C. Capaday et al., DIFFERENTIAL-EFFECTS OF A FLEXOR NERVE INPUT ON THE HUMAN SOLEUS H-REFLEX DURING STANDING VERSUS WALKING, Canadian journal of physiology and pharmacology, 73(4), 1995, pp. 436-449
A conditioning (C) stimulus at group I strength was delivered during s
tanding to the common peroneal (CP) nerve before a test (T) stimulus a
t several C-T intervals ranging from 0 to 150 ms. At sufficiently long
C-T intervals (100-120 ms) the soleus H-reflex was strongly inhibited
despite little, or no change, in the background level of EMG activity
. This finding indicates that a significant portion of the inhibition
occurs at a premotoneuronal level, likely via presynaptic inhibition o
f the Ia-afferent terminals. During standing, at C-T intervals of 100-
120 ms (optimal C-T interval) a conditioning stimulus to the CP nerve
of 1.5 times motor threshold (MT) intensity reduced the soleus II-refl
ex by an average of 45.8% (n = 14 subjects). The conditioning stimulus
always produced a clear inhibition of the II-reflex during standing a
t these C-T intervals. The effects of this conditioning stimulus on th
e soleus II-reflex were then determined in the early part of the stanc
e phase of walking. In contrast to standing, the conditioning stimulus
produced little or no inhibition during the early part of the stance
phase of walking (average inhibition 45.8 vs. 11.6%, n = 14 subjects).
The soleus background EMG, and the soleus and tibialis anterior M-wav
es were essentially the same during standing and walking. Furthermore,
there was no shift of the optimal C-T interval during walking. The di
fference in the effects of the conditioning stimulus was not due to di
fferences in the size of the test II-reflex in each task. It appears t
o be due to a genuine task-dependent change in the input-output proper
ties of the underlying spinal cord circuits. There are at least two, m
utually compatible, explanations of these results. Firstly, during wal
king the intraspinal terminals of the afferent fibres (group Ia and Ib
) conducting the conditioning volley may be presynaptically inhibited,
or their input gated at the interneuronal level. Secondly, on the ass
umption that the conditioning stimulus is acting via the presynaptic i
nhibitory network in the spinal cord, it is possible that during walki
ng this network is saturated as a result of increased central or perip
heral synaptic inputs. Finally, it seems unlikely that differences in
the refractoriness of the CP nerve between the tasks may be involved;
the reasons for this are presented in the discussion.