Muscle Physiology Advanced Study Notes

The ability of muscle to generate heat is independent of its interaction with other tissues, unlike movement, stability, or organ protection which all involve connections with the skeleton or other structures.

Skeletal muscle, unlike cardiac or smooth muscle, does not contract spontaneously. It requires stimulation from the nervous system.

Ca2+ plays a crucial role in muscle contraction, not in the muscle action potential itself. It triggers the release of the myosin binding site on actin, allowing for the interaction that leads to contraction.

T-tubules are extensions of the cell membrane that rapidly transmit the muscle action potential through the muscle fiber. This ensures that all parts of the muscle are excited and contracted simultaneously.

A motor unit containing a smaller number of muscle fibers allows for finer control and more delicate movements.

Curare blocks the transmission of signals at the neuromuscular junction, preventing muscle fibers from receiving the signal to contract, leading to complete paralysis.

A motor nerve contains multiple motor units. Increasing stimulus strength recruits more motor units, resulting in stronger muscle contractions. This is not a violation of the all-or-none law as the law applies to individual muscle fibers, not the entire muscle.

Skeletal muscle is the primary site of heat generation in the body, along with the liver, which plays a role in maintaining core body temperature.

The I-band represents the portion of thin filaments that do not overlap with thick filaments, located on both sides of the Z-line.

The A-band encompasses the entire length of the thick filaments, including the region where they overlap with thin filaments.

During contraction, the A-band remains constant in length, while the I-band shortens as the thin filaments slide over the thick filaments. The Z-lines move closer together to reduce the overall sarcomere length.

Stretching a muscle beyond the point of overlap between thick and thin filaments eliminates the potential for muscle contraction, as there is no longer any interaction between the filaments.

ATP provides the energy required for the myosin head to bind, detach, and re-attach to actin, driving the sliding filament mechanism of muscle contraction.

The energy-dependent rotation of the myosin head during muscle contraction allows it to pull the actin filament towards the center of the sarcomere, resulting in muscle shortening.

The first step in muscle fiber contraction is triggering an action potential at the neuromuscular junction, initiating the cascade of events that lead to muscle activation.

The sarcoplasmic reticulum (SR) is an organelle responsible for storing Ca2+ and releasing it upon receiving a signal from the action potential, triggering the interaction between actin and myosin.

Ca2+ binding to troponin causes a conformational change in tropomyosin, exposing the myosin binding site on actin, allowing myosin to interact with actin and initiate the sliding filament mechanism.

While Ca2+ is present in the sarcoplasm, it allows for the continuous interaction between actin and myosin, leading to continuous muscle contraction. However, Ca2+ removal is necessary for relaxation.

During peak activity, when oxygen-dependent metabolism cannot meet the energy demands, muscles rely on oxygen-independent metabolism to produce ATP. This process leads to the accumulation of lactic acid.

Lactic acid is a byproduct of anaerobic glucose metabolism. It is converted back into glucose during recovery. This process requires oxygen, creating an