Group III and IV muscle afferents: role on central motor drive and clinical implications.

The present review is focused on neural mechanisms responsible of group III and IV muscle afferent actions on central motor drive during physical exercise in both healthy and pathological populations. It seems that these mechanisms contribute to improve muscle performance by regulating the peripheral fatigue development and by avoiding excessive muscle impairments. Therefore, a great deal of attention is paid to their influences on motor unit activation during fatiguing exercise both in human and animal models. Recent evidence indicated that these afferents from a given active muscle could contribute to regulate the motor activity of the homonymous as well as surrounding skeletal muscles by acting at both spinal and supraspinal levels. In addition, given that the recovery of the sensory feedback plays a key role in the improvement of motor function following numerous neuromuscular traumas, the role of these afferents in preclinical and clinical situations is also explored in animal and human models. It is supposed that studying the motor and autonomic functions of group III and IV afferents might help healthcare professionals in the future to find appropriate treatments and rehabilitation programs.

Recovery pattern of motor reflex after a single bout of neuromuscular electrical stimulation session.

We aimed at determining the recovery pattern of neural properties of soleus muscle after a single bout of neuromuscular electrical stimulation (NMES) session. Thirteen subjects performed an NMES exercise (75 Hz, 40 contractions, 6.25 s per contraction). Maximal voluntary contraction (MVC), H-reflex at rest and during voluntary contraction fixed at 60% of MVC (respectively, H(max) and H(sup) ) and volitional (V) wave were measured before and during the recovery period following this exercise [i.e., immediately after, 2 h (H2), 2 days (D2) and 7 days (D7)]. MVC exhibited an immediate and a delayed declines at 2 days (respectively, -29.8±4.6%, P<0.001; -13.0±3.4%, P<0.05). Likewise, V/M(sup) was decreased immediately and 2 days after NMES session (respectively, -43.3±11.6%, P<0.05; 35.3±6.6%, P<0.05). The delayed decrements in MVC and V-wave occurred concomitantly with muscle soreness peak (P<0.001). It could be concluded that motor command alterations after an NMES resistance session contributed to the immediate and also to the delayed decreases in MVC without affecting resting and active H-reflex excitability. These results suggested that spinal circuitry function of larger motoneurons was inhibited by NMES (as indicated by the depressed V-wave responses) contrary to the smaller one (indicated by the unchanged H-reflex responses).

Changes in the soleus muscle architecture after exhausting stretch-shortening cycle exercise in humans.

This study focused on the architectural changes in the muscle-tendon complex during the immediate and secondary (delayed) reductions of performance (bimodal recovery) caused by an exhaustive rebound type stretch-shortening cycle (SSC) exercise. The isometric plantar flexor torque during maximum voluntary contraction (MVC) was measured together with recording of electromyography (EMG) and ultrasonography from the soleus muscle before (BEF), after (AFT), 2 h (2H), 2 and 8 days (2D, 8D) after the SSC exercise (n=8). The performance variables (MVC torque and EMG activation) followed the bimodal recovery patterns. This was not the case in the changes of the fascicle length and muscle thickness. The relative torque changes in MVC correlated positively (R=0.78, P=0.02) to the corresponding averaged EMG changes between BEF and 2H (BEF-->2H); the significance disappeared in the comparison between 2H and 2D (2H-->2D), during which period MVC showed a secondary reduction. The relative torque changes in MVC showed no correlation with the changes in muscle thickness between BEF-2H. However, this correlation between 2H-2D was negative (R=-0.85, P<0.01). The fascicle shortening/average EMG ratio in MVC increased at 2H, and then decreased more at 2D than 2H (P<0.05). Thus, the secondary performance decline was not related to the corresponding EMG reduction but to the increased muscle thickness, which peaked at 2D. The results suggest clearly that the secondary decline in MVC could be related to the increase in muscle volume.

[Peripheral nerve repair: 30 centuries of scientific research]. / La réparation nerveuse périphérique: 30 siècles de recherche.

INTRODUCTION: Nerve injury compromises sensory and motor functions. Techniques of peripheral nerve repair are based on our knowledge regarding regeneration. Microsurgical techniques introduced in the late 1950s and widely developed for the past 20 years have improved repairs. However, functional recovery following a peripheral mixed nerve injury is still incomplete. STATE OF ART: Good motor and sensory function after nerve injury depends on the reinnervation of the motor end plates and sensory receptors. Nerve regeneration does not begin if the cell body has not survived the initial injury or if it is unable to initiate regeneration. The regenerated axons must reach and reinnervate the appropriate target end-organs in a timely fashion. Recovery of motor function requires a critical number of motor axons reinnervating the muscle fibers. Sensory recovery is possible if the delay in reinnervation is short. Many additional factors influence the success of nerve repair or reconstruction. The timing of the repair, the level of injury, the extent of the zone of injury, the technical skill of the surgeon, and the method of repair and reconstruction contribute to the functional outcome after nerve injury. CONCLUSION: This review presents the recent advances in understanding of neural regeneration and their application to the management of primary repairs and nerve gaps.

Evidence that free radical generation occurs during scorpion envenomation.

Although it is well established that symptomatology, morbidity and death following scorpion envenomation are due to increases in neurotransmitter release secondary to toxins binding to voltage-sensitive sodium channels, the mechanism by which venom action is involved in damaging heart, liver, lungs and kidneys remains unclear. We hypothesized that scorpion toxins could induce the generation of high levels of free radicals responsible for membrane damage in organs targeted by venom action. We have investigated lipid peroxidation in different organs, through the evaluation of thiobarbituric acid reactive substances (TBARS), after experimental envenomation of rats by toxic fractions of Androctonus australis Hector venom. We have shown that scorpion toxins cause considerable lipid peroxidation in most vital organs. We also evaluated the protective effects of antioxidants in mice injected with lethal doses of toxins. Among the drugs tested, N-acetylcysteine (NAC) was effective in protecting the mice when injected prior to toxin application. However, the free radical scavenging properties of NAC seem less implicated in these protective effects than its ability to increase the fluidity of bronchial secretions. We therefore conclude that free radical generation only plays a minor role in the toxicity of scorpion venom.

[Metabolic stability and physiological adaptation of muscle under conditions of exercise]. / Métabosensibilité musculaire et adaptations physiologiques au cours de l'exercice.

The first role played by group III (thin myelinated) and group IV (unmyelinated) afferent fibres from skeletal muscle is to transmit nociceptive information from muscle to the central nervous system. The second role of these free endings located in the interstitium of the muscle is to induce cardiovascular and respiratory adjustments during muscular exercise. These respiratory and circulatory responses during muscular exercise may be reflexly induced via muscular afferents. Indeed, static contraction of hindlimb muscles in anaesthetised mammals has been shown to reflexly increase the ventilatory function, the myocardial contractility and heart rate. The mechanical muscle deformation and the accumulation of metabolites in its intersitium are the cause of raised activity in small nerve fibres which in turn induces the physiological responses. It is also admitted that the central locomotor areas on the medullary and spinal neuronal pools control ventilatory and cardiovascular function during exercise. This mechanism is called "central command". Furthermore, adjustments of the locomotor activity during exercise is mediated by the thinly myelinated and unmyelinated fibres with endings in the working muscle. These fibres, also called "metaboreceptor" may be responsible of the coupling between the ventilation and the locomotion. Thickly myelinated muscle afferents (i.e. group I and II) appear to play little role in causing the reflex autonomic responses to contraction.

Effect of muscle electrostimulation on afferent activities from tibialis anterior muscle after nerve repair by self-anastomosis.

Numerous previous studies were devoted to the regeneration of motoneurons toward a denervated muscle after nerve repair by self-anastomosis but, to date, few investigations have evaluated the regeneration of sensory muscle endings. In a previous electrophysiological study (Decherchi et al., 2001) we showed that the functional characteristics of tibialis anterior muscle afferents are affected after self-anastomosis of the peroneal nerve even when the neuromuscular preparation was not chronically stimulated. The present study examines the regeneration of groups I-II (mechanosensitive) and groups III-IV (metabosensitive) muscle afferents by evaluating the recovery of their response to different test agents after self-anastomosis combined or not with chronic muscle stimulation for a 10-weeks period. We compared five groups of rats: C, control; L, nerve lesion without suture; LS, nerve lesion with suture; LSE(m): nerve lesion plus chronic muscle stimulation with a monophasic rectangular current; and LSE(b): nerve lesion plus chronic stimulation with a biphasic current with modulations of pulse duration and frequency, eliciting a pattern of activity resembling that delivered by the nerve to the muscle. Compared to the control group, (1) muscle kept only its original weight in the LSE(b) group, (2) in the LS group the response curve to tendon vibration was shifted toward the highest mechanical frequencies and the response of groups III-IV afferents after fatiguing muscle stimulation lowered, (3) in the LSE(m) group, the pattern of activation of mechanoreceptors by tendon vibrations was altered as in the LS group, and the response of metabosensitive afferents to KCl injections was markedly reduced, (4) in the LSE(b) group, the response to tendon vibration was not modified and the activation of metabosensitive units by increased extracellular potassium chloride concentration was conserved. Both LSE(b) and LSE(m) conditions were ineffective to maintain the post muscle stimulation activation of metabosensitive units as well as their activation by injected lactic acid solutions. Our data indicate that chronic muscle electrostimulation partially favors the recovery of mechano- and metabosensitivity in a denervated muscle and that biphasic modulated currents seem to provide better results.

Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle.

An acute reduction of the oxygen supply to contracting muscles not only affects their metabolism but also modifies their sensorimotor control through changes in afferent discharge of the group I and group III-IV nerve fibers, the latter playing a pivotal role in the protective mechanisms against muscle fatigue. The effects of chronic hypoxemia on the muscle sensitivity are totally unknown. In the present study, group I fibers (mechanosensory afferents) and group III-IV fibers (mechanosensory and chemosensory afferents) from the anterior tibial muscle were recorded in normoxemic and chronic hypoxemic rats. Hypoxemic rats breathed for 45 d a gas mixture containing 9.5 to 10% O(2) in N(2). The data were compared with those obtained in normoxemic animals of the same age. To activate the different muscle afferents, we used different test agents, including electrically induced fatigue (EIF), KCl, lactic acid injections, as well as tendon vibrations. The conduction velocity of all nerve fibers was significantly (p < 0.01) higher in hypoxemic rats than in the normoxemic group. Chronic hypoxemia significantly depressed the response of the group III-IV muscle afferents to KCl injections and even abolished their response to lactic acid and EIF. However, the response to tendon vibrations of the group I afferents was similar in hypoxemic and normoxemic rats. These results suggest that chronic hypoxemia markedly alters the chemosensitivity of the group III-IV muscle afferents, which may explain the higher fatigability of hypoxemic subjects.

Effects of acute hypoxemia on force and surface EMG during sustained handgrip.

Data on the consequences of acute hypoxemia on the strength of contraction are often contradictory. In healthy subjects, we tested the effects of hypoxemia (PaO(2) = 56 mmHg), maintained for a 30-min period, on static handgrip elicited by voluntary effort or direct electrical muscle stimulation, in order to separate the consequences of hypoxemia on central or peripheral factors, respectively. Force was measured during maximal voluntary contractions (MVCs), 60% MVCs sustained until exhaustion, and 1-min periods of electrical muscle stimulation at 60 HZ. The evoked compound muscle action potential (M wave) was recorded in resting muscle and after each period of 60-HZ stimulation or sustained 60% MVC. Power spectrum analysis of surface electromyogram (EMG) was performed during sustained 60% MVC. Compared to normoxemia, acute hypoxemia lowered MVC (-12%, P < 0.01) but enhanced (+38%, P < 0.01) the peak force elicited by electrical muscle stimulation. In resting muscle, hypoxemia had no influence on the M-wave amplitude but lengthened the neuromuscular transmission time(+740 micros, P < 0.05). Hypoxemia did not alter the M wave measured after 60 HZ stimulation and 60% MVC. During sustained 60% MVC, hypoxemia markedly depressed the EMG changes, abolishing the leftward shift of power spectra. These data show that acute hypoxemia reduces MVC through depression of the central drive, whereas it improves the peripheral muscle response to electrical stimulation. In addition, hypoxemia reduces the recruitment of slow firing motor unit, which are highly oxygen-dependent. This could constitute an adaptative muscle response to a reduced oxygen supply.