The stretch reflex arc, depicted in Fig. 9.6, is crucial for the functioning of the stretch reflex. This reflex arc involves inhibitory interneurons, specifically the group Ia inhibitory interneurons, which are unique in receiving input from both the group Ia afferent fibers and Renshaw cells (refer to Fig. 9.12). These interneurons connect with α motor neurons that innervate the antagonist muscles, such as the hamstring muscles, including the semitendinosus muscle, responsible for knee flexion. Other branches of the group Ia afferent fibers synapse with neurons that transmit information to different parts of the brain, particularly the cerebellum and cerebral cortex, regarding the muscle's state.

The organization of the stretch reflex arc ensures the activation of one set of α motor neurons while inhibiting the opposing set, a concept known as reciprocal innervation. Although many reflexes involve reciprocal innervation, it's important to note that other motor control systems can override this pattern through descending motor pathways.

The stretch reflex is highly potent due to its monosynaptic nature. The power of this reflex also stems from the extensive convergence and divergence present in this pathway, which may not be apparent from circuit diagrams like Fig. 9.6 typically used to illustrate reflex pathways. Each group Ia fiber contacts nearly all homonymous α motor neurons, and each α motor neuron receives input from every spindle in the muscle. While the monosynaptic nature makes the group Ia reflex rapid and powerful, it also limits the direct control of activity flow through its reflex arc. However, the central nervous system overcomes this limitation by regulating muscle spindle sensitivity through the γ motor neuron system.

Another reflex related to stretching is the tonic stretch reflex, which can be elicited by passive joint bending. This reflex circuit involves both group Ia and group II afferent fibers from muscle spindles. Group II fibers establish monosynaptic excitatory connections with α motor neurons, but they also excite them through disynaptic and polysynaptic pathways. Under normal circumstances, ongoing activity in the group Ia and group II afferent fibers helps maintain a baseline rate of α motor neuron firing, contributing to muscle tone and posture maintenance. For example, if a soldier standing at attention starts to experience knee flexion due to fatigue, the quadriceps muscle stretches, triggering a tonic stretch reflex that contracts the quadriceps, opposing the flexion and restoring the posture.

The stretch reflexes can be seen as negative-feedback systems regulating muscle length. Changes in the reflex activity counteract alterations in muscle length from a specific equilibrium point. For instance, an increase in muscle length leads to increased firing by group Ia and group II fibers, exciting homonymous α motor neurons and causing muscle contraction to reverse the stretch. On the other hand, passive shortening of the muscle reduces the excitatory drive to the motor neurons, resulting in muscle relaxation. Human joint rotation is facilitated by the coactivation of γ motor neurons during movement, which shifts the spindle's equilibrium point. Additionally, the reflex's gain or strength is low enough for other input to override the stretch reflex.
Fig. 9.6 ), is particularly important with regard to the stretch reflex. These interneurons are identifiable because they are the only inhibitory interneurons •Fig. 9.6 Reflex Arc of the Stretch Reflex. Thepathwaybacktotherectusfemorisinthisarccontainsasinglesynapsewithinthecentralnervoussystem;hence,itisamonosynapticreflex.Theinterneuron,showninblack, isagroupIainhibitoryinterneuron.DRG,dorsalrootganglion.
that receive input from both the group Ia afferent fibers and Renshaw cells (see
Fig. 9.12 ). They end on α motor neurons that innervate the antagonist muscles—in this case, the hamstring muscles, including the semitendinosus muscle—which act to flex the knee. Other branches of the group Ia afferent fibers synapse with yet other neurons that originate ascending pathways that provide various parts of the brain (particularly the cerebellum and cerebral cortex) with information about the state of the muscle.
The organization of the stretch reflex arc guarantees that one set of α motor neurons is activated and the opposing set is inhibited. This arrangement is known as reciprocal innervation. Although many reflexes involve such reciprocal innervation, this type of innervation is not the only possible organization of a motor control system; descending motor pathways can override such patterns.
The stretch reflex is quite powerful, in large part because of its monosynaptic nature. The power of this reflex also derives from the essentially maximal convergence and divergence that exist in this pathway, which is not apparent from the circuit diagrams, such as
Fig. 9.6 , that are typically used to illustrate reflex pathways. That is, each group Ia fiber contacts virtually all homonymous α motor neurons, and each such α motor neuron receives input from every spindle in that muscle. Although its monosynaptic nature makes the group Ia reflex rapid and powerful, it also means that there is relatively little opportunity for direct control of
CHAPTER 9 Organization of Motor Function activity flow through its reflex arc. The CNS overcomes this problem by controlling muscle spindle sensitivity via the γ motor neuron system as described previously.
The Tonic Stretch Reflex
The tonic stretch reflex can be elicited by passive bending of a joint. This reflex circuit includes both group Ia and group II afferent fibers from muscle spindles. Group II fibers make monosynaptic excitatory connections with α motor neurons, but they also excite them through disynaptic and polysynaptic pathways. Normally, there is ongoing activity in the group Ia and group II afferent fibers that helps maintain a baseline rate of firing of α motor neurons; therefore, the tonic stretch reflex contributes to muscle tone. Its activity also contributes to the ability to maintain a posture. For example, if the knee of a soldier standing at attention begins to flex because of fatigue, the quadriceps muscle is stretched, a tonic stretch reflex is elicited, and the quadriceps contracts more, thereby opposing the flexion and restoring the posture.
The foregoing discussion suggests that stretch reflexes can act like a negative-feedback system to control muscle length. By following the stretch reflex arc, it is possible to see that changes in its activity act to oppose changes in muscle length from a particular equilibrium point. For example, if the muscle’s length is increased, there will be an increase in firing by group Ia and group II fibers, which excites homonymous α motor neurons and leads to contraction of the muscle and reversal of the stretch. Similarly, passive shortening of the muscle unloads the spindles and leads to a decrease in the excitatory drive to the motor neurons and thus relaxation of the muscle. So how are humans able to rotate their joints? It is partly because the γ motor neurons are coactivated during a movement and thereby shift the equilibrium point of the spindle and partly because the gain or strength of the reflex is low enough that other input to the motor neuron can override the stretch reflex.