Skeletal Muscles (AQA A-Level Biology): Revision Notes

Contraction of Skeletal Muscle

Antagonistic muscle pairs

Skeletal muscles attach to bones via tendons and work by generating force that moves bones around joints. Since bones are incompressible, muscles can only pull - they cannot push. This creates a requirement for antagonistic muscle pairs that work in opposite directions.

When one muscle in an antagonistic pair contracts, the other relaxes. To reverse the movement, the contracted muscle must relax and return to its original length, while its partner muscle contracts. This coordinated action allows for controlled movement in both directions around joints.

Structure of muscle fibres

Skeletal muscle fibres contain organised arrangements of protein filaments that enable contraction. The functional unit of muscle contraction is the sarcomere, which extends between two Z-lines.

Within each sarcomere are two main types of protein filaments:

• Thick filaments made of myosin protein
• Thin filaments made of actin protein

The arrangement creates distinct bands visible under microscopy:

• A-band: the full length of thick myosin filaments
• I-band: regions containing only thin actin filaments
• H-zone: central region with only thick filaments
• Z-lines: boundaries between adjacent sarcomeres

The sliding filament mechanism

Muscle contraction occurs through the sliding filament mechanism, where thick and thin filaments slide past each other without the filaments themselves shortening. This process causes the sarcomere to shorten while maintaining the length of individual protein filaments.

Evidence supporting the sliding filament mechanism

Microscopic observations of contracting muscle provide clear evidence for the sliding filament theory. During contraction, specific changes occur in the banding pattern:

• The I-band becomes narrower as actin filaments slide further between myosin filaments
• The Z-lines move closer together, reducing overall sarcomere length
• The H-zone becomes narrower as actin filaments overlap more with myosin
• The A-band remains the same width because myosin filament length is unchanged

These observations confirm that filaments slide past each other rather than shortening themselves.

Key proteins in muscle contraction

Three main proteins coordinate the sliding filament mechanism:

Myosin forms the thick filaments and has two distinct components:

• A fibrous protein arranged in filaments containing several hundred molecules
• Globular protein heads that can bind to actin and change shape during contraction

Actin is a globular protein arranged in long chains twisted into a helical strand forming the thin filaments.

Tropomyosin consists of long thin threads wound around actin filaments, acting as a regulatory protein that controls access to binding sites.

Muscle stimulation and contraction mechanism

Muscle stimulation

Muscle contraction begins when an action potential reaches neuromuscular junctions simultaneously across the muscle fibre. This triggers a cascade of events:

• Calcium ion protein channels open in the synaptic knob
• Calcium influx causes synaptic vesicles to fuse with the presynaptic membrane
• Acetylcholine is released into the synaptic cleft
• Acetylcholine binds to receptors on the muscle cell membrane, causing depolarisation

Muscle contraction process

The action potential travels deep into the muscle fibre through T-tubules, which connect to the sarcoplasmic reticulum (specialised endoplasmic reticulum in muscle cells). This system has actively transported calcium ions from the cytoplasm, creating very low calcium concentrations.

The action potential triggers calcium ion channels to open in the sarcoplasmic reticulum, allowing calcium to diffuse into the muscle cytoplasm down a concentration gradient.

The presence of calcium ions causes tropomyosin molecules to shift position, exposing binding sites on actin filaments that were previously blocked.

The cross-bridge cycle

Once binding sites are exposed, myosin heads can attach to actin filaments forming cross-bridges. The detailed mechanism involves a repeating cycle:

This cycle can repeat up to 100 times per second while calcium concentrations remain high, creating smooth muscle contraction through the coordinated action of many cross-bridges.

Muscle relaxation

When nervous stimulation ceases, muscle relaxation occurs through active processes:

• Calcium ions are actively transported back into the sarcoplasmic reticulum using energy from ATP hydrolysis
• Reduced calcium levels allow tropomyosin to block actin binding sites again
• Myosin heads can no longer bind to actin filaments, so contraction stops
• Antagonistic muscles can now pull the relaxed muscle back to its original length

Energy supply during muscle contraction

Muscle contraction requires substantial energy, supplied primarily through ATP hydrolysis. Energy is needed for:

• Movement of myosin heads during the cross-bridge cycle
• Active transport of calcium ions back into the sarcoplasmic reticulum

During intense muscle activity, ATP demand exceeds the rate at which blood can supply oxygen for aerobic respiration. Additional ATP generation occurs through:

Anaerobic respiration: Regenerating ATP from ADP through pyruvate fermentation, though this produces lactate and is less efficient.

Phosphocreatine system: Phosphocreatine acts as an immediate energy store in muscle, rapidly regenerating ATP by donating phosphate groups to ADP. This system provides energy during short bursts of intense activity.

The phosphocreatine store is replenished using phosphate from ATP during periods when the muscle is relaxed, creating an efficient energy buffer system.