Question

Explain why the myosin heads don't bind to the actin when the muscle is at rest. Then, provide a stepby-step explanation of how depolarization of the muscle fiber plasma membrane by ACh leads to the binding of the myosin heads to actin. (That is, explain excitation-contraction coupling.)

Short answer

At rest, myosin heads can't bind to actin due to the presence of tropomyosin blocking binding sites. Depolarization occurs when ACh binds to nicotinic receptors, causing sodium influx and action potential propagation along the sarcolemma. This reaches the T-tubules, causing calcium release from the sarcoplasmic reticulum. Calcium ions bind to troponin, leading to tropomyosin shifting and exposing myosin-binding sites on actin. Finally, myosin heads bind to actin, initiating muscle contraction through excitation-contraction coupling.

Step-by-step solution

Describe the state of skeletal muscle at rest

At rest, the skeletal muscle is in a relaxed state. In this state, the myosin heads are unable to bind to the actin because the binding sites are blocked by the presence of tropomyosin, a protein that covers the binding sites on the actin filaments. Calcium ions, which are required for the binding process, are stored in the sarcoplasmic reticulum, keeping the muscle relaxed.

Describe the role of acetylcholine (ACh) in depolarization

Acetylcholine (ACh) is a neurotransmitter that is released at the neuromuscular junction by the motor neuron. Upon reaching the muscle fiber plasma membrane (sarcolemma), ACh binds to nicotinic receptors, causing an influx of sodium ions (Na+) into the muscle fiber. This results in the depolarization of the sarcolemma.

Explain the propagation of action potential along the sarcolemma

Once the sarcolemma is depolarized, this electrical change (called an action potential) propagates along the length of the muscle fiber. The action potential is transmitted from the sarcolemma into the interior of the muscle fiber through the T-tubules, which are extensions of the sarcolemma.

Describe the release of calcium ions from the sarcoplasmic reticulum

The action potential in the T-tubules causes the voltage-sensitive calcium channels in the sarcoplasmic reticulum to open, resulting in the release of stored calcium ions (Ca2+) into the cytoplasm of the muscle fiber.

Explain the binding of calcium ions to troponin

The released calcium ions bind to the troponin, a protein that is part of the muscle's thin filaments. When calcium ions bind to troponin, it undergoes a conformational change which causes the tropomyosin to shift, exposing the myosin-binding sites on the actin filaments.

Describe the binding of myosin heads to actin

With the myosin-binding sites now exposed, the myosin heads can bind to the actin filaments, forming a cross-bridge. This binding initiates the power stroke, in which the myosin heads pull the actin filaments towards the center of the sarcomere, leading to muscle contraction. This process is called excitation-contraction coupling, as the electrical excitation (action potential) is translated into mechanical contraction.

Key concepts

Skeletal Muscle Physiology

To understand how our muscles work, it's essential to dive into the science of skeletal muscle physiology. This facet of biology deals with the functions of the skeletal muscular system, which includes the mechanics of movement and support.

At rest, each muscle fiber is poised for action, but various checkpoints ensure that energy is not expended unnecessarily. For muscles to contract, a series of steps that begins with a nerve signal must be followed. Kicking off this cascade is the neurotransmitter acetylcholine, but more on that later. The magic of muscle movement is regulated by proteins and ions, making it a beautifully complex ballet on a microscopic scale.

Acetylcholine Neurotransmitter

Acetylcholine (ACh) is the star player when it comes to muscle movement. It's a neurotransmitter released by motor neurons to signal muscle fibers. Its role extends to cognitive functions in the brain, but in the realm of muscles, its job is to act as a chemical messenger.

When ACh is released, it crosses the gap at the neuromuscular junction and binds to receptors on the muscle cell membrane. This leads to an electrochemical reaction that sets the stage for muscle contraction. In short, without ACh, your muscles wouldn't get the memo to move!

Sarcolemma Depolarization

Depolarization of the sarcolemma is akin to flipping a switch to light up a series of Christmas tree lights. This action is where the sarcolemma, the membrane surrounding muscle fibers, responds to the binding of acetylcholine by changing its electrical state.

An influx of sodium ions into the muscle fiber follows, disrupting the balance and triggering an action potential – an electrical pulse that travels the length of the fiber. This process is critical as it sets everything in motion for the muscle to contract. It's the starting gun, if you will, of muscle contraction.

Calcium Ions in Muscle Contraction

Calcium ions are like the key that unlocks muscle contraction. They are usually stored away neatly in the sarcoplasmic reticulum, waiting for the right signal. Once the action potential reaches the T-tubules, calcium channels open up and these ions flood the cell.

What follows is a chain reaction where calcium binds to the troponin on actin filaments, leading to a shift in tropomyosin that exposes the myosin-binding sites. It's a critical moment that turns an electrical signal into an imminent muscle contraction.

Actin and Myosin Interaction

Actin and myosin are the movers and shakers in the muscle contraction process. Actin filaments make up the thin filaments while myosin makes up the thick ones. When the myosin-binding sites are exposed, the myosin heads latch on to actin, creating a cross-bridge.

Following this, a 'power stroke' occurs, pulling the actin inwards and leading to contraction. This interaction is the culmination of excitation-contraction coupling – the connection between the action potential and the muscle fiber's contraction. It's akin to pulling the drawstring of a curtain, bringing actin filaments to the center and tightening the muscle.