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Korthuis RJ. Skeletal Muscle Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011.

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Skeletal Muscle Circulation.

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Chapter 2Anatomy of Skeletal Muscle and Its Vascular Supply


The smallest contractile unit of skeletal muscle is the muscle fiber or myofiber, which is a long cylindrical cell that contains many nuclei, mitochondria, and sarcomeres (Figure 1) [58]. Each muscle fiber is surrounded by a thin layer of connective tissue called the endomysium. Approximately 20–80 of these muscle fibers are grouped together in a parallel arrangement called a muscle fascicle or fiber bundle that is encapsulated by a perimysium, which is thicker than the epimysium enclosing each of the bundled muscle fibers. A distinct muscle is formed by enveloping a large number of muscle fascicles in a thick collagenous external sheath extending from the tendons called the epimysium (Figure 1) [58].

Figure 1. General anatomical structures of skeletal muscle and its vascular supply. See text for explanation.

Figure 1

General anatomical structures of skeletal muscle and its vascular supply. See text for explanation.

Individual muscle fibers are classified by their histologic appearance, rapidity of contraction, and ability to resist fatigue. Slow-twitch or type I fibers are generally thinner, invested by a denser capillary network, and appear red owing to the presence of a large amount of the oxygen-binding protein myoglobin. These type I fibers are resistant to fatigue, relying on oxidative metabolism for energy, and thus exhibit high mitochondrial numbers and oxidative enzyme content, and low glycogen levels and glycolytic enzyme activity. On the other hand, fast-twitch or type II fibers differ among themselves with regard to fatigability. Type IIa fibers share some features with slow-twitch fibers in that they are fatigue-resistant, rely on oxidative metabolism, and contain myoglobin (and thus are red) [20, 58]. However, in contrast to type I slow-twitch cells, type IIa muscle fibers contain abundant glycogen and more mitochondria [20, 58]. These distinctive features ensure adequate ATP generation to compensate for the accelerated rate of ATP hydrolysis in these fast-twitch fibers. Other fast-twitch fibers (type IIb) rely on the energy stored in glycogen and phosphocreatine because they contain fewer mitochondria, have low myoglobin (and thus are white muscle) and oxidative enzyme content, and are invested by a less dense capillary network [20, 58]. As a consequence, type IIb muscle fibers are more easily fatigable.

In addition to dissimilarities in oxidative enzymes, myoglobin and glycogen content, the rate of force development, capillary densities, and fatigability, slow-twitch (type I) and fast-twitch (type IIa and IIb) muscle fibers also differ in the expression of various contractile and regulatory protein isoforms [20, 58, 575]. Indeed, differences in the rate of contraction exhibited by the varied muscle fiber types appear to be correlated with the maximal rate of myosin ATPase activity, which in turn is dependent on the particular myosin heavy chain (MHC) isoform expressed in the various fiber types. That is, each muscle fiber type expresses a specific MHC isoform, the ATPase activity of which corresponds to the rate of contraction in that fiber type. It is also important to emphasize that in most skeletal muscles, individual fascicles are composed of two or more of these fiber types, although one fiber type usually predominates in a given muscle.

As noted above, contractile and regulatory protein isoform expression and mitochondrial density are fine-tuned to meet the functional and energetic demands of the different muscle fiber types. However, comparisons of the mitochondrial complement of proteins expressed in red and white muscle have revealed surprisingly few compositional differences [196]. These results suggest that differences in metabolic demand between red and white muscle are met by adjustments in mitochondrial number and not by significant dissimilarities in the complement of proteins in individual mitochondria within the fibers. In this regard, it is interesting to note that mitochondrial biogenesis is stimulated by exercise, an effect that may be induced in part by β-adrenergic-mediated expression of peroxisome proliferator-activated receptor (PPAR)-γ coactivator 1α (PGC1α) [466].


The vascular inflow to skeletal muscles is provided by primary arteries, which represent the last branches of the arterial supply that arise before entry into the tissue (Figure 1) [32, 58, 602]. The primary arteries are appropriately distributed along the long axis of the muscle and give rise to feed arteries that course toward the epimysium of the muscle at right or oblique angles to the primary arteries. Because feed arteries account for as much as 30–50% of the total resistance to blood flow through skeletal muscle, they represent a significant site for blood flow control proximal to the microvessels that are embedded in the skeletal muscle tissue. Secondary arteriolar branches divide at right angles to these feed vessels and extend longitudinally (Figure 1). The arteriolar network consists of branching vessels that originate from the feed arteries at the point where the latter vessels enter the muscle [137, 372, 714]. Arterioles enter the perimysium and travel perpendicular the muscle fiber axis until giving rise to terminal branches that penetrate the perimysium and immediately branch into numerous capillaries that are embedded in the endomysium and travel parallel to the muscle fiber (Figure 1). The terminal arterioles are the last branches to contain vascular smooth muscle. Thus, the group of capillaries perfused by a terminal arteriole has been termed the microvascular unit, which represents the smallest functional unit for blood flow regulation in skeletal muscle (Figure 1) [32, 58, 602].

Several capillaries surround each muscle fiber, which in cross-section are arranged in a highly variable array around each fiber (Figure 1) [58, 526]. This non-uniform distribution of capillaries around myofibrils, coupled with the fact that the circumference of each muscle fiber is quite variable, indicates that oxygen is non-homogeneously distributed to skeletal muscles, even under conditions of maximal capillary recruitment [47, 48, 584]. However, the capillaries surrounding each muscle fiber are interconnected, with the density of parallel capillary segments increasing toward the venular end of the capillary network, which reduces the inhomogeneity (526, 584). While true capillaries in skeletal muscle are approximately 4 μm in diameter, they taper to a larger diameter as they approach postcapillary venules. Comparison of capillary network anatomy in red and white muscle indicates that the density of surrounding capillaries and the number of interconnections between adjacent capillaries are greater in oxidative muscle [14, 15, 18, 58, 179, 205, 209, 219, 262, 263, 421, 498, 499, 521, 526, 539, 556, 557, 576, 584].

The arrangement of venules and veins is similar to that described for the arterioles and arteries. While the main arterioles and venules are paired, the outflow through a given venule is not derived from its parallel venule, but rather arises from arterioles some distance away (Figure 1).


Terminal lymphatics in skeletal muscle originate as blind endothelial tubes in areas adjacent to postcapillary venules. These vessels penetrate the perimysium and connect to larger lymphatics that are closely associated with paired arterioles and collecting venules. The variously sized lymphatic vessels located inside the muscle lack smooth muscle in their walls, thus relying on muscular movements and pulsation of arterioles to propel lymph centrally [633]. However, contractile lymphatics have been observed on the surface of muscles, which facilitate transport of lymph. Moreover, lymphatics surround larger arteries in skeletal muscle, with arterial pulse pressure providing a force to alternately compress these vessels and propel lymph in a proximal direction.

Copyright © 2011 by Morgan & Claypool Life Sciences.
Bookshelf ID: NBK57140


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