Muscle contraction is the fundamental biological process through which tension is generated within muscle tissue, allowing for movement, posture maintenance, and the propulsion of substances through internal organs. While the body contains three types of muscle tissue (skeletal, cardiac, and smooth), this discussion focuses specifically on the sequence of events governing the voluntary movement of skeletal muscles. Understanding this sequence reveals how an electrical signal from the nervous system translates into physical force.
Initiation The Nerve Impulse
Muscle contraction begins when an action potential travels down a motor neuron, originating in the brain or spinal cord. The motor neuron terminates at the neuromuscular junction (NMJ), a specialized gap near the muscle fiber. When the action potential arrives, it triggers calcium influx into the nerve terminal, causing the release of acetylcholine (ACh) into the junction.
ACh diffuses across the gap and binds to receptors on the muscle fiber’s membrane (sarcolemma). This binding opens ion channels, allowing a rapid influx of positively charged sodium ions (\(\text{Na}^{+}\)) into the muscle cell.
This influx causes a local depolarization, the end-plate potential, which triggers a full action potential across the muscle fiber’s surface. This electrical impulse penetrates deep into the muscle cell.
Excitation and Calcium Release
The action potential travels deep inside the muscle fiber via transverse tubules (T-tubules), which are infoldings of the sarcolemma. T-tubules conduct the electrical wave throughout the cell, ensuring simultaneous activation of contractile elements.
The T-tubules are closely associated with the sarcoplasmic reticulum (SR), which stores high concentrations of calcium ions (\(\text{Ca}^{2+}\)). The electrical signal causes a change in the dihydropyridine receptors (DHPRs) embedded in the T-tubule membrane. In skeletal muscle, these DHPRs are physically linked to the ryanodine receptors (RyRs) on the SR membrane.
This coupling causes the RyRs to open, resulting in a sudden surge of stored \(\text{Ca}^{2+}\) ions into the sarcoplasm. This rapid calcium release is the direct chemical trigger for contraction, linking electrical excitation to mechanical shortening, a process called excitation-contraction coupling.
The Sliding Filament Mechanism
The physical shortening of the muscle is explained by the sliding filament mechanism, detailing how protein filaments interact within the sarcomere. Thick filaments are composed of myosin, and thin filaments are made of actin. In a relaxed muscle, these filaments lie parallel within the sarcomere, the muscle’s functional unit.
Actin filaments contain binding sites that myosin heads must access. In the resting state, these sites are blocked by two regulatory proteins: tropomyosin and troponin.
The \(\text{Ca}^{2+}\) released from the SR binds directly to troponin. This binding causes a conformational change in the troponin complex, pulling tropomyosin away from the active sites on the actin filament. With the sites exposed, the myosin heads attach to the actin, forming a cross-bridge.
The cross-bridge cycle requires energy from adenosine triphosphate (ATP). Before attachment, the myosin head hydrolyzes ATP into ADP and inorganic phosphate (\(\text{P}_{\text{i}}\)), storing energy and placing the head in a “cocked” position. The release of \(\text{P}_{\text{i}}\) triggers the power stroke, where the myosin head pivots and forcefully pulls the actin filament toward the sarcomere center.
Following the power stroke, ADP is released, and the myosin head remains tightly bound to the actin (rigor). A new ATP molecule must bind to the myosin head to cause detachment from the actin filament.
The cycle repeats as the new ATP is hydrolyzed, recocking the myosin head to attach further down the actin. This continuous formation and breaking of cross-bridges shortens the sarcomere, generating tension and causing the muscle to shorten, provided \(\text{Ca}^{2+}\) and ATP remain available.
Muscle Relaxation and Recovery
Contraction stops when the motor neuron ceases sending the action potential. Acetylcholine is rapidly broken down by acetylcholinesterase in the neuromuscular junction, ending the stimulation of the muscle fiber membrane and stopping the electrical signal.
The primary step in relaxation is the swift removal of \(\text{Ca}^{2+}\) from the sarcoplasm. Specialized calcium pumps, such as the Sarcoplasmic Endoplasmic Reticulum Calcium ATPase (SERCA), transport \(\text{Ca}^{2+}\) ions back into the SR storage compartment. This reuptake consumes ATP energy to lower the intracellular calcium concentration.
As the \(\text{Ca}^{2+}\) concentration drops, the ions unbind from troponin. This allows tropomyosin strands to slide back, blocking the myosin binding sites on the actin filaments. Since cross-bridges cannot form, the muscle fibers passively return to their resting length, and tension dissipates.