Muscles and Movement

Movement is one of the defining features of animals. Every movement your body makes — from blinking to running a marathon, from your heartbeat to moving food through your intestines — is powered by muscle. Your body has three distinct types, each designed for a different job. Skeletal muscle (also called striated or voluntary muscle) is what most people think of when they hear "muscle." It is attached to bones by tendons and moves your skeleton. You control it consciously — you decide to raise your arm, kick a ball, or type on a keyboard. Under a microscope it has a striped (striated) appearance because of the regular arrangement of its proteins. Cardiac muscle is found only in the heart. Like skeletal muscle, it is striated — but unlike skeletal muscle, it is involuntary (you cannot decide to stop your heart). Cardiac muscle cells are connected by special junctions called intercalated discs that allow electrical signals to pass rapidly from cell to cell, making the entire heart muscle contract as one coordinated unit. Smooth muscle lines the walls of hollow organs — blood vessels, the digestive tract, the airways, the bladder, and the uterus. It is not striated, and it is involuntary — controlled by the autonomic nervous system and hormones. Smooth muscle contracts more slowly than skeletal muscle but can sustain contractions for long periods. You cannot live without all three: skeletal muscle moves you through the world, cardiac muscle keeps blood moving, and smooth muscle controls the internal processes you never think about.

Inside every skeletal muscle fibre (a single muscle cell) are thousands of parallel myofibrils — rod-like structures that run the length of the cell. Each myofibril is made of repeating units called sarcomeres — the basic unit of muscle contraction. Each sarcomere contains two types of protein filaments: - Actin (thin filaments) — arranged in two strands twisted together - Myosin (thick filaments) — with tiny paddle-like heads projecting outwards The sliding filament theory explains contraction: 1. A nerve signal arrives at the muscle fibre 2. The signal triggers the release of calcium ions (Ca²⁺) from the sarcoplasmic reticulum (a calcium store inside the cell) 3. Calcium binds to a protein called troponin, which shifts another protein (tropomyosin) out of the way — exposing binding sites on actin 4. Myosin heads bind to actin, forming cross-bridges 5. Myosin heads pivot (the "power stroke"), pulling the actin filaments toward the centre — the sarcomere shortens 6. ATP (energy) is used to release and reset the myosin head, ready for the next cycle 7. This cycle repeats hundreds of times per second The actin and myosin filaments themselves do not shorten — they slide past each other. This is why it is called the "sliding filament" theory. The overall shortening of millions of sarcomeres adds up to visible muscle contraction. Rigor mortis — the stiffening of a body after death — occurs because calcium leaks out of the sarcoplasmic reticulum and myosin heads bind to actin permanently, but without ATP, they cannot release. The muscle locks in a contracted state until the proteins begin to break down.

Muscles do not contract on their own — they wait for instructions from nerve cells (motor neurons). The connection point between a motor neuron and a muscle fibre is called the neuromuscular junction. Here is what happens when your brain tells your muscle to contract: 1. An action potential (electrical signal) travels down the motor neuron to its end (axon terminal) 2. The action potential triggers calcium channels to open in the axon terminal 3. Calcium floods in, causing vesicles (little bubbles) full of a chemical called acetylcholine (ACh) to fuse with the membrane and release ACh into the gap between the nerve and muscle (the synaptic cleft) 4. ACh crosses the gap and binds to receptors on the muscle cell membrane 5. This opens ion channels, triggering an action potential in the muscle fibre 6. The muscle action potential spreads throughout the fibre and triggers calcium release and contraction 7. ACh is rapidly broken down by an enzyme called acetylcholinesterase, stopping the signal Why this matters clinically: - Myasthenia gravis is an autoimmune disease where antibodies block ACh receptors at the neuromuscular junction — muscles become weak and fatigable. Treatment includes drugs that inhibit acetylcholinesterase (so ACh lasts longer) and immunosuppressants. - Botulinum toxin (Botox) blocks the release of ACh from the nerve terminal — the muscle cannot receive the signal and is paralysed. Used medically to treat muscle spasms, and cosmetically to reduce facial wrinkles. - Sarin (nerve agent) irreversibly inhibits acetylcholinesterase — ACh builds up continuously, muscles contract permanently and cannot relax. Death occurs from respiratory muscle paralysis.

Not all muscle fibres are the same. Skeletal muscles contain a mix of two main types, in different proportions depending on the muscle's job. Type I fibres (slow-twitch): - Contract slowly but are very resistant to fatigue - Have many mitochondria and a rich blood supply — they use oxygen efficiently to produce ATP (aerobic respiration) - Red in colour (from the oxygen-carrying protein myoglobin) - Ideal for endurance — your postural muscles (holding you upright) and endurance runners' leg muscles are mostly Type I - Marathon runners tend to have a high proportion of Type I fibres Type II fibres (fast-twitch): - Contract rapidly and powerfully but fatigue quickly - Fewer mitochondria — rely more on anaerobic (without oxygen) energy production - Whiter in colour - Ideal for powerful, short bursts — sprinting, jumping, throwing - 100-metre sprinters tend to have a high proportion of Type II fibres Muscle fatigue happens when a muscle can no longer maintain the required force. Causes include: - Depletion of ATP and creatine phosphate (the quick energy stores) - Accumulation of lactate and hydrogen ions (making the muscle environment acidic) — causing the burning sensation in your muscles during intense exercise - Depletion of calcium release from the sarcoplasmic reticulum Creatine phosphate is a rapid energy store in muscle that can instantly regenerate ATP — but only for about 8–10 seconds. This is why a 100m sprint draws primarily on creatine phosphate. After that, the muscle switches to burning glucose (glycolysis) and eventually fat. DOMS (delayed onset muscle soreness) — the ache you feel 24–48 hours after intense exercise — is caused by microscopic tears in muscle fibres from unaccustomed exercise (especially downhill running or weights). During repair, the muscle fibres rebuild slightly larger and stronger. This is the physical basis of exercise-induced muscle growth.

Muscles can only pull — they cannot push. A muscle shortens when it contracts, pulling the bone it is attached to. To move a bone in both directions, muscles are arranged in opposing pairs called antagonistic pairs. Example — the biceps and triceps: - To bend (flex) your elbow: the biceps (front of upper arm) contracts and shortens, pulling the forearm up. Meanwhile the triceps (back of upper arm) relaxes and lengthens. - To straighten (extend) your elbow: the triceps contracts, pulling the forearm back down. The biceps relaxes. - If both contract simultaneously, the arm is locked rigid — useful for stabilising a joint. The roles muscles play during movement: - Agonist (prime mover) — the muscle doing most of the work for a specific movement (biceps during elbow flexion) - Antagonist — the opposing muscle that must relax and stretch (triceps during elbow flexion) - Synergist — a muscle that assists the agonist by stabilising nearby joints - Fixator — a muscle that holds a bone still while others act on it (your core muscles stabilise your spine during limb movements) Tendons and levers: Muscles attach to bones via tendons — tough, flexible cords of collagen. The arrangement of muscle, tendon, and bone creates a lever system that amplifies force or speed depending on the joint. Clinical connection — muscle injuries: A strain is a torn muscle fibre (graded I–III by severity). A rupture is a complete tear of a muscle or tendon (e.g. Achilles tendon rupture — more common in men over 30 doing explosive activity). Duchenne muscular dystrophy (DMD) is a genetic disease where the protein dystrophin — which connects muscle fibres to the surrounding tissue — is absent, causing progressive muscle breakdown from childhood.