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Physiology, Muscle

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Last Update: May 1, 2023.

Introduction

There are three major muscle types found 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 primarily controls movement and posture. Cardiac muscle encompasses the heart, which keeps the human body alive. Smooth muscle is present throughout the gastrointestinal, reproductive, urinary, vascular, and respiratory systems.

Cellular Level

Skeletal muscle constitutes approximately 40% of the total human body weight. Its composition is many individual fibers bundled together into a muscle spindle; this 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 two major classifications of skeletal muscle: 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 their specific function.[1]

The 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] The 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; however, they are arranged in sheets rather than spindles which give this type of muscle a smooth appearance. These cells are present in the walls of many organs such as the lungs, gastrointestinal tract, reproductive organs, blood vessels, and even in the skin.[4]

Function

Whether it is skeletal, cardiac, or smooth, the muscles in the human body function to create force and movement. Skeletal muscles 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 for shortening and propelling 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 subsequently activates ryanodine receptors in the sarcoplasmic reticulum to release even more calcium. Higher quantities of calcium can then bind to the protein troponin that is located on the actin filaments. The calcium-troponin complex displaces the protein tropomyosin from the active site of the actin filament and allows for myosin binding and muscle contraction. Adenosine triphosphate (ATP) is needed to detach myosin from the actin filaments and allow for muscle relaxation.[1]

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

Smooth muscle contraction is not under voluntary control and is done through the 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 that activates the myosin light chain (MLC) kinase to phosphorylate and form cross-bridges between myosin and actin, leading to muscle 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 the normal anatomy and physiology of skeletal muscle cells. The complete or partial absence of the dystrophin protein is the pathologic 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. The 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, making it the highest incidence among the types of 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 results from a reduction of muscle size and 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 the loss of muscle power and immobility issues such as falls, commonly seen in aging populations.[1]

Smooth muscle cells line the entirety of the human vascular system. They exhibit plasticity in response to vascular injury. It is this plasticity that has implications in the disease process of atherosclerosis. Mature smooth muscle cells are involved in the contraction and tone of the vascular system. Cholesterol load demonstrably increases 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 result; 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 the 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]

Review Questions

References

1.
Frontera WR, Ochala J. Skeletal muscle: a brief review of structure and function. Calcif Tissue Int. 2015 Mar;96(3):183-95. [PubMed: 25294644]
2.
Roth GM, Bader DM, Pfaltzgraff ER. Isolation and physiological analysis of mouse cardiomyocytes. J Vis Exp. 2014 Sep 07;(91):e51109. [PMC free article: PMC4828048] [PubMed: 25225886]
3.
Burkhard S, van Eif V, Garric L, Christoffels VM, Bakkers J. On the Evolution of the Cardiac Pacemaker. J Cardiovasc Dev Dis. 2017 Apr 27;4(2) [PMC free article: PMC5715705] [PubMed: 29367536]
4.
Webb RC. Smooth muscle contraction and relaxation. Adv Physiol Educ. 2003 Dec;27(1-4):201-6. [PubMed: 14627618]
5.
Sevrieva I, Knowles AC, Kampourakis T, Sun YB. Regulatory domain of troponin moves dynamically during activation of cardiac muscle. J Mol Cell Cardiol. 2014 Oct;75:181-7. [PMC free article: PMC4169182] [PubMed: 25101951]
6.
Shieh PB. Muscular dystrophies and other genetic myopathies. Neurol Clin. 2013 Nov;31(4):1009-29. [PubMed: 24176421]
7.
Chistiakov DA, Orekhov AN, Bobryshev YV. Vascular smooth muscle cell in atherosclerosis. Acta Physiol (Oxf). 2015 May;214(1):33-50. [PubMed: 25677529]
8.
Robinson P, Liu X, Sparrow A, Patel S, Zhang YH, Casadei B, Watkins H, Redwood C. Hypertrophic cardiomyopathy mutations increase myofilament Ca2+ buffering, alter intracellular Ca2+ handling, and stimulate Ca2+-dependent signaling. J Biol Chem. 2018 Jul 06;293(27):10487-10499. [PMC free article: PMC6036197] [PubMed: 29760186]

Disclosure: Rachel Noto declares no relevant financial relationships with ineligible companies.

Disclosure: Logan Leavitt declares no relevant financial relationships with ineligible companies.

Disclosure: Mary Ann Edens declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK532258PMID: 30335291

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