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Anatomy and physiology of stretching

This is an excerpt from Stretching Anatomy, Second Edition, edited by Arnold Nelson and Jouko Kokkonen.


Learn more about how the body reacts to stretching in
Stretching Anatomy.

Anatomy and Physiology of Stretching

Muscles such as the biceps brachii are complex organs composed of nerves, blood vessels, tendons, fascia, and muscle cells. Nerve cells (neurons) and muscle cells are electrically charged. The resting electrical charge, or resting membrane potential, is negative and is generally around –70 millivolts. Neurons and muscle cells are activated by changing their electrical charges. Electrical signals cannot jump between cells, so neurons communicate with other neurons and with muscle cells by releasing specialized chemicals called neurotransmitters. Neurotransmitters work by enabling positive sodium ions to enter the cells and make the resting membrane potential more positive. Once the resting membrane potential reaches a threshold potential (generally –62 millivolts), the cell becomes excited, or active. Activated neurons release other neurotransmitters to activate other nerves, causing activated muscle cells to contract.

Besides being altered to cause excitation, the membrane potential can be altered to cause either facilitation or inhibition. Facilitation occurs when the resting membrane potential is raised slightly above normal but below the threshold potential. Facilitation increases the likelihood that any succeeding neurotransmitter releases will cause the potential to exceed the threshold. This enhances the chances of the neuron’s firing and activating the target. Inhibition occurs when the resting membrane potential is lowered below the normal potential, thereby decreasing the likelihood of reaching the threshold. Usually this prevents the neuron from activating its target.

To perform work, the muscle is subdivided into motor units. The motor unit is the basic functional unit of the muscle. A motor unit consists of one motor (muscle) neuron and all the muscle cells to which it connects, as few as 4 to more than 200. Motor units are then subdivided into individual muscle cells. A single muscle cell is sometimes referred to as a fiber. A muscle fiber is a bundle of rodlike structures called myofibrils that are surrounded by a network of tubes known as the sarcoplasmic reticulum, or SR. Myofibrils are formed by a series of repeating structures called sarcomeres. Sarcomeres are the basic functional contractile units of a muscle.

The three basic parts of a sarcomere are thick filaments, thin filaments, and Z-lines. A sarcomere is defined as the segment between two neighboring Z-lines. The thin filaments are attached to both sides of a Z-line and extend out from the Z-line for less than one-half of the total length of the sarcomere. The thick filaments are anchored in the middle of the sarcomere. Each end of a single thick filament is surrounded by six thin filaments in a helical array. During muscle work (concentric, eccentric, or isometric), the thick filaments control the amount and direction that the thin filaments slide over the thick filaments. In concentric work, the thin filaments slide toward each other. In eccentric work, the thick filaments try to prevent the thin filaments from sliding apart. For isometric work, the filaments do not move. All forms of work are initiated by the release of calcium ions from the SR, which occurs only when the muscle cell’s resting membrane potential exceeds the threshold potential. The muscle relaxes and quits working when the calcium ions are restored within the SR.

The initial length of a sarcomere is an important factor in muscle function. The amount of force produced by each sarcomere is influenced by length in a pattern similar in shape to an upside-down letter U. As such, force is reduced when the sarcomere length is either long or short. As the sarcomere lengthens, only the tips of the thick and thin filaments can contact each other, and this reduces the number of force-producing connections between the two filaments. When the sarcomere shortens, the thin filaments start to overlap each other, and this overlap also reduces the number of positive force-producing connections.

Sarcomere length is controlled by proprioceptors, or specialized structures incorporated within the muscle organs, especially within the muscles of the limbs. The proprioceptors are specialized sensors that provide information about joint angle, muscle length, and muscle tension. Information about changes in muscle length is provided by proprioceptors called muscle spindles, and they lie parallel to the muscle cells. The Golgi tendon organs, or GTOs, the other type of proprioceptor, lie in series with the muscle cells. GTOs provide information about changes in muscle tension and indirectly can influence muscle length. The muscle spindle has a fast dynamic component and a slow static component that provides information on the amount and rate of change in length. Fast length changes can trigger a stretch, or myotatic, reflex that attempts to resist the change in muscle length by causing the stretched muscle to contract. Slower stretches allow the muscle spindles to relax and adapt to the new longer length.

When the muscle contracts it produces tension in the tendon and the GTOs. The GTOs record the change and rate of change in tension. When this tension exceeds a certain threshold, it triggers the lengthening reaction via spinal cord connections to inhibit the muscles from contracting and cause them to relax. Also, muscle contraction can induce reciprocal inhibition, or the relaxation of the opposing muscles. For instance, a hard contraction of the biceps brachii can induce relaxation within the triceps brachii.

The body adapts differently to acute stretching (or short-term stretching) and chronic stretching (or stretching done multiple times during a week). The majority of current research shows that when acute stretches cause a noticeable increase in a joint’s range of motion, the person can experience either inhibition of the motor nerves, overlengthening of the muscle sarcomeres, or increased length and compliance of the muscle’s tendons. No one is sure of the extent of these changes, but it appears that the muscle shape and cell arrangement, muscle length and contribution to movement, and length of the distal and proximal tendons all play a role. Nevertheless, these transient changes are manifested as decreases in maximal strength, power, and strength endurance. On the other hand, research studies have shown that regular heavy stretching for a minimum of 10 to 15 minutes three or four days a week (chronic stretching) results in the development of increased strength, power, and strength endurance as well as improved flexibility and mobility. Animal studies suggest that these benefits are due in part to increased numbers of sarcomeres in series.

Likewise, research into stretching for injury prevention has shown differences between acute stretching and chronic stretching. Although acute stretching can help an extremely tight person reduce the incidence of muscle strains, the normal person appears to gain minimal injury-prevention benefit from acute stretching. People who are inherently more flexible are less prone to exercise-related injuries, and inherent flexibility is increased with heavy stretching three or four days a week. Because of these differences between acute and chronic stretching, many exercise experts now encourage people to do the majority of their stretching at the end of a workout.


Read more from Stretching Anatomy, Second Edition, by Arnold Nelson and Jouko Kokkonen.



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