Muscle contraction is the event of tension creation in muscle fibre due to actin and myosin filament slide resulting in either shortening or lengthening of the muscle. The process has significant implications for many functions of physiology: it enables voluntary movements, such as posture and heat generation, and involuntary actions like the heart beating and interior organ functions, including digestion. There are three types of muscle tissue in the human body: skeletal muscles that provide for body movements, cardiac muscle found in the heart organ, which brings about rhythmic contractions to pump blood, and lastly, the smooth muscles found in the walls of internal organs that control such involuntary movements as peristalsis in the digestive tract.
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The anatomy of muscles is discussed below-
Skeletal muscle fibers are rather long, cylindrical cells that bear several nuclei at the periphery. They are covered with a plasma membrane called the sarcolemma. The sarcolemma envelops the sarcoplasm and within it, there are many myofibrils.
These are rod-like structures lying parallel to each other in the muscle fibre and composed of repeated units known as sarcomeres. These consist of the contractile proteins, actin and myosin.
Sarcomere is rightly viewed as a portion of the muscle fibre existing between two successive and running Z-lines. Comprising overlapping thin and thick filaments, their interaction with actin and myosin, respectively, gives rise to the contraction and subsequent relaxation of muscles.
The mechanism of muscle contraction is discussed below-
The neuromuscular junction is, literally speaking, a chemical synapse between the motor neuron and the skeletal muscle fibre. Derivation from the neuron axon ending, crossing the synaptic cleft, comes to rest at the motor end plate within the muscle fibre.
When the action potential reaches the axon terminal, acetylcholine is released into the synaptic cleft. Sometime later, ACh will bind to the receptors present on the motor end plate and finally depolarize it, which generates an action potential into the muscle fibre.
Role of calcium ions
The action potential travels down the sarcolemma and into the T-tubules, and then the Ca²⁺ is released from the Sarcoplasmic Reticulum into the Sarcoplasm.
Role of troponin and tropomyosin
This Ca²⁺ now combines with Troponin wherein, on a conformational change, the Tropomyosin exposes the myosin-binding site on Actin hence facilitating cross-bridge formation
Steps involved in excitation-contraction coupling
Action Potential reaches the T-tubules
Release of Ca²⁺ from the Sarcoplasmic Reticulum.
Ca²⁺ binds with troponin; this use causes a change in the position of the tropomyosin.
Myosin-binding sites on the actin are exposed, and contraction is initiated.
Binding of myosin to actin
When the myosin-binding sites on the actin filaments become available, energized myosin heads bind to these exposed sites, forming cross-bridges.
Power stroke
The myosin head pivots to return to its previous position, taking the attached actin filament towards the mid-sarcomere; it releases ADP and phosphate.
Detachment of myosin
A newly bound ATP into the myosin head releases the myosin head from the actin filament.
Re-cocking of the myosin head
Hydrolysis replenishes the energy of the myosin head so that it is cocked again and hence at the beginning of another cycle.
The energy for muscle contraction is discussed below-
It provides energy for the cross-bridge cycle of muscle contraction. The binding of ATP to myosin heads allows the myosin heads to detach from actin after the completion of a power stroke. Hydrolysis re-energizes the myosin heads so that they are ready to go through another cycle of binding and pulling.
Creatine phosphate
This high-energy compound gives its phosphate group directly back to ADP with great velocity, thereby regenerating a certain amount of ATP. This is an abbreviated form but instantaneous energy for contraction, sufficient activity to last about 10 seconds.
Glycolysis
Because this pathway is anaerobic, it degrades glucose to pyruvate directly by yielding 2 ATP molecules per glucose molecule. The energy yield from glycolysis caters to fleeting, very intense bursts of activities but results in the accumulation of lactic acid and thus muscle fatigue.
Aerobic respiration
This process takes place inside the mitochondria. Oxygen is used in completely oxidizing glucose, fatty acids, and amino acids into carbon dioxide and water. In this process, a quite significant amount of ATP is generated. Aerobic Respiration is effective and, by continuously supplying ATP can last for a longer period with moderate-intensity activities.
The steps involved in muscle contraction are:
The neuromuscular junction releases acetylcholine as a consequence of a muscle fibre being excited by a nerve impulse. After this, an action potential is generated within the muscle fibre.
The impulse travels down the sarcolemma and into the T-tubules, triggering an increased release of calcium ions from the sarcoplasmic reticulum.
Calcium binds to troponin; tropomyosins, entrained with the former, get out of the way and thus expose the binding sites for myosin to bind and actin.
The myosin head binds the actins forming the cross-bridges and undergoes a "power stroke", pulling the actin toward the center of the sarcomere.
ATP binds myosin, releasing this protein from actin and recocking it for another cycle.
According to the sliding filament theory, sliding of thin filaments—actin—and thick filaments—myosin—past each other accounts for muscle contraction and hence shortens the sarcomere and, in consequence, the muscle Fiber. Thus, myosin heads will attach to actin, pulling it in—the actin filaments—toward the centre, thereby shortening the sarcomere to create tension. Because this event continually repeats in the presence of calcium ions and ATP, it leads to muscle contraction.
The entering into the activity of calcium ions during muscle contraction occurs by its binding to troponin on the actin filaments. This conformational change of the troponin causes a repositioning of tropomyosin, which moves off the myosin-binding sites on the actin filaments and opens these binding sites so that myosin heads can bind and institute the cross-bridge cycle that eventually results in muscle contraction.
Isotonic muscle contraction is one in which there is a change in the length of the muscle while developing force; hence, it can be further divided into two kinds: a concentric contraction, which results in muscle shortening, or an eccentric contraction, which results in muscle lengthening. Isometric contractions are muscle contractions that develop force without a change in the length of a muscle; this occurs due to holding a weight at some fixed position. Both are critical components of many forms of physical activity and muscle functions.
Common muscle contraction disruptions include muscular dystrophies, which is the progressive muscle weakening in the case of Duchenne muscular dystrophy; myasthenia gravis, an autoimmune disorder in which fatigability and generalised muscular weakness are factors; muscle cramps or spasms, in which involuntary contractions result; and finally, fibromyalgia, related aching and tenderness of the muscles.
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