# Muscle contraction

Muscle contraction is a fundamental biological process that allows organisms to move and perform various bodily functions. It is primarily explained by the **sliding filament theory**.

#### Types of Muscle Tissue

There are three main types of muscle tissue in the body:

* **Skeletal muscle** (also called striated, striped, or voluntary muscle): This type is attached to bones by tendons and is used for movement, such as the biceps and triceps moving the lower arm. It is described as **neurogenic**, meaning it contracts when stimulated by impulses from motor neurones.
* **Cardiac muscle**: Found only in the heart, it contracts without conscious control. Cardiac muscle is **myogenic**, meaning it can contract and relax without receiving signals from nerves.
* **Smooth muscle**: Found in the walls of internal organs (excluding the heart), such as the stomach, intestine, blood vessels, and airways, and contracts without conscious control. It also typically contracts in response to motor neurones, but smooth muscle in arteries can contract when stretched by blood pressure without nervous system input.

The following summary primarily focuses on **skeletal muscle contraction**, which is detailed extensively in the sources.

#### Structure of Skeletal Muscle

Skeletal muscle is highly organized for contraction:

* **Muscle fibers**: Skeletal muscle is made up of large bundles of long cells called muscle fibers. These are specialized cells containing many nuclei (multinucleate or syncytium).
* **Sarcolemma**: The cell membrane of a muscle fiber. It folds inwards across the muscle fiber to form **transverse (T) tubules**, which help spread electrical impulses throughout the sarcoplasm.
* **Sarcoplasm**: The cytoplasm of a muscle cell.
* **Sarcoplasmic Reticulum (SR)**: A network of internal membranes running through the sarcoplasm. It stores and releases **calcium ions (Ca2+)**, which are crucial for muscle contraction.
* **Mitochondria**: Muscle fibers contain many mitochondria to provide the **ATP** needed for muscle contraction.
* **Myofibrils**: Long, cylindrical organelles within muscle fibers, specialized for contraction.
  * **Myofilaments**: Myofibrils contain bundles of **thick myosin filaments** and **thin actin filaments**.
  * **Sarcomere**: The basic contractile unit of a myofibril, marked by **Z-lines** at its ends.
  * **Banding Pattern**: Under an electron microscope, myofibrils show alternating dark and light bands:
    * **A-bands (dark)**: Contain thick myosin filaments and some overlapping thin actin filaments.
    * **I-bands (light)**: Contain only thin actin filaments.
    * **H-zone**: A lighter area within the A-band, containing only myosin filaments.
    * **M-line**: The middle of the myosin filaments, located in the center of the H-zone.

#### Sliding Filament Theory: Mechanism of Contraction

Muscle contraction occurs as myosin and actin filaments slide over one another, shortening the sarcomeres; the myofilaments themselves do not contract.

1. **Nerve Impulse Arrival at Neuromuscular Junction**: An action potential from a motor neurone arrives at the **neuromuscular junction**, a specialized cholinergic synapse between a motor neurone and a muscle cell.
2. **Neurotransmitter Release**: The action potential stimulates **voltage-gated calcium ion channels** to open in the presynaptic neurone, causing calcium ions (Ca2+) to diffuse into the synaptic knob. This influx causes **synaptic vesicles** (containing the neurotransmitter **acetylcholine (ACh)**) to fuse with the presynaptic membrane and release ACh into the **synaptic cleft** by exocytosis.
3. **Postsynaptic Depolarization**: ACh diffuses across the synaptic cleft and binds to specific **cholinergic receptors** (nicotinic cholinergic receptors) on the postsynaptic membrane (called the **sarcolemma** or motor end plate). This binding causes **sodium ion channels to open**, leading to an influx of sodium ions into the muscle cell. This influx causes **depolarization** of the sarcolemma.
4. **Action Potential Propagation and Ca2+ Release**: The depolarization spreads down the T-tubules to the sarcoplasmic reticulum (SR). This causes the SR to release stored calcium ions (Ca2+) into the sarcoplasm surrounding the myofibrils.
5. **Tropomyosin Displacement**: The influx of calcium ions triggers muscle contraction by binding to **troponin**. This binding causes the troponin molecule to change shape, which then pulls the associated **tropomyosin** (a protein coiled around the actin filament) out of the **actin-myosin binding site** on the actin filament.
6. **Cross-bridge Formation**: With the binding sites exposed, the **myosin heads** can now bind to the actin filaments, forming a bond called an **actin-myosin cross-bridge**.
7. **Power Stroke**: Calcium ions also activate **ATP hydrolase (ATPase)**, an enzyme on the myosin head, which hydrolyses ATP into ADP and inorganic phosphate (Pi). The energy released from ATP causes the myosin head to bend or tilt (the "power stroke"), which pulls the actin filament along in a rowing action towards the center of the sarcomere. This shortens the sarcomere, pulling the Z-lines closer together. During this process, the **I-band gets shorter**, and the **H-zone gets shorter**, while the **A-band stays the same length**.
8. **Cross-bridge Breaking and Reattachment**: Another ATP molecule binds to the myosin head, providing energy to **break the actin-myosin cross-bridge**, causing the myosin head to detach from the actin filament. The myosin head then returns to its starting position and reattaches to a different binding site further along the actin filament, ready for another power stroke. This cycle of attachment, movement, detachment, and reattachment repeats rapidly as long as calcium ions are present.
9. **Relaxation**: When nervous stimulation stops, calcium ions leave their binding sites on troponin and are actively transported back into the sarcoplasmic reticulum (this also requires ATP). This causes the troponin and tropomyosin molecules to return to their original positions, blocking the actin-myosin binding sites again. With no myosin heads attached, the actin filaments slide back to their relaxed position, lengthening the sarcomere.

#### Energy for Muscle Contraction

Muscle contraction is an **energy-requiring process** that uses a lot of ATP. ATP is rapidly used up and must be continually generated. ATP can be generated in three main ways:

1. **Aerobic respiration**: The primary source of ATP for muscle contraction, especially during long periods of low-intensity exercise. It occurs in the mitochondria.
2. **Anaerobic respiration**: Produces ATP rapidly by glycolysis, converting pyruvate to lactate. It is good for short bursts of hard exercise but leads to lactate build-up and muscle fatigue.
3. **ATP-phosphocreatine (PCr) system**: Generates ATP very quickly by phosphorylating ADP with a phosphate group from phosphocreatine. This system is used for short bursts of vigorous exercise but PCr runs out quickly.

#### Reflex Arcs and Speed of Conduction

Nervous communication allows rapid responses to stimuli. A **reflex arc** is the pathway of neurones (sensory, relay, motor) linking receptors to effectors in a rapid, involuntary response.

* **Speed of conduction** of action potentials along an axon is affected by:
  * **Myelination**: The myelin sheath acts as an electrical insulator, forcing action potentials to "jump" from one **node of Ranvier** to the next (saltatory conduction). This significantly increases the speed of transmission (up to 50 times faster).
  * **Axon diameter**: Larger diameter leads to faster conduction.
  * **Temperature**: Higher temperature increases conduction speed, but denaturing of proteins above 40°C causes speed to decrease.
* **All-or-Nothing Principle**: If a stimulus reaches a certain **threshold**, an action potential will always fire with the same voltage change. If the threshold is not reached, no action potential occurs.
* **Refractory Period**: After an action potential, there is a brief period where the neurone cannot be excited again. This ensures action potentials are **discrete**, limits their **frequency**, and ensures **unidirectional** transmission.

#### Synaptic Transmission

Neurones communicate at **synapses** by releasing chemical messengers called **neurotransmitters** into the **synaptic cleft**. This process is **unidirectional** because neurotransmitters are released only from the presynaptic side and receptors are only on the postsynaptic side.

* **Acetylcholinesterase (AChE)**, an enzyme, rapidly breaks down ACh in the synaptic cleft to ensure the response is short-lived and does not keep stimulating the postsynaptic neurone.
* **Summation**: Synapses can integrate information through **spatial summation** (neurotransmitters from many neurones are added) and **temporal summation** (impulses arrive quickly from the same neurone).
* **Inhibitory Synapses**: Some synapses release neurotransmitters that **hyperpolarize** the postsynaptic membrane (make it more negative), preventing action potential generation.
* **Drugs** can affect synaptic transmission, for example, nerve gases stop ACh from being broken down, leading to loss of muscle control.