Role of small diameter afferents in reflex inhibition during human muscle fatigue.

Abstract

SUMMARY1. Previous work has shown that the H reflex excitability of the human soleus motoneurones is reduced during fatigue and is accompanied by a corresponding decrease in electromyographic (EMG) activity during maximal voluntary contractions. These findings were consistent with the existence of a reflex whereby xmotoneurones are inhibited by sensory input from the fatigued muscle.2. To elucidate the contribution of different-sized afferents in such reflex inhibition, compression of the sciatic nerve was used in an attempt to block large myelinated afferents prior to fatigue. 3. Fatigue of the soleus muscle was induced under ischaemic conditions by intermittent electrical stimulation at 15 Hz in ten healthy subjects. These subjects also participated in a control test in which the compression block was followed by ischaemia without fatigue.4. Following nerve compression alone, both the mean maximal plantarflexion torque and the associated EMG for all ten subjects declined by 18-8+ 162% (S.D.) and 13 4 + 17 2 %, respectively. 5. Following fatigue, there were five subjects in whom the large afferents remained blocked and the experimental findings were consistent with the existence of reflex inhibition during fatigue. The mean maximal plantarflexion torque decreased further by 36 2 + 7 6 % from the value following the compression block compared to a decrease of 5-0 + 9-9 % in the ischaemia control. The mean EMG associated with these contractions also decreased from post-block values by 56 8 + 19-6 % following fatigue and by only 6-4 + 8-0 % following ischaemia alone.6. The peripheral excitability of the neuromuscular junction and muscle fibre membrane was adequate following fatigue as evidenced by only modest changes in the M wave (muscle compound action potential). The descending motor drive was deemed sufficient because of the absence of any large interpolated twitches superimposed upon the maximal voluntary contraction in all but two subjects.7. The declines in maximal plantarflexion torque and the associated EMG activity were very similar to those found in a previous study in which the sensory input was unaltered. The findings demonstrated that any reflex inhibition of the o-motoneurone

Behaviour of short and long latency reflexes in fatigued human muscles.

“…Because of the slow time course of the H reflex decrease during fatigue, it is suggested that this is induced by muscle metabolic or chemical processes which could be mediated by small diameter afferents from the fatigued muscle (Garland, 1991). This conclusion is supported by our finding that the H reflex decrease does not recover as long as ischaemia is maintained (cf.…”

Fatigue-Sensitive Afferents Inhibit Extensor but Not Flexor Motoneurons in Humans

“…The reduced motoneuronal excitability probably contributes to the decline in the discharge rate of single motor units and the development of central fatigue that occurs with sustained MVCs. The reduction in motoneuron firing rates observed in many studies (Grimby et al, 1981;Bigland-Ritchie et al, 1983;Gandevia et al, 1990) has often been attributed to reflex inhibition from group III and IV muscle afferents (Woods et al, 1987;Garland, 1991). In the current study, when ischemia was maintained after fatiguing contractions of elbow extensors, CMEPs in triceps failed to recover.…”

“…Much of the indirect evidence favoring a reflex inhibitory pathway mediated by group III and IV muscle afferents has been obtained for other physiological extensors. For example H-reflexes evoked in ankle plantarflexors are depressed after fatigue (Garland and McComas, 1990;Garland, 1991;Loscher et al, 1996;Walton et al, 2002;Kuchinad et al, 2004). We suggested previously that the discrepancy between results based on the H-reflex and that for the CMEP in elbow flexors (Butler et al, 2003) could be attributable to presynaptic inhibition of group Ia afferent volleys by group III and IV muscle afferents (Pettorossi et al, 1999;Rossi et al, 1999;Rudomin and Schmidt, 1999).…”

“…When firing of group III and IV muscle afferents is maintained after fatiguing exercise by muscle ischemia, the recovery of the discharge rates of motoneurons is prevented (Bigland-Ritchie et al, 1986;Woods et al, 1987). The tendon jerk and H-reflex are also reduced by fatigue (Garland and McComas, 1990;Garland, 1991;Duchateau and Hainaut, 1993;Walton et al, 2002;Kuchinad et al, 2004), and a contraction-induced spinal inhibition may operate between synergists (Sacco et al, 1997). These studies suggest that group III and IV muscle afferent feedback from the fatiguing muscle can reflexly depress or inhibit motoneuronal firing rates.…”

Effects of muscle action type on corticospinal excitability and triceps surae muscle-tendon mechanics

“…Additionally, fascicle length afferent information coming from the muscle spindles can also be ruled out as possible excitability modulator, since FL was the same among the experimental protocols. (4) small diameter afferents (i.e chemosensors and nociceptors; Gandevia 1998;Garland et al 1991) should play if any a small role as the maximal effort duration was small (Min:2.35s/Max:3.4s) and the recovery time between trials was long (3 minutes). The torque analysis for each trial throughout the testing session showed no significant effect of fatigue (see methods), therefore it seems that the effort to rest ratio probably was not enough to cause metabolite accumulation and induce peripheral fatigue; (5) corticospinal descending drive produced by TMS reduced PSI of Ia terminals of a relaxed muscle (Meunier & Pierrot-Deseilligny 1998) suggesting that the same cortical sites both activate MNs of a given pool and depress primary afferent depolarization interneurons.…”