TL;DR: The results of the study do not support the assumption that a painful muscle lesion is followed by an activation of the gamma‐loop that leads to an increase in musle tone, and may offer an explanation for the weakness and — in chronic cases — the reflex atrophy of lesioned muscles.
Abstract: The study was undertaken to test the widely held hypothesis that a painful lesion of the skeleto-motor system leads to an increase in the neuromuscular component of muscle tone by activating gamma-motoneurones in the affected region. In chloralose-anaesthetized cats, artificial myositis was induced in the lateral gastrocnemius-soleus (LGS) muscle and several hours later the impulse activity was recorded from single gamma-motoaxons supplying the medial gastrocnemius (MG) muscle. Under the conditions of the study, the majority of the fusimotor neurones had a resting activity and could be readily excited by natural stimuli. In contrast to the assumptions of the working hypothesis, the gamma-motoneurones in the myositis animals were not activated but showed a strong inhibition; both resting activity and excitability by electrical and natural stimuli were decreased. Additional recordings from fusimotor neurones of a flexor muscle (tibialis anterior, TA) demonstrated that in the preparation used, the behaviour of the flexor gamma-motoneurones was different from extensor ones in that the former usually had no resting activity and did not respond to natural stimuli. The only discernible effect of a myositis of the LGS muscle on the TA gamma-motoneurones was a decrease in their electrical reflex threshold. The results of the study do not support the assumption that a painful muscle lesion is followed by an activation of the gamma-loop that leads to an increase in muscle tone. Instead, the data may offer an explanation for the weakness and--in chronic cases--the reflex atrophy of lesioned muscles.
TL;DR: The abnormal response to prolonged vibration stimulation could represent abnormal gamma loop in the quadriceps femoris muscle of the uninjured side in patients with ACL rupture since the normal response of maximal voluntary contraction and I-EMG to prolonged vibrations could not be evoked without normal function of the gamma loop.
Abstract: KONISHI, Y., H. KONISHI, and T. FUKUBAYASHI. Gamma Loop Dysfunction in Quadriceps Contralateral Side in Patients with Ruptured ACL. Med. Sci. Sports Exerc., Vol. 35, No. 6, pp. 897–900, 2003. Purpose: The aim of our study was to test for any neurophysiological abnormality in the gamma loop in the quadriceps femoris muscle on the uninjured side of patients with unilateral rupture of the anterior cruciate ligament (ACL). Methods: Maximal voluntary contraction of knee extension and integrated electromyography (I-EMG) of the vastus medialis, vastus lateralis, and rectus femoris were measured in the uninjured limb of 13 patients with unilateral ACL rupture and 10 normal subjects, before and after 20-min vibration stimulation applied to the infrapatellar tendon. Results: The mean percentage changes of maximal voluntary contraction and I-EMG in quadriceps femoris of the uninjured side of patients with ACL rupture were significantly different from those of the control group. Maximal voluntary contraction and I-EMG after prolonged vibration stimulation did not decrease as much as those of the control group even though the same protocol of vibration stimulation was applied. Conclusion: The abnormal response to prolonged vibration stimulation could represent abnormal gamma loop in the quadriceps femoris muscle of the uninjured side in patients with ACL rupture since the normal response of maximal voluntary contraction and I-EMG to prolonged vibration stimulation could not be evoked without normal function of the gamma loop. Key Words: VIBRATION STIMIULATION, ACL INJURY, REFLEX INHIBITION, EMG
TL;DR: The recurrent extrafusal contractions in movements of this type are initiated by the fast direct alpha route, but individual contraction phases generally last long enough to be influenced subsequently by the coactivated fusimotor loop through the spindles.
Abstract: Single unit activity in primary spindle afferent nerve fibres from finger and foot flexors was recorded with tungsten microelectrodes inserted into the median and peroneal nerves of healthy subjects. During voluntary fast alternating finger and foot movements, simulating the tremor of Parkinsonism, two types of discharges were seen in the Ia afferent fibres: (1) stretch responses occurring during the flexor relaxation phases, and (2) discharges occurring during the flexor contraction phases. Contrary to the stretch responses the spindle contraction discharges could be eliminated by a partial lidocaine block of the muscle nerve proximal to the recording site, indicating that they resulted from fusimotor activation of intrafusal fibres. On the basis of the temporal relations between the beginning and end of individual EMG-bursts, the start of the spindle contraction discharges and the latency of the stretch reflex in the muscles concerned, the following conclusions were drawn: the recurrent extrafusal contractions in movements of this type are initiated by the fast direct alpha route, but individual contraction phases generally last long enough to be influenced subsequently by the coactivated fusimotor loop through the spindles. It is postulated that this gamma loop influence during alternating movements helps to keep flexor and extensor muscles working in a regular reciprocal fashion with contractions adjusted in strength to the external loads.
TL;DR: It is concluded that the early inhibition of the soleus H-reflex is only due to suprasegmental activity, whereas during the secondary part of the inhibition there is a supplementary inhibitory action brought about by Ia fibres from tibialis anterior.
Abstract: Variations of the soleus H-reflex were studied during voluntary isometric or anisometric contractions of the tibialis anterior in man. At the onset of isometric contractions there was a weak inhibition of the soleus H-reflex, which was not related to the force of the tibialis anterior contraction. 110 msec after the onset of the EMG activity, the inhibition became secondarily more marked and was then related to the force of the contraction. This secondary potentiation of the H-reflex inhibition is brought about by group I fibres activity, since it was markedly reduced during is-chemia of the leg. It persisted during local muscular fatigue, this indicating that Ib fibres from tibialis anterior are not involved and that, by the process of elimination, group Ia fibres must be responsible for the supplementary secondary inhibition. It is concluded that the early inhibition is only due to suprasegmental activity, whereas during the secondary part of the inhibition there is a supplementary inhibitory action brought about by Ia fibres from tibialis anterior. The secondary potentiation of the inhibition is therefore likely to be produced via the gamma loop.