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Muscle cell
Muscle cell
Muscle cell
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Muscle cell
General structure of a skeletal muscle cell and neuromuscular junction:
Details
LocationMuscle
Identifiers
Latinmyocytus
MeSHD032342
THH2.00.05.0.00002
FMA67328
Anatomical terms of microanatomy

A muscle cell, also known as a myocyte, is a mature contractile cell in the muscle of an animal.[1] In humans and other vertebrates there are three types: skeletal, smooth, and cardiac (cardiomyocytes).[2] A skeletal muscle cell is long and threadlike with many nuclei and is called a muscle fiber.[3] Muscle cells develop from embryonic precursor cells called myoblasts.[1]

Skeletal muscle cells form by fusion of myoblasts to produce multinucleated cells (syncytia) in a process known as myogenesis.[4][5] Skeletal muscle cells and cardiac muscle cells both contain myofibrils and sarcomeres and form a striated muscle tissue.[6]

Cardiac muscle cells form the cardiac muscle in the walls of the heart chambers, and have a single central nucleus.[7] Cardiac muscle cells are joined to neighboring cells by intercalated discs, and when joined in a visible unit they are described as a cardiac muscle fiber.[8]

Smooth muscle cells control involuntary movements such as the peristalsis contractions in the esophagus and stomach. Smooth muscle has no myofibrils or sarcomeres and is therefore non-striated. Smooth muscle cells have a single nucleus.

Structure

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The unusual microscopic anatomy of a muscle cell gave rise to its terminology. The cytoplasm in a muscle cell is termed the sarcoplasm; the smooth endoplasmic reticulum of a muscle cell is termed the sarcoplasmic reticulum; and the cell membrane in a muscle cell is termed the sarcolemma.[9] The sarcolemma receives and conducts stimuli.

Skeletal muscle cells

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Main article: Skeletal muscle fibers
Diagram of skeletal muscle fiber structure

Skeletal muscle cells are the individual contractile cells within a muscle and are more usually known as muscle fibers because of their longer, threadlike appearance.[10] Broadly there are two types of muscle fiber performing in muscle contraction, either as slow twitch (type I) or fast twitch (type II).

A single muscle, such as the biceps brachii in a young adult human male, contains around 253,000 muscle fibers.[11] Skeletal muscle fibers are the only muscle cells that are multinucleated with the nuclei usually referred to as myonuclei. This occurs during myogenesis with the fusion of myoblasts, each contributing a nucleus to the newly formed muscle cell or myotube.[12] Fusion depends on muscle-specific proteins known as fusogens called myomaker and myomerger.[13]

A striated muscle fiber contains myofibrils consisting of long protein chains of myofilaments. There are three types of myofilaments: thin, thick, and elastic, that work together to produce a muscle contraction.[14] The thin myofilaments are filaments of mostly actin and the thick filaments are of mostly myosin, and they slide over each other to shorten the fiber length in a muscle contraction. The third type of myofilament is an elastic filament composed of titin, a very large protein.

In striations of muscle bands, myosin forms the dark filaments that make up the A band. Thin filaments of actin are the light filaments that make up the I band. The smallest contractile unit in the fiber is called the sarcomere, which is a repeating unit within two Z bands. The sarcoplasm also contains glycogen which provides energy to the cell during heightened exercise, and myoglobin, the red pigment that stores oxygen until needed for muscular activity.[14]

The sarcoplasmic reticulum, a specialized type of smooth endoplasmic reticulum, forms a network around each myofibril of the muscle fiber. This network is composed of groupings of two dilated end-sacs called terminal cisternae, and a single T-tubule (transverse tubule), which bores through the cell and emerge on the other side; together these three components form the triads that exist within the network of the sarcoplasmic reticulum, in which each T-tubule has two terminal cisternae on each side of it. The sarcoplasmic reticulum serves as a reservoir for calcium ions, so when an action potential spreads over the T-tubule, it signals the sarcoplasmic reticulum to release calcium ions from the gated membrane channels to stimulate muscle contraction.[14][15]

In skeletal muscle, at the end of each muscle fiber, the outer layer of the sarcolemma combines with tendon fibers at the myotendinous junction.[16][17] Within the muscle fiber pressed against the sarcolemma are multiply flattened nuclei; embryologically, this multinucleate condition results from multiple myoblasts fusing to produce each muscle fiber, where each myoblast contributes one nucleus.[14]

Cardiac muscle cells

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Main article: Cardiac muscle

The cell membrane of a cardiac muscle cell has several specialized regions, which may include the intercalated disc, and transverse tubules. The cell membrane is covered by a lamina coat which is approximately 50  nm wide. The laminar coat is separable into two layers; the lamina densa and lamina lucida. In between these two layers can be several different types of ions, including calcium.[18]

Cardiac muscle, like skeletal muscle, is also striated, and the cells contain myofibrils, myofilaments, and sarcomeres as the skeletal muscle cell. The cell membrane is anchored to the cell's cytoskeleton by anchor fibers that are approximately 10  nm wide. These are generally located at the Z lines so that they form grooves, and transverse tubules emanate. In cardiac myocytes, this forms a scalloped surface.[18]

The cytoskeleton is what the rest of the cell builds off of and has two primary purposes: the first is to stabilize the topography of the intracellular components, and the second is to help control the size and shape of the cell. While the first function is important for biochemical processes, the latter is crucial in defining the surface-to-volume ratio of the cell. This heavily influences the potential electrical properties of excitable cells. Additionally, deviation from the standard shape and size of the cell can have a negative prognostic impact.[18]

Smooth muscle cells

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Main article: Smooth muscle
Further information: Basal electrical rhythm

Smooth muscle cells are so-called because they have neither myofibrils nor sarcomeres and therefore no striations. They are found in the walls of hollow organs, including the stomach, intestines, bladder and uterus, in the walls of blood vessels, and in the tracts of the respiratory, urinary, and reproductive systems. In the eyes, the ciliary muscles dilate and contract the iris and alter the shape of the lens. In the skin, smooth muscle cells such as those of the arrector pili cause hair to stand erect in response to cold temperature or fear.[19]

Smooth muscle cells are spindle-shaped with wide middles and tapering ends. They have a single nucleus and range from 30 to 200 micrometers in length. This is thousands of times shorter than skeletal muscle fibers. The diameter of their cells is also much smaller, which removes the need for T-tubules found in striated muscle cells. Although smooth muscle cells lack sarcomeres and myofibrils, they do contain large amounts of the contractile proteins actin and myosin. Actin filaments are anchored by dense bodies (similar to the Z discs in sarcomeres) to the sarcolemma.[19]

Development

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Main article: Myogenesis

A myoblast is an embryonic precursor cell that differentiates to give rise to the different muscle cell types.[20] Differentiation is regulated by myogenic regulatory factors, including MyoD, Myf5, myogenin, and MRF4.[21] GATA4 and GATA6 also play a role in myocyte differentiation.[22]

Skeletal muscle fibers are made when myoblasts fuse together; muscle fibers therefore are cells with multiple nuclei, known as myonuclei, with each cell nucleus originating from a single myoblast. The fusion of myoblasts is specific to skeletal muscle, and not cardiac muscle or smooth muscle.

Myoblasts in skeletal muscle that do not form muscle fibers dedifferentiate back into myosatellite cells. These satellite cells remain adjacent to a skeletal muscle fiber, situated between the sarcolemma and the basement membrane[23] of the endomysium (the connective tissue investment that divides the muscle fascicles into individual fibers). To re-activate myogenesis, the satellite cells must be stimulated to differentiate into new fibers.

Myoblasts and their derivatives, including satellite cells, can now be generated in vitro through directed differentiation of pluripotent stem cells.[24]

Kindlin-2 plays a role in developmental elongation during myogenesis.[25]

Function

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Muscle contraction in striated muscle

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Main article: Muscle contraction

Skeletal muscle contraction

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When contracting, thin and thick filaments slide past each other by using adenosine triphosphate. This pulls the Z discs closer together in a process called the sliding filament mechanism. The contraction of all the sarcomeres results in the contraction of the whole muscle fiber. This contraction of the myocyte is triggered by the action potential over the cell membrane of the myocyte. The action potential uses transverse tubules to get from the surface to the interior of the myocyte, which is continuous within the cell membrane. Sarcoplasmic reticula are membranous bags that transverse tubules touch but remain separate from. These wrap themselves around each sarcomere and are filled with Ca2+.[26]

Excitation of a myocyte causes depolarization at its synapses, the neuromuscular junctions, which triggers an action potential. With a singular neuromuscular junction, each muscle fiber receives input from just one somatic efferent neuron. Action potential in a somatic efferent neuron causes the release of the neurotransmitter acetylcholine.[27]

When the acetylcholine is released, it diffuses across the synapse and binds to a receptor on the sarcolemma, a term unique to muscle cells that refers to the cell membrane. This initiates an impulse that travels across the sarcolemma.[28]

When the action potential reaches the sarcoplasmic reticulum, it triggers the release of Ca2+ from the Ca2+ channels. The Ca2+ flows from the sarcoplasmic reticulum into the sarcomere with both of its filaments. This causes the filaments to start sliding and the sarcomeres to become shorter. This requires a large amount of ATP, as it is used in both the attachment and release of every myosin head. Very quickly, Ca2+ is actively transported back into the sarcoplasmic reticulum, which blocks the interaction between the thin and thick filaments. This, in turn, causes the muscle cell to relax.[28]

There are four main types of muscle contraction: isometric, isotonic, eccentric, and concentric.[29] Isometric contractions are skeletal muscle contractions that do not cause movement of the muscle, and isotonic contractions are skeletal muscle contractions that do cause movement. Eccentric contraction is when a muscle moves under a load. Concentric contraction is when a muscle shortens and generates force.

Cardiac muscle contraction

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See also: Bowditch effect

Specialized cardiomyocytes in the sinoatrial node generate electrical impulses that control the heart rate. These electrical impulses coordinate contraction throughout the remaining heart muscle via the electrical conduction system of the heart. Sinoatrial node activity is modulated, in turn, by nerve fibers of both the sympathetic and parasympathetic nervous systems. These systems act to increase and decrease, respectively, the rate of production of electrical impulses by the sinoatrial node.

Evolution

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Further information: Evolution and Adaptation

The evolutionary origin of muscle cells in animals is highly debated: One view is that muscle cells evolved once, and thus all muscle cells have a single common ancestor. Another view is that muscles cells evolved more than once, and any morphological or structural similarities are due to convergent evolution, and the development of shared genes that predate the evolution of muscle – even the mesoderm (the germ layer) that gives rise to muscle cells in vertebrates).

Schmid & Seipel (2005)[30] argue that the origin of muscle cells is a monophyletic trait that occurred concurrently with the development of the digestive and nervous systems of all animals, and that this origin can be traced to a single metazoan ancestor in which muscle cells are present. They argue that molecular and morphological similarities between the muscle cells in non-bilaterian Cnidaria and Ctenophora are similar enough to those of bilaterians that there would be one ancestor in metazoans from which muscle cells derive. In this case, Schmid & Seipel argue that the last common ancestor of Bilateria, Ctenophora and Cnidaria, was a triploblast (an organism having three germ layers), and that diploblasty, meaning an organism with two germ layers, evolved secondarily, because they observed the lack of mesoderm or muscle found in most cnidarians and ctenophores. By comparing the morphology of cnidarians and ctenophores to bilaterians, Schmid & Seipel were able to conclude that there were myoblast-like structures in the tentacles and gut of some species of cnidarians and the tentacles of ctenophores. Since this is a structure unique to muscle cells, these scientists determined, based on the data collected by their peers, that this is a marker for striated muscles similar to that observed in bilaterians. The authors also remark that the muscle cells found in cnidarians and ctenophores are often contested due to the origin of these muscle cells being the ectoderm rather than the mesoderm or mesendoderm.

The origin of true muscle cells is argued by other authors to be the endoderm portion of the mesoderm and the endoderm. However, Schmid & Seipel (2005)[30] counter skepticism about whether the muscle cells found in ctenophores and cnidarians are "true" muscle cells, by considering that cnidarians develop through a medusa stage and polyp stage. They note that in the hydrozoans' medusa stage, there is a layer of cells that separates from the distal side of the ectoderm, which forms the striated muscle cells in a way similar to that of the mesoderm; they call this third separated layer of cells the ectocodon. Schmid & Seipel argue that, even in bilaterians, not all muscle cells are derived from the mesendoderm: Their key examples are that in both the eye muscles of vertebrates and the muscles of spiralians, these cells derive from the ectodermal mesoderm, rather than the endodermal mesoderm. Furthermore, they argue that since myogenesis does occur in cnidarians with the help of the same molecular regulatory elements found in the specification of muscle cells in bilaterians, there is evidence for a single origin for striated muscle.[30]

In contrast to this argument for a single origin of muscle cells, Steinmetz, Kraus, et al. (2012)[31] argue that molecular markers such as the myosin II protein used to determine this single origin of striated muscle predate the formation of muscle cells. They use an example of the contractile elements present in the Porifera, or sponges, that do truly lack this striated muscle containing this protein. Furthermore, Steinmetz, Kraus, et al. present evidence for a polyphyletic origin of striated muscle cell development through their analysis of morphological and molecular markers that are present in bilaterians and absent in cnidarians, ctenophores, and bilaterians. Steinmetz, Kraus, et al. showed that the traditional morphological and regulatory markers such as actin, the ability to couple myosin side chains phosphorylation to higher concentrations of the positive concentrations of calcium, and other MyHC elements are present in all metazoans not just the organisms that have been shown to have muscle cells. Thus, the usage of any of these structural or regulatory elements in determining whether or not the muscle cells of the cnidarians and ctenophores are similar enough to the muscle cells of the bilaterians to confirm a single lineage is questionable according to Steinmetz, Kraus, et al. Furthermore, they explain that the orthologues of the Myc genes that have been used to hypothesize the origin of striated muscle occurred through a gene duplication event that predates the first true muscle cells (meaning striated muscle), and they show that the Myc genes are present in the sponges that have contractile elements but no true muscle cells. Steinmetz, Kraus, et al. also showed that the localization of this duplicated set of genes that serve both the function of facilitating the formation of striated muscle genes, and cell regulation and movement genes, was already separated into striated muscle and non-muscle MHC. This separation of the duplicated set of genes is shown through the localization of the striated much to the contractile vacuole in sponges, while the non-muscle much was more diffusely expressed during developmental cell shape and change. Steinmetz, Kraus, et al. found a similar pattern of localization in cnidarians, except with the cnidarian N. vectensis having this striated muscle marker present in the smooth muscle of the digestive tract. Thus, they argue that the pleisiomorphic trait of the separated orthologues of much cannot be used to determine the monophylogeny of muscle, and additionally argue that the presence of a striated muscle marker in the smooth muscle of this cnidarian shows a fundamentally different mechanism of muscle cell development and structure in cnidarians.[31]

Steinmetz, Kraus, et al. (2012)[31] further argue for multiple origins of striated muscle in the metazoans by explaining that a key set of genes used to form the troponin complex for muscle regulation and formation in bilaterians is missing from the cnidarians and ctenophores, and 47 structural and regulatory proteins observed, Steinmetz, Kraus, et al. were not able to find even on unique striated muscle cell protein that was expressed in both cnidarians and bilaterians. Furthermore, the Z-disc seemed to have evolved differently even within bilaterians, and there is a great deal of diversity of proteins developed even between this clade, showing a large degree of radiation for muscle cells. Through this divergence of the Z-disc, Steinmetz, Kraus, et al. argue that there are only four common protein components that were present in all bilaterians muscle ancestors and that of these for necessary Z-disc components only an actin protein that they have already argued is an uninformative marker through its pleisiomorphic state is present in cnidarians. Through further molecular marker testing, Steinmetz et al. observe that non-bilaterians lack many regulatory and structural components necessary for bilaterian muscle formation and do not find any unique set of proteins to both bilaterians and cnidarians and ctenophores that are not present in earlier, more primitive animals such as the sponges and amoebozoans. Through this analysis, the authors conclude that due to the lack of elements that bilaterian muscles are dependent on for structure and usage, non-bilaterian muscles must be of a different origin with a different set of regulatory and structural proteins.[31]

In another take on the argument, Andrikou & Arnone (2015)[32] use the newly available data on gene regulatory networks to look at how the hierarchy of genes and morphogens and another mechanism of tissue specification diverge and are similar among early deuterostomes and protostomes. By understanding not only what genes are present in all bilaterians but also the time and place of deployment of these genes, Andrikou & Arnone discuss a deeper understanding of the evolution of myogenesis.[32]

In their paper, Andrikou & Arnone (2015)[32] argue that to truly understand the evolution of muscle cells, the function of transcriptional regulators must be understood in the context of other external and internal interactions. Through their analysis, Andrikou & Arnone found that there were conserved orthologues of the gene regulatory network in both invertebrate bilaterians and cnidarians. They argue that having this common, general regulatory circuit allowed for a high degree of divergence from a single well-functioning network. Andrikou & Arnone found that the orthologues of genes found in vertebrates had been changed through different types of structural mutations in the invertebrate deuterostomes and protostomes, and they argue that these structural changes in the genes allowed for a large divergence of muscle function and muscle formation in these species. Andrikou & Arnone were able to recognize not only any difference due to mutation in the genes found in vertebrates and invertebrates, but also the integration of species-specific genes that could also cause divergence from the original gene regulatory network function. Thus, although a common muscle patterning system has been determined, they argue that this could be due to a more ancestral gene regulatory network being co-opted several times across lineages with additional genes and mutations causing very divergent development of muscles. Thus, it seems that the myogenic patterning framework may be an ancestral trait. However, Andrikou & Arnone explain that the basic muscle patterning structure must also be considered in combination with the cis regulatory elements present at different times during development. In contrast with the high level of gene family apparatuses structure, Andrikou and Arnone found that the cis-regulatory elements were not well conserved both in time and place in the network, which could show a large degree of divergence in the formation of muscle cells. Through this analysis, it seems that the myogenic GRN is an ancestral GRN with actual changes in myogenic function and structure possibly being linked to later co-opting of genes at different times and places.[32]

Evolutionarily, specialized forms of skeletal and cardiac muscles predated the divergence of the vertebrate/arthropod evolutionary line.[33] This indicates that these types of muscle developed in a common ancestor sometime before 700 million years ago (mya). Vertebrate smooth muscle was found to have evolved independently from the skeletal and cardiac muscle types.

Invertebrate muscle cell types

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The properties used for distinguishing fast, intermediate, and slow muscle fibers can be different for invertebrate flight and jump muscles.[34] To further complicate this classification scheme, the mitochondrial content, and other morphological properties within a muscle fiber, can change in a tsetse fly with exercise and age.[35]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Muscle cell

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A muscle cell, also known as a myocyte, is the specialized contractile cell that forms the basic structural and functional unit of all muscle tissues in the body, enabling movement, circulation, and other vital processes through the generation of force via contraction. These cells are categorized into three distinct types—skeletal, , and —each exhibiting unique structural features, control mechanisms, and physiological roles tailored to their locations and functions. cells, which are striated and multinucleated, are responsible for voluntary movements and are attached to bones via tendons. cells, also striated but involuntary, form the myocardium of the heart and are interconnected by intercalated discs to ensure synchronized contractions. cells, non-striated and involuntary, line the walls of hollow organs and blood vessels, facilitating functions such as and vascular tone regulation. At the cellular level, all muscle cells share core components for contraction, including actin and myosin filaments that interact in a sliding mechanism triggered by calcium ions, though the organization and regulation differ by type. Skeletal muscle cells are elongated, cylindrical fibers ranging from 10 to 100 micrometers in diameter and up to several centimeters long, containing multiple nuclei and organized into sarcomeres that give them their characteristic striations under microscopy. These cells feature a highly developed sarcoplasmic reticulum for calcium storage and T-tubules that propagate action potentials deep into the fiber for rapid, uniform contraction. In contrast, cardiac muscle cells are shorter and branched, with a single central nucleus, and rely on gap junctions in intercalated discs for electrical coupling, allowing the heart to function as a unified pump. Smooth muscle cells are spindle-shaped with a single nucleus, lacking sarcomeres but possessing dense bodies and caveolae that anchor filaments and aid in calcium signaling, enabling slower, sustained contractions. Muscle cells develop from mesodermal precursors through myogenesis, a process involving transcription factors like MyoD and Myf-5 that drive cell fusion and differentiation. Skeletal muscle arises from somites and limb bud mesoderm, forming multinucleated syncytia during embryogenesis. Cardiac muscle differentiates from the cardiogenic mesoderm and becomes functional early in fetal development, around day 32 of gestation. Smooth muscle originates from diverse embryonic layers depending on the organ, such as mesoderm for vascular smooth muscle. Functionally, contraction in skeletal muscle follows the sliding filament theory, where neural excitation releases calcium to bind troponin, exposing myosin-binding sites on actin for cross-bridge cycling. Cardiac contraction is modulated by the autonomic nervous system and hormones, featuring a prolonged action potential for tetanic prevention. Smooth muscle contraction is often initiated by autonomic nerves or circulating factors, involving calmodulin-mediated myosin light chain phosphorylation. These adaptations underscore the versatility of muscle cells in maintaining , with comprising about 40% of body mass in adults and playing key roles in and posture. Disruptions in muscle cell function contribute to conditions like muscular dystrophies, cardiomyopathies, and vascular disorders, highlighting their .

Structure and Classification

Skeletal muscle cells

Skeletal muscle cells, also known as muscle fibers or myofibers, are elongated, cylindrical, multinucleated cells that form the functional units of skeletal muscles responsible for voluntary movement. These fibers arise from the fusion of multiple myoblasts during development, resulting in syncytial structures that can extend up to 30 cm in length in certain muscles like the sartorius, with diameters ranging from 10 to 100 micrometers. The multiple nuclei within each fiber are characteristically located at the periphery, just beneath the sarcolemma, the plasma membrane of the muscle cell. This multinucleated organization supports the large size and extensive contractile apparatus of the fibers, enabling powerful and coordinated contractions for locomotion and posture maintenance. A defining feature of cells is their striated appearance, caused by the highly organized arrangement of —the repeating units of the contractile apparatus—aligned within myofibrils that run parallel to the fiber's long axis. fibers are classified into two main types based on their contractile and metabolic properties: Type I (slow-twitch) fibers, which are oxidative and fatigue-resistant, suited for activities like sustained posture or ; and Type II (fast-twitch) fibers, which are primarily glycolytic and generate rapid, powerful contractions for short bursts of activity, such as sprinting or . Type II fibers can be further subdivided into Type IIa (fast oxidative-glycolytic, with moderate ) and Type IIx (fast glycolytic, with high power but low fatigue resistance), allowing muscles to adapt to diverse functional demands. The striations and fiber type distribution contribute to the precise control of force and speed in voluntary movements, with organization detailed further in discussions of contractile proteins. Human skeletal muscles contain varying numbers of these fibers; for example, the typically has approximately 253,000 fibers in young adults, organized into where each fiber is innervated by a single at a specialized called the . This junction ensures precise, all-or-none activation of fibers within a motor unit, facilitating graded force production through recruitment of multiple units for voluntary actions like arm flexion. Surrounding the fibers are layers of that provide structural support and transmit contractile forces: the endomysium envelops individual fibers, the perimysium bundles fibers into fascicles, and the encases the entire muscle. Additionally, skeletal muscle fibers are associated with satellite cells—quiescent stem cells located between the and —that play a crucial role in muscle maintenance and repair by proliferating and fusing with damaged fibers to restore function.

Cardiac muscle cells

Cardiac muscle cells, also known as cardiomyocytes, are specialized striated muscle cells that form the contractile tissue of the heart. These cells are typically branched and cylindrical, with lengths ranging from 50 to 100 micrometers and diameters of about 25 micrometers, allowing for efficient packing within the myocardial wall. Unlike skeletal muscle fibers, each cardiac muscle cell contains a single, centrally located nucleus, which facilitates coordinated gene expression across the interconnected network. The striated appearance arises from the organized arrangement of contractile proteins within the cells, enabling powerful and rhythmic contractions essential for heart function. A defining feature of cardiac muscle cells is the presence of intercalated discs, which are specialized junctions located at the ends of the cells where they connect to adjacent cardiomyocytes. These discs include desmosomes and fascia adherens for mechanical coupling, providing structural integrity to withstand the repetitive stretching and contracting of the heart. Gap junctions within the intercalated discs allow for electrical coupling by permitting the direct passage of ions and small molecules between cells, ensuring synchronized depolarization across the myocardium. This dual mechanical and electrical connectivity transforms individual cells into a functional , critical for efficient propagation of action potentials. Within cardiac muscle cells, myofibrils are composed of repeating sarcomeres, similar to those in , which consist of overlapping and filaments responsible for contraction. However, the excitation-contraction coupling in cardiac cells features unique arrangements of and the (SR) optimized for rapid calcium handling. in cardiac muscle are larger and positioned at the Z-lines of sarcomeres, forming dyads with the SR rather than the triads seen in , which enhances calcium influx from extracellular sources and release from intracellular stores. The SR surrounds the myofibrils closely, storing and releasing calcium ions efficiently to trigger contractions, with additional calcium entering via L-type channels during each beat to sustain the process. Certain cardiac muscle cells exhibit autorhythmicity, the intrinsic ability to generate spontaneous action potentials without external stimulation, a property most prominent in pacemaker cells of the . These specialized cells, derived from the same lineage as contractile cardiomyocytes, possess unique expressions, such as funny currents (If) and calcium channels, that drive slow during , leading to rhythmic firing at rates of 60-100 beats per minute. This autorhythmic capability initiates the heartbeat and propagates through the network to coordinate ventricular contraction.

Smooth muscle cells

Smooth muscle cells are , or spindle-shaped, uninucleated structures that typically measure 30 to 200 micrometers in length and 3 to 10 micrometers in width. These cells lack the organized sarcomeres found in striated muscle, resulting in a smooth, non-striated appearance under light microscopy. Instead, their contractile apparatus consists of thin filaments and thicker filaments arranged in an oblique, crisscrossing pattern throughout the , enabling a more diffuse and flexible force generation. The filaments insert into dense bodies, which are discrete, electron-dense protein aggregates scattered throughout the and along the plasma , serving to anchor the filaments and transmit contractile forces across the cell. Intermediate filaments, primarily composed of desmin, link these dense bodies to one another and to the , forming a cytoskeletal network that enhances mechanical stability and efficient force propagation to adjacent cells and . Smooth muscle is categorized into single-unit and multi-unit types based on cellular organization and coordination. Single-unit smooth muscle features cells electrically coupled by gap junctions containing connexins, promoting coordinated, wave-like activity resembling a functional , as observed in the tunica media of the . Multi-unit smooth muscle, by contrast, comprises discrete cells with independent neural innervation and no widespread gap junctions, allowing precise, individual control, such as in the pupillary constrictor muscle of the iris. These cells are predominantly situated in the tunica media of walls, the muscularis layers of the digestive tract, and the bronchial walls of airways, where their elongated form and attachments facilitate sustained circumferential tension. The plasma membrane of smooth muscle cells contains numerous caveolae, flask-shaped invaginations rich in and that cluster L-type voltage-gated calcium channels, supporting localized calcium handling essential for structural integrity during prolonged activity.

Development and Regeneration

Embryonic development

Muscle cells originate from distinct regions of the during early embryogenesis. Skeletal muscle cells derive from the paraxial mesoderm, specifically the somites, which form along the , while cells and most cells arise primarily from the splanchnic layer of the , with some cells deriving from and other mesodermal sources. Progenitor cells from these mesodermal origins undergo migration and commitment to the myogenic lineage, primarily regulated by the paired box transcription factors and Pax7. In skeletal muscle development, -expressing cells in the dermomyotome of somites migrate to sites of muscle formation, such as the limb buds, where Pax7 further specifies cell precursors and myogenic progenitors. plays a predominant role in early embryonic , driving and migration of myoblasts, whereas Pax7 is essential for fetal muscle growth and the establishment of a progenitor pool. Differentiation of these myogenic progenitors into mature muscle cells is orchestrated by the myogenic regulatory factors (MRFs), a family of basic helix-loop-helix transcription factors including Myf5, , myogenin, and MRF4. Myf5 and initiate commitment to the myogenic lineage by activating muscle-specific in proliferating myoblasts, while myogenin and MRF4 promote terminal differentiation and the withdrawal from the . These factors function in a hierarchical and partially redundant manner, with Myf5 being the earliest expressed during somitogenesis to specify myoblasts. In , mononucleated myoblasts fuse to form multinucleated myotubes, a process critical for generating the syncytial structure of muscle fibers. This fusion occurs after MRF activation, involving molecules and cytoskeletal rearrangements to align and merge myoblasts. For , cardioblasts from the coalesce bilaterally and fuse to form the primitive heart tube around the midline, establishing the linear structure that undergoes subsequent looping and chamber formation. cells differentiate from mesenchymal progenitors primarily in the , with additional contributions from cells for certain vascular types; these progenitors respond to local inductive signals, such as epithelial-mesenchymal interactions and TGF-β signaling, to form contractile layers around developing organs and vessels without myoblast fusion. In embryos, somitogenesis begins during the third week post-fertilization, with the first somites appearing around day 20 and continuing until week 5, providing the initial pool of progenitors. Myotube formation in commences by weeks 7-8, marking the onset of primary , while the primitive heart tube assembles by the end of week 3. These processes are modulated by signaling pathways such as Wnt and Notch, which refine progenitor specification; Wnt signaling promotes myogenic commitment in somitic cells, whereas Notch inhibits premature differentiation to maintain the progenitor state.

Postnatal growth and regeneration

Postnatal muscle growth primarily occurs through , where fibers increase in size in response to mechanical stimuli such as resistance exercise. This involves the addition of s and an expansion in their cross-sectional area, driven by signaling pathways activated by mechanical tension, metabolic stress, and muscle damage. Hormones like insulin-like growth factor-1 (IGF-1) and nutrients further support protein synthesis, leading to net muscle mass gains without significant in adults. In contrast, —characterized by reduced number and size—arises from disuse, such as immobilization, or aging-related , involving upregulated via the ubiquitin-proteasome system and impaired mitochondrial function. , affecting up to 50% of individuals over 80, accelerates muscle loss through chronic and anabolic resistance, diminishing force production. Muscle regeneration in postnatal life relies heavily on satellite cells, quiescent stem cells marked by Pax7 expression that reside between the basal lamina and sarcolemma of muscle fibers. Upon injury, such as strains or trauma, these cells activate, proliferate as Pax7-positive myoblasts, and differentiate into myocytes that fuse with damaged fibers or form new myofibers, restoring structure and function. This process is robust in skeletal muscle, enabling repair after acute damage through coordinated expression of myogenic regulatory factors like MyoD and myogenin. Cardiac muscle, however, exhibits minimal regenerative capacity postnatally; injury typically leads to cardiomyocyte apoptosis and replacement by fibrotic scar tissue via fibroblast activation, impairing contractility due to the limited proliferation of terminally differentiated cardiomyocytes. Smooth muscle regeneration is intermediate, often involving dedifferentiation and proliferation of existing cells rather than dedicated stem cells. Recent advances in muscle regeneration target satellite cell limitations and genetic defects. Stem cell therapies, particularly using mesenchymal stem cells (MSCs) derived from or , enhance repair by secreting paracrine factors that promote satellite cell activation and reduce in models of and . Ongoing clinical trials as of 2025 indicate that MSCs can improve functional outcomes in muscular dystrophies through mechanisms supporting myoblast fusion and vascularization. For (DMD), CRISPR-Cas9 editing of the gene has progressed to phase I/II trials, where editing of patient myoblasts restores expression, with preclinical data indicating up to 60% functional protein recovery and reduced in animal models. A 2025 trial update reports safe delivery via AAV vectors, with initial human results showing modest restoration in limb muscles.

Molecular Components

Contractile proteins and filaments

Muscle cells rely on specialized contractile proteins organized into filaments to generate force and enable contraction. The primary proteins include and , which form thick and thin filaments, respectively, interacting via the cross-bridge cycle to produce mechanical work from . These filaments are arranged differently in striated (skeletal and cardiac) versus , influencing contractility across cell types. Thick filaments consist of myosin II, a hexameric protein with two heavy chains and four light chains. Each heavy chain (~200-220 kDa) features a globular motor head with actin- and nucleotide-binding sites, a neck region serving as a lever arm, and a coiled-coil tail for filament assembly. The light chains (essential and regulatory, ~15-20 kDa) stabilize the neck and modulate activity. Myosin II exhibits ATPase activity in its head domain, hydrolyzing ATP to ADP and inorganic phosphate, which powers conformational changes and force generation during the power stroke. Isoforms vary by muscle type, with fast skeletal myosin showing higher ATPase rates (~30 s⁻¹) compared to slow cardiac (~5-6 s⁻¹), adapting to physiological demands like speed versus endurance. Thin filaments are polymers of , associated with regulatory proteins and in striated muscle. exists as globular monomers (G-actin, ~42 kDa) that polymerize into double-helical filamentous structures (F-actin, ~7 nm diameter), forming the core of thin filaments anchored at Z-lines. , a coiled-coil dimer (~40 kDa), binds along F-actin, spanning seven actin subunits and sterically blocking myosin-binding sites in the relaxed state. The complex, comprising three subunits, regulates this interaction: (TnC, ~18 kDa) binds calcium ions to initiate contraction; (TnI, ~21 kDa) inhibits actin-myosin binding at low calcium by anchoring in a blocked position; and (TnT, ~31 kDa) links the complex to . Calcium binding to TnC induces TnI release, pivoting to expose myosin sites. In striated muscle, these filaments organize into s, the basic contractile units (~2-3 μm long). Thin filaments anchor at Z-lines, defining boundaries, and extend into the isotropic I-band before overlapping thick filaments in the anisotropic A-band. The A-band spans the full length of thick filaments, with the central H-zone (lacking thin filament overlap) flanked by regions of partial overlap. , a giant elastic protein (~3-4 MDa), spans from Z-line to M-line, aligning filaments and providing passive elasticity via its extensible I-band region (tandem immunoglobulin and PEVK domains), which generates restoring force (0-5 pN per molecule) to maintain integrity during stretch. Smooth muscle lacks sarcomeres, featuring a non-sarcomeric arrangement of - filaments in dense bodies and oblique lattices for isotropic contraction. Regulatory proteins caldesmon and calponin modulate interactions: caldesmon (~87-93 kDa), an - and -binding protein, cross-links filaments, inhibits activity, and maintains myosin spacing to balance force without calcium sensitization. Calponin (~34 kDa), -associated, reduces shortening velocity and stabilizes filaments but does not directly regulate force or calcium sensitivity. These adaptations support sustained, low-energy contractions in organs like blood vessels. The cross-bridge cycle kinetics underpin force generation, where total force FF arises from the number of attached bridges nn, force per bridge ff, and displacement dd:
F=n⋅f⋅dF = n \cdot f \cdot d
This models collective head contributions during ATP-driven cycling. The length-tension relationship, describing how varies with length, follows Hill's equation for force-velocity dynamics:
(F+a)(v+b)=(F0+a)b(F + a)(v + b) = (F_0 + a)b
where FF is , vv is , F0F_0 is maximum isometric , and aa, bb are muscle-specific constants shaping the hyperbolic curve. This equation reveals molecular insights into cross-bridge attachment rates and energy efficiency.

Energy production and metabolism

Muscle cells across types—skeletal, cardiac, and smooth—exhibit high energy demands to support contraction, relaxation, and maintenance, with ATP as the currency generated through specialized biochemical pathways and organelles. Mitochondria are central to this process, particularly in oxidative fibers; in , slow-twitch Type I fibers contain high mitochondrial densities (up to 12.2 µmol/L in ), enabling sustained aerobic activity, while fast-twitch Type II fibers have lower densities (1.9 µmol/L in gracilis) suited for brief, intense efforts. cells feature even higher mitochondrial volume fractions (~35%), supporting continuous pumping via β-oxidation and , whereas cells maintain lower densities (~3-5%) for tonic contractions with efficient, primarily oxidative ATP production from glucose. ATP production relies on interconnected systems: the phosphocreatine shuttle provides rapid resynthesis through -mediated transfer (with stores exceeding ATP by 4-fold in ), delivers anaerobic ATP with lactate as a byproduct (dominant in Type II fibers rich in stores), and via the Krebs cycle yields efficient aerobic energy (prevalent in Type I fibers and cardiac cells). , abundant in slow-twitch and cardiac fibers, facilitates and diffusion to mitochondria, enhancing aerobic capacity during prolonged activity. In , supports biosynthetic needs under stress, but oxidative pathways predominate for contractile energy, with adaptations like increased compensating for disruptions. in these pathways, such as for or glycolytic enzymes, follow Michaelis-Menten kinetics, where reaction velocity vv is given by v=Vmax⁡[S]Km+[S]v = \frac{V_{\max} [S]}{K_m + [S]} with Vmax⁡V_{\max} as maximum rate, [S] as substrate concentration, and KmK_m as the Michaelis constant indicating enzyme-substrate affinity. Glucose metabolism exemplifies ATP yields: anaerobic glycolysis nets ~2 ATP per glucose molecule, Glucose+2ADP+2Pi→2Lactate+2ATP+2H+,\text{Glucose} + 2 \text{ADP} + 2 \text{P}_i \rightarrow 2 \text{Lactate} + 2 \text{ATP} + 2 \text{H}^+, while full aerobic oxidation produces ~36 ATP through combined glycolysis, Krebs cycle, and electron transport. A significant portion of ATP sustains homeostasis, particularly via the sarco/endoplasmic reticulum Ca²⁺-ATPase () pump, which reuptakes Ca²⁺ into the for relaxation and consumes ~70% of total ATP in active muscle cells across types. Fatigue mechanisms impair this balance: lactate buildup from anaerobic glycolysis causes and inhibits contractile proteins, while calcium dysregulation—from impaired function or SR release—reduces force generation and exacerbates energy depletion. These processes highlight metabolic specialization, with Type I fibers resisting fatigue through oxidative resilience and myoglobin-mediated oxygen buffering.

Function and Contraction

Skeletal muscle contraction

Skeletal muscle contraction begins at the neuromuscular junction, where an action potential arriving at the motor neuron terminal triggers the release of acetylcholine from synaptic vesicles into the synaptic cleft. This neurotransmitter binds to nicotinic acetylcholine receptors on the postsynaptic muscle fiber membrane, opening ligand-gated sodium channels and generating a localized depolarization known as the end-plate potential. The end-plate potential, typically exceeding the threshold for an action potential, depolarizes the adjacent sarcolemma, initiating a propagating action potential along the muscle fiber surface and deep into the transverse tubules (T-tubules). The action potential in the activates dihydropyridine receptors (DHPRs), which serve as voltage sensors and physically couple to ryanodine receptors (RyRs) on the (SR) membrane, triggering the release of stored calcium ions into the . This calcium release, part of excitation-contraction coupling, raises cytosolic calcium concentration rapidly; the calcium binds to on the thin filaments, inducing a conformational change that shifts away from the myosin-binding sites on . Exposure of these sites enables myosin heads from the thick filaments to form cross-bridges with , initiating the power stroke powered by . The explains the mechanism of shortening, where successive cross-bridge cycles cause and filaments to slide past each other, reducing length without altering filament overlap proportions during contraction. In this process, the detached myosin head hydrolyzes ATP to ADP and inorganic , reattaching to a new site farther along the thin filament to generate force and displacement. A single elicits a brief twitch contraction, characterized by rapid rise and fall in tension due to transient calcium elevation, whereas high-frequency stimulation (typically 50-100 Hz) causes temporal summation of twitches, fusing into a sustained that produces 3-4 times greater force than a single twitch. Muscle relaxation follows of the and reuptake of calcium into the SR by the sarco/endoplasmic reticulum Ca²⁺-ATPase () pump, which uses ATP to transport calcium against its gradient, lowering cytosolic levels and allowing to re-cover binding sites, detaching cross-bridges. The rate of relaxation influences movement efficiency, as seen in the force-velocity relationship, where maximal force is achieved at zero velocity (isometric conditions) and decreases hyperbolically as shortening velocity increases, reflecting cross-bridge cycling dynamics. This relationship, first described experimentally in frog , underscores how balances force and speed for voluntary actions like locomotion.

Cardiac muscle contraction

Cardiac muscle contraction is characterized by its autorhythmic and synchronized nature, initiated by specialized pacemaker cells in the sinoatrial (SA) node. These cells exhibit spontaneous diastolic depolarization during phase 4 of the action potential, driven primarily by the funny current (I_f), a hyperpolarization-activated mixed Na^+-K^+ inward current that activates upon repolarization and contributes to the gradual membrane depolarization. This process is complemented by the calcium clock mechanism, where spontaneous sarcoplasmic reticulum (SR) Ca^{2+} releases elevate cytosolic Ca^{2+}, activating the Na^+-Ca^{2+} exchanger (N_CX) to further depolarize the membrane and open L-type Ca^{2+} channels, culminating in the action potential upstroke. The action potential generated in the SA node propagates rapidly across the cardiac myocardium through gap junctions located in the intercalated discs, enabling electrical coupling and coordinated contraction of cardiomyocytes as a functional . Unlike , cardiac action potentials feature a prolonged plateau phase (phase 2) lasting approximately 200 ms due to sustained Ca^{2+} influx, resulting in a longer refractory period that prevents summation of contractions and , ensuring complete relaxation between beats to allow ventricular filling. Excitation-contraction coupling in cardiac muscle relies on (CICR), where opens L-type Ca^{2+} channels in the , permitting a small influx of extracellular Ca^{2+} that triggers ryanodine receptors on the SR to release a much larger store of Ca^{2+} into the . This amplified Ca^{2+} transient binds to , facilitating cross-bridge cycling between and for contraction. The majority of contractile Ca^{2+} is sourced from the SR via this CICR process, with termination occurring through SR Ca^{2+}- reuptake and extrusion mechanisms to restore diastolic levels. The Frank-Starling mechanism intrinsically adjusts to venous return by linking preload to contractile force; increased stretches sarcomeres, enhancing Ca^{2+} sensitivity and SR Ca^{2+} release, thereby augmenting without altering characteristics. This length-dependent activation ensures that the heart matches output to input, maintaining circulatory balance during varying hemodynamic demands. Autonomic nervous system modulation fine-tunes cardiac contraction: sympathetic stimulation via norepinephrine binding to β1-adrenergic receptors activates the cAMP-PKA pathway, increasing I_f, L-type Ca^{2+} current, and SR Ca^{2+} handling to elevate and contractility. Conversely, parasympathetic input through vagal release of on M2 receptors inhibits adenylate cyclase, reducing cAMP and slowing SA node depolarization to decrease rate and atrial force.

Smooth muscle contraction

Smooth muscle contraction is a slower, more sustained process compared to striated muscle, enabling functions such as maintaining vascular tone and facilitating . It is primarily regulated by changes in intracellular calcium concentration, which modulates the interaction between and filaments through phosphorylation-dependent mechanisms. Unlike , smooth muscle lacks and relies on (MLCK) for activation, allowing for graded and adaptable force generation. Contraction in smooth muscle is triggered by neural, hormonal, or mechanical stimuli. Autonomic nerves release neurotransmitters like norepinephrine or , which bind to G protein-coupled receptors on the , leading to or direct modulation of ion channels. Hormonal signals, such as norepinephrine from the , similarly activate receptors to initiate signaling cascades. Stretch of the muscle tissue can also provoke contraction by activating mechanosensitive ion channels, resulting in membrane . This opens voltage-gated calcium channels, primarily L-type channels, allowing extracellular calcium influx, while intracellular release from the via inositol trisphosphate (IP3) or ryanodine receptors further elevates cytosolic calcium levels. The influx of calcium binds to calmodulin, forming a calcium-calmodulin complex that activates MLCK. This kinase the regulatory light chain of myosin II at serine 19 (and sometimes threonine 18), increasing the enzyme's activity and enabling the formation of cross-bridges between myosin heads and actin filaments. The resulting cross-bridge cycling generates sliding force and shortening of the muscle cell, producing contraction. This step allows for precise control, as the extent of phosphorylation correlates with the degree of force development. A key feature of smooth muscle is the latch state, which permits energy-efficient maintenance of tone. In this state, dephosphorylated remains attached to , sustaining force with minimal even as calcium levels and decrease. This is facilitated by pathways such as RhoA/Rho-kinase, which inhibit myosin light chain (MLCP), preventing rapid and allowing prolonged contraction without continuous energy expenditure. Relaxation occurs when calcium is sequestered back into the or extruded via pumps like the plasma membrane Ca2+-ATPase, reducing the calcium-calmodulin complex. Simultaneously, MLCP dephosphorylates myosin light chains, detaching cross-bridges and allowing filaments to slide apart; factors like enhance this by increasing cGMP and activating MLCP. Smooth muscle contractions vary by type and organization. Phasic contractions are rhythmic and transient, as seen in the where they drive through periodic depolarizations. Tonic contractions are sustained and steady, characteristic of vascular maintaining diameter. These differences arise from variations in calcium handling and phosphatase activity, with tonic muscles exhibiting greater latch-state stability. is classified as single-unit or multi-unit based on coordination: single-unit , such as in the gut or , functions as a with gap junctions (connexins) enabling electrical and synchronized contractions across cells. Multi-unit , found in the iris or , consists of independently innervated cells that contract individually without widespread , allowing finer control.

Evolution

Origins in early animals

Muscle cells are believed to have first appeared approximately 600–700 million years ago during the early diversification of metazoans, coinciding with the period. Fossil evidence from this era, such as the ~560-million-year-old Haootia quadriformis from Newfoundland, , reveals impressions interpreted as muscle-like contractile structures, suggesting that simple muscular constrictors predated the by tens of millions of years. These findings indicate that basic contractile tissues were already present in soft-bodied organisms, enabling primitive and potentially contributing to the ecological success of early animal lineages. Ctenophores also exhibit early muscle systems, with recent research (as of 2025) confirming their neuromuscular organization and contributing to debates on metazoan phylogeny. The monophyletic origin of muscle cells traces back to choanoflagellate-like unicellular ancestors, where the core - contractile machinery was already established as a conserved feature across eukaryotes. This system, involving filaments and motors for cell and , was co-opted in early metazoans to form multicellular contractile apparatuses. Molecular studies confirm that II subclasses, including those for smooth and striated muscle types, diverged prior to the metazoan radiation, providing a foundational toolkit for muscle . The evolution of the heavy chain (MyHC) played a pivotal role in this process, with ancient duplications enabling specialization in contractile function. In cnidarians, such as (e.g., Aurelia and Clytia ), MyHC homologs support striated-like muscles used for , featuring organized myofibrils that resemble bilaterian counterparts but with distinct ultrastructural arrangements. These cnidarian muscles highlight the early deployment of MyHC variants in non-bilaterian metazoans, underscoring their conserved role in metazoan locomotion. Debates persist regarding the versus of muscle cells, with evidence for a single origin of basic contractility contrasted by independent evolutions of specialized types. Schmid and Seipel (2005) proposed a monophyletic descent of striated muscle from a triploblastic cnidarian-like , based on shared developmental regulators and cnidarian striations. In contrast, Steinmetz et al. (2012) argued for polyphyletic origins of striated muscles, citing genomic and ultrastructural differences between cnidarian and bilaterian lineages, suggesting . Across bilaterians, myogenic regulatory factors (MRFs), such as and Myf5 homologs, remain highly conserved, reinforcing a shared genetic framework for muscle specification despite these divergences.

Diversification in vertebrates and invertebrates

In vertebrates, diversification of striated skeletal and cells, enabling specialized contractile functions in locomotion and circulation, respectively, was facilitated by duplications, particularly in the heavy chain (MyHC) family, which produced multiple isoforms tailored to specific muscle types; for instance, distinct fast and slow MyHC isoforms support varying contraction speeds in skeletal muscles across lineages. cells contribute to visceral and vascular contractility without striations, with MyHC isoforms adapted for sustained contractions. In , muscle cell organization diverged earlier, with cnidarians featuring epithelio-muscular cells integrated into epithelial layers of the and , where myofibrils lie parallel to the body surface for simple body wall contractions. Bilaterian exhibit further specializations: non-striated muscles predominate in mollusks and , often with oblique striations in flight muscles that enhance power output through asynchronous contraction, while nematodes possess obliquely striated muscles adapted for body undulation. These muscle types reflect adaptations to hydrostatic or exoskeletal locomotion, contrasting with striations. Key evolutionary divergences in muscle cells occurred around 550 million years ago during the bilaterian radiation, marking the protostome-deuterostome split, where myosins evolved distinct heavy chain structures and alternative splicing patterns compared to myosins, influencing filament assembly and contractility. In , for example, myosin heavy chain genes underwent lineage-specific expansions to support diverse muscle functions, differing from the isoform multiplicity in . These changes highlight how post-bilaterian expansions drove muscle specialization across phyla. Adaptations in muscle isoforms further illustrate diversification; in , fast MyHC isoforms in flight muscles enable exceptionally rapid actomyosin kinetics for high-frequency wing beats, while slower isoforms support muscles, reflecting selective pressures for aerial locomotion. Regeneration capacity also varies phylogenetically, with planarians (flatworms) exhibiting high regenerative potential through neoblast stem cells that replenish muscle tissues, in contrast to the limited satellite cell-mediated repair in mammals, where often predominates post-injury. These variations underscore evolutionary trade-offs in muscle resilience across animal lineages.

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