All skeletal muscles contractions occur as a result of conscious effort originating in the brain. The brain sends electrochemical signals through the nervous system to the motor neuron that innervates several muscle fibers.In the case of some reflexes, the signal to contract can originate in the spinal cord through a feedback loop with the grey matter.
Chemical synapse formed by the contact between a motor neuron and a muscle fiber. The neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. Acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing the depolarization of the muscle fiber. It causes the release of Ca2+ from sarcoplasmic reticulum into the cytosol.
The sliding filament theory explains the mechanism of muscle contraction based on muscle proteins that slide past each other to generate movement. According to the sliding filament theory, the myosin (thick) filaments of muscle fibers slide past the actin (thin) filaments during muscle contraction, while the two groups of filaments remain at relatively constant length.
One zone of the repeated sarcomere arrangement, the "A band," remained relatively constant in length during contraction. The A band contains thick filaments of myosin, which suggested that the myosin filaments remained central and constant in length while other regions of the sarcomere shortened. The investigators noted that the "I band," rich in thinner filaments made of actin, changed its length along with the sarcomere. These observations led them to propose the sliding filament theory, which states that the sliding of actin past myosin generates muscle tension. Because actin is tethered to structures located at the lateral ends of each sarcomere called z discs or "z bands," any shortening of the actin filament length would result in a shortening of the sarcomere and thus the muscle. Filament sliding occurs by cyclic attachment and detachment of myosin on actin filaments. Contraction occurs when the myosin pulls the actin filament towards the centre of the A band, detaches from actin and creates a force (stroke) to bind to the next actin molecule. This sequence is known as the cross-bridge cycle.
All events and facts about the theory summarized:
1. Muscle activation: The motor nerve stimulates an action potential (impulse) to pass down a neuron to the neuromuscular junction. This stimulates the sarcoplasmic reticulum to release calcium into the muscle cell.
2. Muscle contraction: Calcium floods into the muscle cell binding with troponin allowing actin and myosin to bind. The actin and myosin cross bridges bind and contract using ATP as energy.
3. Recharging: ATP is re-synthesised (re-manufactured) allowing actin and myosin to maintain their strong binding state
4. Relaxation: Relaxation occurs when stimulation of the nerve stops. Calcium is then pumped back into the sarcoplasmic reticulum breaking the link between actin and myosin. Actin and myosin return to their unbound state causing the muscle to relax. Alternatively relaxation (failure) will also occur when ATP is no longer available.