Muscle contraction events describing the sliding-filament concept are listed as follows.
ATP binds to a myosin head and forms ADP + P i. When ATP binds to a myosin head, it is converted to ADP and P i, which remain attached to the myosin head.
Ca 2+ exposes the binding sites on the actin filaments. Ca 2+ binds to the troponin molecule, causing tropomyosin to expose positions on the actin filament for the attachment of myosin heads.
When attachment sites on the actin are exposed, the myosin heads bind to actin to form cross bridges.
ADP and P i are released, and a sliding motion of actin results. The attachment of cross bridges between myosin and actin causes the release of ADP and P i. This, in turn, causes a change in the shape of the myosin head, which generates a sliding movement of the actin toward the center of the sacromere. This pulls the two Z discs together, effectively contracting the muscle fiber to produce a power stroke.
ATP causes the cross bridges to unbind. When a new ATP molecule attaches to the myosin head, the cross bridge between the actin and myosin breaks, returning the myosin head to its unattached position.
Without the addition of a new ATP molecule, the cross bridges remain attached to the actin filaments. This is why corpses become stiff with rigor mortis (new ATP molecules are unavailable).
Action potential generates release of acetylcholine. When an action potential of a neuron reaches the neuromuscular junction, the neuron secretes the neurotransmitter acetylcholine (Ach), which diffuses across the synaptic cleft.
Action potential is generated on the motor end plate and throughout the T tubules. Receptors on the motor end plate, a highly folded region of the sarcolemma, initiate an action potential. The action potential travels along the sarcolemma throughout the transverse system of tubules.
Sarcoplasmic reticulum releases Ca 2+. As a result of the action potential throughout the transverse system of tubules, the sarcoplasmic reticulum releases Ca 2+.
Myosin cross bridges form. The Ca 2+ released by the sarcoplasmic reticulum binds to troponin molecules on the actin helix, prompting tropomyosin molecules to expose binding sites for myosin cross‐bridge formation. If ATP is available, muscle contraction begins.
The latent period is the time required for the release of Ca 2+.
The contraction period represents the time during actual muscle contraction.
The relaxation period is the time during which Ca 2+ are returned to the sarcoplasmic reticulum by active transport.
The refractory period is the time immediately following a stimulus. This is the time period when a muscle is contracting and therefore will not respond to a second stimulus. Since this is occurring at the same time as the contraction, it does not appear on the myogram as a separate event.
Figure 1.The phases of a myogram.
A staircase effect (treppe) is produced if each successive stimulus occurs after the relaxation period of the previous stimulus (refer to Figure 1b). Each successive muscle contraction is greater than the previous one, up to some maximum value. In addition to the accumulation of Ca 2+, other factors, such as increases in temperature and changes in pH, may contribute to this “warming up” effect commonly employed by athletes.
Wave (temporal) summation occurs if consecutive stimuli are applied during the relaxation period of each preceding muscle contraction (refer to Figure 1c). In this case, each subsequent contraction builds upon the previous contraction before its relaxation period ends.
Incomplete tetanus, also called unfused tetanus, occurs when the frequency of stimuli increases (refer to Figure 1d). Successive muscle contractions begin to blend, almost appearing as a single large contraction.
Complete tetanus, also called fused tetanus, occurs when the frequency of stimuli increases still further (refer to Figure 1d). In this case, individual muscle contractions completely fuse to produce one large muscle contraction.
Strength of stimulus. Muscle contractions intensify when more motor neurons stimulate more muscle fibers. This effect, called recruitment or multiple motor unit summation, is also responsible for fine motor coordination, because by continually varying the stimulation of specific muscle fibers, smooth body movements are maintained.
Length of muscle fiber contraction. Because a muscle is attached to bones, muscle contraction is restricted to lengths that are between 60 percent and 175 percent of the length that produces optimal strength. This range of muscle lengths limits myosin cross bridges and actin to positions only where they overlap and thus can generate contractions.
Isotonic contractions occur when muscles change length during a contraction. Picking up a book is an example.
Isometric contractions occur when muscles do not change length during a contraction. When holding a book in midair, muscle fibers produce a force, but no motion is generated.
Slow fibers contract slowly, have a high endurance, and are red from their rich blood supply. However, they do not produce much strength. These fibers are used for long‐distance running.
Fast fibers contract rapidly, fatigue rapidly, and are white because the blood supply is limited. They generate considerable strength. These fibers are used for short‐distance running.
Muscle tone. In any relaxed skeletal muscle, a small number of contractions continuously occur. Observed as firmness in a muscle, these contractions maintain body posture and increase muscle readiness.
Muscle fatigue. Muscle fibers stop contraction when inadequate amounts of ATP are available. Lack of oxygen and glycogen and the accumulation of lactic acid (a byproduct of ATP production in the absence of oxygen), together with the lack of ATP, all contribute to muscle fatigue.