9.4: Muscle Fiber Contraction and Relaxation
- Page ID
- 61564
- Describe the components involved in a muscle contraction
- Explain how muscles contract and relax
- Describe the sliding filament model of muscle contraction
The sequence of events that result in the contraction of an individual muscle fiber begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP (Figure \(\PageIndex{1}\)). As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.
Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma and T-tubules, and closes the voltage-gated calcium channels in the SR. Ca++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands. A muscle also can stop contracting when it runs out of ATP and becomes fatigued (Figure \(\PageIndex{2}\)).
The molecular events of muscle fiber shortening occur within the fiber’s sarcomeres (see Figure \(\PageIndex{3}\)). The contraction of a striated muscle fiber occurs as the sarcomeres, linearly arranged within myofibrils, shorten as myosin heads pull on the actin filaments.
The region where thick and thin filaments overlap has a dense appearance, as there is little space between the filaments. This zone where thin and thick filaments overlap is very important to muscle contraction, as it is the site where filament movement starts. Thin filaments, anchored at their ends by the Z-discs, do not extend completely into the central region that only contains thick filaments, anchored at their bases at a spot called the M-line. A myofibril is composed of many sarcomeres running along its length; thus, myofibrils and muscle cells contract as the sarcomeres contract.
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.
Interactive Link Questions
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.
Answer: (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.
Review Questions
Q. In relaxed muscle, the myosin-binding site on actin is blocked by ________.
A. titin
B. troponin
C. myoglobin
D. tropomyosin
Answer: D
Q. The cell membrane of a muscle fiber is called ________.
A. myofibril
B. sarcolemma
C. sarcoplasm
D. myofilament
Answer: B
Q. Thin and thick filaments are organized into functional units called ________.
A. myofibrils
B. myofilaments
C. T-tubules
D. sarcomeres
Answer: D
Critical Thinking Questions
Q. What causes the striated appearance of skeletal muscle tissue?
A. Dark A bands and light I bands repeat along myofibrils, and the alignment of myofibrils in the cell cause the entire cell to appear striated.
Glossary
- aerobic respiration
- production of ATP in the presence of oxygen
- ATPase
- enzyme that hydrolyzes ATP to ADP
- creatine phosphate
- phosphagen used to store energy from ATP and transfer it to muscle
- glycolysis
- anaerobic breakdown of glucose to ATP
- lactic acid
- product of anaerobic glycolysis
- oxygen debt
- amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction
- power stroke
- action of myosin pulling actin inward (toward the M line)
- pyruvic acid
- product of glycolysis that can be used in aerobic respiration or converted to lactic acid