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Muscular system

The muscular system is the biological network of tissues in the human body composed of specialized contractile cells called muscle fibers, primarily responsible for enabling movement, maintaining posture, and generating heat through contraction.^[1]^[2] It consists of three distinct types of muscle: skeletal muscle, which is voluntary and striated; cardiac muscle, which is involuntary and striated; and smooth muscle, which is involuntary and non-striated.^[2]^[3] These muscle types differ in structure, location, and control mechanisms but collectively support essential physiological processes.^[2] Skeletal muscles, the most abundant type, attach to bones via tendons and facilitate voluntary actions such as walking, lifting, and facial expressions, while also stabilizing joints and contributing to body support.^[4]^[5] Cardiac muscle, found exclusively in the walls of the heart, contracts rhythmically and involuntarily to pump blood throughout the circulatory system, ensuring continuous circulation without fatigue under normal conditions.^[3]^[2] Smooth muscles line the walls of internal organs like the digestive tract, blood vessels, and airways, enabling involuntary processes such as peristalsis for digestion, vasoconstriction, and regulation of airflow during respiration.^[2]^[3] Beyond locomotion, the muscular system plays critical roles in homeostasis and metabolism; for instance, muscle contractions produce approximately 85% of the body's heat, aiding thermoregulation, and antagonistic pairs of muscles work in opposition to produce coordinated movements while preventing injury.^[1] It also supports respiration by driving the diaphragm and intercostal muscles to facilitate breathing, and integrates with other systems like the nervous and skeletal systems for precise control and force generation.^[6] Overall, the muscular system accounts for approximately 40% of total body weight in adults and is essential for survival, with its efficiency relying on energy from ATP and interactions with connective tissues like fascia.^[2]

Overview

Definition and Functions

The muscular system is the biological network of tissues responsible for generating force and enabling movement in the human body, consisting primarily of three types of muscle: skeletal, cardiac, and smooth.^[2] These muscles facilitate both voluntary actions, such as walking, and involuntary processes, like heartbeat regulation.^[1] Collectively, the muscular system accounts for approximately 40% of total body weight in adults, with skeletal muscles alone numbering over 600 and forming the bulk of this mass.^[7] The primary functions of the muscular system include force generation for locomotion and manipulation of the environment, maintenance of posture and joint stability, and heat production through metabolic activity during contractions.^[1] Additionally, it supports vital organ functions, such as the cardiac muscle's role in pumping blood via the heart and smooth muscle's contribution to peristalsis in the digestive tract.^[2] These roles ensure essential physiological processes, from basic mobility to thermoregulation. The muscular system integrates closely with other body systems to achieve its functions effectively. It collaborates with the skeletal system to produce coordinated movements by attaching to bones via tendons, allowing leverage and support.^[1] The nervous system provides control through neural signals that initiate contractions, while the circulatory system delivers oxygen and nutrients to muscles and removes waste products.^[8] Muscle mass varies significantly by factors such as sex, age, and fitness level; for instance, it typically comprises about 38% of body weight in males compared to 31% in females, declines with advancing age due to sarcopenia, and increases with regular physical training in athletes.^[9]^[10]

Evolutionary and Comparative Aspects

The muscular system originated from mesodermal tissue in early bilaterians over 550 million years ago, where muscle cells likely played a central role in the evolution of mesoderm by enabling control of swimming and body shape through contractile apparatus.^[11]^[12] In bilaterians, the dichotomy between smooth and striated myocytes emerged as a fundamental feature, with smooth muscles providing slow, sustained contractions and striated muscles enabling rapid, forceful movements.^[13] This distinction became more pronounced in chordates around 500 million years ago, where striated muscles evolved alongside the notochord and vertebral column, supporting more complex locomotion in early vertebrates.^[14] Comparatively, invertebrate muscular systems often rely on non-striated, smooth-like muscles integrated with hydrostatic skeletons, as seen in annelids like earthworms, where circular and longitudinal muscle layers generate peristaltic waves by altering internal fluid pressure for burrowing and crawling.^[15]^[16] In contrast, vertebrates developed segmented skeletal muscles attached to a bony endoskeleton, allowing precise, lever-based movements; for example, avian flight muscles are highly specialized for power output with asynchronous contraction in insects and synchronous striated fibers in birds, differing from the endurance-oriented slow-twitch fibers predominant in mammalian locomotor muscles.^[17]^[18] Human adaptations reflect further evolutionary refinements tied to bipedalism, with the gluteal muscles—particularly the gluteus maximus—enlarging and reorienting to stabilize the pelvis and enable efficient upright walking and running by countering trunk tilt during single-leg support.^[19]^[20] The expansion of the human brain also drove adaptations in fine motor control muscles, such as those in the hands, enhancing dexterity for tool manipulation through increased neural integration and individuated finger movements.^[21]^[22] Key molecular components like actin and myosin proteins are highly conserved across phyla, forming the core contractile machinery from invertebrates to vertebrates and underscoring the ancient origins of muscle function.^[23]^[24] Vertebrate cardiac muscle represents a unique innovation, featuring striated sarcomeres specialized for rhythmic, involuntary contractions that support closed circulatory systems, absent in invertebrates with open circulation.^[25]^[26]

Anatomy

Macroscopic Structure

The human muscular system at the macroscopic level consists primarily of skeletal muscles organized into two main groups: axial muscles, which support the head, neck, and trunk by originating on the axial skeleton, and appendicular muscles, which facilitate movement of the limbs by attaching to the appendicular skeleton.^[27]^[28] Each skeletal muscle is composed of bundles of fascicles, which are groups of muscle fibers wrapped in connective tissue layers, including the perimysium around fascicles and the epimysium enveloping the entire muscle to form a discrete organ-like structure.^[29]^[30] Skeletal muscles typically attach to bones or other structures via tendons, with one end designated as the origin—the more fixed or proximal attachment point—and the other as the insertion—the more movable or distal point that moves during contraction.^[29] For example, the biceps brachii muscle originates from the supraglenoid tubercle and coracoid process of the scapula and inserts via its tendon onto the radial tuberosity of the radius, allowing flexion at the elbow and supination of the forearm.^[31] These attachments enable muscles to act across joints, transmitting force to produce movement while maintaining structural integrity through the tough, fibrous nature of tendons.^[29] Muscles exhibit diverse shapes and architectures that influence their functional properties, such as speed or force production, determined by the arrangement of fascicles relative to the tendon's line of action. Fusiform muscles, with fibers running parallel to the long axis, like the biceps brachii, prioritize shortening velocity and range of motion over force.^[32] In contrast, pennate muscles feature fibers oriented at an angle to a central tendon, as in the gastrocnemius, which enhances force generation by packing more fibers into a smaller volume, ideal for powerful actions like plantarflexion.^[33]^[32] Convergent muscles, such as the pectoralis major, have fibers fanning out from a broad origin to a narrower insertion, allowing versatile movements like arm adduction and flexion across a wide range.^[34] Skeletal muscles are named according to standardized conventions that reflect their anatomical and functional characteristics, often using Latin or Greek roots for precision in medical and scientific contexts. Names may indicate location, such as tibialis anterior for its position on the anterior tibia; action, like flexor carpi radialis, which flexes the wrist on the radial side; or relative size, as in gluteus maximus, the largest muscle of the buttocks.^[35] These naming systems aid in identifying over 600 skeletal muscles in the adult human body, most of which occur in bilateral pairs to ensure symmetrical movement and postural balance.^[29]^[35] Deep fascia, a dense connective tissue layer external to the epimysium, encases groups of muscles into functional compartments, such as the anterior and posterior compartments of the leg, preventing friction and directing forces during contraction while compartmentalizing the limbs for specialized actions.^[30] This organization supports the overall integration of the muscular system with the skeletal framework, enabling coordinated locomotion and stability.^[29]

Microscopic Structure

Muscle tissue is composed of specialized cells known as myocytes, which vary in nuclear configuration across types. Skeletal muscle fibers are long, cylindrical, and multinucleated due to the fusion of multiple myoblasts during development, forming a true syncytium.^[36] In contrast, cardiac muscle cells (cardiomyocytes) are typically mononucleated with a single, centrally located nucleus, though they form a functional syncytium through interconnections, while smooth muscle cells are spindle-shaped and also mononucleated with a central nucleus.^[37] These cellular features support the structural integrity and functional demands of each muscle type under microscopic examination.^[38] In striated muscle types—skeletal and cardiac—the functional unit is the sarcomere, a repeating segment along myofibrils that imparts the characteristic striated appearance visible under light microscopy. The sarcomere is bounded by Z-lines, which anchor thin actin filaments; the A-band represents the length of thick myosin filaments, with the central H-zone containing only myosin and the M-line bisecting it to connect myosin tails. Overlapping actin and myosin in the A-band creates darker regions, while the I-band consists of actin filaments exclusive to each sarcomere half, appearing lighter.^[4] This banded pattern arises from the precise hexagonal lattice arrangement of actin and myosin, essential for the organized architecture observed in electron micrographs.^[39] Key organelles within myocytes include the sarcoplasmic reticulum (SR), a specialized endoplasmic reticulum that stores calcium ions, and transverse tubules (T-tubules), which are invaginations of the plasma membrane facilitating rapid signal transmission deep into the cell. Mitochondria are abundant, particularly in oxidative muscle fibers, providing ATP for cellular maintenance and contraction readiness.^[40] T-tubules align at the A-I junction in skeletal muscle, associating closely with SR terminal cisternae to form triads.^[41] Connective tissue sheaths integrate myocytes into functional units: the endomysium, a delicate layer of reticular fibers and basal lamina, surrounds individual muscle fibers; the perimysium encases bundles of fibers (fascicles), containing fibroblasts, collagen, and elastic fibers for structural support; and the epimysium envelops the entire muscle, blending with tendons.^[30] These layers not only provide mechanical strength but also house nerves, blood vessels, and lymphatics.^[29] Myofibrils, composed of aligned sarcomeres, serve as the primary contractile elements within the cytoplasm (sarcoplasm) of myocytes, occupying up to 80% of the cell volume in skeletal muscle. Adjacent to skeletal muscle fibers lie satellite cells, mononucleated stem cells residing between the plasma membrane and basal lamina, which contribute to regeneration by proliferating and fusing with damaged fibers.^[42] This microscopic organization ensures both contractility and repair potential across muscle tissues.^[43]

Types of Muscle Tissue

Skeletal Muscle

Skeletal muscle tissue, also known as striated voluntary muscle, is primarily located throughout the body where it attaches to bones via tendons, enabling precise control over body movements and posture. These muscles span joints, with one end typically fixed (origin) and the other movable (insertion), allowing for actions such as limb extension and flexion. Under voluntary control, skeletal muscle is innervated by the somatic nervous system, which transmits signals from the central nervous system to initiate contractions for activities like walking or lifting.^[4]^[44] The fundamental units of skeletal muscle are long, cylindrical fibers that can extend up to several centimeters in length and range from 10 to 100 micrometers in diameter; these fibers are multinucleated, formed by the fusion of myoblasts during development, and display a characteristic striated appearance due to the organized arrangement of contractile proteins into sarcomeres. Skeletal muscles contain a mix of fiber types adapted to different demands: Type I fibers, or slow-twitch oxidative fibers, rely on aerobic metabolism for sustained, low-power contractions and exhibit high fatigue resistance, making them ideal for endurance activities; in contrast, Type II fibers, or fast-twitch glycolytic fibers (including subtypes like IIa and IIx), generate rapid, high-force contractions using anaerobic pathways but fatigue more quickly, suiting explosive movements. The proportion of these fiber types varies by muscle and individual, influencing overall performance capabilities.^[4]^[4]^[45] Innervation occurs through motor units, defined as a single alpha motor neuron and all the skeletal muscle fibers it supplies, allowing graded force production by recruiting varying numbers of units; finer control in muscles like those in the eye involves small motor units with few fibers, while larger units in postural muscles like the quadriceps innervate hundreds. At the neuromuscular junction, the motor neuron terminal releases acetylcholine upon action potential arrival, binding to receptors on the muscle fiber's sarcolemma to depolarize the membrane and propagate the signal for contraction. This synaptic transmission ensures precise, voluntary activation without involuntary interference.^[4]^[46] Skeletal muscle demonstrates remarkable adaptability, undergoing hypertrophy—increased fiber size and protein synthesis—in response to resistance exercise, enhancing strength and volume; for instance, the quadriceps femoris muscle, responsible for knee extension during activities like standing or jumping, shows significant hypertrophy after targeted training regimens such as leg extensions. Comprising approximately 40% of total body mass in humans, skeletal muscle plays a critical role in metabolism and thermoregulation, with fatigue resistance differing markedly by fiber type—Type I fibers enduring prolonged activity through efficient oxygen use, while Type II fibers excel in short bursts but tire rapidly due to lactic acid buildup.^[47]^[48]

Cardiac Muscle

Cardiac muscle, also known as myocardium, forms the thick muscular walls of the heart's chambers and is essential for generating the rhythmic contractions that propel blood through the circulatory system. Unlike skeletal muscle, it operates involuntarily and exhibits autorhythmicity, meaning it can initiate its own contractions without external neural stimulation, primarily through specialized pacemaker cells located in the sinoatrial node. These pacemaker cells spontaneously depolarize, setting the heart's intrinsic rhythm at approximately 60-100 beats per minute in adults.^[37]^[49]^[50] Structurally, cardiac muscle fibers are short, branched, and striated, similar to skeletal muscle in their arrangement of sarcomeres but adapted for continuous activity. The fibers are interconnected end-to-end by intercalated discs, specialized junctions that include gap junctions for electrical coupling—allowing ions to pass rapidly between cells, thus enabling the heart to contract as a unified syncytium—and desmosomes for mechanical adhesion, which anchor actin filaments and maintain structural integrity during forceful contractions. Many cardiac myocytes are binucleated, a feature arising from incomplete cytokinesis during development, which supports their large size and high metabolic demands.^[51]^[52]^[53] Innervation of cardiac muscle is provided exclusively by the autonomic nervous system, with no somatic motor units as seen in skeletal muscle. Sympathetic nerves, via norepinephrine release, accelerate heart rate and enhance contractility by increasing calcium influx, while parasympathetic nerves, primarily through the vagus nerve and acetylcholine, slow the heart rate by hyperpolarizing pacemaker cells. This modulation fine-tunes the autorhythmic baseline without directly initiating contractions.^[54]^[55] Cardiac muscle is highly specialized for aerobic metabolism, with mitochondria comprising 30-40% of the cell volume to efficiently generate ATP for unrelenting activity. Transverse tubules (T-tubules) are positioned at the Z-lines rather than the A-I junction, and they are larger and less numerous than in skeletal muscle, facilitating synchronized calcium release across the fiber network. Contractions are myogenic, triggered intrinsically, and protected by a prolonged refractory period—lasting about 250 milliseconds—that prevents tetanus and ensures complete relaxation for ventricular filling during diastole.^[56]^[37]^[50]

Smooth Muscle

Smooth muscle is a type of involuntary muscle tissue found in the walls of hollow organs and structures throughout the body, including blood vessels, the digestive tract, airways, urinary bladder, and uterus, where it facilitates functions such as peristalsis for moving contents through the gastrointestinal tract and vasoregulation to control blood flow.^[57] Unlike skeletal muscle, smooth muscle operates without conscious control, enabling sustained contractions that maintain organ tone and support essential visceral processes.^[58] Structurally, smooth muscle cells are spindle-shaped and uninucleated, arranged in sheets or bundles with actin and myosin filaments oriented obliquely rather than in the striated sarcomere pattern of skeletal or cardiac muscle, resulting in a non-striated appearance under light microscopy.^[58] Instead of Z-lines, these cells feature dense bodies and intermediate filaments that anchor the contractile apparatus to the cell membrane and transmit force across the tissue.^[59] This organization allows for widespread force distribution, supporting the muscle's role in modulating the diameter of tubes and vessels.^[60] Smooth muscle is classified into two main types based on its functional organization and response to stimuli: single-unit and multi-unit. Single-unit smooth muscle, common in the digestive tract and uterus, consists of interconnected cells joined by gap junctions that enable electrical coupling and synchronized contractions as a functional syncytium, often triggered by spontaneous pacemaker activity or stretch.^[57] In contrast, multi-unit smooth muscle, found in structures like the iris of the eye, large arteries, and the ciliary muscle of the eye, features individual cells that contract independently due to discrete innervation, lacking extensive gap junctions and responding primarily to neural or hormonal signals.^[59] This distinction allows single-unit muscle to generate coordinated waves of contraction for propulsion, while multi-unit muscle provides precise, graded control.^[57] Innervation of smooth muscle is primarily provided by the autonomic nervous system, with sympathetic and parasympathetic fibers releasing neurotransmitters such as norepinephrine and acetylcholine to modulate contraction and relaxation, though smooth muscle can also respond directly to circulating hormones like epinephrine for broader regulation of tone.^[58] Hormonal influences, including those from the endocrine system, further integrate smooth muscle activity with systemic needs, such as adjusting vascular resistance during stress.^[57] A key characteristic of smooth muscle is its ability to maintain prolonged tension with minimal energy expenditure through the latch state, a mechanism where cross-bridges between actin and myosin remain attached after initial phosphorylation, allowing sustained contraction without continuous ATP hydrolysis or calcium influx.^[57] This feature makes smooth muscle highly fatigue-resistant and efficient for tonic activities, such as maintaining blood pressure or bladder fullness, with contractions that are slower in onset and speed compared to striated muscle but capable of lasting hours or days.^[58]

Physiology

Excitation-Contraction Coupling

Excitation-contraction coupling (ECC) refers to the physiological process that links the electrical excitation of a muscle cell membrane to the subsequent mechanical contraction of its myofibrils, primarily mediated by calcium ions (Ca²⁺) as a key signaling molecule across all muscle types.^[61] This coupling ensures rapid and coordinated responses to neural or hormonal stimuli, with variations tailored to the functional demands of skeletal, cardiac, and smooth muscles.^[61] In skeletal muscle, ECC is initiated by a neural trigger at the neuromuscular junction, where the neurotransmitter acetylcholine is released from the motor neuron axon terminal and binds to nicotinic receptors on the muscle fiber's sarcolemma, generating an end-plate potential that depolarizes the membrane and propagates an action potential.^[62] The action potential travels along the sarcolemma and invaginates into the fiber via transverse tubules (T-tubules), where it activates dihydropyridine receptors (DHPRs, or L-type Ca²⁺ channels) in the T-tubule membrane.^[62] These DHPRs form a direct physical linkage with ryanodine receptors (RyR1) on the sarcoplasmic reticulum (SR), the intracellular Ca²⁺ store, leading to conformational changes that open RyR1 channels and release stored Ca²⁺ into the cytosol without requiring extracellular Ca²⁺ influx—a process known as depolarization-induced Ca²⁺ release.^[62] The released Ca²⁺ binds to troponin C on the thin filaments, inducing a conformational change in the troponin-tropomyosin complex that shifts tropomyosin away from the myosin-binding sites on actin, thereby permitting cross-bridge formation and contraction initiation.^[62] This mechanism allows for tetanic contractions through rapid summation of action potentials, enabling sustained force generation in skeletal muscle.^[62] Cardiac muscle ECC shares structural similarities with skeletal muscle, including T-tubules and SR, but relies on a different trigger and amplification step suited to its involuntary, rhythmic nature.^[63] Action potentials originate in pacemaker cells of the sinoatrial node and propagate through gap junctions to cardiomyocytes, depolarizing the sarcolemma and opening L-type Ca²⁺ channels (DHPRs) to allow extracellular Ca²⁺ influx during the plateau phase.^[63] This influx acts as a trigger for Ca²⁺-induced Ca²⁺ release (CICR) via RyR2 channels on the SR, where small local releases termed "Ca²⁺ sparks" synchronize into global Ca²⁺ transients that propagate through the cell.^[63] The elevated cytosolic Ca²⁺ binds to troponin C, similar to skeletal muscle, causing a conformational change in the regulatory proteins to expose actin binding sites and initiate contraction.^[63] A key difference is the long refractory period of the cardiac action potential, which prevents summation of contractions and tetanus, ensuring alternating systole and diastole for effective pumping.^[63] In smooth muscle, ECC is more variable and often modulated by both neural and hormonal inputs, lacking the organized T-tubules and SR of striated muscles, with signal propagation relying on caveolae—small invaginations of the plasma membrane—and a less developed SR.^[64] Triggers include autonomic innervation via varicosities that release neurotransmitters like norepinephrine onto adrenergic receptors, or hormones such as angiotensin II binding to G-protein-coupled receptors, leading to membrane depolarization or direct intracellular signaling that opens voltage-gated or receptor-operated Ca²⁺ channels for influx, supplemented by Ca²⁺ release from the SR through inositol trisphosphate receptors (IP3R) or RyRs.^[64] The cytosolic Ca²⁺ binds to calmodulin, forming a Ca²⁺-calmodulin complex that activates myosin light chain kinase (MLCK), which phosphorylates the regulatory light chain of myosin II, inducing a conformational change that enables myosin to interact with actin and generate force.^[64] Unlike striated muscles, smooth muscle contractions are typically slower and can be tonic (sustained) without tetanus, reflecting its role in prolonged activities like vascular tone regulation.^[64]

Mechanisms of Contraction

The sliding filament model describes the fundamental mechanism of muscle contraction in striated muscles, where actin thin filaments slide past myosin thick filaments within the sarcomere, leading to its shortening and overall muscle contraction. This model, proposed by Huxley and Hanson in 1954 based on electron microscopy and X-ray diffraction studies of frog sartorius muscle, posits that the overlap between actin and myosin increases during contraction without changes in filament lengths. The process generates force through interactions between myosin heads and actin binding sites, shortening the sarcomere from a resting length of approximately 2.5 μm to as little as 1.6 μm.^[65] Central to this model is the cross-bridge cycle, a series of biochemical and mechanical steps powered by ATP hydrolysis that enables myosin heads to interact with actin. In the cycle, a myosin head in a high-energy state binds to an actin filament forming a cross-bridge, undergoes a power stroke that pulls the actin filament toward the sarcomere center, and then detaches upon ATP binding; without ATP, the muscle enters a rigor state with persistent cross-bridges, as observed in rigor mortis. This cycle, detailed by Huxley and Simmons in 1971 through quick-release experiments on frog muscle fibers, repeats rapidly, with each cross-bridge contributing to force generation and filament sliding. The biochemical sequence, elucidated by Lymn and Taylor in 1971 using in vitro assays, confirms that ATP hydrolysis occurs after detachment, resetting the myosin head for reattachment. Muscle contraction is tightly regulated to prevent constant activity. In striated muscles (skeletal and cardiac), calcium ions bind to troponin, inducing a conformational change that shifts tropomyosin away from actin's myosin-binding sites, allowing cross-bridge formation; this Ca²⁺-troponin-tropomyosin system was identified by Ebashi in the 1960s through extraction studies from rabbit skeletal muscle.^[66] In smooth muscle, regulation occurs primarily via phosphorylation of the regulatory light chain of myosin by Ca²⁺-calmodulin-dependent myosin light chain kinase (MLCK), enhancing myosin's ATPase activity and actin interaction; this mechanism was established by Adelstein and colleagues in the 1970s using purified turkey gizzard myosin.^[67] Force generation is modulated by the length-tension relationship, where maximal isometric tension occurs at optimal sarcomere lengths of 2.0-2.2 μm due to maximal actin-myosin overlap, as demonstrated by Gordon, Huxley, and Julian in 1966 through laser diffraction measurements on single frog muscle fibers.^[68] Beyond this range, tension decreases: below 2.0 μm due to double overlap of thin filaments, and above 3.6 μm due to no overlap. Contractions vary by type—isometric, where muscle tension increases without length change (e.g., holding a weight steady), and isotonic, where length changes under constant tension (concentric shortening or eccentric lengthening).^[69] The relationship between force and shortening velocity is hyperbolic, described by Hill's equation: (F + a)v = b(F_0 - F), where F is load, v is velocity, F_0 is maximal isometric force, and a and b are constants; derived by Hill in 1938 from heat and tension measurements in frog sartorius muscle, it reflects that force is proportional to the number of cross-bridges while velocity inversely relates to load. In skeletal muscle, a single action potential elicits a twitch—a brief contraction—while high-frequency stimulation causes summation leading to tetanus, a sustained maximal contraction due to incomplete relaxation between twitches. Cardiac muscle, however, exhibits no true tetanus because its prolonged refractory period (lasting nearly the full twitch duration) prevents summation of contractions, ensuring rhythmic beating without sustained fusion.^[70]

Energy Metabolism

The muscular system relies on adenosine triphosphate (ATP) as the primary energy currency for contraction, with production pathways varying by demand intensity and duration to match the needs of different muscle types.^[71] These pathways include immediate, anaerobic, and aerobic systems, ensuring efficient energy supply during rest, short bursts, or sustained activity.^[72] The phosphocreatine (PCr) shuttle provides the fastest ATP regeneration for immediate high-intensity demands, such as sprinting, by transferring a phosphate group from PCr to ADP via creatine kinase, yielding an equimolar amount of ATP but depleting stores within 5-10 seconds of maximal effort.^[73] This system buffers ATP levels without oxygen or metabolic byproducts, bridging the gap until other pathways activate.^[74] For moderate to intense efforts lasting up to a few minutes, anaerobic glycolysis dominates in oxygen-limited conditions, converting glucose or glycogen to pyruvate and then lactate, netting only 2 ATP per glucose molecule while producing lactate as a byproduct to regenerate NAD+ for continued flux.^[75] This pathway supports rapid energy needs in fast-twitch fibers but leads to acidosis and fatigue if prolonged.^[76] Aerobic metabolism, predominant during endurance activities, occurs in mitochondria through the Krebs cycle and electron transport chain, oxidizing substrates like glucose, fatty acids, or lactate to produce up to 36 ATP per glucose molecule—far more efficient than anaerobic glycolysis—while requiring oxygen delivery via blood.^[77] Fatty acids often serve as the main fuel in resting or low-intensity states, enhancing long-term sustainability.^[78] Muscle fiber types exhibit distinct metabolic profiles: Type I (slow oxidative) fibers, abundant in mitochondria and myoglobin, prioritize aerobic pathways for fatigue-resistant, low-power output suited to posture and endurance; Type II (fast glycolytic) fibers, with fewer mitochondria, favor anaerobic glycolysis for high-power, short-duration contractions but fatigue quickly due to lactate accumulation.^[4] Type IIa fibers blend both, offering intermediate oxidative capacity.^[79] Cardiac muscle, operating continuously, relies almost entirely on aerobic metabolism—over 95% of ATP from oxidative phosphorylation—using fatty acids as the primary substrate under normal conditions to meet its high, unrelenting energy demands.^[78] Glucose and lactate contribute during stress, but the heart's dense capillary network ensures efficient oxygen supply.^[74] After intense exercise, excess post-exercise oxygen consumption (EPOC), formerly termed oxygen debt, elevates metabolism to restore homeostasis: it clears accumulated lactate via hepatic gluconeogenesis or oxidation, replenishes PCr stores, and resaturates myoglobin and hemoglobin with oxygen.^[80] This recovery phase can last minutes to hours, depending on exercise severity.^[72] Myoglobin, a heme protein in skeletal and cardiac muscle cytoplasm, binds and stores oxygen for diffusion to mitochondria during contraction, desaturating at activity onset to maintain supply when blood flow lags.^[81] Concentrations are highest in oxidative fibers, buffering against transient hypoxia.^[82] Aerobic capacity is quantified by VO2 max, the maximum rate of oxygen uptake during exhaustive exercise, reflecting integrated muscle mitochondrial density, capillary supply, and cardiovascular output—typically 35-40 mL/kg/min in untrained adults and up to 80 mL/kg/min in athletes.^[83] Higher VO2 max correlates with superior endurance performance.^[84] Prolonged excessive anaerobic metabolism, as in overtraining or extreme exertion, risks rhabdomyolysis—a breakdown of muscle fibers releasing myoglobin and enzymes into blood, potentially causing renal failure—due to unchecked lactate buildup, ionic imbalances, and energy depletion.^[85] This underscores the need for balanced training to favor aerobic adaptations.^[86]

Functions

Movement and Locomotion

The muscular system enables movement and locomotion primarily through the coordinated actions of skeletal muscles, which generate force to produce motion at joints. Skeletal muscles operate in agonist-antagonist pairs, where the agonist muscle contracts to initiate a movement while the antagonist relaxes to allow it, ensuring smooth and controlled motion. For instance, the biceps brachii acts as the agonist to flex the elbow during arm bending, while the triceps brachii serves as the antagonist to extend it, preventing uncontrolled motion through reciprocal relaxation.^[87] Synergist muscles, such as the brachialis assisting the biceps, provide fine control and stability by supporting the primary action or countering unwanted movements at adjacent joints.^[88] In gait and locomotion, leg muscles drive the cyclic patterns of walking and running through phased contractions coordinated by the nervous system. During the walking cycle, the gluteus maximus and hamstrings extend the hip as the stance leg pushes off, while the quadriceps control knee flexion during swing, enabling forward propulsion.^[89] Reciprocal inhibition, mediated by spinal interneurons, ensures that contraction of one muscle group, such as the quadriceps during knee extension, inhibits its antagonist, the hamstrings, to facilitate efficient stride without opposition.^[90] In running, these patterns intensify, with faster recruitment of fast-twitch fibers in muscles like the gastrocnemius for explosive push-off, adapting the gait to higher speeds and impacts.^[91] Upper body muscles contribute to locomotion by maintaining balance and enabling manipulation. Arm swing during walking and running, driven by the deltoids and latissimus dorsi, counterbalances the rotational forces from leg motion, stabilizing the torso and conserving energy.^[92] In the hands, intrinsic muscles such as the interossei and lumbricals facilitate precise grip and object manipulation by adjusting finger positions and stabilizing joints during prehensile tasks, allowing for tasks like tool use while moving.^[93]^[94] Biomechanically, the body functions as a system of levers, with joints serving as fulcrums, bones as rigid levers, and muscles as force generators to amplify motion. Most human movements involve third-class levers, where the effort arm (muscle insertion to fulcrum) is shorter than the load arm, providing speed and range but requiring greater force, as seen in elbow flexion.^[95] In activities like jumping, the quadriceps generate peak forces of approximately 5 times body weight at the knee to propel the body upward, demonstrating the system's capacity for high power output through coordinated multi-joint action.^[96] Training induces adaptations in the muscular system that enhance force production for locomotion via increased motor unit recruitment and neural efficiency. Resistance and plyometric exercises improve the ability to recruit high-threshold motor units, boosting peak force in activities like sprinting.^[97] Sprinters develop greater fast-twitch fiber hypertrophy and power output for short bursts, while marathoners adapt with enhanced slow-twitch fiber endurance and mitochondrial density for sustained locomotion, illustrating activity-specific physiological changes.^[98] These adaptations draw on energy metabolism pathways for prolonged activity, such as aerobic processes supporting endurance running.^[97]

Posture and Stability

The muscular system plays a crucial role in maintaining posture and stability by counteracting gravitational forces through sustained muscle activation and reflexive adjustments. Antigravity muscles, such as the erector spinae along the spine, are essential for upholding upright posture by extending the vertebral column and resisting forward flexion. Core muscles, including the abdominals and obliques, contribute to trunk stability by providing a muscular corset that supports the spine and pelvis, enabling balanced weight distribution during static positions.^[99]^[100]^[101] Reflex mechanisms, particularly the stretch reflex, facilitate automatic postural corrections via muscle spindles, which detect changes in muscle length and trigger rapid contractions to restore equilibrium. For instance, the knee-jerk reflex demonstrates this process, where stretching the quadriceps activates spindles, leading to monosynaptic excitation of motor neurons and leg extension to prevent collapse. These reflexes ensure continuous fine-tuning of muscle tone, known as tonus, which involves low-level, asynchronous contractions in antigravity muscles during quiet standing.^[102]^[103] Balance integration relies on the interplay between vestibular inputs from the inner ear and proprioceptors in muscles and joints, which coordinate muscle responses in the neck and legs to maintain equilibrium. Vestibular signals modulate balance-correcting responses in muscles like the paraspinals and quadriceps, with proprioceptive feedback from trunk movements further refining activation patterns across different muscle groups. This sensory-motor integration allows for adaptive stability without conscious effort.^[104] Pathological conditions highlight the importance of muscular balance; for example, imbalance favoring back extensors, such as the erector spinae, over weak abdominal flexors can lead to increased lumbar lordosis, exaggerating the spinal curve and predisposing individuals to low back pain. Such imbalances disrupt postural alignment, illustrating how muscular weakness compromises overall stability.^[105] A key aspect of postural maintenance is the constant low-level contraction of skeletal muscles, which accounts for approximately 20% of resting energy expenditure, underscoring the energetic cost of stability. Furthermore, robust postural muscles enhance injury prevention by absorbing external forces and maintaining joint alignment, reducing strain on supporting structures during everyday activities.^[106]^[107]

Thermoregulation and Other Roles

The muscular system contributes to thermoregulation primarily through shivering thermogenesis in skeletal muscle, where rapid, involuntary contractions generate heat to counteract cold exposure and maintain core body temperature. This mechanism is the dominant source of heat production in cold-stressed adult humans, involving asynchronous activation of motor units to maximize efficiency without coordinated movement.^[108] Intense shivering can elevate metabolic heat output to 3-5 times basal levels, approximately 250-500 W, significantly above basal levels, by hydrolyzing ATP in muscle fibers primarily for thermal rather than mechanical purposes.^[108] Skeletal muscle also supports thermoregulation at rest through its substantial contribution to basal metabolism, accounting for 20-30% of total resting energy expenditure via low-level futile cycles, such as calcium pumping and substrate cycling, which dissipate energy as heat without net work.^[109] This ongoing metabolic activity underscores muscle's role as a key organ in whole-body energy homeostasis, independent of overt contraction.^[110] Non-shivering thermogenesis in skeletal muscle provides an additional, adaptive heat-generating pathway that parallels the uncoupling protein 1-mediated process in brown adipose tissue (BAT), allowing sustained thermoregulation without the fatigue of shivering.^[111] In this mechanism, muscle mitochondria uncouple oxidative phosphorylation to produce heat directly, enhancing energy expenditure during chronic cold exposure or metabolic stress, much like BAT's role in rodents and neonates.^[112] Exercise further amplifies this by inducing excess post-exercise oxygen consumption (EPOC), which boosts metabolic rate for hours afterward—up to 15% above baseline in moderate sessions—through elevated oxygen use for recovery processes like lactate clearance and ion homeostasis.^[80] Beyond thermoregulation, smooth muscle fulfills visceral support roles, such as maintaining vascular tone through sustained tonic contractions that regulate peripheral resistance and blood pressure.^[113] This contractile activity in arterial walls responds to neural and humoral signals, ensuring stable systemic circulation essential for oxygen delivery. Cardiac muscle, in turn, drives systemic circulation by rhythmically contracting to propel blood through the heart's chambers, enabling nutrient distribution and waste removal across all bodily functions.^[37] Other specialized muscular roles include control of continence via smooth and skeletal muscle sphincters; for instance, the urethral sphincter complex modulates urine outflow from the bladder, preventing involuntary leakage during pressure increases.^[114] In the eye, the ciliary muscle—a smooth muscle ring—enables visual focus by contracting to adjust the lens shape for accommodation on near objects.^[115] Laryngeal muscles, comprising both intrinsic and extrinsic groups, coordinate vocal fold adduction and tension for phonation, producing the vibrations necessary for speech and sound generation.^[116]

Development and Maintenance

Embryonic Development

Skeletal muscle arises primarily from the paraxial mesoderm, which segments into somites during early embryogenesis. The dermomyotome layer of each somite gives rise to myogenic progenitor cells that migrate to form the myotome, where they proliferate and differentiate into myoblasts. These myoblasts fuse to create multinucleated myofibers, establishing the basic structure of skeletal muscles; this process, known as primary myogenesis, begins around week 4 in human embryos and continues with secondary myogenesis to form additional fiber types.^[117] Cardiac muscle develops from the cardiogenic mesoderm, a region of the splanchnic lateral plate mesoderm located in the anterior embryo. Progenitor cells from the first heart field (FHF) form the initial linear heart tube by week 3–4, while the second heart field (SHF) contributes to outflow tract, right ventricle, and atrial septation through later addition of cells. These cardiomyocytes differentiate and interconnect via intercalated discs to enable synchronized contractions, with the process regulated by transcription factors like Nkx2.5 and Gata4.^[118] The embryonic development of smooth muscle tissue begins with progenitor cells derived from the lateral plate mesoderm, particularly the splanchnic layer, which gives rise to visceral smooth muscle in organs such as the gastrointestinal tract and blood vessels.^[119] Vascular smooth muscle cells (SMCs) exhibit multiple embryological origins, including contributions from the lateral plate mesoderm, neural crest cells for certain arterial segments, and secondary heart field progenitors, reflecting the diverse locations of smooth muscle in the body.^[120] Unlike skeletal muscle, smooth muscle does not arise from paraxial mesoderm somites but instead from these more lateral mesodermal populations, ensuring targeted formation in hollow organs and vasculature.^[121] The myogenesis of smooth muscle involves the direct differentiation of undifferentiated mesenchymal cells into contractile smooth muscle cells, bypassing the myoblast fusion characteristic of skeletal muscle formation. These mesenchymal progenitors, originating from the mesoderm, undergo proliferation and commitment to the smooth muscle lineage, maturing into spindle-shaped cells that express contractile proteins. Innervation occurs after initial tissue formation, with neural crest-derived nerves integrating into smooth muscle layers to enable autonomic control.^[119] In human embryos, this process commences early; for instance, primitive smooth muscle layers in the developing gut and major vessels appear by the end of the fourth week, with more defined differentiation by weeks 5–6 as organogenesis progresses.^[120] Genetic regulation of smooth muscle development is orchestrated by key transcription factors that promote lineage specification and patterning. Serum response factor (SRF), often in complex with myocardin, is essential for activating smooth muscle-specific genes like ACTA2 (encoding α-smooth muscle actin) and MYH11 (smooth muscle myosin heavy chain), driving differentiation from mesenchymal precursors.^[121] Hox genes contribute to regional patterning along the anterior-posterior axis, ensuring appropriate smooth muscle distribution in visceral structures, while signaling pathways such as TGF-β and Notch refine cell fate decisions during migration and assembly.^[122] Critical events include the migration of smooth muscle precursors into developing organ primordia, such as the foregut and limb buds, where they form concentric layers around epithelial structures. Disruptions in these processes can lead to congenital anomalies, including vascular malformations or agenesis of smooth muscle in hollow organs like the esophagus.^[120]

Growth, Repair, and Aging

Muscle growth, or hypertrophy, primarily occurs through resistance exercise, which activates satellite cells—Pax7-positive progenitor cells located between the basal lamina and sarcolemma of muscle fibers—to proliferate and fuse with existing myofibers, thereby increasing fiber cross-sectional area.^[123] This process enhances muscle protein synthesis and leads to net gains in muscle mass, with studies showing that mechanical loading from exercise stimulates satellite cell expansion and myonuclear addition, essential for sustained hypertrophy.^[124] Conversely, disuse atrophy results from prolonged inactivity, such as bed rest, causing a rapid loss of 1-2% of muscle mass per week due to reduced protein synthesis and increased proteolysis, particularly in antigravity muscles like the quadriceps.^[125] Muscle repair following injury involves a coordinated response where satellite cells activate, proliferate, and differentiate to fuse with damaged fibers, restoring structure and function; these Pax7+ cells are indispensable for efficient regeneration, as their ablation impairs recovery.^[126] Inflammation plays a critical role in this process, with macrophages infiltrating the injury site to clear necrotic debris through phagocytosis and secrete growth factors that promote satellite cell activation and myoblast fusion.^[127] M1 pro-inflammatory macrophages dominate early to resolve damage, transitioning to M2 anti-inflammatory phenotypes that support tissue remodeling and inhibit excessive fibrosis. Aging leads to sarcopenia, characterized by a progressive loss of 20-50% of skeletal muscle mass by the eighth decade of life, accompanied by diminished strength and function due to reduced regenerative capacity.^[128] This decline stems partly from satellite cell senescence, where aged progenitors exhibit impaired proliferation and self-renewal, exacerbated by chronic low-grade inflammation and altered niche signaling.^[129] Hormonal factors influence these processes; testosterone promotes muscle growth by enhancing protein synthesis and satellite cell activity in young adults, while declining levels contribute to age-related atrophy.^[130] Similarly, insulin-like growth factor-1 (IGF-1) supports repair by stimulating myoblast proliferation and differentiation, countering degeneration in damaged muscle.^[131] Nutrition, particularly adequate protein intake (1.2-1.6 g/kg body weight daily), boosts muscle protein synthesis rates, aiding both growth and maintenance across the lifespan.^[132] Emerging stem cell therapies, leveraging engineered myogenic progenitors, show promise for enhancing repair in degenerative conditions like Duchenne muscular dystrophy (DMD), with phase 1/2 trials as of 2025 demonstrating improved dystrophin expression and muscle function without severe adverse events.^[133] Resistance training effectively mitigates sarcopenia by increasing muscle mass and strength in older adults, activating satellite cells and countering atrophy through progressive overload protocols.^[134]

Clinical Significance

Major Disorders

The muscular system is affected by a range of disorders that compromise muscle structure, function, and energy production, leading to symptoms such as weakness, pain, and reduced mobility. These include genetic conditions like muscular dystrophies, autoimmune inflammatory myopathies, metabolic defects impairing energy metabolism, and other acquired or age-related pathologies. While some are inherited and progressive from childhood, others arise later in life or from external triggers, with varying prevalence influenced by genetics and demographics.^[135] Muscular dystrophies represent a primary genetic category, characterized by progressive degeneration due to defects in muscle membrane proteins. Duchenne muscular dystrophy (DMD) arises from mutations in the DMD gene on the X chromosome, resulting in absent dystrophin protein, which stabilizes muscle fibers during contraction; this X-linked recessive disorder typically manifests in boys during early childhood with proximal muscle weakness and pseudohypertrophy. Its incidence is approximately 1 in 3,500 to 5,000 male live births.^[136]^[135] Becker muscular dystrophy (BMD), a milder allelic variant, involves in-frame mutations producing truncated but partially functional dystrophin, leading to later onset and slower progression of similar symptoms.^[137] Limb-girdle muscular dystrophies (LGMD) comprise diverse autosomal forms caused by mutations in genes encoding sarcoglycans or other membrane-associated proteins, primarily affecting shoulder and hip girdle muscles; their collective prevalence is estimated at 1 in 14,500 to 123,000 individuals.^[138]^[135] Inflammatory myopathies involve immune-mediated muscle damage, often with systemic features. Polymyositis and dermatomyositis are autoimmune conditions driven by T-cell infiltration and cytokine release targeting muscle fibers, causing symmetric proximal weakness; dermatomyositis uniquely includes characteristic skin rashes such as heliotrope eyelids.^[139] Inclusion body myositis, predominantly affecting individuals over age 50, features vacuolar degeneration with amyloid-like inclusions and rimmed vacuoles in muscle biopsies, alongside chronic inflammation, making it the most common myopathy in older adults and often refractory to immunosuppression.^[139]^[140] Metabolic myopathies disrupt muscle energy pathways, typically unmasking symptoms during physical exertion. McArdle disease (glycogen storage disease type V) stems from autosomal recessive mutations in the PYGM gene, abolishing muscle glycogen phosphorylase and preventing glycogenolysis, which manifests as exercise-induced cramps, fatigue, and myoglobinuria without fixed weakness.^[141] Mitochondrial myopathies, caused by mutations in mitochondrial or nuclear DNA affecting oxidative phosphorylation, impair ATP production in muscle, resulting in proximal weakness, ptosis, and lactic acidosis exacerbated by endurance activities.^[142] Other notable disorders include autoimmune and traumatic conditions impacting neuromuscular transmission or muscle integrity. Myasthenia gravis is an autoimmune disease where antibodies against acetylcholine receptors at the neuromuscular junction block neurotransmission, producing fatigable weakness in ocular, bulbar, and limb muscles that worsens with repetitive use.^[143] Rhabdomyolysis entails acute skeletal muscle necrosis, often triggered by trauma, extreme exertion, or ischemia, releasing myoglobin, potassium, and creatine kinase into circulation, which can precipitate renal failure if severe.^[144] Sarcopenia, a universal age-related process involving progressive loss of muscle mass (approximately 1-2% annually after age 50) and strength due to hormonal, nutritional, and denervation factors, contributes to frailty and falls, with prevalence rising to 10-50% in those over 80 years.^[145] Recent therapeutic progress includes the 2023 FDA accelerated approval of Elevidys (delandistrogene moxeparvovec), an AAV-based gene therapy delivering a micro-dystrophin transgene, which was expanded in 2024 for patients aged 4 years and older with confirmed DMD mutations (excluding those with exon 8 and/or 9 deletions), regardless of ambulatory status, marking the first such intervention for this disorder.^[146]^[147]

Diagnosis and Management

Diagnosis of muscular system disorders typically involves a combination of clinical evaluation and specialized tests to assess muscle function, structure, and underlying genetic causes. Electromyography (EMG) is a key diagnostic tool that measures the electrical activity of muscles and nerves, helping to differentiate myopathic from neurogenic disorders by detecting abnormal patterns during rest and contraction.^[148] Muscle biopsy provides histological analysis, revealing characteristic changes such as dystrophic features, fiber necrosis, or inflammatory infiltrates in conditions like muscular dystrophies.^[149] Magnetic resonance imaging (MRI) of muscles is used to identify patterns of involvement, inflammation, or fatty replacement, aiding in the localization of affected areas and guiding biopsy sites.^[150] Genetic testing, including next-generation sequencing (NGS), is essential for confirming mutations, such as those in the dystrophin gene for Duchenne muscular dystrophy (DMD).^[149] Blood tests serve as initial screening tools for muscle damage and autoimmune involvement. Elevated serum creatine kinase (CK) levels are a hallmark of muscle injury in dystrophies, reflecting breakdown of muscle fibers and often correlating with disease severity.^[151] In inflammatory myopathies like myositis, autoantibodies such as anti-Jo-1 or anti-Mi-2 are detected, supporting diagnosis and monitoring response to therapy.^[152] Management of muscular disorders emphasizes slowing progression, maintaining function, and addressing complications through pharmacological, rehabilitative, and supportive strategies. Corticosteroids, such as prednisone, are standard for reducing inflammation and preserving muscle strength in conditions like DMD and myositis, with daily regimens shown to delay loss of ambulation.^[148] Eteplirsen, an antisense oligonucleotide, is approved for DMD patients with exon 51 mutations amenable to skipping, administered weekly via intravenous infusion to promote dystrophin production and attenuate respiratory decline.^[153] Physical therapy plays a crucial role in optimizing mobility, preventing contractures through stretching, and enhancing endurance via low-impact exercises tailored to the patient's capacity.^[154] Emerging therapies aim to address genetic roots of disorders like DMD. As of 2025, CRISPR-Cas9 gene editing trials, including the MUSCLE trial for HG302 initiated in December 2024 by HuidaGene Therapeutics and exploratory studies like CRD-TMH-001 by Cure Rare Disease, target dystrophin mutations by correcting the DMD gene in patient cells, with preclinical and early-phase studies demonstrating restored protein expression in animal models.^[155]^[156] Stem cell-based approaches, including myoblast transplantation, are under investigation to regenerate muscle tissue, though challenges like immune rejection persist in clinical trials.^[157] Supportive care integrates multidisciplinary interventions to improve quality of life. Orthotics, such as ankle-foot braces, stabilize gait and reduce fall risk in ambulatory patients with progressive weakness.^[158] Noninvasive ventilation supports respiratory function in advanced stages, extending survival by managing nocturnal hypoventilation.^[159] Comprehensive multidisciplinary teams, involving neurologists, pulmonologists, and therapists, coordinate holistic management to optimize outcomes across physical, cardiac, and nutritional domains.^[160] Prognosis for muscular disorders varies by type and access to care; in DMD, modern interventions like corticosteroids and ventilation have extended median survival to around 30 years.^[161] For age-related sarcopenia, preventive resistance exercise programs effectively mitigate muscle loss by enhancing strength and function in older adults.^[162]

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Biochemistry, Glycolysis - StatPearls - NCBI Bookshelf - NIH
Anaerobic respiration results in the production of 2 ATP molecules.[5] Glucose is a hexose sugar, meaning it is a monosaccharide with six carbon atoms and six ...
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Jul 31, 2023 · In poorly oxygenated tissue, glycolysis produces 2 ATP by shunting pyruvate away from mitochondria and through the lactate dehydrogenase ...
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Misconceptions about Aerobic and Anaerobic Energy Expenditure
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Cardiac Metabolism and Its Interactions with Contraction, Growth ...
The heart is capable of utilizing all classes of energy substrates, including carbohydrates, lipids, amino acids and ketone bodies, for ATP production in the ...
[79]
Skeletal muscle fiber type: using insights from ... - PubMed Central
Skeletal muscle fibers are classified as slow-twitch (type 1) and fast-twitch (type 2), with fast-twitch further divided into 2A, 2X, and 2B subtypes.Missing: fatigue | Show results with:fatigue
[80]
Effect of exercise intensity, duration and mode on post ... - PubMed
In the recovery period after exercise there is an increase in oxygen uptake termed the 'excess post-exercise oxygen consumption' (EPOC), consisting of a ...
[81]
Biochemistry, Myoglobin - StatPearls - NCBI Bookshelf - NIH
Myoglobin facilitates oxygen diffusion. Myoglobin desaturates at the onset of muscle activity, which increases oxygen's diffusion gradient from the capillaries ...
[82]
Myoglobin and Mitochondria: A relationship bound by Oxygen and ...
Oxygen storage. The most accepted function of myoglobin is that of a temporary store of oxygen. Studies of working skeletal muscle show that upon the onset of ...
[83]
V̇O2max and Aerobic Fitness - Sports Medicine - UC Davis Health
VO 2 max, the maximum rate of oxygen consumption measured during incremental exercise, is the gold standard measure of aerobic fitness.
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AEROBIC CAPACITY AS AN INDICATOR IN DIFFERENT KINDS OF ...
Maximal oxygen uptake (VO2 max) refers to the intensity of aerobic processes, and actually represents the capacity of the organism to utilize at a certain ...
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Exercise-induced rhabdomyolysis mechanisms and prevention - NIH
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Muscle agonist–antagonist interactions in an experimental joint model
Contractions of agonist and antagonist muscle groups generate movement around a limb joint, and during any movement, the muscle antagonists change their ...
[88]
Physiology of Stretching - Flexibility - MIT
When an agonist contracts, in order to cause the desired motion, it usually forces the antagonists to relax (see section Cooperating Muscle Groups). This ...
[89]
Spinal Control of Locomotion: Individual Neurons, Their Circuits and ...
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[90]
Spinal reciprocal inhibition in human locomotion
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[91]
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Jul 26, 2025 · The skeletal muscles of the hand enable movement of the hand and fingers. These muscles are categorized into extrinsic and intrinsic groups.
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Nov 27, 2001 · Many of the hand's intrinsic muscles attach to the extensor mechanism. Activity in any of these muscles produces force that the extensor ...
[95]
Biomechanics of human movement and its clinical applications
Human movement is achieved by a complex and highly coordinated mechanical interaction between bones, muscles, ligaments and joints within the musculoskeletal ...
[96]
Hip and knee joint loading during vertical jumping and push jerking
The hip experienced a mean peak loading of 5.5-8.4 × body weight and the ankle 8.9-10.0 × body weight. Interpretation. The magnitudes of the total (resultant) ...
[97]
Adaptations to Endurance and Strength Training - PubMed Central
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[98]
Fast-Twitch Vs. Slow-Twitch Muscle Fiber Types + Training Tips
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[100]
The role of the antigravity musculature during quiet standing in man
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The Impact Of Core Stability Exercises On Standing , Functional ...
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Spinal Reflexes and Descending Motor Pathways (Section 3 ...
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An imbalance in trunk muscle strength can influence significantly lordotic curve of lumbar spine and might be one risk factor for potential low back pain.
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Resting Energy Expenditure - an overview | ScienceDirect Topics
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The Role of Neuromuscular Control of Postural and Core Stability in ...
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Shivering thermogenesis in humans: Origin, contribution and ...
This review focuses primarily on the most important contributor of heat production in cold-exposed adult humans, shivering skeletal muscles.
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Skeletal muscle metabolism is a major determinant of resting energy ...
These findings suggest that differences in resting muscle metabolism account for part of the variance in metabolic rate among individuals.
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Skeletal Muscle Thermogenesis and Its Role in Whole Body Energy ...
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[112]
Muscle Non-shivering Thermogenesis and Its Role in the Evolution ...
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[113]
The crosstalk between BAT thermogenesis and skeletal muscle ...
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[114]
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[115]
Anatomy, Abdomen and Pelvis, Sphincter Urethrae - StatPearls - NCBI
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[116]
Anatomy, Head and Neck: Eye Muscles - StatPearls - NCBI Bookshelf
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Anatomy, Head and Neck: Laryngeal Muscles - StatPearls - NCBI
The laryngeal muscles are critical to voice production, breathing, and airway protection during swallowing. These muscles are categorized into intrinsic and ...Introduction · Structure and Function · Muscles · Physiologic Variants
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[121]
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Satellite cell dynamics during skeletal muscle hypertrophy
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One Week of Bed Rest Leads to Substantial Muscle Atrophy and ...
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[125]
An absolute requirement for Pax7-positive satellite cells in acute ...
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The Many Roles of Macrophages in Skeletal Muscle Injury and Repair
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The age-related loss of skeletal muscle mass and function - NIH
Longitudinal studies show that in people aged ∼75 y, muscle mass is lost at a rate of 0.64–0.7%/y in women and 0.8–0.98%/y in men (Mitchell et al., 2012).
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This review discusses data pertaining to the satellite cell responses and function in aging skeletal muscle, and the impact that three compounds: resveratrol, ...
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The therapeutic potential of IGF-I in skeletal muscle repair - PMC
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[131]
Nutrition and muscle protein synthesis: a descriptive review - PMC
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Stem/progenitor cell-based therapy for Duchenne muscular dystrophy
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Muscular Dystrophy - StatPearls - NCBI Bookshelf - NIH
Feb 26, 2024 · Mutations in the caveolin-3 gene cause autosomal dominant limb-girdle muscular dystrophy. ... Genetic epidemiology of Duchenne and Becker muscular ...
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Duchenne Muscular Dystrophy - StatPearls - NCBI Bookshelf
As DMD is inherited in an X-linked recessive manner, boys are more frequently affected than girls. The estimated incidence is 1 in 3600 male live-born infants.
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Becker Muscular Dystrophy - StatPearls - NCBI Bookshelf
Jan 30, 2024 · Becker muscular dystrophy (BMD) is an X-linked recessive disorder involving dystrophin gene mutation, resulting in progressive muscle degeneration.
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The Limb–Girdle Muscular Dystrophies: Is Treatment on the Horizon?
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Dermatomyositis, Polymyositis and Inclusion Body Myositis - NCBI
Dermatomyositis (DM), polymyositis (PM) and inclusion body myositis (IBM) belong to the heterogeneous group of the inflammatory myopathies and are ...Introduction · Clinical Aspects · Histopathology · Immunopathogenesis
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[142]
Myasthenia Gravis - StatPearls - NCBI Bookshelf - NIH
Myasthenia gravis is an autoimmune disorder affecting the neuromuscular junction. It manifests as a generalized muscle weakness which can involve the ...
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Rhabdomyolysis - StatPearls - NCBI Bookshelf - NIH
Rhabdomyolysis is a clinical syndrome characterized by skeletal muscle breakdown and the release of intracellular components such as myoglobin, creatine ...Continuing Education Activity · Pathophysiology · History and Physical · Evaluation
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Sarcopenia: Definition, Epidemiology, and Pathophysiology - PMC
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[145]
FDA Approves First Gene Therapy for Treatment of Certain Patients ...
Jun 22, 2023 · FDA Approves Elevidys, a gene therapy for the treatment of pediatric patients 4 through 5 years of age with Duchenne muscular dystrophy ...Missing: delandistrogene moxeparvovec
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Neuromuscular imaging in inherited muscle diseases - PMC
MRI is frequently used to describe muscle involvement patterns, which aids in narrowing of the differential diagnosis and distinguishing between dystrophic and ...
[149]
Biomarkers in Inflammatory Myopathies—An Expanded Definition
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Autoantibodies in Myositis. How to Achieve a Comprehensive ... - NIH
Antibody levels correlate with creatine kinase levels and strength in anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase-associated autoimmune myopathy.
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Eteplirsen Treatment for Duchenne Muscular Dystrophy
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What are the treatments for muscular dystrophy (MD)? | NICHD
Nov 9, 2020 · Studies show that daily treatment with prednisone can increase muscle strength and respiratory function and slow the progression of weakness in ...
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Gene Editing for Duchenne Muscular Dystrophy - PubMed Central
Apr 12, 2025 · The CRISPR system has emerged as a ground-breaking gene-editing tool, offering promising therapeutic potential for Duchenne muscular dystrophy (DMD).
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Cell therapy for Duchenne muscular dystrophy - NIH
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[155]
Development and Economic Evaluation of a Patient-Centered Care ...
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Diagnosis and management of Duchenne muscular dystrophy, part 2
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Developing multidisciplinary clinics for neuromuscular care and ...
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Prognostic indicators of disease progression in Duchenne muscular ...
The median life expectancy at birth is around 30 years [12]. At present, there is no cure for DMD, and standard of care is mainly aimed at managing disease ...
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Nevertheless, aerobic, resistance, and combined exercise training regimes have been shown to produce the most beneficial preventive and therapeutic effects.