Sports Medicine Tip: Understanding Flexibility
Understanding flexibility starts with a basic knowledge of cellular muscle anatomy. Of particular importance is the basic unit of muscle cell (the sarcomere) an the three primary inhibitory prociceptors: the Golgi tendon organ (GTO), the muscle spindle and the Pacinian corpuscles.
Myofibrils have the ability to change length, because they are constructed of overlapping strands of protein polymers called actin (the thin strands) and myosin (the thicker strands). The boundaries are called Z lines, to which the actin filaments are attached. In the center of the sarcomere are the myosin strands which, during contraction, can pull the Z lines closer together by attaching to the actin filaments with specialized heads called “cross bridges”. These cross bridges function much like boat oars as they reach out attach and pull on the actin filaments, causing the Z lines to move toward one another.
When you strech a muscle, the opposite occurs. During the stretch, the fibers elongate as each sarcomere extends to the point where no overlap between the thick and thin filaments exists at all (specialized elastic filaments comprised of titin keep the sarcomere together in the absence of overlap). At this point, the remaining stress is taken up by the surrounding connective tissue. If the stretch tension escalates beyond this point, microscopic tears develop both in the connective tissues and within the sarcomere itself. Such micro-traumatic injuries eventually heal, but a cost of scarification and micro-adheresions that may leave the muscle fiber less capable of contraction and extension.
Research conducted at the University of London suggests that during periods of prolonged muscle elongation, the body detects a reduction in the overlap between action and myosin, and synthesizes new sarcomeres at the ends of the myofilaments in order to reestablish proper overlap. Greater overlap means improved force production potential, so this may be an important reason for anyone to include stretching in their programs.
The neuromuscular system has built in safeguards against severe muscular injury. These safeguards take the form of proprioceptors that can sense changes in muscle tension. When these changes are too sudden, too intense or both, the proprioceptors act to inhibit the nerveous impulse sent to the muscle. There are three primary proprioceptors involved in the strecht inhibition: the Glogi tendon organ (GTO), the Pacinian corpuscle and the muscle spindle.
The Golgi tendon organ is located at the musculo-tendonous junction, and detects the magnitude of mechanical stress of this location. When excessive tension develops, the GTO causes the motor cortex of the brain to shut off muscle contraction. The GTO is not sensitive to the rate of force development, only to the absolute value of tension that develops within the muscle.
Pacinian corpuscles are small, elliptical bodies, which lien in the deep layers of the skin, in close proximity to the GTOs. Tehy are sensitive to quick movement and deep pressure. As compared to the GTO and muscle spindle, the inhibitory role of this organ is not well understood.
The muscle spindle is actually a specialized muscle fiber, which detects excessive stretch within the muscle. Muscles responsible for fine movements contain more muscle spindles than do muscles responsible for gross movements. Unlike GTO, the muscle spindle does not relay on signals through the motor cortex; as such, it is not considered a feedback loop, but rather an inhibitory knob. Resetting the muscle spindle is the mechanism of PNF and contract-relax stretching methods.
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