Muscle contraction allows for movement, posture maintenance, and blood circulation. It involves the generation of tension within muscle cells, which may or may not result in shortening. The sliding filament model explains how muscles achieve this. This model describes how protein filaments within muscle cells interact and slide past one another to produce force and facilitate movement.
Fundamental Structures of Muscle Contraction
The basic contractile unit of a muscle fiber is the sarcomere, which repeats along the length of the muscle. Each sarcomere is defined by Z-discs, which anchor the thin protein filaments. These thin filaments are composed of actin, arranged as two coiled strands.
Interspersed with the thin actin filaments are thicker filaments, made of the protein myosin. Each myosin molecule features a long tail and two globular heads, which interact with actin. The organized arrangement of these filaments within the sarcomere creates distinct regions: the A-band, encompassing the entire length of the thick myosin filaments, and the I-band, containing only the thin actin filaments. A central H-zone exists within the A-band where only myosin is present.
The Contraction Process
Muscle contraction begins with myosin heads forming attachments to actin filaments, creating cross-bridges. Following this attachment, the “power stroke” occurs. During the power stroke, the myosin head pivots, pulling the actin filament inward towards the center of the sarcomere. This action generates the mechanical force for muscle shortening.
After the power stroke, a molecule of adenosine triphosphate (ATP) binds to the myosin head, causing it to detach from the actin filament. Without ATP, the myosin heads would remain bound to actin, leading to a rigid state, as seen in rigor mortis. The bound ATP is then hydrolyzed into adenosine diphosphate (ADP) and inorganic phosphate. The released energy “re-cocks” the myosin head, returning it to a high-energy position and preparing it to bind to another site on the actin filament for the next contraction cycle.
During this process, individual actin and myosin filaments do not physically shorten. Instead, they slide past one another, drawing the Z-discs closer together and causing the overall shortening of the sarcomere and the entire muscle. This repetitive cycle of attachment, pulling, detachment, and re-cocking, powered by ATP, drives muscle contraction.
Initiating and Regulating Contraction
Muscle contraction is initiated by a signal from the nervous system. A nerve impulse travels along a motor neuron to a specialized junction with the muscle fiber. At this neuromuscular junction, acetylcholine is released, binding to receptors on the muscle fiber’s membrane. This triggers an electrical signal, an action potential, which spreads across the muscle cell surface and into T-tubules.
The action potential’s arrival at the T-tubules causes the release of calcium ions (Ca2+) from the sarcoplasmic reticulum (SR), a specialized internal storage network within the muscle cell. Calcium ions control muscle contraction.
In a relaxed muscle, proteins troponin and tropomyosin are positioned on the actin filaments, blocking sites where myosin heads would bind.
When calcium ions are released, they bind to troponin. This binding changes the shape of the troponin-tropomyosin complex, causing tropomyosin to shift. The shift uncovers the myosin-binding sites on the actin filaments, allowing myosin heads to attach and begin the cross-bridge cycle. Muscle relaxation occurs when the nerve signal ceases and calcium ions are actively pumped back into the sarcoplasmic reticulum, causing tropomyosin to again block the myosin-binding sites on actin.