Introduction
The sliding filament theory illustrated the process of muscle contraction. Namely, it explains how muscle tension occurs when the actin proteins slide past the motor proteins, myosin. To exemplify the theoretical framework, it is essential to highlight the structure of the muscle itself.
Muscle Structure
Each muscle consists of multiple muscle fibers. Each of the muscle fibers, on the other hand, consists of myofibrils. The myofibrils are units within the muscle cells. They consist of myofilaments, protein chains within cells.
Two of the ones that participate in muscle contraction are actin, which is the thinner protein, and myosin, which is the thicker one. These structural characteristics are essential in generating tension. However, the contraction process is more complex and requires the aforementioned sliding phenomenon.
Mechanism Behind Contracting Muscles
Sarcomere and Sarcolemma
For the muscle to contract, actin and myosin must bind. This generates the sarcomere, the smallest contractile unit. However, binding requires several steps, as barriers exist in the connection of the proteins above. Nerve impulses, also known as action potentials, occur in the sarcolemma.
The sarcolemma is the plasma membrane of the previously mentioned myofibril. Namely, the motor neuron transmits a signal that travels through the motor axon to the axon terminal (Powers et al., 2021). The said signal aims to reach the muscle fiber of the motor unit.
The chemical synapse between the two is called the neuromuscular junction. It consists of the presynaptic and the postsynaptic membranes. They, however, are not connected. The space between the two is called the synaptic cleft. As a result, the neuron releases the neurotransmitter acetylcholine (ACh).
Acetylcholine
ACh binds to existing receptors, opening sodium (Na) channels. The sodium released facilitates a positive change that ultimately depolarizes the sarcolemma and the tubes within the muscle fiber. As a result of the depolarization process, Calcium (Ca) is released.
Calcium and Troponin
The calcium reaches the sarcoplasmic reticulum, which stores the element. The presence of calcium is crucial for the interaction between myosin and actin. However, at this stage, myosin still cannot bind to actin. This phenomenon is attributed to tropomyosin, which helps maintain troponin (Powers et al., 2021).
The binding of calcium indeed triggers the release of troponin, which ultimately leads to the movement of tropomyosin. However, as mentioned earlier, the actin proteins must slide past the myosin. Thus, it is to be in a favorable position, bind to the synoptic end bulbs of the actin, and move it.
ADP and Phosphate
The binding is established through the hydrolysis of ATP into ADP and phosphate. When they get disconnected from the myosin, a power stroke occurs. The process is initiated when myosin binds to the synaptic end bulbs of the actin. The ADP and phosphate are then released, the myosin head returns to its original position, and the actin slides as a result. The sliding of the actin molecule is called the power stroke. This phenomenon is linked to the production of force.
Conclusion
Thus, alterations in the bridge formed as a result of actin and myosin binding are at the core of the sliding filament theory. This explanation of the molecular mechanism highlights the structures, elements, and processes that are essential in muscle contraction.
References
Powers, J. D., Malingen, S. A., Regnier, M., & Daniel, T. L. (2021). The sliding filament theory since Andrew Huxley: Multiscale and multidisciplinary muscle research. Annual Review of Biophysics, 50(1), 373–400.