Terminal cisternae are structures adjacent to T-tubules in muscle cells.
Groups of these structures, along with T-tubules, form triads.
Triads play a crucial role in calcium ion communication essential for muscle contraction.
Skeletal muscle contraction is initiated by action potentials traveling from the nervous system to muscle cells.
Action potentials propagate through T-tubules, leading to calcium release from the sarcoplasmic reticulum (SR).
This calcium release triggers the contraction of myofibrils and therefore the entire muscle.
In muscles, even at rest, skeletal muscles hold posture and keep the body balanced.
The contraction occurs in a coordinated manner across multiple muscle fibers, enhancing movement effectiveness.
Muscle contraction involves various structural levels: myofibrils → muscle cells (myocytes) → fascicles → entire muscle organs.
Myofibrils consist of stacked units called sarcomeres, composed of thick (myosin) and thin (actin) filaments.
Sarcomeres are the smallest functional units where muscle contraction occurs. They are characterized by:
A Band: Region with thick myosin filaments.
I Band: Region with only thin actin filaments.
Myosin heads bind to exposed sites on actin filaments, forming cross-bridges.
The myosin heads perform a power stroke powered by ATP, pulling actin filaments towards the center of the sarcomere, shortening the muscle.
Myosin detach from actin when a new ATP molecule binds.
Myosin heads reset to their original position, ready to bind again if calcium is present.
Calcium ions are key regulators in muscle contraction; they bind to the troponin-tropomyosin complex, uncovering binding sites for myosin.
ATP is essential for both cross-bridge formation and relaxation. Muscle fatigue occurs when ATP availability diminishes.
Muscle relaxation occurs after stimulation ceases: calcium ions are reabsorbed, restoring troponin-tropomyosin blockage over actin binding sites.
Myosin heads detach, and muscle fibers return to a resting state.