in hindlimb (left) and intestine (right) during 10% hemorrhage in dogs with aortic nerves cut. Iliac and superior mesenteric artery perfused at constant flow.

From Donald and Shepherd 130


Figure 25.

Effect of hypercapnea on inhibition of hindlimb and renal vascular resistance by aortic and cardiopulmonary mechanoreceptors in anesthetized rabbits. Left: vagal and carotid sinus nerves cut prior to aortic nerve block by cooling. Right: carotid sinus and aortic nerves cut prior to cold block of cervical vagal nerves. Note greater augmentation by hypercapnea of inhibitory influence of both systems on renal but not on hindlimb vascular resistance.

From Donald and Shepherd 130


Figure 26.

Vascular responses to vagal cold block before and after removal of lungs. Dog on cardiopulmonary bypass, with arterial baroreceptors denervated, vagi cut at diaphragm, and heart removed. One hindlimb and kidney were perfused at constant pressure of 120 mmHg. Cooling the cervical vagi to 0°C with lungs artificially ventilated caused an increase in aortic blood pressure and a decrease in renal and hindlimb blood flow. Removal of lungs resulted in an increase in aortic pressure and a decrease in renal and hindlimb blood flow (RF, HL). There was no further change with vagal cooling.

From Shepherd 438, by permission of the American Heart Association, Inc


Figure 27.

Effect of passive raising of legs of a normal subject on circulation through forearm. With leg raising, forearm blood flow increases. This was due to increase in muscle blood flow, since the O2 content of the blood draining forearm muscles increased (deep vein) but not that of the blood draining forearm skin (superficial vein). Increased flow was due to reflex dilatation, because blocking sympathetic nerves to the forearm vessels with local anesthetic prevented flow increase. Dilatation was not affected by atropine, indicating that it was caused by decreased activity of noradrenergic fibers and not by activation of cholinergic fibers. Reflex dilatation was caused by displacement of blood from the legs, since it was prevented by inflation of thigh cuffs to suprasystolic pressure prior to leg raising. Because arterial mean and pulse pressures were unchanged and central venous pressure increased, muscle vasodilatation is attributed to receptor excitation somewhere in the heart and lungs.

From Donald and Shepherd 130


Figure 28.

Effect of leg exercise in aortic stenosis. Reflex vasoconstrictor response seen in normal subjects and in patients with mitral stenosis is replaced by a vasodilator response in aortic stenosis. Dots, responses in individual patients. Horizontal lines, means of responses in each group.

From Mark et al. 344


Figure 29.

Blood flow during supine leg exercise in a subject with a normal and a sympathectomized forearm.

From Bevegård and Shepherd 52


Figure 30.

Reproduction of tracings obtained during experiment with a dog hindlimb perfused at constant flow. Vasoconstrictive responses to lumbar trunk stimulation at 6 cycles/s were recorded at rest, at intervals during 65 min of exercise, and 16 min after termination of exercise. Perfusion flows at rest, exercise, and recovery were 84, 285, and 78 ml/min, respectively.

From Rowlands and Donald 420, by permission of the American Heart Association, Inc


Figure 31.

Effect of increased sympathetic outflow to forearm blood vessels on blood flow through forearm during and after rhythmic exercise of forearm muscles. Increased sympathetic outflow induced by application of subatmospheric pressure to lower body (continuous suction).

From Strandell and Shepherd 461


Figure 32.

Effect of increased sympathetic outflow to forearm blood vessels on O2 saturation in a deep forearm vein during rhythmic exercise of forearm muscle. Increased sympathetic outflow induced by application of subatmospheric pressure to lower body (lower‐body suction).

From Strandell and Shepherd 461


Figure 33.

Average response of forearm blood flow (4 expts) to infusion of norepinephrine (Nor, 0.75 μg/min) into left brachial artery. Left: before α‐blockade. Center: during α‐blockade with phentolamine (1,600 μg/min ia). Right: during combined α‐ and β‐blockade with phentolamine (1,600 μg/min ia) and propranolol (10.0 μg/min ia). •, Blood flow in left or experimental forearm; ○, blood flow in right or control forearm; ▪, mean arterial blood pressure.

From Brick et al. 71


Figure 34.

Effect of echo stress test on heart rate, mean arterial blood pressure, forearm and calf blood flow, and resistances. Average values in 6 normal supine subjects.

From Rusch, Shepherd, et al. 422, by permission of the American Heart Association, Inc


Figure 35.

Changes in forearm blood flow and heart rate during moderately severe leg exercise (1,200 kg · m−1 · min−1); average values for 8 studies in 3 normal trained subjects.

From Bevegård and Shepherd 52


Figure 36.

Longitudinal sections through hypothalamus and midbrain of the dog. A: sites at which electrical stimulation produced noncholinergic dilator responses restricted to vasculature of the leg above the paw. B: sites at which electrical stimulation produced noncholinergic dilator responses restricted to vasculature of the paw. Filled star, sites at which electrical stimulation elicited antihistamine‐sensitive vasodilatation. Filled circle, sites at which electrical stimulation elicited antihistamine‐resistant vasodilatation. MI, massa intermedia; P, pituitary stalk; S, substantia nigra. Although stimulation was done in planes 2–5 mm lateral to the midline, diagrams are shown as midline sections for convenience.

From Lang et al. 310, by permission of the American Heart Association, Inc


Figure 37.

Left: separate perfusion of right and left hindlimbs at constant flow (1 dog). Measurement of mean aortic and limb perfusion pressure. Decrease in left leg perfusion pressure in response to stimulation of isolated left anterior spinal nerve root at level of L6. Right: blood flow measurement in right (R) and left (L) hindlimbs perfused at constant aortic (A) pressure (1 dog). Increase in blood flow in right leg in response to stimulation of right anterior nerve root.

From Donald and Ferguson 128, by permission of the American Heart Association, Inc
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Article Title: Circulation to Skeletal Muscle
 

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John T. Shepherd. Circulation to Skeletal Muscle. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 319-370. First published in print 1983. doi: 10.1002/cphy.cp020311