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INVITED REVIEW
HIGHLIGHTED TOPICS
Skeletal and Cardiac Muscle Blood Flow
1Hypertension Division, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390; and 2The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519
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ABSTRACT |
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 TOP ABSTRACT VASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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muscle contraction; sympathetic nerves; motor nerves; vasoconstriction; vasodilation
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VASCULAR RESISTANCE OF SKELETAL MUSCLE |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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In the absence of sympathetic nerve activity, vasomotor tone in the resistance network of skeletal muscle at rest represents the interaction between myogenic contraction of smooth muscle cells in response to blood pressure (16) and the modulating influence of the endothelium, e.g., through release of NO in response to luminal shear stress exerted by the flowing blood (15). Under these conditions, the resting tone of resistance vessels is typically 50–70% of their maximal diameter (40, 94). The initial vascular response to motor unit activation is dilation of the terminal arterioles (17, 84), which promotes the extraction of available oxygen (2) by increasing the surface area for diffusion through capillary recruitment (44). However, as metabolic demand increases, greater total delivery of oxygen is required to support the aerobic production of ATP. This increase in total blood flow is achieved by the progressive dilation of successively larger and more proximal branches of the resistance network (27, 30). Indeed, direct observations have confirmed that as motor unit recruitment and work intensity increase, vasodilation "ascends" progressively from distal arterioles, through intermediate branches, and into proximal arterioles and feed arteries (94, 98). The initiation of ascending vasodilation has been linked to muscle fiber recruitment (94, 98) and is mediated by cell-to-cell conduction of a vasodilator signal along the vessel wall (37, 78).
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SYMPATHETIC INNERVATION OF SKELETAL MUSCLE VASCULATURE |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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A limitation to studying the role of sympathetic innervation in whole muscles of animals and intact limbs of humans is that the precise location and extent of vasoconstriction within the resistance network can be difficult to ascertain. Thus complementary studies in rodents and cats have used intravital microscopy to determine specific segmental vasomotor responses to SNA. In resting muscles, sympathetic nerve stimulation constricts all resistance vessels. Increasing the stimulus frequency of SNA from 0.5 Hz through 16 Hz produces a full range of vasoconstriction mediated primarily through the release of norepinephrine (5, 21, 50, 60, 95). However, there is a rank order of responsiveness to SNA that varies with location in the resistance network. For example, in the rat cremaster muscle, small arterioles readily constrict at all frequencies of SNA, with maximal responses obtained at 4 Hz, whereas large arterioles constrict progressively over the entire frequency range through 16 Hz (60). In the hamster retractor muscle, the absolute decreases in vessel diameter during SNA are largest in feed arteries and progressively smaller in first- through third-order arterioles. However, when these responses to SNA are normalized to the respective resting diameters, the magnitude of vasoconstriction is largest in the distal branches and smallest in the proximal branches (50, 95).
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SYMPATHETIC ESCAPE IN RESTING MUSCLE AND THE DISTRIBUTION OF ADRENORECEPTOR SUBTYPES |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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1- and 2-adrenoreceptors on smooth muscle cells within the resistance network. In the rat cremaster muscle, constriction of smaller, distal branches of the arteriolar network is controlled mainly by 2-adrenoreceptors, which appear to be relatively more susceptible to metabolic inhibition (3, 24). In contrast, constriction of larger proximal arterioles and feed arteries are controlled by both 1- and 2-adrenoreceptors (24). Whether the microcirculation of other muscles in animals or in humans is characterized by similar spatial distributions and functional roles of the -adrenoreceptor subtypes is not known and requires further study. However, findings from a recent study in which -adrenoreceptor antagonists were infused into the forearm of conscious human subjects indicate that both 1- and 2-adrenoreceptors contribute to the component of basal vasomotor tone that is caused by tonic SNA (19).
There are three recognized subtypes of 1-adrenoreceptors (1A, 1B, 1D) and of 2-adrenoreceptors (2A/D, 2B, 2C) (32). However, the relative contributions of each receptor subtype to sympathetic vasoconstrictor responses in skeletal muscle have yet to be defined, as do the signaling pathways through which they exert their respective effects in the microcirculation of skeletal muscle. Many vessels express more than one -adrenoreceptor subtype, and there may be redundancy in respective signaling events, making it difficult to dissect functional roles for individual receptor subtypes by use of the pharmacological tools presently available. Nevertheless, selective receptor agonists and antagonists have linked constrictor responses of large arterioles in the rat cremaster muscle to 1D- and 2A/D-adrenoreceptors (85). An alternative approach to define the role of respective vascular adrenoreceptors is to study mice that have been genetically engineered to selectively eliminate one or more of these receptor subtypes (67). In turn, findings from transgenic animals can provide valuable new insight for defining and investigating vasoactive signaling pathways in humans (73, 88).
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ACTIVATION OF MUSCLE SYMPATHETIC NERVES DURING EXERCISE |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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CONSTITUTIVE SYMPATHETIC VASOCONSTRICTION IN EXERCISING MUSCLES |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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-adrenoreceptors, demonstrating ongoing sympathetic restraint of blood flow to the active muscles (6, 8, 41, 58, 61). Furthermore, activation of postjunctional -adrenoreceptors by SNA or with -agonist infusion reduces blood flow in exercising muscles, demonstrating the potential for sympathetic control of muscle blood flow during muscular activity (20, 41, 42, 59, 68, 69, 71, 72, 80, 83, 86, 90, 91, 93, 95). During dynamic exercise of the knee extensors in humans, peak blood flow in the active muscle can increase up to 100-fold above resting values (2). Thus, during intense whole body exercise, restriction of blood flow by increasing SNA to active muscles (in addition to other vascular beds) may be integral to prevent this large capacity for vasodilation from surpassing the ability of cardiac output to maintain systemic arterial blood pressure (70). However, blood flow in exercising muscles generally increases despite concomitant sympathoexcitation. This raises another key question: is the responsiveness of the resistance vasculature to SNA altered in exercising muscle? |
IS SYMPATHETIC VASOCONSTRICTION MODULATED IN EXERCISING MUSCLE? |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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A key factor affecting the interpretation of some of these studies is the use of resistance to quantify vasomotor responses (70). It is difficult to compare changes in resistance between resting and exercising skeletal muscle because resistance (pressure/flow) is inversely and therefore nonlinearly related to flow (47, 57). Thus a given change in blood flow will produce a much smaller change in calculated resistance when superimposed on a high baseline flow vs. a low baseline flow, which leads to an underestimation of the true magnitude of the vascular response under high-flow conditions. In contrast, vascular conductance (flow/pressure) is related linearly to blood flow. In this case, a given change in flow produces the same change in conductance irrespective of the baseline level of flow. However, even though conductance provides a more accurate assessment of vascular responsiveness when baseline flows differ, it does not solve all of the problems associated with comparing responses between conditions of low and high muscle blood flows.
Another key concern is whether vasomotor responses are expressed as absolute or relative changes from baseline. For example, when a given increase in SNA evokes the same absolute decrease in conductance in resting and exercising muscle, the relative decrease is smaller in exercising muscle because of its higher baseline blood flow. Moreover, an equivalent absolute reduction in conductance for resting and exercising muscle could suggest that exercise does not affect vascular responsiveness to SNA. However, the smaller relative decrease in conductance in exercising muscle leads to the opposite conclusion! To directly address the influence of vasodilation and elevated blood flow per se on sympathetic responsiveness, some investigators have administered vasodilator stimuli in resting muscle to match the increases in blood flow induced by exercise (20, 68, 86, 87, 93, 95). These important control experiments have consistently shown that, as baseline diameter, flow, or conductance increases in resting muscle (via graded vasodilator administration), the vasoconstrictor response to sympathetic activation is either enhanced (absolute response) or unchanged (relative response). In contrast, in exercising muscles with equivalent vasodilation, the constrictor responses to SNA are attenuated significantly when expressed in either absolute or relative terms. These well-controlled studies provide convincing evidence that sympathetic vasoconstriction can be attenuated in exercising skeletal muscle. Furthermore, this attenuation is not an artifact of data expression nor is it due to a nonspecific effect of vasodilation. This conclusion leads to the question of how sympathetic vasoconstriction is actually modulated during exercise.
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MECHANISMS UNDERLYING FUNCTIONAL SYMPATHOLYSIS |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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-adrenoreceptor agonists in exercising muscle (3, 4, 9, 20, 65, 68, 87, 88). These findings collectively suggest that a major locus of functional sympatholysis is at the level of the postjunctional vascular -adrenoreceptors and/or their underlying intracellular signaling pathways in smooth muscle cells.
It is unlikely that 
-adrenoreceptors play a significant role in functional sympatholysis because their blockade has no effect on functional sympatholysis in mice (89) and the vasodilation produced by infusion of the -agonist isoproterenol in resting muscle does not attenuate sympathetic vasoconstriction in rats (86). In addition to norepinephrine, sympathetic nerves also release ATP, which causes vasoconstriction by activating P2X purinoreceptors. A recent study in dogs suggests that P2X purinoreceptor vasoconstriction also is attenuated in exercising muscle (7). Whether similar mechanisms modulate P2X purinoreceptor and -adrenoreceptor vasoconstriction in active muscle remains to be determined.
Spatial relationships.
The interaction between muscle contraction and SNA in controlling vessel diameter is graded with the intensity of the respective stimuli and with the location of vessel branches within the resistance network (27, 52, 95). In contracting muscle of cats and hamsters, the vasoconstrictor response to SNA is attenuated to a greater extent in distal vs. proximal resistance microvessels (27, 95). The physiological importance of this proximal shift in resistance, from downstream to upstream arterioles, is that the dilation of distal vessels promotes maximal extraction of oxygen when flow is restricted in proximal segments. In consonance with these observations, the vasoconstriction mediated by 2-adrenoreceptors is more susceptible to attenuation than that of 1-adrenoreceptors in exercising muscle of rats and dogs (3, 9, 87), which closely corresponds to the preferential expression of 2-adrenoreceptors on the distal arterioles described earlier for the rat cremaster muscle (24). In humans, a greater susceptibility of 2- vs. 1-adrenoreceptor-mediated vasoconstriction to attenuation is apparent in exercising leg muscles (100) but not in exercising forearm muscles (68). Other factors that may contribute to regional differences in microvascular reactivity in exercising muscle include differences in vessel wall stress (28), the nature of smooth muscle coupling to endothelium (74), and physical proximity to vasodilator metabolites.
Temporal aspects. Both motor unit recruitment and SNA increase with exercise; however, this synchrony has been difficult to study with experimental models. Therefore, in most studies examining functional sympatholysis, the vasoconstrictor stimulus is superimposed during steady-state exercise, which precludes evaluation of the time required for muscle contractions to modulate sympathetic vasoconstriction. Two recent studies in humans in which SNA was increased before the start of exercise suggest that sympathetic vasoconstriction may be attenuated within the first 30 s of muscle contractions (18, 92). Studies in dogs have also found that sympathetic vasoconstriction was reduced during contractions of durations as brief as 4 s (43) and that the modulation of vasoconstriction in active muscle was transient, paralleling increases in arterial K+ concentration, but not H+ concentration or osmolality (4). In light of recognized differences in the mediators responsible for the onset vs. maintenance of functional vasodilation (33), these findings raise the question whether different mechanisms modulate sympathetic vasoconstriction during the course of an exercise bout. Additional work is needed to resolve such "components" of functional sympatholysis.
Metabolic mechanisms. Because functional sympatholysis is confined to the active muscles and is graded to the intensity of the exercise, the search for the underlying mechanisms has focused primarily on local factors related to changes in muscle metabolism. Approaches commonly used to identify potential mechanisms include 1) establishing temporal associations between metabolite concentrations and functional sympatholysis; 2) determining whether sympathetic vasoconstriction in resting muscle is attenuated by mimicking exercise-induced changes in the local metabolic environment; and 3) determining whether functional sympatholysis is impaired either by inhibiting the production of particular metabolites in active muscle or the action of these metabolites on specific cellular signaling pathways. The regulation of smooth muscle cell contraction during SNA is summarized briefly first for reference.
Activation of -adrenoreceptors causes contraction of vascular smooth muscle by a depolarization-induced increase in intracellular Ca2+ that is derived from the extracellular fluid through voltage-dependent L-type Ca2+ channels and internally from the sarcoplasmic reticulum via inositol 1,4,5-trisphosphate receptors (32, 53). Smooth muscle contraction also can be altered independent of Ca2+ via thin-filament regulation and phosphorylation of various regulatory proteins (82, 99). Whereas 1-adrenoreceptor signaling mobilizes both intra- and extracellular Ca2+, 2-adrenoreceptors rely mainly on extracellular Ca2+ (53, 54). Thus contraction mediated by 2-adrenoreceptors is susceptible to modulation by events that preferentially inhibit influx of extracellular Ca2+. One such event may be the activation of membrane K+ channels, which hyperpolarize smooth muscle cells, thereby reducing Ca2+ entry through the voltage-dependent Ca2+ channels (39).
During muscle contraction, K+ is released from the active skeletal muscle cells. Increases in extracellular K+ concentration ([K+]o) can promote smooth muscle hyperpolarization by activating inward-rectifying K+ channels and stimulating Na+-K+ pump activity in the plasma membrane (62). These actions of elevated [K+]o may explain the impaired sympathetic vasoconstriction observed in the resting skeletal muscle of dogs perfused with blood made hyperkalemic to reflect the exercise-induced increase in [K+]o (4, 11). Alternatively, increased [K+]o may act to inhibit norepinephrine release from sympathetic nerves. Of the various K+ channels expressed in vascular smooth muscle, the ATP-sensitive K+ (KATP) channel is uniquely regulated by cellular metabolism and is activated by hypoxia, ischemia, acidosis, and by endogenous vasodilators such as prostacyclin, adenosine, and NO (62). Pharmacological activation of KATP channels has a greater inhibitory effect on the vasoconstrictor response to 2- vs. 1-adrenoreceptor activation (85, 86), making this an attractive candidate for mediating functional sympatholysis. Indeed, KATP channel blockade has been shown to enhance sympathetic vasoconstriction in the contracting hindlimb of rats (86) and augment spontaneous vasomotor tone in arterioles of the hamster cremaster muscle (38). However, a concern in defining the role of specific ion channels in the regulation of vascular resistance is resolving which of the cell types expressing the channel of interest mediates the vascular response. For example, KATP channels are expressed in smooth muscle, endothelial cells, and skeletal muscle (62). Although this resolution is difficult to achieve by conventional pharmacological interventions, such limitations open the doors for selective genetic and molecular interventions.
Of the numerous metabolic signals generated in exercising muscle, only a few have been examined as potential mediators of functional sympatholysis. At present, neither adenosine nor prostaglandins appear to be obligatory for functional sympatholysis (20, 34, 69, 90, 93). In contrast, a study in humans has implicated local tissue hypoxia as an important factor in the attenuated vasoconstrictor response to SNA in exercising muscle (34). This effect of hypoxia may be enhanced by physiologically relevant increases in [K+]o (81), indicating the potential for additive or synergistic effects of metabolic signals on vascular regulation in exercising muscle. Another factor that is reported to mediate functional sympatholysis in rodents (88–90) and in some (13, 73), but not all (20), human studies is NO. The predominant source of NO that modulates sympathetic vasoconstriction appears to be the neuronal isoform of NO synthase (29, 88, 89), which is abundantly expressed in skeletal muscle fibers. NO may act to antagonize sympathetic vasoconstriction by a variety of mechanisms such as facilitating KATP channel activation (56, 90) or reducing phosphorylation of regulatory myosin light chain (29), which is a key determinant of smooth muscle contraction (99).
Additional mechanisms for modulating sympathetic vasoconstriction.
Negative feedback from the endothelium (e.g., NO release) during -adrenoreceptor activation of adjacent smooth muscle cells can attenuate sympathetic vasoconstriction in isolated arterioles (22, 101). Stimulation of endothelial cells can also produce smooth muscle cell hyperpolarization through release of autacoids that activate K+ channels in smooth muscle (12). Furthermore, the conduction of vasodilation can attenuate sympathetic vasoconstriction (45), with hyperpolarization initiated and conducted along the endothelium and into the surrounding smooth muscle cells through myoendothelial gap junctions (23, 78). These signaling pathways provide alternative mechanisms through which exercise-induced increases in metabolites and blood flow can influence smooth muscle contraction. Although many of these regulatory events have been defined in isolated vessels and cellular preparations, a great deal remains to be learned with respect to how and where vasoactive signals produced during exercise actually modulate the ability of SNA to produce vasoconstriction.
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CONCLUSION AND FUTURE RESEARCH DIRECTIONS |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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-adrenoreceptor subtypes, skeletal muscle fiber types, active muscle mass, aging, and training status. In accord with the regulation of functional hyperemia (33, 46), it is likely that the modulation of sympathetic vasoconstriction by exercising muscle does not depend on any single mechanism but reflects the spatial and temporal interactions of multiple signaling events that work in concert to modulate vascular responsiveness. Furthermore, the findings that functional sympatholysis is impaired in several diseases, including muscular dystrophy (73, 88) and experimental heart failure (91), lead to the hypothesis that derangements of sympathetic neural control may contribute to the exercise intolerance observed in these and other pathophysiological conditions. Innovative approaches in both animals and humans are required to address these unresolved issues and to fully appreciate the integrative nature of the interaction between local vasodilatory factors and sympathetic vasoconstrictor activity in exercising muscle. |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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FOOTNOTES |
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REFERENCES |
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TOPABSTRACTVASCULAR RESISTANCE OF SKELETAL...SYMPATHETIC INNERVATION OF...SYMPATHETIC ESCAPE IN RESTING...ACTIVATION OF MUSCLE SYMPATHETIC...CONSTITUTIVE SYMPATHETIC...IS SYMPATHETIC VASOCONSTRICTION...MECHANISMS UNDERLYING FUNCTIONAL...CONCLUSION AND FUTURE RESEARCH...GRANTSREFERENCES |
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1- and 2-adrenergic vasoconstriction is blunted in contracting human muscle. J Physiol 547: 971–976, 2003.-adrenergic vasoconstriction in human limbs. J Appl Physiol 95: 2370–2374, 2003.2D-adrenergic receptor contraction of arteriolar smooth muscle and reversal of contraction in hypoxia. Circ Res 76: 53–63, 1995.2-adrenergic vasoconstriction during contraction of glycolytic, not oxidative, rat hindlimb muscle. Am J Physiol Heart Circ Physiol 266: H920–H929, 1994.-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle. Proc Natl Acad Sci USA 95: 15090–15095, 1998.-syntrophin-mediated sarcolemmal localization of neuronal nitric oxide synthase. Circ Res 92: 554–560, 2003.1-Adrenergic signaling mechanisms in contraction of resistance arteries. Rev Physiol Biochem Pharmacol 150: 91–139, 2003.[Medline]
-adrenergic vasoconstriction in exercising human thigh muscles. J Physiol 555: 545–563, 2004.This article has been cited by other articles:
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) to promote the opening of plasma membrane Ca2+ channels as well as release of Ca2+ from internal stores, resulting in vasoconstriction. Contractile activity can antagonize vasoconstriction by reducing neurotransmitter release from sympathetic terminals and/or by attenuating sympathetically mediated increases in intracellular Ca2+ concentration in VSMC. The contractile apparatus in VSMC also is modulated by various kinase and phosphatase activities (*P) and by changes in sensitivity to intracellular Ca2+ concentration.