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Muscle fatigue occurs when a muscle can no longer contract in response to signals from the nervous system. The exact causes of muscle fatigue are not fully known, although certain factors have been correlated with the decreased muscle contraction that occurs during fatigue. ATP is needed for normal muscle contraction, and as ATP reserves are reduced, muscle function may decline. This may be more of a factor in brief, intense muscle output rather than sustained, lower intensity efforts. Lactic acid buildup may lower intracellular pH, affecting enzyme and protein activity. Imbalances in Na + and K + levels as a result of membrane depolarization may disrupt Ca ++ flow out of the SR. Long periods of sustained exercise may damage the SR and the sarcolemma, resulting in impaired Ca ++ regulation.

Intense muscle activity results in an oxygen debt    , which is the amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction. Oxygen is required to restore ATP and creatine phosphate levels, convert lactic acid to pyruvic acid, and, in the liver, to convert lactic acid into glucose or glycogen. Other systems used during exercise also require oxygen, and all of these combined processes result in the increased breathing rate that occurs after exercise. Until the oxygen debt has been met, oxygen intake is elevated, even after exercise has stopped.

Relaxation of a skeletal muscle

Relaxing skeletal muscle fibers, and ultimately, the skeletal muscle, begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the gates in the SR where Ca ++ was being released. ATP-driven pumps will move Ca ++ out of the sarcoplasm back into the SR. This results in the “reshielding” of the actin-binding sites on the thin filaments. Without the ability to form cross-bridges between the thin and thick filaments, the muscle fiber loses its tension and relaxes.

Muscle strength

The number of skeletal muscle fibers in a given muscle is genetically determined and does not change. Muscle strength is directly related to the amount of myofibrils and sarcomeres within each fiber. Factors, such as hormones and stress (and artificial anabolic steroids), acting on the muscle can increase the production of sarcomeres and myofibrils within the muscle fibers, a change called hypertrophy, which results in the increased mass and bulk in a skeletal muscle. Likewise, decreased use of a skeletal muscle results in atrophy, where the number of sarcomeres and myofibrils disappear (but not the number of muscle fibers). It is common for a limb in a cast to show atrophied muscles when the cast is removed, and certain diseases, such as polio, show atrophied muscles.

Disorders of the …

Muscular system

Duchenne muscular dystrophy (DMD) is a progressive weakening of the skeletal muscles. It is one of several diseases collectively referred to as “muscular dystrophy.” DMD is caused by a lack of the protein dystrophin, which helps the thin filaments of myofibrils bind to the sarcolemma. Without sufficient dystrophin, muscle contractions cause the sarcolemma to tear, causing an influx of Ca ++ , leading to cellular damage and muscle fiber degradation. Over time, as muscle damage accumulates, muscle mass is lost, and greater functional impairments develop.

DMD is an inherited disorder caused by an abnormal X chromosome. It primarily affects males, and it is usually diagnosed in early childhood. DMD usually first appears as difficulty with balance and motion, and then progresses to an inability to walk. It continues progressing upward in the body from the lower extremities to the upper body, where it affects the muscles responsible for breathing and circulation. It ultimately causes death due to respiratory failure, and those afflicted do not usually live past their 20s.

Because DMD is caused by a mutation in the gene that codes for dystrophin, it was thought that introducing healthy myoblasts into patients might be an effective treatment. Myoblasts are the embryonic cells responsible for muscle development, and ideally, they would carry healthy genes that could produce the dystrophin needed for normal muscle contraction. This approach has been largely unsuccessful in humans. A recent approach has involved attempting to boost the muscle’s production of utrophin, a protein similar to dystrophin that may be able to assume the role of dystrophin and prevent cellular damage from occurring.

Chapter review

A sarcomere is the smallest contractile portion of a muscle. Myofibrils are composed of thick and thin filaments. Thick filaments are composed of the protein myosin; thin filaments are composed of the protein actin. Troponin and tropomyosin are regulatory proteins.

Muscle contraction is described by the sliding filament model of contraction. ACh is the neurotransmitter that binds at the neuromuscular junction (NMJ) to trigger depolarization, and an action potential travels along the sarcolemma to trigger calcium release from SR. The actin sites are exposed after Ca ++ enters the sarcoplasm from its SR storage to activate the troponin-tropomyosin complex so that the tropomyosin shifts away from the sites. The cross-bridging of myposin heads docking into actin-binding sites is followed by the “power stroke”—the sliding of the thin filaments by thick filaments. The power strokes are powered by ATP. Ultimately, the sarcomeres, myofibrils, and muscle fibers shorten to produce movement.

The release of calcium ions initiates muscle contractions. Watch this video to learn more about the role of calcium. (a) What are “T-tubules” and what is their role? (b) Please also describe how actin-binding sites are made available for cross-bridging with myosin heads during contraction.

(a) The T-tubules are inward extensions of the sarcolemma that trigger the release of Ca ++ from SR during an Action Potential. (b) Ca ++ binds to tropomyosin, and this slides the tropomyosin rods away from the binding sites.

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Questions & Answers

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Anatomy is the identification and description of the structures of living things
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Anatomy is the study of the structure of the body, while physiology is the study of the function of the body. Anatomy looks at the body's organs and systems, while physiology looks at how those organs and systems work together to keep the body functioning.
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Enzymes are proteins that help speed up chemical reactions in our bodies. Enzymes are essential for digestion, liver function and much more. Too much or too little of a certain enzyme can cause health problems
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the normal temperature is 37°c or 98.6 °Fahrenheit is important for maintaining the homeostasis in the body the body regular this temperature through the process called thermoregulation which involves brain skin muscle and other organ working together to maintain stable internal temperature
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anaemia is the decrease in RBC count hemoglobin count and PVC count
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Organ Systems Of The Human Body (Continued) Organ Systems Of The Human Body (Continued)
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It is made up of three layers, the epidermis, dermis, and the hypodermis, all three of which vary significantly in their anatomy and function. The skin's structure is made up of an intricate network which serves as the body's initial barrier against pathogens, UV light, and chemicals, and mechanical
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Diabetes is a chronic (long-lasting) health condition that affects how your body turns food into energy. Your body breaks down most of the food you eat into sugar (glucose) and releases it into your bloodstream. When your blood sugar goes up, it signals your pancreas to release insulin. Insulin act
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Rheumatoid arthritis (RA) Scleroderma. Granulomatosis with polyangiitis (GPA) Churg-Strauss syndrome. Lupus. Microscopic polyangiitis. Polymyositis/dermatomyositis. Marfan syndrome.
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(CO) amount of blood pumped by each ventricle during one minute; equals HR multiplied by SV
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SV- Stroke Volume HR- Heart Rate
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Cardiac output is the amount of blood pumped by the heart in one minute. It's calculated by multiplying the heart rate (the number of times the heart beats in one minute) by the stroke volume (the amount of blood pumped out by the heart with each beat). So, cardiac output = heart rate x stroke volum
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Source:  OpenStax, Anatomy & Physiology. OpenStax CNX. Feb 04, 2016 Download for free at http://legacy.cnx.org/content/col11496/1.8
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