muscle that is made up of myofilaments, actin and myosin. Other organelles in the myofibers include the sarcolemma (plasma membrane), t-tubules, sarcoplasmic reticulum, and the mitochondria. In terms of physiology, skeletal muscles take many steps to contract a muscle.
First, an electrical impulse or action potential from the central nervous system triggers a muscle contraction. When this happens, acetylcholine (ACH) serves as a neurotransmitter, sending the signal to the neuromuscular junction. The impulse is then propagated down the sarcolemma and through the t-tubules. As this signal travels down the t-tubules, Calcium (Ca2+) is released from the sarcoplasmic reticulum to the sarcomere, one unit of contraction with actin and myosin and z-lines on each side. Calcium binds to the troponin protein, located on the actin filament. This allows tropomyosin to move, exposing the myosin head binding sites on actin. When the myosin heads bind to actin, this is known as the cross bridge. ADP and Pi molecules are released, causing myosin to pull on actin. This movement is known as the power stroke. To stop the contraction, ATP binds to the myosin head, and myosin detaches from actin, stopping the contraction. After the impulse or action potential ceases, Calcium returns to the sarcoplasmic reticulum and tropomyosin return, covering myosin binding sites on
actin. Now as muscles continue to contract, muscles will eventually undergo muscle fatigue. Muscle fatigue is the decline in the ability of the myofibers to generate force. There are two types of muscle fatigue, neural fatigue and metabolic fatigue. Unlike metabolic fatigue, neural fatigue affects the nerves, as they become tired of “firing” signals to the muscle. This can happen for many reasons, including dehydration, over exercising, lack of recovery (sleep), and other reasons. However, this type of muscle fatigue is less common amongst most people. Metabolic fatigue is the reduction in the capability to contract and generate force. This is caused by either (or both) the shortage of substrates and/or the accumulation of metabolites. Substrates are the cell’s fuel toward muscle contraction, consisting of molecules, such as ADP, ATP, creatine phosphate, and glycogen, all necessary in muscle contractions. ADP is a key to stimulating the power stroke movement, ultimately contracting the muscle, while ATP is necessary to stop the muscle contraction. Creatine phosphate and glycogen are molecules involved in different types of cellular respiration, a chemical process inside the cell, producing more ATP. As all of these molecules are a major key to muscular contraction, lack of these substrates causes the muscle to fatigue and gradually decline in contraction force. Metabolites are byproducts of the muscular contraction process. The main byproduct is lactic acid, produced during anaerobic respiration to create ATP. As lactic acid builds up, the accumulation of lactate in the cell interferes with Calcium release from the sarcoplasmic reticulum. Finally, temperature of a muscle has a fair effect on the muscle’s ability to contract. Muscles are able to contract to their fullest when they are at an ideal, normal body temperature. Increases/decreases in body temperature cause the rate of the production of ATP for muscle contractions to decrease because of the change inn body temperature. Because of this decrease in ATP, muscles may fatigue quicker in colder/warmer temperatures than normal.