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Skeletal Muscle

Skeletal muscle is the main muscle type in our body and makes up approximately 40% of our total body weight.

A skeletal muscle consists of muscle fibres. One muscle fibre is approximatels 100 µm in diameter and consists of several nuclei and many mitochondria. Each muscle fibre contains myofibrils. These are approximately 1 µm in diameter. Muscle fibres are made up of many muscle cells.

The myofibril is organised in repeating units called sarcomeres. These contain thick and thin filaments; these may be viewed under a microscope, and for this reason they are also known as striated muscle cells. The thick and thin filaments are made up of two different proteins called actin and myosin. The actin filaments are the thin and flexible filaments and the myosin filaments are the thick filaments. Thick filaments consist of the protein myosin II which forms a globular head and fibrous tail. The thin filaments are formed from G-actin monomers which polyermise to form F-actin [1].  Each G-actin has a myosin-heading binding site which is blocked during muscle relaxation by the protein tropomyosin. Tropomyosin winds around the F-actin in association with troponin. Troponin consists of 3 subunits; I, T and C. The I and T subunits bind to the tropomyosin blocking the myosin-head binding sites by holding the tropomyosin in position. The C subunit binds to calcium ions after their release from the sarcoplasmic reticulum during muscle stimulation. Muscle contraction occurs when the thin filaments slide along the thick filament by hydrolysing ATP [2] by what is known as the Sliding Filament Theory.

Contraction in a muscle cell is propagated by an action potential travelling along a motor neurone and arriving at a Synapse; it is mediated by sodium ions. The voltage gradient causes voltage-gated calcium ion channels in the presynaptic neurone to open, triggering vesicles containing neurotransmitters, specifically acetylcholine, to travel towards the sarcolemma; fusing with the membrane and releasing acetylcholine into the synaptic cleft [3]. They diffuse across the cleft where they bind to specific receptors called nicotinic cholinergic receptors on the sarcolemma, where the depolarisation travels along the membrane and deep into the cell via T-tubules [4]. Therefore it allows the sarcoplasmic reticulum to become depolarised, releasing calcium ions and triggering muscle contraction to take place by the sliding filament theory [5]

Skeletal muscles are able to undergo muscle hypertrophy during increased physical exercise, e.g. in athletes. As well as this, muscles are also able to undergo atrophy when the muscles are underused, such as in someone who is immobilized by paralysis or linb injury.

Cardiac Muscle

Cardiac Muscle is composed of smaller interconnection cells with single nucleus per cell instead of long multinucleate cells in skeletal muscle. Interconnection which appears as dark lines under microscope is known as intercalated discs. These interconnections make the cardiac muscle cells to form single functioning unit called myocardium. Some cardiac muscle cells generate electric impulses which spread across the gap junctions from cell to cell by itself this enables cell contractions in the myocardium[6].

Cardiac muscle fibers are electrically coupled to each other and consequently excitation of one cardiac muscle fiber triggers a series of action potentials throughout all of the muscle fibers in the cardiac muscle, hence allowing cardiac muscle to contract as one entity, much like single-unit smooth muscle cells. The strength of the cardiac muscle is further enhanced by the fact that action potentials are maintained in cardiac muscles cells considerably longer than in skeletal muscle fibers; cardiac muscle cells remain depolarized for several hunder milliseconds whilst a nerve or skeletal muscle fiber is depolarizaed for several milliseconds. The significantly longer depolarization span in cardiac muscles induces a longer refractory period which inhibits "circus movements" of constant re-excitation around the wall of the heart. [7]

Cardiac muscles are able to undergo muscle hypertrophy both as a result of increased physiological demand and as a result of some disease processes.

Smooth Muscle

A smooth muscle cell's location are mainly on the walls of hollow organs such as the urinary, reproductive, intestinal and respiratory tracts of both females and males. They also contribute to other major functions such as peristalsis and vasoconstriction. Due to the smooth muscle cell having many different functions the cells are organised into two groups. These are catagorized as:  multi-unit smooth muscles or single-unit smooth muscles. The majority of smooth muscle is of the single-unit type for simultaneous contraction within organs.  

Single unit smooth muscle cells are electrically coupled, so that the stimulation of one cell leads to the stimaulation of a nearby cell. This results in a wave of contraction as can be evidenced in peristalsis. Some smooth muscles cells have pacemaker activity and can depolarise without external stimuli and these are the sort of cells that may initiate the wave of contraction.

Multi unit smooth cells, however, are not electrically coupled and hence the contraction of one cell does not neccesarily mean the contraction of cells that are adjascent. Multiunit smooth cells can be found in the Iris of the eye and the Vas deferens in the male genital tract. [8]

Unlike skeletal muscles they are 2 to 10 µm and have only one nuclei. They contain similar components to both cardiac and skeletal muscle cells; myosin, actin and tropomyosin but they do not have troponin. Instead, the myosin-head binding sites on the actin filaments are blocked by the protein calmodulin. When calcium ions are released from the extracellular fluid, 4 calcium ions bind to the protein calmodulin. This activates an enzyme - myosin light chain kinase - which phosphorylates the regulatory light chain myosin-heads. This activates myosin ATPase activity enabling cross-bridge formation and consequently muscular contraction.[9] The non-striated cells contain more actin than myosin in the fibre composition. Therefore, there is a larger proportion of thin filaments than thick filaments in smooth muscles than striated muscles. 

The mode of control is mostly governed by the autonomic nervous system, meaning it is an involuntary control. Whereas, the skeletal muscles are innervated by the somatic nervous system control. The neuron can make contact with the smooth muscle cell at many points on the cell. This forms a swelling called a varicosity which contains the components for vesicular neurotransmitter release. The multiunit smooth muscle's cells each receive a nervous input and act independently to each other. The single unit muscle cells recieve a nervous input together and due to the many gap junctions electrical communication and take place. This allows the cells to act in unison[10].  

Smooth muscles are able to undergo both muscle hypertrophy and muscle hyperplasia in response to increasing demands of heavier workloads. Hyperplasia is usually the major response. Muscle atrophy also occur in smooth muscles, as in the uterine smooth muscle after menopause, indicating that the status of uterine smooth muscle is under hormonal control.


  1. Freeman S. (2007), Biological Science, 3rd edition. San Francisco, Benjamin-Cummings Pub Co
  2. Berg J., Tymoczko J and Stryer L. (2001) Biochemistry, 5th edition, New York: WH Freeman.
  3. Bowness E, Braid K, Brazier J, Burrows C, Craig K, Gillham R, Towle J. (2009), A2-level Biology The Revision Guide Exam Board AQA, page 57-60, Newcastle-upon-Tyne: CGP books.
  4. Bowness E, Braid K, Brazier J, Burrows C, Craig K, Gillham R, Towle J. (2009), A2-level Biology The Revision Guide Exam Board AQA, page 57-60, Newcastle-upon-Tyne: CGP books.
  5. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. (2008), Molecular Biology of The Cell, page 1028-1029, 5th edition, New York:Garland Science.
  6. Raven, P.H. and Johnson, G.B. (1999) Biology(5th ed.) P915 WCB/McGraw-Hill
  7. Moffet, Moffett, Schauf(1993)Human Physiology, 2nd Edition, St. Louis, p313-314
  8. Bruce M. Koeppen and Bruce A Stanton (2008) Berne and Levy Physiology, 6th edition, Philadelphia: Moseby Elsevier.
  9. Guyton A, Hall J, 1997, Human Physiology and Mechanisms of Disease, 6th Edition, W.B. Saunders Company.
  10. Animal Physiology, Second Edition, Richard W.Hill Michigan State University, Gordon A. Wyse University of Massachusetts Amherst, Margaret Anderson Smith College,
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