The body of the organ is made up of braided strands of collagen that are less compact than elsewhere in the tendon and are encapsulated. The capsule is connected in series with a group of muscle fibers at one end, and merge into the tendon proper at the other. Each capsule is about long, has a diameter of about, and is perforated by one or more afferenttype Ib sensory nerve fibers, which are large myelinated axons that can conduct nerve impulses very rapidly. Inside the capsule, the afferent fibers lose their medullary sheaths, branch, intertwine with the collagen fibers, and terminate as flattened leaf-like endings between the collagen strands.
Function
When the muscle generates force, the sensory terminals are compressed. This stretching deforms the terminals of the Ib afferent axon, opening stretch-sensitive cation channels. As a result, the Ib axon is depolarized and fires nerve impulses that are propagated to the spinal cord. The action potential frequency signals the force being developed by 10-20 extrafusal muscle fibers in the muscle. Average level of activity in a tendon organ population is representative of the whole muscle force. The Ib sensory feedback generates spinal reflexes and supraspinal responses which control muscle contraction. Ib afferents synapse with interneurons that are within the spinal cord that also project to the braincerebellum and cerebral cortex. The autogenic inhibition reflex assists in regulating muscle contraction force. It is associated with the Ib. Tendon organs signal muscle force through the entire physiological range, not only at high strain. During locomotion, Ib input excites rather than inhibits motoneurons of the receptor-bearing muscles, and it affects the timing of the transitions between the stance and swing phases of locomotion. The switch to autogenic excitation is a form of positive feedback. The ascending or afferent pathways to the cerebellum are the dorsal and ventral spinocerebellar tracts. They are involved in the cerebellar regulation of movement.
History
Until 1967 it was believed that Golgi tendon organs had a high threshold, only becoming active at high muscle forces. Consequently, it was thought that tendon organ input caused "weightlifting failure" through the clasp-knife reflex, which protected the muscle and tendons from excessive force. However, the underlying premise was shown to be incorrect by James Houk and Elwood Henneman in 1967.