Myofibrils are the fundamental, rod-like organelles that make up muscle cells, which are also known as muscle fibers. These structures are responsible for the primary function of muscle: contraction. Contained within each muscle fiber are numerous myofibrils, running parallel to each other along the length of the cell. Their coordinated action generates the force required for all voluntary movements, from walking to lifting.
Structural Components of a Myofibril
A closer look at a myofibril reveals it is constructed from repeating functional units called sarcomeres. These sarcomeres are arranged end-to-end along the entire length of the myofibril, and their structure gives skeletal muscle its characteristic striped, or striated, appearance. The sarcomere itself is composed of two main types of protein filaments: thick filaments and thin filaments.
The thick filaments are primarily made of a protein called myosin, which is responsible for generating force. Each myosin molecule has a long rod shape with a globular head that binds to specific sites on the thin filaments. The thin filaments are composed mainly of actin. These actin strands act as a track or “ladder” along which the myosin heads can “climb” to shorten the muscle.
The interaction between actin and myosin is regulated by two other proteins associated with the thin filaments: troponin and tropomyosin. In a relaxed muscle, tropomyosin is positioned to block the binding sites on the actin strands, preventing the myosin heads from attaching. Troponin is a protein complex that holds the tropomyosin in this blocking position.
The Mechanism of Muscle Contraction
The process of muscle contraction is initiated by a signal, typically a nerve impulse, that travels to the muscle cell. This signal triggers the release of calcium ions from a specialized storage structure within the cell called the sarcoplasmic reticulum. They bind to the troponin proteins located on the thin filaments.
This binding of calcium to troponin causes a change in the shape of the troponin complex. This change pulls the attached tropomyosin strand away from the actin filament’s binding sites. With these sites now exposed, the myosin heads are free to attach to the actin, forming a connection known as a cross-bridge.
Once the cross-bridge is formed, the myosin head performs a “power stroke,” pivoting and pulling the thin actin filament toward the center of the sarcomere. This action shortens the sarcomere and, collectively, the entire muscle fiber. Detaching from the actin to reset for another cycle requires energy in the form of adenosine triphosphate (ATP). The myosin head uses ATP to release from the actin, re-cock, and prepare to attach again, continuing the sliding process as long as calcium and ATP are present.
Myofibrils and Muscle Growth
Muscles increase in strength and size primarily through a process called myofibrillar hypertrophy. This process involves an increase in both the number and the diameter of myofibrils within each muscle fiber. It is a direct adaptation to physical stress, like resistance training, where muscles challenged with heavier loads are signaled to create more of these force-producing units.
The growth in muscle fiber girth occurs as existing myofibrils are stimulated by the stress placed on the sarcomeres. This stress can cause the myofibrils to split, effectively increasing their number. An adult’s muscle cells can contain approximately 2,000 myofibrils each, a significant increase from the 50 or so found in a fetus, illustrating the adaptive potential of muscle tissue.
It is useful to distinguish myofibrillar hypertrophy from another type of muscle growth called sarcoplasmic hypertrophy. Sarcoplasmic hypertrophy involves an increase in the volume of the fluid, or sarcoplasm, within the muscle cell, along with non-contractile components. While this can increase the overall size of the muscle, it does not contribute to strength in the same direct way that adding more myofibrils does. Myofibrillar hypertrophy is the adaptation for enhanced muscular strength.
Myofibril Damage and Repair
The soreness experienced after a strenuous workout is directly related to the microscopic processes happening within the myofibrils. Intense or novel exercise, particularly movements that involve eccentric contractions (lengthening the muscle under load), causes micro-tears and damage to the myofibril structures. This exercise-induced damage is a normal part of the muscle adaptation process.
This damage to the myofibrils and the surrounding structures initiates an inflammatory response within the muscle. The body’s natural repair mechanisms are activated to clean out the damaged tissue and begin rebuilding the protein filaments. This process is what leads to Delayed Onset Muscle Soreness (DOMS), the characteristic muscle pain and stiffness that typically peaks 24 to 48 hours after a workout.
The repair cycle is fundamental for muscle growth and strengthening. As the body repairs the micro-tears, it doesn’t just return the myofibrils to their previous state; it often reinforces them, making them stronger and more resilient to future stress. With proper nutrition to supply the necessary protein building blocks and adequate rest to allow the repair processes to unfold, this cycle of damage and repair is what ultimately leads to the myofibrillar hypertrophy and increased strength discussed previously.