Elongation-shortening Cycle: Function, Tasks, Role & Diseases

In the stretch-shortening cycle (DVZ), an eccentric stretch of a muscle is followed by a concentric contraction of the same muscle, which conserves energy and uses the kinetic energy from the stretch. The DVZ plays an important role in reactive movements and is triggered by muscle flexibility and the stretch reflex. Disorders of the cycle present as part of the extrapyramidal syndrome.

What is the stretch-shortening cycle?

The DVZ plays an important role in reactive movements and is triggered by muscle flexibility and the stretch reflex. The stretch-shortening cycle is a mode of operation of the neuromuscular system. In this process, the activated muscle is first stretched against its working direction, which is also known as eccentric muscle work. Following the eccentric work, there is an automatic shortening of the stretched muscle, which is known as the concentric mode of work. The stretch-shortening cycle can be fast or slow. The fast cycle occurs, for example, during sports movements. Because muscle has plastic and elastic properties, contractions automatically and immediately follow stretching. That is, eccentric muscle work must be immediately followed by concentric muscle work. Contraction of the musculature occurs well before the muscle adapts to the stretch. The stretch-shortening cycle uses the stored energy from the stretching movement and thus makes the concentric work particularly energy-saving and fast. In this way, particularly large force development is achieved. The cycle depends primarily on the flexibility of the tendons and ligaments. Contraction is initiated within the stretch-shortening cycle by the muscle spindles, which initiate the stretch reflex in the form of a motor response to the stretch stimulus.

Function and task

Before the onset of a stretch, a muscle is pre-activated in the sense of pre-innervation. This creates what is known as short range elastic stiffness (SRES). For a short time, this stiffness enables the muscle to resist stretching. Short Range Elastic Stiffness is predominantly due to the muscle’s actin-myosin bridges, which provide short-term resistance to stretch. The resistance of the bridges decreases with continued stretch because of what is called bridge strain. During stretching, the muscle is also additionally activated at the level of the stretch reflex. This increases the contractile force because of additional cross-bridge formation. The contractile parts of the muscle, i.e. actin and myosin, thus increase stiffness. In addition, the tendons of the muscle are lengthened due to stretching. The so-called stretch reflex is an intrinsic reflex that induces contraction when a muscle is stretched, thus adjusting the muscle length. Like any reflex, the stretch reflex begins with a stimulus, in this case the stretch stimulus, which is detected by the muscle spindles. The muscle spindles are sensory cells of deep sensitivity and are connected to the central nervous system via afferent nerve pathways. There, the excitation is switched to efferent motor nerve pathways that initiate contraction of the muscle. In this way, an eccentric stretch in the human body is responded to by a concentric muscle contraction. The kinetic energy from the stretch is now used for the contraction. While many sources speak of kinetic energy being stored in connective tissue, just as many assume it is stored in tendons. The tendon is nearly ideally elastic and is said to be capable of storing kinetic energy because of this property. The kinetic energy is generated in the eccentric phase of the movement and is now released again. Thus, the stretch-shortening cycle has a force-intensifying effect compared to purely concentric muscle work. The force of the stretch-shortening cycle cannot be achieved by purely voluntary muscle work. To trigger the cycle, the tendons must be maximally stretched. Only at maximum stretch does the body fear a tendon rupture and initiate contraction for protective reasons. Thus, high extensibility leads to a stretch-shortening cycle that is more difficult to trigger.

Diseases and disorders

The stretch-shortening cycle is especially crucial for reactive strength. This refers to the force to perform reactive movements, which is different from spontaneous force.Reactive strength, and thus also the stretch-shortening cycle, can be promoted by means of plyometric training. From person to person, the stretch-shortening cycle can thus differ to a certain extent and depends, for example, on the training condition. Differences in the cycle therefore do not have to be due to a disease. However, any neuromuscular disease can have a negative effect on the stretch-shortening cycle. After sports injuries, for example, reactive strength is limited. In plyometrics, the stretch reflex is promoted physiotherapeutically after injuries of this type. Weakened reflex ability can refer to neuropathies in addition to sports injuries. These are diseases of the peripheral nervous system that do not have a traumatic cause. In addition, all reactive movements are impaired in the hypokinetic-rigid variant of the extrapyramidal syndrome. Disorders of the extrapyramidal system in the central nervous system are noticeable, for example, in Parkinson’s disease, chorea, or ballism. In addition, drugs such as neuroleptics affect the extrapyramidal motor system. In addition to ataxias, tremors or start inhibitions, tendencies to fall are a typical symptom of the syndrome. The extrapyramidal system is a neuroanatomical structure in which higher-level motor control processes take place. Thus, not all motor control processes are located in the pyramidal tract of the pyramidal system. All control processes outside the pyramidal system are grouped together as activities of the extrapyramidal system, including, for example, the stretch reflex as part of the stretch-shortening cycle. In this context, all lesions of the extrapyramidal system can affect the stretch-shortening cycle. This is true for bacterial and autoimmunological inflammatory, as well as tumor-related, degenerative, trauma-related, and infarct-related damage to the neurological structure.