The contraction of skeletal muscle includes ultra structural and biochemical events.
1. Ultra structural events (Biophysics of muscle contraction). HE Huxley and AF Huxley in 1954 proposed a theory to explain the process of muscular contraction. This theory is known as sliding filament theory, which is now generally accepted. This theory states that the acting (thin) filaments slide over the myosin (thick) filaments to penetrate deeper into the A bands in the contracting muscle fiber. The thin filaments meet in the centre of the macromere. As such the width of the A band remains constant.
However, the bands shorten and ultimately disappear. This shortens the sarcomere. As all the sacromeres of the myofibril shorten simultaneously the muscle fibre shortens. However, the filaments do not undergo any alteration in length. It is though that the cross bridges on the thick filaments might pull the thin filaments while muscle is contracted, but during relaxation these cross bridges disappear. Thus contraction and relaxation of muscles are brought about by the repetitive formation and breakage of cross bridges respectively.
The proteins, troponin and tropomyosin, which are closely associated with acting, are also important in regulating the attachment of acting to the cross bridges.
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2. Biochemical events (Biochemistry of muscles contraction). Albert Szent Gyorgyi ana other worked out the biochemical events associated with the muscles contraction. These biochemical events are summarised below:
(z) The nerve impulse stimulates a muscle fibre at the neuromuscular junction or motor end plate, producing acetylcholine.
(ii) Acetylcholine brings out the release of calcium ions from the sarcopiasmic reticulum of the muscle into the interior of muscle fibre.
(Hi) Myosin now binds with acting to form act myosin in the presence of ATP and calcium ions.
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(iv) Energy for muscles contraction is provided by hydrolysis of ATP by myosin ATP-ase enzyme. This hydrolysis produces ADP, inorganic phosphate and energy (used in muscles contraction). Phosphocreatine donated its high energy and phosphate to ADP, producing ATP. Phosphocreatine serves as an energy source for a few seconds for metabolic processes in the muscles cells to begin to produce greater quantities of ATP. Phosphocreatine is again formed in relaxing muscle by using ATP produced by carbohydrate oxidation.
(v) At the end of muscle contraction, the conversion of ADP into ATP takes place. The muscle is rich in glycogen which is broken down into lactic acid through a series of reaction (glycol sis) and liberates energy. Some of this energy is used for the reformation of phosphocreatine and also for the conversion of 4/5th of lactic acid back into glycogen. The 15th of lactic acid is oxidised to water and carbon dioxide. These reactions taking place in the muscles and liver, are proposed by Cori and Cori, hence known as Cori’s cycle.
During strenuous exercise, the muscle does not get sufficient oxygen to meet its energy needs immediately. So it contracts an aerobically and accumulates lactic acid produced by anaerobic glycolysis. During recovery, the oxygen consumption of muscle exceeds. The extra oxygen consumed during recovery is called oxygen debt of the muscle. It is used in oxidising the accumulated lactic acid aerobically and in restoring the depleted creatine phosphate and ATP in the muscle fibre. A small part of oxygen debt also goes to myoglobin which binds and stores oxygen for future use. For extra oxygen, deep and rapid breathing occurs carrying more oxygen into the lungs and eventually to the tissues.
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The reduction in to force of contraction of a muscle after prolonged stimulation is called muscle fatigue. The accumulation of lactic acid leads to muscle fatigue. Pain is experienced in the fatigued muscle. The site of fatigue is the junction between nerve and muscle. A muscle gets fatigued sooner after a strenuous exercise than after a mild exercise. Fatigued muscle needs extra oxygen to dispose off excess lactic acid. This results in the disappearance of fatigue.
Increase in the size of muscle cells is called hypertrophy. The increase is due to increase in the number of filaments in the sarcomeres in number of mitochondria and in the amount of sarcoplasm but it does not involve the division of muscle cells.
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Reduction in the size of individual muscle cells is called atrophy. In atrophy the number of filaments and mitochondria and the amount of sarcoplasmic reticulum are reduced. A lack of exercise or immobilization of muscles leads to atrophy.
Birds and mammals have in their skeletal muscles two kinds of striated muscle fibre; red or slow muscle fibre and white or fast muscle fibres.
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(a) Red muscle fibres’. These muscle fibres are dark red which is due to the presence of red haemoprotein called hypertrophy. The reduction in the size of muscle cells is called myoglobin. Myoglobin binds and stores oxygen as oxymyolobin in the red firbres. Oxymyoglobin releases oxygen for utilization during muscle contraction. Red muscle fibres are rich in mitochondria. They carry out considerable aerobic oxidation. These muscle fibres have slow rate of contraction. Red muscle fibres perform sustained work at a slow rate but for a long time. Extensor muscles on the back of the human body are very rich in muscle fibres. Some flight muscles of birds are red muscles.
(b) White muscle fibres: They are much thicker. These muscles are lighter in colour as they do not have myoglobin. White muscle fibres are poorer in mitochondria. They depend mainly on anaerobic oxidation (glycolysis) or energy production. These muscle fibres have a fast rate of contraction. White muscle fibres are specialized for very fast and strenuous work for a short time only. The muscles for eye ball movements are very rich in white muscle fibres. Flight muscles which are used in short fast flying such as in sparrow are white muscles.