Biomedical subjects
Publications and source records attributed to R S Person.
Main mechanisms of muscle contraction control: recruiting of motor units and changes of their firing rate are discussed in the review. Relative contribution of these mechanisms at different types of muscular activity (tonic contraction, vibration reflex, locomotion) is considered.
Firing of motor units of human soleus, triceps brachii and rectus femoris muscles was studied. Standard deviations of interspike intervals against mean intervals were plotted during voluntary muscle contraction and tonic vibration reflex. There was no significant difference between the results obtained under these conditions.
Cross-correlograms (CCGs) of action potentials of single motor unit (MU) pairs of soleus, triceps br. and 1 interosseus dors muscles were plotted. The CCGs of 21 pairs from 126 pairs studied during voluntary muscle contraction revealed peaks at a zero point, the peak width being less than or equal to 5 ms (short-term synchronization). During the tonic vibration reflex of the soleus and triceps br. muscles there were 12 synchronized MU pairs from 86 studied pairs. The CCGs of MU 1 and 2 interosseus dors. muscles revealed the synchronization in 4 pairs from 10 studied pairs. The "strength" of synchronization in all MU pairs was low: usually no more than 6% of all impulses coincided above the probability of accidental coincidences. The short-term synchronization is, presumably, a result of common input to different motoneurons from branches of the last-order premotoneuron nerve fibres. The long-term synchronization of MUs was revealed in the CCGs. This synchronization is supposedly caused by the muscle fatigue during the experiment.
The influence of a short inhibitory volley on firing motoneurons of soleus and ext. carpi uln. was studied in human experiments and the results obtained were used as a basis for simulation. An increase of the interspike interval (ISI) depended on the timing of inhibitory volley arrival and silent period (SP) duration was studied. The ability of the individual motoneuron to respond to inhibitory volley by prolongation of ISI influenced the SP duration. Two parameters were crucial: the duration of the part of ISI where the inhibition was efficient in increasing the ISI (d) and the maximal increase of ISI (delta x max). The latter corresponded to the inhibitory volley arrival at the very end of ISI. If d less than delta x max the SP = d; if d greater than delta x max the SP = delta x max. In the case of variable ISIs those relations should be applied to the smallest ISI among the ISI distribution. Therefore the SP duration depended not only on the mean ISI of a motoneuron, but on ISI variability as well.
The tonic vibration reflex was evoked in the human soleus muscle, the range of vibration frequencies was 30-180 Hz. The potentials of single motor units (MUs) were picked up. At low frequencies (to 70-80 Hz) the potentials of all MUs under study correlated with vibration stimuli. This showed the existence of ripples in the excitatory inflow to motoneurons. With an increase of the vibration frequency the correlation disappeared. In the voluntarily contracted muscle the correlation was revealed at higher vibration frequencies than in the relaxed muscle. Since the vibration is known to depress monosynaptic reflexes from primary spindle endings, it is suggested that the correlation of motoneuron discharges and vibration stimuli at low vibration frequency is, apparently, a result of the activation of secondary spindle endings which via short synaptic pathways evoked discrete EPSPs in motoneurons.
Recurrent inhibition was studied by antidromic stimulation of Renshaw's cells. 25 normal subjects and 74 patients with CNS lesions accompanied by movement disturbances were examined. During weak voluntary contraction of the soleus muscle, the stimuli were applied to motor fibers of the n. tibialis (weak M-response was evoked). In normal subjects, the stimulation was followed by short-latency suppression of the EMG background activity of the muscle brought about by recurrent inhibition. The same inhibition was revealed in patients with spastic paresis caused by pyramidal system lesion. However, the stimulation failed to evoke the recurrent inhibition in patients with movement disturbances caused by brain stem and cerebellum lesions, including patients with hypotonia.
Analysis of poststimulus histograms and interspike intervals of firing motor units showed that the burst following the silent period under evoked muscle contraction is the result of synchronous motoneuron escape from inhibition. Under strong evoked isotonic muscle contraction a true facilitation was revealed. The latency of this facilitation was too long for spinal monosynaptic reflex related to spindles elongation at the muscle relaxation stage.
Isotonic contractions of human hand muscles were elicited by nerve stimulation and the silent period was studied on single motor units employing post-stimulus histograms. At submaximal M-response (up to 70% of M-maximum) the motoneurons under study were not stimulated and thus the after-hyperpolarization was excluded from the experiment. Under these conditions the latency of the silent period was not less than 60 ms and the silent period parameters were similar to those after subthreshold for M-response nerve stimulation and to those after skin stimulation. The experiments proved that neither recurrent inhibition nor spindle unloading affected the spinal centres of muscles under study.
The probability of motor unit discharges and changes in the inter-spike interval duration before the voluntary contraction were studied on m. soleus of human beings. A strong motoneuron facilitation was revealed 15-20 ms before the burst of potentials in EMG and only in some experiments a weak facilitation took place earlier (30-50 ms before the burst). So, "tuning" (H-reflex increasing) 60 ms before the voluntary contraction may be regarded as a result of H-reflex presynaptic disinhibition.
The method of post-stimulus histograms of the single motor unit potentials permits the under-threshold facilitation to be revealed and the antidromic blocking of H-reflex to be avoided up to sub-maximal for M-response stimuli. The H-reflex was revealed only under abnormal conditions and was not observed in the noraml subjects. In the experiments the motoneurons responded to impulses from above, therefore the inhibition of the motoneurons itself cannot be a mechanism of the H-reflex inhibition. The alternative explanation is the presynaptic inhibition.
Motor unit (MU) potentials of m. triceps br. of healthy subjects and patients with myasthenia gravis were recorded during slight isometric contractions. MU potentials were visually identified, semi-automatically coded and automatically led in the digital computer. In myasthenia the mean frequency of the MU discharges and SD of the interspike intervals were higher than in healthy states, the difference being not great, but significant. The interspike interval hystograms of single MUs were unchanged (normal). So the disturbances in pattern of motoneurone activity in myasthenia were mild. Proserin raised the muscle contraction strength and normalized the interspike interval variability but did not lower the frequency of MU discharges. The increase of the frequency may be accounted for the reduction of Renshaw inhibition.
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