There are no direct connections between nerves that make muscles contract (motor neurons) and skeletal muscle fibers. When a motor neuron depolarizes, an electrical current (the action potential) is passed down the nerve fiber.
Upon reaching the end of the neuron, the impulse causes the release of the neurotransmitter, acetylcholine.
The acetylcholine binds with receptors on the muscle membrane which are in close proximity to the neuron (the motor end plate).
The binding of the acetylcholine to the muscle membrane allows for the initiation of an action potential (which promotes the passing of an electrical current) on the muscle membrane.
A special enzyme, acetylcholinesterase, breaks down the released acetylcholine so that it cannot continue to bind to the muscle membrane. In this way, the nerve controls the action of the muscle such that the muscle can only generate a current when the nerve has first generated a current.
Once the muscle membrane has been excited by the electrical current, the same current causes the release of calcium (Ca++) by specialized storage sites throughout the muscle (called the sarcoplasmic reticulum). The released Ca++ comes into contact with the contractile machinery of the muscle fiber and muscle contraction can begin.
The presence of Ca++ allows for the interaction of two major proteins in the muscle, actin and myosin. In the resting state, these proteins (which have a natural affinity for each other) are prevented from coming into contact.
Two other proteins, troponin and tropomyosin, form a complex weave between the actin and myosin, and prevent contact. When Ca++ enters the picture, the shape of the troponin-tropomyosin complex changes, and now actin and myosin can come into contact with each other.
The shape of the myosin molecule is very complex. Actually, a globular head on myosin attaches to a long stalk on the major portion of the myosin molecule. Numerous heads exist on a single myosin molecule. This head is flexible and attaches to the actin molecule. The head allows for energy requiring movement of the actin molecule along the myosin molecule.
It can be considered a ratchet because it detaches from the binding site on actin after the power stroke, goes back to its original orientation, and attaches to another binding site on actin, further down the molecule. This process slides the actin filament along the myosin filament and is known as the sliding filament theory of muscle contraction. It was initially proposed by A.F. Huxley in 1957.
Energy for the reorientation and movement of the myosin head comes from the molecule ATP. Oddly enough, stopping the process of muscle contraction also requires energy. The saying ‘it takes energy to relax’, is certainly true for skeletal muscle.
Muscle contraction stops when Ca++ is removed from the immediate environment of the myofilaments. The sarcoplasmic reticulum actively pumps Ca++ back into itself and this requires utilization of ATP. Troponin-tropomyosin reassume their inhibitory position between the actin and myosin molecules once Ca++ is removed.
It is important to remember that the above scenario applies for groups of individual muscle fibers which, with their motor neuron, are called motor units. When a muscle is required to contract during exercise not all motor units are used (or recruited).
Most movements require only a fraction of the total power available from an entire muscle. Consequently, our motor system grades the intensity of muscle contraction by recruiting various numbers of motor units. Even during maximal shortening contractions (so called concentric contractions) it is doubtful that all motor units are recruited.
Energy Supply for Muscle Contraction
ATP, adenosine triphosphate (there are three phosphates in ATP), is not stored to a great degree in cells. Once muscle contraction starts the regeneration of ATP must occur rapidly. There are three primary sources of ATP which, in order of their utilization, are creatine phosphate (CP), anaerobic glycolysis, and oxidative phosphorylation.
Energy from ATP derives from cleaving of the terminal phosphate of the ATP molecule. The resulting molecule is called ADP, adenosine diphosphate. Creatine phosphate converts ADP back to ATP by donating its phosphate in the presence of an enzyme which is called either creatine kinase (CK) or creatine phosphokinase (CPK). The reaction of CP with ADP to form ATP is very rapid but short lived, since the cell does not store high amounts of CP.
However during short, high intensity contractions, CP serves as the major source of energy. This form of energy generation is often called alactic anaerobic because it neither produces lactate nor requires oxygen. It is of paramount importance in sports requiring bursts of speed or power such as sprints of 10 seconds or less in duration.
As soon as muscle contraction starts, the process of anaerobic glycolysis also begins. Anaerobic glycolysis does not contribute as large an amount of energy as CP in the short term, but its contribution is likely to last from 30 to 60 seconds. During glycolysis, locally stored muscle glycogen and possibly some blood born glucose, supply the substrate for energy generation.
No oxygen is required so the process is called anaerobic. Lactic acid (lactate is the salt) is formed as the end product of pure anaerobic glycolysis.
Sufficient lactic acid formation can lower the pH of the cell to the extent that metabolism is turned off in the cell. The major substrate for anaerobic glycolysis is glycogen, so prior hard exercise without adequate repletion of glycogen is going to limit further high intensity, short term work by muscles.
The final, and virtually limitless supply of energy, comes from the process of oxidative phosphorylation. Maximum energy production rates from oxidative phosphorylation are not as high as from glycolysis. Aerobic events like the marathon are run at a considerably slower pace than a 440 because of this fact.
The substrates for oxidative metabolism are primarily glucose and fat (free fatty acids, not cholesterol), although protein can also act as an energy source through intermediate conversions to glucose, glucose precursors or free fatty acids. Because fat can be metabolized aerobically, most well nourished humans have a near limitless supply of energy for low intensity exercise. Limitation of low intensity exercise is rarely due to substrate depletion, although depletion of muscle glycogen may also result in fatigue during aerobic events. The reasons for this are beyond the scope of this description.
We also have an article that has a somewhat more detailed look at energy supply for muscle.