The reflex that opposes changes in muscle force is called the inverse myotatic reflex. Similar to how the stretch reflex regulates muscle length, the inverse myotatic reflex, or group Ib reflex, helps maintain force levels in a muscle. For example, in the upper part of the leg, the group Ib reflex arc begins with the Golgi tendon organ receptor, which detects muscle tension. Golgi tendon organs are found at the junction of the tendon and muscle fibers and are in series with the muscle fibers, unlike the parallel arrangement of muscle spindles. These Golgi tendon organs are innervated by group Ib afferent fibers that wrap around bundles of collagen fibers in the muscle tendon. Hyperactive stretch reflexes can cause involuntary rhythmic movements such as tremors and clonus. While the negative feedback action of the stretch reflex can stabilize the limb at a certain position, external disturbances can lead to the stretch reflex circuit becoming a source of instability, resulting in rhythmic movements like clonus. Clonus is triggered by a sustained muscle stretch in individuals with spinal cord damage. Normally, a sustained muscle stretch increases activity in group Ia and group II fibers, which after a delay causes a muscle contraction opposing the stretch. However, the muscle does not fully return to its initial length due to the stretch reflex gain being less than 1. This partial compensation then decreases the activity in group Ia and group II fibers, causing the limb to lengthen again, leading to a repeating cycle. The delay is crucial in setting up this oscillation as it allows the feedback signal to continue even after the muscle has compensated, resulting in an overcompensation that leads to the next overcorrection. However, because the reflex gain is typically much less than 1, this oscillation usually dies out quickly, and the muscle reaches an intermediate length. In contrast, when descending motor pathways are damaged, changes in spinal cord connectivity and increased neuronal excitability result in a hyperactive reflex, which is equivalent to raising the gain of the stretch reflex close to 1. In this case, the successive overcompensations are much larger, leading to an overt but transient oscillation known as clonus. If the gain equals 1, the clonus does not die out but persists as long as the initial stretch stimulus is maintained.
The inverse myotatic reflex acts to oppose changes in the level of force in the muscle. Just as the stretch reflex can be thought of as a feedback system to regulate muscle length, the inverse myotatic, or group Ib, reflex can be thought of as a feedback system to help maintain force levels in a muscle. With the upper part of the leg as an example, the group Ib reflex arc is depicted in
Fig. 9.7.
The arc starts with the Golgi tendon organ receptor, which senses the tension in the muscle. Golgi tendon organs are located at the junction of the tendon and the muscle fibers and thus lie in series with the muscle fibers, in contrast to the parallel arrangement of the muscle spindles (see
Fig. 9.2 ). Golgi tendon organs have a diameter of about 100 µm and a length of about 1 mm. A Golgi tendon organ is innervated by the terminals of group Ib afferent fibers. These terminals wrap about bundles of collagen fibers in the tendon of a muscle (or in tendinous inscriptions within the muscle).
Hyperactivestretchreflexescanleadtotremorsandclonus,whicharetypesofinvoluntaryrhythmicmovements.Althoughthenegative-feedbackactionofthestretchreflexcanhelpstabilizethelimbataparticularposition,ifanexternalperturbationtothelimboccurs,theconductiondelaybetweentheinitiatingstimulus(musclestretch)andtheresponse(musclecontraction)cancausethestretchreflexcircuittobeasourceofinstabilitythatleadstorhythmicmovements.Specifically,clonusiselicitedbyasustainedstretchofamuscleinapersonwhohasspinalcorddamage.Normally,animposedsustainedstretchonamuscleelicitsanincreaseingroupIaandgroupIIfiberactivity,whichafteradelaycausesacontractioninthemusclethatopposesthestretchbutdoesnotcompletelyreturnthemuscletoitsinitiallengthbecausethegainofthestretchreflexismuchless than1.*
Thispartialcompensation,inturn,leadstoadecreaseingroupIaandgroupIIfiberactivity,whichcausesthelimbtolengthenagain,butnotfully.ThislengtheningonceagainincreasesgroupIaandgroupIIfiberactivity,andsoon.Thedelayisessentialinsettingupthisoscillationbecauseitcausesthefeedbacksignaltocontinueevenafterthemusclehascompensatedandthusresultsinanovercompensationthatleadstothenextovercorrection.However,becausethereflexgainisnormallymuchlessthan1,thisoscillationnormallydiesoutquickly(theovercompensationsdecreaseinamplituderapidly),andthemusclecomestorestatanintermediatelength.Incontrast,whendescendingmotorpathwaysaredamaged,theresultingchangesinspinalcordconnectivityandincreasesinneuronalexcitabilityresultinahyperactivereflex(whichisequivalenttoraisingthegainofthestretchreflexcloseto1).Inthiscase,thesuccessiveovercompensationsaremuchlarger,andanovertbuttransientoscillationcanbeobserved(clonus).Ifthegainequals1,theclonusdoesnotdieoutbutratherpersistsforaslongastheinitialstretchstimulusismaintained.
*Ingeneral,gain ofasystemisdefinedasitsoutputforagiveninput.Inthiscase,theinputtothesystemistheimposedstretch,andtheoutputismovementcausedbythestretchreflex–evokedcontraction.