Skeletal Muscles

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Skeletal muscles


Skeletal muscles have transverse striations and are under conscious or voluntary control by the somatic nervous system .



Skeletal muscles are often attached to bone, although this is not always the case. Tendons are a common means of attaching skeletal muscle to bone; they are composed of collagen, a structurally strong yet flexible substance. A muscle's origin is the end that moves least on contraction; the other end is referred to as the insertion. There is a large range of muscle sizes, types, and functions. Most human muscles have muscle fibers arranged parallel to a tendon. A unipinnate muscle, however, has all of its muscle fibers inserted at an angle into one side of a tendon.


Skeletal muscles are made up of bundles (called fascicles) of individual muscle fibers lined with connective tissue. Each muscle fiber is a giant multinucleated cell, formed by the fusion of myoblasts (muscle cell precursors) during development. Muscle fibers contain approximately one thousand myofibrils, tubular organelles that appear striated under a microscope ; each myofibril is surrounded by a system of vesicles called the sarcoplasmic reticulum. The striations are due to alternating bands of light and dark regions called bands. The light regions are called I-bands, while the dark regions are called A-bands. A dividing line that runs through the A-band is called the Z-line, and the region between successive Z-lines is called the sarcomere.

The sarcomere is the functional unit of skeletal muscle and is associated with muscle contraction . It is composed primarily of two different contractile proteins : actin (or thin filaments) and myosin (or thick filaments). The filaments are arranged in an organized array so that their overlapping pattern produces the striations visible from under a microscope. The light I-bands are formed by actin filaments that are rooted at the Z-line, while the dark A-bands are composed of myosin filaments that overlap the actin filaments to varying degrees based on the extent of muscle contraction. The region in which there is no overlap (i.e., groups of actin filaments) in the center part of the A-band is called the H-band.



In a resting muscle, opposing actin filaments overlap myosin filaments only partially, resulting in the characteristic H-band. When a muscle contracts, however, the opposing actin filaments slide along the myosin filaments and are pushed together so that the H-bands (and I-bands) become narrower, while the A-bands remain the same length. The result is that the Z-lines come closer together without the actual length of the filaments changing. This mode of action is called the sliding filament mechanism.

The sliding filament mechanism is regulated by the binding of adenoside triphosphate (ATP) to myosin. ATP is a molecule present in all living cells that acts as an energy source. When ATP is not bound to myosin, projections along the myosin filaments called heads remain tightly bound to actin and therefore no sliding takes place (and subsequently, no muscle contraction). When ATP binds to myosin, however, a series of steps causes the myosin head to temporarily dissociate and change its conformation so that the actin and myosin filaments move relative to one another. This process, actively repeated in the many sarcomeres in a muscle fiber, results in muscle contraction.

Muscle contraction is also regulated by the calcium ion. A nerve impulse results in calcium being released from the sarcoplasmic reticulum. The calcium binds to various proteins that in turn cause conformational changes that expose the myosin-binding sites on the actin filaments so that contraction may occur.

Lactic acid fermentation

Glucose is a major fuel for most organisms; when energy is needed, glucose can be quickly released from the body's stores and processed metabolically to produce ATP. This metabolic process occurs optimally under high-oxygen (aerobic) conditions. When oxygen cannot be replenished to the muscles as fast as it is being used (as in short bursts of extreme activity), glucose can be broken down anaerobically (under no- or low-oxygen conditions). Use of this pathway, however, leads to a buildup of the byproduct lactic acid in the muscles; this buildup causes muscle pain and cramps—uncontrollable shortening and hardening of muscle tissue—and limits the period of intense activity.

Role in human health

Neuromuscular disorders typically manifest themselves with one of four classes of symptoms (or any combination of the four):

  • Weakness: Muscle weakness may be specific to a particular part of the body (i.e., neck, shoulder, arm, hand, leg, hip, etc.) or it may be generalized. Weakness may be caused by brain damage from a stroke or tumor, damage to the spinal cord , damage to a single nerve, or psychological problems.
  • Fatigue: Individuals may suffer from chronic fatigue because of major depression, multiple sclerosis , stroke, neuromuscular transmission failure, or psychosomatic illness.
  • Pain: Like muscle weakness, muscle pain may be specific (e.g., due to an muscle abscess ) or general; it may also have a psychosomatic origin (i.e., associated with anxiety or depression).
  • Cramps: Muscle pain caused by cramps is distinct from general muscle pain in that it often occurs in healthy individuals and causes intense pain.

Common diseases and disorders

  • Spasmodic torticollis: This disease is characterized by painful spasms of the neck muscles that force the head to rotate and/or tilt. Its cause is usually unknown although occasionally conditions such as infections of the nervous system, tumors of the neck, or hyperthyroidism cause spasmodic torticollis.
  • Fibromyalgia : Syndromes associated with fibromyalgia are characterized by localized or general pain or stiffness in muscles, tendons, and ligaments. There is no known cause for fibromyalgia but stress , inadequate sleep, injury, infections, and other conditions have been associated.
  • Muscular dystrophy : The most common dystrophies (Duchenne's and Becker's) cause weakness in the muscles in or around the torso. In the case of Duchenne's muscular dystrophy (DMD), joint and muscle contractures develop in the form of cramps and amassment of fibrous tissue (including progressive destruction of muscle fibers).
  • Tetanus: The bacillus Clostridium tetani produces a toxin called tetanospasmin that causes persistent spasms in the muscles of the jaw (hence the name "lockjaw"), the back, and/or the site of infection.
  • Sports injuries: Muscle, ligament, and tendon injuries can be caused by inaccurate training advice, abnormalities in body structures, and overexertion. Common muscular injuries include ankle sprains, shin splints, hamstring injuries, and weightlifter's back. Such injuries can often be prevented by warming up before exercise , cooling down after exercise, performing strengthening and stretching exercises, and wearing protective gear.


Actin —A contractile protein that forms thin filaments in myofibrils; forms the I-band of the sarcomere.

Adenosine triphosphate (ATP) —A molecule present in all living organisms that acts as an energy source.

Fascicle —Bundles of muscle fibers surrounded by connective tissue.

Muscle fibers —Tubular multinucleated cells containing approximately one thousand contracting myofibrils.

Myofibrils —Tubular organelles found in muscle fibers that appear striated under a microscope; they are surrounded by a system of vesicles called the sarcoplasmic retictulum, important in the regulation of muscle contraction.

Myosin —A contractile protein that forms thick filaments in myofibrils; forms the A-band of the sarcomere with some overlap with actin filaments.

Sarcomere —The functional unit of muscle contraction; composed of striated bands of contractile proteins (actin and myosin).



Kakulas, B. A. "Pathologic Aspects of Muscle Contracture." In Exercise Intolerance and Muscle Contracture, edited by Georges Serratrice, Jean Pouget, and Jean-Philippe Azulay. France: Springer-Verlag, 1999.

McComas, Alan J. Skeletal Muscle Form and Function. Champaign, IL: Human Kinetics, 1996.

Schapira, Anthony H. V., and Robert C. Griggs, eds. Muscle Diseases. Woburn, MA: Butterworth-Heinemann, 1999.


Muscular Dystrophy Association. 3300 E. Sunrise Drive, Tucson, AZ 85718. (800) 572-1717. <>.


Berkow, Robert, Mark H. Beers, Andrew J. Fletcher, and Robert M. Bogin, eds. "Bone, Joint, and Muscle Disorders." The Merck Manual of Medical Information: Home Edition. 2001. <>.

Stéphanie Islane Dionne