The myofibril is the fundamental component responsible for the power and movement generated by muscles throughout the body. These rod-like organelles exist inside every muscle cell, or muscle fiber, giving the tissue its ability to contract. Myofibrils are the physical machinery that converts chemical energy into mechanical force, enabling everything from the subtlest facial expression to the most strenuous physical activity. This microscopic architecture is the reason skeletal muscle tissue has its characteristic striated, or striped, appearance when viewed under a microscope.
Defining the Myofibril and Its Context
Muscle tissue is organized hierarchically, starting with the whole muscle organ. The muscle is composed of bundles known as fascicles, which are groups of individual muscle fibers. These muscle fibers are single, elongated muscle cells where the myofibrils reside. A single muscle fiber can contain hundreds to thousands of myofibrils running parallel to its long axis, measuring between 1 and 2 micrometers in diameter. The myofibril is bathed in the sarcoplasm, the muscle cell’s cytoplasm, and is closely associated with the sarcoplasmic reticulum (SR), a specialized internal membrane system that stores calcium ions. This close relationship ensures that the release and retrieval of calcium from the sarcoplasmic reticulum directly control the myofibril’s contraction cycle.
The Sarcomere—The Core Unit of Structure
The myofibril is composed of thousands of repeating segments called sarcomeres, which are the smallest functional units of muscle contraction. The striated look of muscle tissue comes from the precise, alternating arrangement of thick and thin protein filaments within these sarcomeres. Each sarcomere is defined by two Z-discs, which act as the boundaries and anchor points for the thin filaments. The main components are two types of myofilaments: the thick filaments, made primarily of the protein myosin, and the thin filaments, made mostly of the protein actin. The A-band is the central, darker region of the sarcomere that spans the entire length of the thick myosin filaments. The I-band is the lighter region containing only the thin actin filaments, extending from the Z-disc toward the center. The H-zone is found within the A-band where only thick filaments are present, while the M-line is a structure in the very middle of the H-zone that anchors the thick myosin filaments.
The Mechanism of Muscle Contraction
The process of muscle contraction is explained by the Sliding Filament Theory, which describes how the sarcomere shortens without the thick or thin filaments themselves changing length. The process begins when a nerve impulse signals the muscle fiber, causing the sarcoplasmic reticulum to release calcium ions (Ca\(^{2+}\)) into the sarcoplasm. These calcium ions bind to the regulatory protein troponin, located on the thin actin filament. This binding causes a shift in tropomyosin, which then exposes the myosin-binding sites on the actin filament.
With the binding sites exposed, the heads of the thick myosin filaments attach to the actin, forming cross-bridges. Adenosine triphosphate (ATP) powers the subsequent action. The hydrolysis of ATP causes the myosin head to pivot, a movement known as the power stroke. This pulls the thin actin filament toward the M-line in the center of the sarcomere. After the power stroke, a new ATP molecule binds to the myosin head, causing the cross-bridge to detach. The cycle repeats as long as calcium and ATP are available. The cumulative effect of these power strokes causes the Z-discs to be pulled closer together, shortening the sarcomere and, consequently, the entire myofibril and muscle fiber.
Myofibrils and Muscle Adaptation
The structure of myofibrils is dynamic and changes in response to physical demands, a process known as muscle adaptation. Muscle growth, or hypertrophy, occurs when the muscle fiber increases in diameter due to the addition of new myofibrils. This growth is achieved by adding new sarcomeres in parallel to the existing ones, which increases the total number of actin-myosin cross-bridges available to generate force.
Muscle atrophy, or wasting, involves the degradation and loss of myofibril components, leading to a decrease in muscle fiber size. This breakdown is an active process mediated by specific cellular pathways, including the ubiquitin-proteasome system. For example, the protein MuRF1 targets components of the thick myosin filaments for degradation, leading to the loss of contractile material. Intense exercise can also cause micro-tears, which are minor damage to the myofibrils; the subsequent repair and rebuilding process drives the muscle to adapt and become stronger.