The two reflex arcs can function synergistically. For example, when knee extensors start to fatigue during maintained posture, the force pulling on the patellar tendon decreases. This decline in force reduces the activity of Golgi tendon organs in the tendon. As a result, the excitability of the α motor neurons to the rectus femoris muscle is enhanced, reversing the decrease in force caused by fatigue. At the same time, bending of the knee stretches the knee extensors and activates the afferent fibers from the muscle spindles. These fibers excite the same α motor neurons. Thus, coordinated action of afferent fibers from both the muscle spindle and Golgi tendon organ help oppose the decrease in contraction of the rectus femoris muscle due to fatigue and maintain the standing posture.

The flexion reflex is initiated by the activation of sensory receptors, including nociceptors, which send signals to the spinal cord through afferent fibers known as flexion reflex afferent (FRA) fibers. In flexion reflexes, these afferent volleys cause excitatory interneurons to activate α motor neurons that supply the flexor muscles in the same limb and inhibit the α motor neurons that supply the antagonistic extensor muscles. This pattern of activity leads to flexion of one or more joints in the stimulated limb. Additionally, commissural interneurons elicit the opposite pattern of activity in the contralateral side of the spinal cord, resulting in extension of the opposite limb, known as the crossed extension reflex. In lower limbs (or both forelimbs and hind limbs in quadrupeds), the crossed extension reflex helps maintain balance by enabling the contralateral limb to support the additional load when the flexed limb is lifted.

After damage to the descending motor pathways, hyperactive stretch reflexes can lead to spasticity, characterized by significant resistance to passive limb rotation. In this condition, the clasp-knife reflex may be observed. Initially, attempts to rotate a limb about a joint are met with high resistance. However, as the applied force increases, there comes a point where the resistance suddenly dissipates, and the limb rotates easily. This change in resistance is caused by reflex inhibition. The group Ib reflex arc suggests that increased activity in this pathway may underlie the sudden release of resistance. The clasp-knife reflex was once thought to be triggered by the activation of Golgi tendon organs, which were believed to have a high threshold for muscle stretch. However, it is now understood that the activation of other high-threshold muscle receptors supplying the fascia around the muscle is responsible for this reflex. Signals from these receptors activate interneurons that lead to the inhibition of the corresponding motor neurons.

Flexion reflexes are considered a type of withdrawal reflex because they typically bring the affected limb closer to the body and away from a painful stimulus.
Functionally, however, the two reflex arcs can act synergistically, as the following example shows. Recall that the Golgi tendon organs monitor force levels across the tendon that they supply. If during maintained posture (such as standing at attention) knee extensors (such as the rectus femoris muscle) begin to fatigue, the force pulling on the patellar tendon declines. The decline in force reduces the activity of Golgi tendon organs in this tendon. Because the group Ib reflex normally inhibits the α motor neurons to the rectus femoris muscle, reduced activity of the Golgi tendon organs enhances the excitability of (i.e., disinhibits) the α motor neurons and thereby helps reverse the decrease in force caused by the fatigue. Simultaneously, bending of the knee stretches the knee extensors and activates the afferent fibers from the muscle spindles, which then excite the same α motor neurons. Thus coordinated action of afferent fibers from both the muscle spindle and Golgi tendon organ help oppose the decrease in contraction of the rectus femoris muscle due to fatigue and thereby work together to maintain the standing posture.
The flexion reflex starts with activation of one or more of a variety of sensory receptors, including nociceptors, whose signals can be carried to the spinal cord via a variety of afferent fibers, including group II and group III fibers, collectively called the flexion reflex afferent (FRA) fibers. In flexion reflexes, afferent volleys (1) cause excitatory inter-neurons to activate the α motor neurons that supply the flexor muscles in the ipsilateral limb and (2) cause inhibitory interneurons to inhibit the α motor neurons that supply the antagonistic extensor muscles (
Fig. 9.9).
This pattern of activity causes one or more joints in the stimulated limb to flex. In addition, commissural interneurons evoke the opposite pattern of activity in the contralateral side of the spinal cord (see
Fig. 9.9 ), which results in extension of the opposite limb, the crossed extension reflex. For lower limbs in humans (or for both forelimbs and hind limbs in quadrupeds), the crossed extension part of the reflex helps in maintaining balance by enabling the contralateral limb to be able to support the additional load that is transferred to it when the flexed limb is lifted.
Afterdamagetothedescendingmotorpathways,hyperactivestretchreflexesmayresultinspasticity,inwhichthereislargeresistancetopassiverotationofthelimbs.Inthiscondition,itmaybepossibletodemonstratewhatiscalledtheclasp-knife reflex. Whenspasticityispresent,attemptstorotatealimbaboutajointinitiallymeethighresistance.However,iftheappliedforceisincreased,therecomesapointatwhichtheresistancesuddenlydissipatesandthelimbrotateseasily.Thischangeinresistanceiscausedbyreflexinhibition.ThegroupIbreflexarcsuggeststhatrisingactivityinthispathwaycouldunderliethesuddenreleaseofresistance,andindeed,theclasp-knifereflexwasonceattributedtotheactivationofGolgitendonorganswhenthesereceptorswerethoughttohaveahighthresholdtomusclestretch.However,thetendonorganshavesincebeenshowntobeactivatedatverylowlevelsofforceandarenolongerthoughttocausetheclasp-knifereflex.Itisnowthoughtthatthisreflexiscausedbytheactivationofotherhigh-thresholdmusclereceptorsthatsupplythefasciaaroundthemuscle.Signalsfromthesereceptorscausetheactivationofinterneuronsthatleadtoinhibitionofthehomonymousmotorneurons.
Because flexion typically brings the affected limb in closer to the body and away from a painful stimulus, flexion reflexes are a type of withdrawal reflex. In