Muscles and Movement (OCR A-Level Biology A): Revision Notes

Muscles and Movement

Introduction to muscle-driven movement

The brain and central nervous system coordinate all body movements through a complex network of sensory input and motor output. Movement can occur as a direct environmental response or to maintain body posture. The brain processes information from various sense organs, including stretch receptors within the muscles themselves, before sending coordinated signals to multiple muscles via motor neurones travelling through the spinal cord.

In vertebrates, movement depends on skeletal joints operated by muscles arranged in antagonistic pairs. This arrangement is necessary because muscles generate force only through contraction. Since an individual muscle cannot both flex and extend a joint, a second muscle working in opposition is required to return the joint to its original position.

Skeletal muscle structure

Three distinct muscle types exist in the human body: skeletal (also termed striated or voluntary), smooth (also termed involuntary), and cardiac. Skeletal muscle, responsible for moving joints, possesses a highly organized and complex structure.

Skeletal muscle displays a hierarchical organization. Multiple muscle fibres bundle together to form a fascicle, and numerous fascicles combine to create the complete muscle. Although termed muscle "cells," these fibres are actually multinucleate structures formed through the fusion of several cells during development.

Transverse tubules (T tubules) are sarcolemma extensions that penetrate deep into the fiber, conducting electrical impulses rapidly throughout the cell. The fiber contains numerous myofibrils, which are the actual contractile elements. High ATP demand during contraction necessitates abundant mitochondria within each fiber.

Myofibril structure and the sarcomere

Myofibrils contain bundles of protein filaments that slide past one another during contraction. Two types of myofilaments exist: thick filaments composed primarily of myosin protein, and thin filaments composed primarily of actin protein. Both myosin and actin function as cytoskeletal components in many cell types.

The regular alternating arrangement of thick and thin filaments creates the characteristic striped appearance giving skeletal muscle its alternative name: striated muscle. Darker bands represent regions where filaments overlap.

The repeating contractile unit along the myofibril is the sarcomere, bounded by Z lines at each end. Within each sarcomere:

• Z line: attachment point for thin filaments
• I band: region containing only thin filaments (appears lighter)
• A band: region containing thick filaments, including overlap with thin filaments (appears darker)
• H zone: central region containing only thick filaments
• M line: center of the sarcomere where thick filaments attach

The sliding filament model

The sliding filament theory explains muscle contraction through relative movement of thick and thin filaments, which slide past each other without changing their individual lengths. Understanding this mechanism requires examination of the filament structures in detail.

Myosin thick filaments possess projections called myosin heads capable of binding to actin and generating movement. The thin filaments contain actin molecules arranged in a twisted chain, with tropomyosin protein wound around them. Troponin protein molecules attach to tropomyosin at regular intervals.

In relaxed muscle, tropomyosin physically blocks myosin-binding sites on actin, preventing myosin heads from attaching. When calcium ions become available, they bind to troponin, causing a conformational change that moves tropomyosin away from the binding sites.

During contraction, the I band and H zone become noticeably narrower as thin filaments slide toward the sarcomere center. The A band maintains constant width because thick filament length remains unchanged.

Mechanism of muscle contraction

When a nerve impulse arrives at a muscle fiber, the following sequence produces contraction:

The nerve impulse depolarizes the sarcolemma. T tubules rapidly transmit this depolarization throughout the entire fiber. The depolarization triggers voltage-gated calcium channels in the sarcoplasmic reticulum to open, releasing $\text{Ca}^{2+}$ ions into the sarcoplasm.

Calcium ions bind to troponin molecules, causing them to change shape. This conformational change pulls tropomyosin away from myosin-binding sites on actin, exposing them.

Myosin heads bind to the newly exposed sites on actin. This binding triggers release of $\text{ADP}$ and inorganic phosphate ($\text{P}_i$) already present in the myosin heads. Release of these products causes the myosin heads to bend, creating a power stroke that pulls the thin filaments toward the sarcomere center.

Fresh $\text{ATP}$ molecules bind to myosin heads, causing them to detach from actin. The myosin head then functions as an ATPase enzyme, hydrolyzing $\text{ATP}$ into $\text{ADP}$ and $\text{P}_i$. Energy from this hydrolysis resets the myosin head to its extended position, ready to bind to the next myosin-binding site along the actin filament.

This cycle repeats continuously while calcium ions remain available, pulling thin filaments progressively toward the sarcomere center. The cumulative shortening of all sarcomeres produces contraction of the entire muscle.

When nerve impulses cease, calcium ions are actively pumped back into the sarcoplasmic reticulum. Without calcium, troponin returns to its original shape, allowing tropomyosin to block the myosin-binding sites again, and the muscle relaxes.

Energy supply for muscle contraction

$\text{ATP}$ plays an essential role in muscle contraction, with muscles requiring substantial quantities. Muscle fibers contain numerous mitochondria that normally provide sufficient $\text{ATP}$ through aerobic respiration. During vigorous exercise, however, $\text{ATP}$ supplies may become inadequate. Muscles employ several strategies to address this:

Myoglobin serves as an oxygen storage protein within muscles. This pigment releases oxygen only when surrounding oxygen concentration drops very low, providing an emergency oxygen reserve for aerobic respiration.

Anaerobic respiration can support muscles for short periods during intense activity. This process provides nearly all energy for brief strenuous bursts but releases far less ATP per glucose molecule than aerobic respiration, making it inefficient for sustained activity.

The ATP-creatine phosphate system provides additional $\text{ATP}$ for very brief periods. Creatine phosphate ($\text{PCr}$) stored in muscle fibers can rapidly donate phosphate to convert $\text{ADP}$ into $\text{ATP}$:

$\text{ADP} + \text{PCr} \rightarrow \text{ATP} + \text{Cr}$

This reaction produces no lactate, thus avoiding muscle fatigue. However, creatine phosphate stores are extremely limited, depleting within a few seconds and providing $\text{ATP}$ only for very short bursts of maximum activity.

The neuromuscular junction

Skeletal muscle contraction occurs under nervous control through impulses traveling along motor neurones. Where a motor neurone meets muscle tissue, a specialized synapse called a neuromuscular junction forms.

Neuromuscular junctions share similarities with nerve synapses but possess several distinctive features:

Acetylcholine functions as the neurotransmitter at all somatic motor neurones, whereas different nerve synapses employ various neurotransmitters. The postsynaptic membrane (the muscle fiber motor end plate) is extensively folded to increase surface area, allowing many more receptors than in nerve synapses. In nerve synapses, a single impulse may fail to trigger a postsynaptic action potential if threshold is not reached. In contrast, a single impulse at a neuromuscular junction invariably causes muscle fiber contraction.

The neuromuscular junction operates through the following mechanism:

An impulse arriving at the motor neurone terminal causes calcium ion influx, triggering release of acetylcholine from synaptic vesicles into the synaptic cleft. Acetylcholine diffuses across the narrow cleft and binds to cholinergic receptors on the motor end plate.

This binding generates an impulse that spreads across the entire sarcolemma of the muscle fiber. Depolarization simultaneously travels down all T tubules throughout the fiber. T tubule depolarization directly couples to the contraction mechanism by opening voltage-gated calcium channels in the surrounding sarcoplasmic reticulum.

$\text{Ca}^{2+}$ ions diffuse from the sarcoplasmic reticulum among the myofibrils, where they bind to troponin to initiate contraction. Acetylcholinesterase enzyme in the synaptic cleft then breaks down acetylcholine, preventing continuous stimulation unless additional impulses arrive.

When the sarcolemma, T tubules, and sarcoplasmic reticulum are no longer depolarized, calcium ions are actively pumped back into the sarcoplasmic reticulum, terminating contraction.

Types of muscle tissue

Fast-twitch and slow-twitch muscle fibres

Voluntary (skeletal or striated) muscles can be consciously controlled, though their actions may occur subconsciously (such as during posture maintenance). Skeletal muscles may contain one or both of two fiber types:

Fast-twitch muscle fibres contract rapidly but fatigue quickly. Slow-twitch muscle fibres contract more slowly but resist fatigue for extended periods. Some muscles consist entirely of one fiber type, while many contain both. For example, leg muscles contain slow-twitch fibers that contract continuously for posture maintenance, plus fast-twitch fibers that can be recruited for rapid leg movements.

Smooth (involuntary) muscle

Smooth muscle (also called involuntary muscle) controls many internal organs without conscious control. It lacks the striations characteristic of skeletal muscle, though it does contain actin and myosin filaments arranged differently.

Smooth muscle forms part of the walls of various internal organs including the gut, bladder, uterus, and blood vessels. It controls processes such as gut peristalsis and arterial diameter regulation. Smooth muscle cells possess a much simpler structure than striated muscle. The cells are smaller, spindle-shaped, and contain only a single nucleus.

Cardiac muscle

Cardiac muscle exists exclusively in the heart. This specialized striated muscle possesses several unique properties:

Cardiac muscle is myogenic, meaning it contracts without requiring external nervous or hormonal stimulation. It beats rhythmically on its own, though the autonomic nervous system can regulate beating rate. Muscle fibers branch to form an interconnected network extending through atrial and ventricular walls.

Cardiac muscle never fatigues and contracts continuously throughout an organism's entire lifetime (exceeding $2 \times 10^9$ contractions over an average human lifespan). Fibers connect to each other via specialized junctions called intercalated discs, which permit depolarization to transfer directly from cell to cell.

Continuous cardiac muscle contraction requires substantial energy, so cells are densely packed with mitochondria to generate the necessary $\text{ATP}$.

Summary diagram

This sarcomere diagram illustrates key structures in relaxed muscle: Z lines define sarcomere boundaries, the A band contains thick filaments, I bands contain only thin filaments, and the H zone contains only thick filaments in the sarcomere center.

During contraction, the H zone and I band narrow as thin filaments slide toward the M line. The A band width remains constant because thick filament length does not change.