Stretch Receptors: Structure, Function & Diseases

Stretch receptors measure tension in tissues to detect stretch in a muscle or organ. Their main function is overstretch protection, which is provided by the monosynaptic stretch reflex. The stretch receptors may show structural changes in the context of various muscle diseases.

What are stretch receptors?

Receptors are proteins of human tissues. They respond to specific stimuli in their environment with depolarization and convert the stimulus impulse into a bioelectrical action potential. Receptors are therefore the target molecules of a body cell and belong to the signaling devices of organs or organ systems. The so-called mechanoreceptors react to mechanical stimuli from the environment and make them processable for the central nervous system. The proprioceptors are primary sensory cells and belong to the mechanoreceptors. They are mainly responsible for the body’s own perception and correspond to free nerve endings. The group of proprioceptors includes the receptors of the muscle spindle. These sensory cells play a role primarily for the monosynaptic stretch reflex and are accordingly also called stretch receptors. Muscle spindle are thus stretch receptors of skeletal muscles that respond to mechanical stretch. They measure muscle length enabling differential and reflex movements. Interacting with the stretch receptors are the Ruffini and Vater-Pacini corpuscles in the joint capsule.

Anatomy and structure

The muscle spindles are located in the skeletal musculature. They are composed of intrafusal muscle fibers. These fibers lie parallel to those of skeletal muscle. Nuclear chain fibers are composed of cell nuclei arranged in a chain-like fashion. Nuclear sac fibers are a collection of distended cell nuclei. All muscle spindles are composed of five to ten striated muscle fibers in a connective tissue sheath. In humans, spindles are between one and three millimeters long. The spindles are found at various locations in the body. On the muscle fibers of the leg extensor, for example, there are up to a thousand muscle spindles in the thigh, which can reach a length of almost ten millimeters. The more muscle spindles, the more finely the associated muscle can move. In the non-contractile center of the muscle spindles lie primarily afferent sensory nerve fibers that serve to record stimuli. These fibers are also known as Ia fibers. They wrap around the middle portions of the intrafusal fibers and are also called anulospiral terminals. The efferent nerve fibers of the muscle spindle are so-called gamma neurons, which control the sensitivity of the spindle.

Function and tasks

Stretch receptors primarily protect muscles and organs from stretch damage. To do this, they trigger the monosynaptic stretch reflex, which reflexively moves the associated muscle against the direction of stretch. This reflex response must occur as close in time as possible to the stretch. For this purpose, the afferents of the muscle spindle run almost exclusively via the fast-conducting nerve fibers of type Ia and are monosynaptically connected via the spinal cord. To interconnect otherwise would delay the protective reflexes of the stretch receptors. Class II nerve fibers permanently record muscle length. They belong to the secondary innervation. The action potential frequency in the Ia fibers is always proportional to the measured muscle length or tissue tension. The action potential frequency is also related to the rate of length change due to stretch. Because of these relationships, muscle spindles are also called PD sensors. A change in the length of the muscle activates the alpha-motoneuron of the stretched muscle and at the same time activates the gamma-motoneuron. Thus, the fibers of the working muscle shorten parallel to the intrafusal fibers. In this way, there is a constant sensitivity of the spindle. When a muscle is stretched, the stretch also reaches the muscle spindle. The Ia fibers then generate an action potential and transport it via the spinal nerve to the posterior horn of the spinal cord. Via a synaptic connection in the anterior horn of the spinal cord, the impulse from the stretch receptors is projected monosynaptically to α-motoneurons. They cause the skeletal muscle fibers of the stretched muscle to contract briefly. Muscle length is further controlled via the γ-spindle loop. The intrafusal muscle fibers are cross-linked with γ-motoneurons at the contractile end.When these motor neurons are activated, contraction occurs at the muscle spindle ends and the center is stretched. Thus, the Ia fibers again generate an action potential. After passing through the spinal cord, this triggers a contraction of the skeletal muscle fibers, which relaxes the muscle spindle. The process continues until the Ia fibers detect no stretch.

Diseases

Diseases based on muscle spindle senescence have not been reported to date. However, because of their complexity as receptor organs, such diseases are quite likely. In the context of peripheral neuropathies, enlargement or aplasia of spinal ganglion cells or of medullary and sensory nerve fibers sometimes occurs. These phenomena could affect the development of stretch receptors. The absence of a particular transcription factor may also show negative effects on the development of the stretch receptors in some circumstances. In contrast, demyelinating forms of neuropathy are not associated with alterations of muscle spindles. In return, the muscle spindles may be affected by specific muscle diseases and thus show morphological changes. This specifically includes neurogenic muscle atrophy. Muscle atrophies are characterized by a reduction in the circumference of the skeletal muscles and are a reaction to reduced strain. In the neurogenic form of muscle atrophy, the reduced strain is caused by the nervous system or certain neurons and can thus occur, for example, in the context of the degenerative disease ALS. The fine tissue of the muscle spindles changes in a thread-like manner in muscle atrophies. Many other diseases alter the muscle spindles. However, the fine-tissue structure of the stretch receptors and their diseases has not been particularly well studied to date because of its high complexity.