Muscle Types and Mechanics Overview

The process that triggers muscle contraction in the nervous system. It begins with an action potential (AP) on the axon terminal of a motor neuron, leading to acetylcholine secretion.

The motor neuron releases acetylcholine into the synapse, which then binds to receptors on the muscle fiber, leading to a graded potential.

The specialized region of the muscle fiber's plasma membrane where acetylcholine receptors are located.

A change in the membrane potential that is proportional to the strength of the stimulus, which can be either excitatory or inhibitory.

If the depolarizing graded potential reaches a threshold, an action potential is initiated, which travels along the muscle fiber.

Deeply invaginated extensions of the muscle fiber's plasma membrane that carry the action potential into the interior of the muscle fiber.

A specialized network of membranes within the muscle fiber that stores calcium ions.

The action potential triggers the release of calcium ions from the sarcoplasmic reticulum into the cytoplasm of the muscle fiber.

Specific binding sites on the actin filaments that interact with myosin heads during contraction.

A protein that covers actin active sites in a resting muscle, preventing myosin-actin interactions.

Small protein fibers to which calcium binds, to “turn off” the tropomyosin barrier and allow myosin-actin interactions.

The attachment of myosin heads to actin active sites, initiating the sliding filament process of muscle contraction.

The basic contractile unit of a muscle fiber, composed of overlapping actin and myosin filaments.

The ends of a sarcomere, where actin filaments attach.

Thin protein filaments that are arranged parallel to each other in the sarcomere.

Thick protein filaments that are situated in the center of the sarcomere.

The region in a sarcomere where both actin and myosin filaments overlap.

The region in a sarcomere that contains only actin filaments.

The region in a sarcomere that contains only myosin filaments.

The narrow, dark band in the center of the sarcomere.

The connection formed between a myosin head and an actin active site.

The theory describing how muscle contraction occurs through the sliding of actin and myosin filaments.

The breakdown of glycogen into glucose, requiring no oxygen.

A molecule that rapidly provides ATP for muscle contraction, but only for short durations.

The breakdown of glucose into ATP without oxygen, producing a small amount of ATP.

Creatine Phosphokinase, an enzyme that is released when muscle cells are damaged.

Protein that stores oxygen in muscle cells allowing initial aerobic cellular respiration if oxygen supply is limited.

A process occurring without oxygen, producing a small amount of ATP.

Occurs due to lack of ATP and buildup of lactic acid, not primarily from lactic acid buildup.

Breakdown of glycogen (stored glucose) into glucose for energy; major energy source in the beginning of exercise.

Oxygen-dependent processes that create a large amount of ATP.

Metabolic pathway that breaks down glucose to pyruvate and a small amount of ATP; initial stage of both aerobic and anaerobic respiration.

Release of energy from glucose without oxygen, producing lactic acid as a byproduct.

A process needing oxygen, creatine phosphate replacement, lactic acid oxidation, and glycogen replenishment.

Release of energy from glucose with oxygen, producing CO2, H2O, and a large quantity of ATP; occurs in mitochondria.

The extra oxygen needed after exertion to restore energy stores and remove waste products.

The stiffening of muscles after death due to lack of ATP.

Major energy source used after glycogen and blood glucose is depleted; occurs via aerobic respiration.

During muscle contraction, the release of ADP from the myosin head allows the cross-bridge to detach from the thin filament.

After the cross-bridge detaches, myosin needs to be re-energized to prepare for the next contraction cycle. This requires ATP.

During muscle contraction, the sarcomere (the basic unit of a muscle) shortens, but the length of the myofilaments does not change.

When a muscle contracts, the H-zone and I-band within the sarcomere may disappear because of the overlapping of myofilaments.

During muscle contraction, the length of the A-band does not change significantly.

The process by which a muscle receives a nervous signal and responds by contracting.

Skeletal muscle fibers need a nerve impulse to contract.

The point where a motor neuron connects to a muscle fiber.

The body becomes stiff approximately 12-15 hours after death due to cellular decomposition.

Virus destroying motor neurons, leading to muscle weakness and paralysis. A vaccine exists.

Abnormal high-frequency action potentials on motor neurons, causing involuntary muscle contractions (often due to ion imbalances).

Genetic disease (more common in males), causing progressive degeneration of skeletal and cardiac muscles, weakening muscles and potentially leading to death.

Autoimmune disease where motor end plates are destroyed, leading to a loss of acetylcholine receptors, causing muscle weakness.

Bacterial disease caused by Clostridium tetani producing neurotoxins in anaerobic conditions. A vaccine exists.

Food-borne illness caused by Clostridium botulinum producing a neurotoxin that prevents Acetylcholine (ACh) release, causing flaccid paralysis.

Chemical that blocks ACh receptors on the sarcolemma, causing paralysis, potentially leading to asphyxiation.

Chemicals that inhibit acetylcholinesterase, leading to a buildup of ACh, causing paralysis and other severe effects.

Muscle cells fuse to form long, multinucleated fibers; this process is called syncytium.

Increase in the size of existing muscle fibers (not more fibers); often through exercise, but not necessarily directly caused by exercise.