Muscle fibers contract and relax through a complex process involving the interaction of muscle proteins, the nervous system, and chemical signals. The contraction and relaxation of muscles are governed by the sliding filament theory, which explains how muscle fibers shorten and lengthen to produce movement.
1. Structure of a Muscle Fiber
A muscle fiber (also called a muscle cell) is made up of smaller units called myofibrils, which are composed of repeating sections called sarcomeres. Sarcomeres are the basic functional units of muscle contraction and contain two primary protein filaments:
- Actin (thin filaments)
- Myosin (thick filaments)
These filaments slide past each other during contraction and relaxation.
2. The Role of Calcium and ATP
For a muscle to contract and relax, two critical elements are involved:
- Calcium ions (Ca²⁺)
- Adenosine triphosphate (ATP)
- Calcium: Calcium is released from the sarcoplasmic reticulum (a storage organelle in muscle cells) when a muscle receives a signal to contract.
- ATP: ATP is the energy currency that powers the muscle contraction and relaxation processes.
3. Muscle Contraction (Sliding Filament Theory)
Here’s how muscle fibers contract:
a. Nerve Signal and Action Potential
- The process starts when the brain or spinal cord sends an electrical signal (action potential) through motor neurons to the muscle fibers.
- When the action potential reaches the muscle fiber, it travels along the sarcolemma (the muscle fiber membrane) and into the T-tubules (tiny tubes inside the cell). This allows the signal to reach all parts of the fiber quickly.
b. Release of Calcium
- The action potential triggers the sarcoplasmic reticulum to release calcium ions into the cytoplasm of the muscle fiber.
- Calcium binds to troponin, a regulatory protein located on the actin filaments.
c. Expose Binding Sites
- When calcium binds to troponin, it causes a shift in the position of another protein called tropomyosin, which is blocking the binding sites on actin.
- With the tropomyosin out of the way, the myosin heads (on the thick myosin filaments) can now bind to the exposed binding sites on the actin filaments.
d. Cross-Bridge Formation and Power Stroke
- Once myosin heads bind to actin, they form cross-bridges. The myosin heads then pivot, pulling the actin filaments toward the center of the sarcomere, which shortens the muscle fiber. This movement is called the power stroke.
- During the power stroke, ATP is broken down into ADP (adenosine diphosphate) and inorganic phosphate (Pi), releasing energy.
e. Detach and Re-cock
- After the power stroke, a new ATP molecule binds to the myosin head, causing it to release from the actin filament.
- The ATP is then broken down, and the myosin head “cocks” back into its original position, ready to form another cross-bridge and repeat the cycle.
f. Repeat
- This cycle of binding, pulling, and releasing (powered by ATP) continues as long as calcium is present in the muscle fiber and the muscle is being stimulated by nerve signals.
- As the myosin heads continue to pull on the actin filaments, the sarcomere shortens, and the entire muscle fiber contracts.
4. Muscle Relaxation
For the muscle to relax, the process must be reversed:
a. Calcium Removal
- After the signal from the nervous system stops, calcium ions are actively pumped back into the sarcoplasmic reticulum (using ATP).
- As calcium levels in the muscle fiber drop, calcium ions detach from troponin.
b. Re-covering of Binding Sites
- When calcium leaves, tropomyosin moves back into its blocking position on the actin filaments, preventing myosin from binding to actin.
c. Muscle Fiber Lengthens
- With no cross-bridge formation, the actin and myosin filaments slide back to their relaxed positions. The sarcomere lengthens, and the muscle fiber relaxes.
5. Summary of Muscle Contraction and Relaxation
- Contraction: The release of calcium ions allows myosin heads to bind to actin filaments, and ATP powers the sliding motion, shortening the muscle fiber.
- Relaxation: When calcium is pumped back into the sarcoplasmic reticulum, tropomyosin blocks the actin binding sites, preventing further myosin binding, and the muscle fiber returns to its resting length.