Physiology, Muscle

Article Author:
Rachel Noto
Article Editor:
Mary Ann Edens
Updated:
10/27/2018 12:31:44 PM
PubMed Link:
Physiology, Muscle

Introduction

There are 3 major muscle types in the human body: skeletal, cardiac, and smooth muscle. Each muscle type has unique cellular components, physiology, specific functions, and pathology. Skeletal muscle is an organ that controls movement and posture. Cardiac muscle encompasses the heart, which keeps the human body alive. Smooth muscle is located throughout the gastrointestinal, reproductive, urinary, vascular, and respiratory systems.

Cellular

Skeletal muscle constitutes approximately 40% of the total human body weight. It is comprised of many individual fibers that are bundled together into a muscle spindle; this is what gives the skeletal muscle a striated appearance. A single muscle fiber is composed mostly of actin and myosin fibers covered by a cell membrane (sarcolemma). These fibers are the functional unit of the organ, leading to contraction and relaxation. There are 2 major classifications of skeletal muscle; these include Type I (slow oxidative) and Type II (fast twitch). The vast diversity in the makeup of skeletal muscle leads to variations in speed and length of contractions in different muscle groups depending on specific function.[1]

Cardiac muscle or myocardium is an involuntary, striated muscle that encloses the chambers of the heart. It is comprised of individual cardiomyocytes, which are similar in structure to skeletal muscle. Each cardiomyocyte contains cytoskeletal and contractile elements, all of which are connected through intercalated discs. These are highly adherent complexes, which allow the cardiac muscle cells to receive rapid electrical transmission and contract as a single unit.[2] Cardiac muscle also contains specialized cardiac pacemaker cells that lie within the myocardium. These cells allow for cardiac tissue to depolarize without external stimuli intrinsically.[3]

The cells of smooth muscle are also composed of actin and myosin fibers, but they are arranged in sheets rather than spindles to give the muscle a smooth appearance. These cells are contained in the walls of many organs such as the lungs, gastrointestinal tract, reproductive organs, blood vessels, and even in the skin.[4]

Function

Muscle in the human body, whether it is skeletal, cardiac or smooth, functions to create force and movement. Muscles of the skeleton support the bones to maintain posture as well as control voluntary movement. Skeletal muscle also contributes to energy metabolism and storage. Cardiac muscle propels blood and leads to proper oxygenation and maintenance of each cell that comprises the human body. Smooth muscle is located throughout the body and uses contractile force to shorten and propel various contents across the lumen of the multiple organ systems in which it is involved.

Mechanism

Action potentials from nerve fibers of the central nervous system depolarize muscle down the length of the sarcolemma to the innermost fibers through a transverse tubule (T tubule) system. The action potential responds with a dihydropyridine receptor on the T tubule; this acts as a voltage sensor allowing for calcium to be released. Calcium then activates ryanodine receptors in the sarcoplasmic reticulum to release even more calcium. Higher quantities of calcium can then bind to the protein troponin located on the actin fibers. The calcium-troponin complex displaces the protein tropomyosin from the active site of the actin filament and allows for myosin binding and muscle contraction. ATP is needed to detach myosin from actin and allow for relaxation.[1]

Similarly to skeletal muscle, cardiac muscle is triggered by calcium binding to troponin in the actin filaments of the cardiomyocyte. This then removes tropomyosin and allows for the binding of myosin to actin and eventual contraction. The significant difference between cardiac and skeletal muscle is in cardiomyocytes automaticity. Specialized cardiac pacemaker cells located in the sinoatrial (SA) node are responsible for creating cardiac muscle contraction. These act to trigger action potentials which allow for sodium and potassium influx as well as calcium release from the sarcoplasmic reticulum. The cardiac muscle can then contract as a single unit.[5]

Smooth muscle contraction is not under voluntary control and is done so through autonomic regulation of a calcium-calmodulin interaction. Contraction begins through a change in action potential or activation of mechanical stretch receptors in the plasma membrane. Intracellular calcium is increased and combines with the protein calmodulin. It is this complex which activates the myosin light chain (MLC) kinase to phosphorylate and form cross-bridges between myosin and actin, leading to contraction. Some smooth muscle maintains tone, which is caused by a constant phosphorylation level in the absence of external potentials. A decrease in intracellular calcium levels induces relaxation.[4]

Clinical Significance

Muscular dystrophy is a progressive genetic myopathy, which leads to degeneration of normal anatomy and physiology of skeletal muscle cells. The complete or partial absence of the dystrophin protein is the mechanism of both Becker and Duchenne muscular dystrophy. Dystrophin is a protein that is associated with the filaments of skeletal muscle. Dystrophin provides structure and support to the sarcolemma of the monofilament. Lack of dystrophin protein leads to damage in the supporting sarcolemma, weakness and eventual atrophy of healthy muscle fibers. Duchenne muscular dystrophy affects up to 1 in 3600 boys, which makes it the highest incidence upon the muscular dystrophies. Many with Duchenne have a low life expectancy because there is currently no treatment available. Management of these disorders is purely supportive. The most common cause of death in these individuals is cardiorespiratory failure.[6]

 Sarcopenia is the loss of muscle mass and atrophy that is associated with aging. It has been attributed to a reduction of muscle size as well as a reduction in satellite cells, mitochondrial numbers, and elasticity. Sarcopenia is seen in increasing numbers with advancing age but is not universal. Sarcopenia varies in degree of physical activity, gender, and race. It can attribute to loss of muscle power and immobility issues such as falls, commonly seen in aging populations.[1]

Smooth muscle cells can be found lining the entirety of the human vascular system. They have been shown to exhibit plasticity in response to vascular injury. It is this plasticity that has been implicated in the disease process of atherosclerosis. Mature smooth muscle cells are involved in contraction and tone in the vascular system. Cholesterol load has been shown to increase stress on endothelial cells, leading to vascular injury. This damage changes the vascular smooth muscle from the inactive contractile state to the pro-inflammatory response state. Smooth muscle cell proliferation and remodeling then results, this leads to the fibrous capsule formation seen in atherosclerosis.[7]

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder caused by genetic variants that code for a portion of the contractile element of the cardiomyocyte. These mutations allow for heightened myofilament calcium sensitivity, thickening of the interventricular septum and eventual obstruction of blood flow. Although commonly asymptomatic, symptoms of obstruction can result in chest pain during exertion, tachycardia with shortness of breath, syncope, and sudden cardiac death. HOCM is the most commonly inherited cardiac disorder with a prevalence of 1 in 500. It is the leading cause of sudden death in young individuals and currently has no cure.[8]


References

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[2] Roth GM,Bader DM,Pfaltzgraff ER, Isolation and physiological analysis of mouse cardiomyocytes. Journal of visualized experiments : JoVE. 2014 Sep 7     [PubMed PMID: 25225886]
[3] Burkhard S,van Eif V,Garric L,Christoffels VM,Bakkers J, On the Evolution of the Cardiac Pacemaker. Journal of cardiovascular development and disease. 2017 Apr 27     [PubMed PMID: 29367536]
[4] Webb RC, Smooth muscle contraction and relaxation. Advances in physiology education. 2003 Dec     [PubMed PMID: 14627618]
[5] Sevrieva I,Knowles AC,Kampourakis T,Sun YB, Regulatory domain of troponin moves dynamically during activation of cardiac muscle. Journal of molecular and cellular cardiology. 2014 Oct     [PubMed PMID: 25101951]
[6] Shieh PB, Muscular dystrophies and other genetic myopathies. Neurologic clinics. 2013 Nov     [PubMed PMID: 24176421]
[7] Chistiakov DA,Orekhov AN,Bobryshev YV, Vascular smooth muscle cell in atherosclerosis. Acta physiologica (Oxford, England). 2015 May     [PubMed PMID: 25677529]
[8] Robinson P,Liu X,Sparrow A,Patel S,Zhang YH,Casadei B,Watkins H,Redwood C, Hypertrophic cardiomyopathy mutations increase myofilament Ca{sup}2 {/sup} buffering, alter intracellular Ca{sup}2 {/sup} handling, and stimulate Ca{sup}2 {/sup}-dependent signaling. The Journal of biological chemistry. 2018 Jul 6     [PubMed PMID: 29760186]