Muscles gain versus atrophy

Although al cells are capable of some sort of movement, the dominant function of several cell types is to generate motile forces through contractions. In these specialized contractile cells, motile forces are generated by the interaction of the proteins actin and myosin.

Certain forms of contractile cell function as single-cell contractile Units: Myoepithelial cells are an important component of certain secretory glands where they function to expel secretions from glandular acini; pericytes are smooth muscle-like cells that surround blood vessels; myofibroblasts are cells that have a contractile role in addition to being able to secrete collagen. Other forms of contractile cell function by forming multicellular contractile units termed muscles. Such muscle cells can be grouped into three major types: cardiac, smooth and skeletal.

Cardiac muscle provides the rhythmic contractility of the heart; is striated. Skeletal muscle is striated muscle responsible for the movement of the skeleton and certain organs such as the eye globe and the tongue. Unlike other types, smooth muscle is not striated and forms the muscular component of internal organs such as those of the gastrointestinal, vascular and urogenittal systems. Of these three types, skeletal muscle is under voluntary control, but the smooth and cardiac types are not under voluntary as a system of neurohormonal components influences their movement.

In these muscle types, the muscle cells are surrounded by an external lamina which is connected to internal contractile proteins via link proteins. This external lamina binds individual muscle cells into a single functional mass. MUSCLE GAIN VERSUS ATROPHY The concept of muscle gain and atrophy are interposing concepts that revolve around the adaptive changes muscle suffers in the face of stress, injury and/or disease. Muscle gain Muscle gain is a function of hypertrophy, hyperplasia or both. Hyperplasia is an increase in the number of cells or tissues which result in increased volume of the organ.

This can only take when the cell is capable of synthesizing DNA for mitosis to take place. On the other hand, hypertrophy is increase in the size of the cells without cell division. These mechanisms can occur in the presence or absence of disease. For example, exercise and rest are condition capable of causing muscle gain in the absence of disease while heart failure is a pathologic condition sequel to cardiac hypertrophy. This concept is compared between the skeletal and cardiac muscle types: Although a wide spectrum of disease may affect muscle, the numbers of pathologic reactions differ and are relatively limited in number.

Fiber hypertrophy occurs in response to increased load, either in the setting of exercise or in pathologic conditions where muscle fibers are injured [ Carpenter, 2001]. The cardiac muscle is considered a terminally differentiated muscle whose increase in size is usually as a result of hypertrophy and not hyperplasia. In this case, increased mechanical work owing to pressure or volume overload cause the rate of protein synthesis to increase, sarcomere and mitochondrial number escalate and the dimension of each myocyte widens.

This culminates in an enlarged heart. The extent of this hypertrophy varies with underlying etiology and reflects the nature and strength of the stimulus. There are also molecular and cellular changes which initially promote heart function but later contribute to failure of the heart{Johnatty, 2000]. Muscle loss Muscle loss is a function of atrophy. The shrinkage in the size of the cell resulting from loss of cell substance is atrophy.

This is seen in skeletal muscles as segmental necrosis [destruction of a portion of the length of a muscle cell which may be accompanied by phagocytosis and cellular infiltration. The loss of muscle fibers is followed by fatty infiltration and collagen deposition; vacuolation, alterations in structural proteins or organelles and accumulation of intracytoplamic deposits may also be seen in many diseases. Muscle atrophy could result from prolonged immobilization, bed rest, muscle injury, nerve damage, diabetes, joint diseases like rheumatoid arthritis, infections like tuberculosis etc.

[Pasumarthi, 2002] Conclusion Muscle can increased in size or otherwise due to reaction to stress, injury and/or disease. It depicts change in the cell components particularly the organelles. REFERENCES Pasumarthi KBS Field Lj Cardiomyocyte cell cycle regeneration. Circ Res 90;1044, 2002 Johnatty SE et al: Identification of genes regulated during mechanical load-induced cardiac hypertrophy J Mol Cell Cardiol 32:805, 2000 Carpenter S. et al. Pathology of skeletal muscle, 2nd Ed. Oxford England, Oxford University Press 2001, p 662

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