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.
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
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.
1. In relaxed muscle, the myosin-binding site on actin is blocked by ________.
A) titin
B) troponin
C) myoglobin
D) tropomyosin
D
2. According to the sliding filament model, binding sites on actin open when ________.
A) creatine phosphate levels rise
B) ATP levels rise
C) acetylcholine levels rise
D) calcium ion levels rise
D
3. The cell membrane of a muscle fiber is called ________.
A) myofibril
B) sarcolemma
C) sarcoplasm
D) myofilament
B
4. Muscle relaxation occurs when ________.
A)calcium ions are actively transported out of the sarcoplasmic reticulum
B) calcium ions diffuse out of the sarcoplasmic reticulum
C) calcium ions are actively transported into the sarcoplasmic reticulum
D) calcium ions diffuse into the sarcoplasmic reticulum
C
5. During muscle contraction, the cross-bridge detaches when ________.
A) the myosin head binds to an ADP molecule
B) the myosin head binds to an ATP molecule
C) calcium ions bind to troponin
D) calcium ions bind to actin
C
6. Thin and thick filaments are organized into functional units called ________.
A) myofibrils
B) myofilaments
C) T-tubules
D) sarcomeres
D
1. How would muscle contractions be affected if skeletal muscle fibers did not have T-tubules?
Without T-tubules, action potential conduction into the interior of the cell would happen much more slowly, causing delays between neural stimulation and muscle contraction, resulting in slower, weaker contractions.
2. What causes the striated appearance of skeletal muscle tissue?
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.
3. How would muscle contractions be affected if ATP was completely depleted in a muscle fiber?
Without ATP, the myosin heads cannot detach from the actin-binding sites. All of the “stuck” cross-bridges result in muscle stiffness. In a live person, this can cause a condition like “writer’s cramps.” In a recently dead person, it results in rigor mortis.