Musculoskeletal System Overview

Skeletal muscles attach to bones directly or via tendons.

The stationary attachment point of a muscle during contraction.

The attachment point of a muscle that moves during contraction.

Pairs of muscles that work opposite to each other at a joint.

The process of muscle contraction where filaments slide past each other.

A muscle cell, also called a myocyte, containing bundles of myofibrils.

An elongated structure within a muscle fiber (cell), composed of thick and thin myofilaments.

Thread-like structures composing myofibrils; categorized as thick (myosin) or thin (actin).

A protein that forms the thin myofilaments in muscle fibers.

A protein that forms the thick myofilaments in muscle fibers.

The smallest functional unit of muscle contraction, located between two Z-lines.

A protein disc that separates sarcomeres; crucial for muscle contraction.

A bundle of muscle fibers within a muscle.

A muscle cell; also called a muscle fiber

The plasma membrane of a muscle cell (myocyte).

Myofibrils shorten as the sarcomeres within them contract.

No, myofilaments themselves do not shorten. They slide past each other.

The A band is the region of the sarcomere that contains both thick and thin filaments. It maintains a constant width during contraction.

The I band consists of only thin filaments. It shortens during contraction.

The H zone is the central region of the A band containing only thick filaments. It narrows during contraction.

Myosin forms the thick filaments. It has globular heads that bind to actin and generate force to slide the filaments.

Actin forms the thin filaments. It interacts with myosin heads to facilitate sliding.

ATP provides energy for myosin heads to bind to and release from actin, powering the sliding process.

The hydrolysis of ATP by myosin activates the head, preparing it for the power stroke.

After ATP hydrolysis, ADP and inorganic phosphate (Pi) remain bound to the myosin head. This allows the head to bind to actin, forming a cross-bridge.

The power stroke is the movement of the myosin head, pulling the actin filament towards the center of the sarcomere. This is driven by the release of ADP and Pi.

The power stroke stops when ATP binds to the myosin head, causing it to detach from actin.

After ATP binds and the myosin detaches from actin, the myosin head returns to its original conformation. This is ready for another cycle.

The presence of ATP and calcium ions regulate the cross-bridge cycle. Calcium allows actin and myosin to interact, while ATP provides the energy for the cycle.

The repeated cycle of myosin binding, pulling, and detaching from actin, fueled by ATP, results in the sliding of filaments past each other, shortening the sarcomere and causing muscle contraction.

Without ATP, the myosin head remains bound to actin, causing the muscle to become stiff and rigid, leading to rigor mortis.

Tropomyosin blocks the myosin binding sites on actin filaments when the muscle is relaxed.

Troponin binds to calcium and moves tropomyosin aside, exposing the myosin binding sites on actin.

High calcium levels in the muscle fiber cytoplasm trigger muscle contraction by binding to troponin.

In low calcium levels, tropomyosin prevents the formation of cross-bridges between actin and myosin, keeping the muscle relaxed.

In high calcium levels, troponin binds to calcium, moving tropomyosin aside and allowing cross-bridge formation, leading to muscle contraction.

The sarcoplasmic reticulum within muscle fibers stores and releases calcium ions that control muscle contraction.

Motor neurons stimulate muscle contraction by releasing acetylcholine at the neuromuscular junction, which initiates a cascade leading to calcium release from the sarcoplasmic reticulum.

The arrival of a nerve impulse at the neuromuscular junction causes the muscle fiber membrane to depolarize, triggering a series of events leading to calcium release from the sarcoplasmic reticulum.

The heart's ability to generate its own rhythm through specialized muscle cells (pacemakers), independent of nervous signals.

The autonomic nervous system modifies (speeds up or slows down) the heart's pacemakers, but doesn't initiate the heartbeat.

Smooth muscle is simple, spindle-shaped, found in internal organs, controlled by the autonomic nervous system, and arranged in sheets.

Smooth muscle cells are connected via gap junctions allowing electrical signals to spread throughout the sheet. This ensures coordinated contraction.

The plasma membrane of smooth muscle cells is sensitive to stretch. Stretching the muscle triggers depolarization and contraction.

Smooth muscle plays a key role in various bodily functions, including digestion (food movement) and blood vessel constriction and dilation.

ACh binds to receptors on the sarcolemma, causing sodium ions (Na+) to flow into the muscle cell, generating an action potential.

Calcium (Ca++) is vital for muscle contraction. It releases from the sarcoplasmic reticulum and binds to troponin, exposing actin binding sites allowing myosin to bind and initiate the power stroke.