Зміни скорочувальної властивості м’яза і модуляція сегментарних рефлексів при розвитку м’язової втоми

Bugaychenko L.A. - Fatigue effects on muscle cotractility and segmental reflexes. - Manuscript.

Thesis for a candidate's degree on the speciality 03.00.13 - physiology of animals and humans. - Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, 2005.

Thesis in view reveals some fatigue effects on muscle contraction dynamics and basic segmental reflexes.

Effects of wide-range fatigue were studied on transient and steady force components of eccentric contraction of cat gastrocnemius. Gastrocnemius muscle was activated by distributed stimulation of dissected ventral root (VR) L7 with rate of 10/s per filament. Active muscle was stretched through trapezoidal ramp with different velocities (1.25, 2.5, 10 mm/s). Fatiguing sessions consisted of standard test repetitions every 2 minutes. Normalized transient and steady components of extra force (fresh-state value = 1) were respectively 0.77±0.04 and 0.78±0.02 at 30% muscle tension drop, 0.27±0.04 and 0.55±0.02 at 60% muscle tension drop. Both transient and steady components have equal shares in extra force of eccentric contraction during moderate fatigue (up to 30% muscle tension drop); further pronouncing of fatigue entailed diminution of transient component share and corresponding augmentation of steady component one. Falling phase of transient component was subjected to fatigue and velocity of preceding lengthening in similar manner. We are speculated that steady component as reflection of actin-myosin affinity improvement during muscle stretching is less exposed to fatigue than cross-bridge rate.

Further we have explored lengthening and shortening trajectories under servo-control of external load during spatial spreading effects of fatigue from active to inactive parts in the cat gastrocnemius muscle. Conditioning fatiguing contractions (CFC) of a part of gastrocnemius muscle were evoked through stimulation of the cut VR S1 with rate 50 s^-1 during 20 s followed by 10 s of rest, over 10 - 30 min. To test activation of a non-active part of this muscle the distributed stimulation of dissected VR L7 with rate of 10 s^-1 per filament was applied. After achieving by the muscle a steady-state level of isometric contraction, a quick transition to isotonic condition was produced. Transient responses of shortening and lengthening were analyzed in terms of the two-component model including the fast inertialess and slow aperiodic components. Test duration was 12 s, time intervals between tests consisted of 3 min. CFC reduced isometric force of the tested part of muscle as well as the velocity of shortening and lengthening. The muscle lengthening had been slowing down with development of the fatigue effects; the final steady value of the muscle length in transients was reduced, while weight of the inertialess component increased. Slowing of shortening was accompanied by reduction of the final length amplitude and the time constants of aperiodic component were increased. We suppose that diffusion of metabolites from active to inactive muscle fibers was the major reason for contractility deterioration.

To ascertain possible alterations of motoneurons activity due to homonomous muscle fatigue, the monosynaptic reflex (MSR) and stretch reflex were monitored.

Responses of gastrocnemius-soleus (G-S) motoneurones to stretches of the homonymous muscles were recorded intracellularly in decerebrate cats before, during and after fatiguing stimulation (FST) of G-S muscles. VR L7 and S1 were cut, and FST was applied to VR S1, a single FST session including 4-5 repetitions of 12-s periods of regular 40 s^-1 stimulation. Muscle stretches consisted of several phases of slow sinusoidal shortening-lengthening cycles and intermediate constant lengths. The maximal stretch of the muscles was 8.8 mm above the rest length. Effects of FST on excitatory postsynaptic potentials (EPSPs) and spikes evoked by the muscle stretches were studied in 12 motoneurones from 10 experiments. Stretch-evoked EPSPs and firing were predominantly suppressed after FST, with the exception of a post-contraction increase of the first EPSP after FST, which was most likely due to after-effects in the activity of muscle spindle afferents. The post-fatigue suppression of EPSPs and spike activity was followed by restoration within 60 - 100 s. Additional bouts of FST augmented the intensity of post-fatigue suppression of EPSPs, with the spike activity sometimes disappearing completely. FST itself elicited EPSPs at latencies suggesting activation of muscle spindle group Ia afferents via stimulation of в-fibres. The suppression of the stretch-evoked responses most likely resulted from fatigue-evoked activity of group III and IV muscle afferents. Presynaptic inhibition could be one of the mechanisms involved, but homosynaptic depression in the FST-activated group Ia afferents may also have contributed.

In decerebrate cats, changes in MSR of G-S motoneurones were studied after FST of the G-S muscles. MSRs were evoked by stimulation of Ia fibres in the G-S nerve and recorded from a filament of VR L7. FST (intermittent 40 s?1 stimulation for 10-12 min) was applied to the distal part of the cut VR S1. FST reduced MSR amplitudes to 0.64 ± 0.04 (mean ±S.E.M.) of the prefatigue values. The suppression remained stable for approximately 25 min and then MSR amplitudes gradually returned towards the normal. To test for the involvement of presynaptic and recurrent inhibition, MSRs were conditioned by stimulation of the nerve to the posterior biceps and semitendinosus (PBSt) muscles or a filament of VR L7, respectively. The intensity of presynaptic inhibition (reduction of the normalized value of MSR amplitude during conditioning) increased from 0.19 ± 0.02 in prefatigue to 0.44 ± 0.04 within a 5.3-18.2 min interval after FST, followed by a recovery. In contrast, the intensity of recurrent inhibition first diminished from 0.23 ± 0.02 in prefatigue to 0.15 ± 0.01 within 15.6-30.1 min after FST and then gradually recovered. Both primary afferent depolarization and the intensity of antidromic discharges in primary afferents increased with the presynaptic inhibition intensity. These results demonstrate a fatigue-related suppression of Ia excitation of synergistic motoneurones, probably arising from the activation of group III and IV afferents. The effects could in part be due to increased presynaptic inhibition, while recurrent inhibition plays a minor role.

Key words: muscle fatigue, monosynaptic reflex, stretch reflex, presynaptic inhibition, recurrent inhibition, dynamics of muscle contraction.

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