A&P Ch9 ~ Muscles And Muscle Tissue ~ MasteringA&P HW

Excitation, in this case, refers to the propagation of action potentials along the sarcolema. (These action potentials set off a series of events that lead to a contraction)

Calcium release from the sarcoplasmic reticulum initiates the contraction. (Sarcoplasmic reticulum is the specific name given to the smooth endoplasmic reticulum in muscle cells. It is especially abundant and convoluted in skeletal muscle cells. It functions in the storage, release, and reuptake of calcium ions)

A series of proteins that control calcium release. (When action potentials propagate along T-tubules, a voltage-sensitive protein changes shape and triggers a different protein to open it's channels, resulting in the release of calcium from the terminal cisternae.)

transverse or T tubules (T tubules penetrate a skeletal muscle fiber and provide a pathway for excitation into the interior. )

Calcium ions. (Action potentials propagating down the T-tubule cause a voltage-sensitive protein to change shape. This shape change opens calcium release channels in the sarcoplasmic reticulum, allowing calcium ions to flood the sarcoplasm. This flood of calcium ions is directly responsible for the coupling of excitation to contraction in skeletal muscle fibers.)

Typically, hundreds of skeletal muscle fibers are innervated by a single motor neuron. (There are many more skeletal muscle fibers than there are motor neurons. The ratio of neurons to fibers varies from approximately one to ten to approximately one to thousands.)

An action potential in the motor neuron causes ACh to be released into the synaptic cleft. Binding of ACh to sarcolemma receptors initiates graded potentials. (An action potential traveling down a motor neuron arrives at the axon terminal and causes exocytosis of the neurotransmitter ACh into the synaptic cleft. ACh diffuses into the synaptic cleft, binds to the receptor proteins on the junctional folds of the muscle sarcolemma (motor end plate), and initiates graded potentials. These graded potentials sum to an action potential, thus initiating excitement of the muscle fiber)

It allows calcium to exit the sarcoplasmic reticulum and enter the cytosol. (As the action potential propagates, it changes the shape of T tubule proteins. These proteins are linked to calcium channels in the terminal cisterns of the sarcoplasmic reticulum. When these proteins' calcium channels open, a massive amount of calcium flows into the cytosol)

Calcium binds to troponin, which moves tropomyosin and exposes the myosin-binding sites on actin. (The thin filament in a sarcomere is composed of actin, troponin, and tropomyosin. Troponin and tropomyosin are attached to one another, both overlaying actin. When a muscle is relaxed, tropomyosin blocks actin's myosin-binding sites. Calcium binds to troponin, initiating a shape change that removes the blocking action of tropomyosin. This exposes the myosin-binding sites on actin to the myosin heads for cross bridging)

Myosin heads bind to the newly exposed myosin-binding sites on actin to form across bridges. (Contraction begins when myosin binds to actin and forms cross bridges)

A series of events in which an electrical stimulus is conveyed to a muscle fiber to enact contraction.

1. Action potential is generated at the sarcolemma. 2. Action potential goes down the T tubule. 3. Voltage-gated tubule protein changes shape. 4. Calcium ion channels open. 5. Calcium exits the cistern into sarcoplasm. 6. Calcium binds to troponin. 7. Actin sites are exposed. 8. Cross bridges form between actin and myosin.