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.

Vitamin D3 improves respiratory adjustment to fatigue and H-reflex responses in paraplegic adult rats.

We previously demonstrated that vitamin D2 (ergocalciferol) triggers axon regeneration in a rat model of peripheral nerve transection. In order to confirm the regenerative potential of this neuroactive steroid, we performed a study in which vitamin D3 (cholecalciferol) was delivered at various doses to paralytic rats. After spinal cord compression at the T10 level, rats were given orally either vehicle or vitamin D3 at the dose of 50 IU/kg/day or 200 IU/kg/day. Three months later, M and H-waves were recorded from rat Tibialis anterior muscle in order to quantify the maximal H-reflex (H(max)) amplitude. We also monitored the ventilatory frequency during an electrically induced muscle fatigue known to elicit the muscle metaboreflex and an increase in respiratory rate. Spinal cords were then collected, fixed and immunostained with an anti-neurofilament antibody. We show here that vitamin D-treated animals display an increased number of axons within the lesion site. In addition, rats supplemented with vitamin D3 at the dose of 200 IU/kg/day exhibit (i) an improved breathing when hindlimb was electrically stimulated; (ii) an H-reflex depression similar to control animals and (iii) an increased number of axons within the lesion and in the distal area. Our data confirm that vitamin D is a potent molecule that can be used for improving neuromuscular adaptive mechanisms and H-reflex responses.

[Pulmonary function testing of 156 children exposed to automobile pollution in the municipality of Cotonou]. / Evaluation Du DEM(25) Chez 156 Enfants Exposes A La Pollution Automobile Dans La Municipalite De Cotonou.

AIMS: To evaluate the risk of disruption of distal airways in children exposed to pollutants automobiles. MATERIAL AND METHODS: Study included 156 children selected assigned in groups "Most Exposed" and "Less Exposed" separated respectively 15 meters and 150 meters of road traffic. Children in both groups were subjected to lung function tests before and after an exercise test that was to perform a series of flexion / extension of the knees to the fatigue. FEV and MEF(25) were parameters selected. RESULTS: Change in FEV post exercise of each group is below 5%. The group "Less Exposed" presented a mean value of MEF(25) before exercise similar to that recorded after exercise. Within the group "Most Exposed", the mean value of MEF(25) post exercise is significantly lower than that observed at rest of 8.65%. CONCLUSION: The fact of living permanently near the traffic, poses serious risks of disruption of the distal airways.

Fin swimming improves respiratory gas exchange.

Data in the literature suggest that compared to dry-land exercise fin swimming might delay the activation of the anaerobic metabolism. To verify this hypothesis, we explored indirect indices such as the oxygen pulse (VO(2)/HR), carbon dioxide production (VCO(2)), and ventilatory threshold, comparing fin swimming exercise to dry-land cycling. Thirteen participants, experienced or inexperienced in fin swimming, completed an incremental fin swimming exercise and a maximal exercise on a cycloergometer with breath-by-breath measurements of heart rate (HR), ventilation (VE), tidal volume (VT), VO(2), VCO(2), and VO(2)/HR and determination of the ventilatory threshold and maximal oxygen uptake (VO(2)max). Compared to dry-land cycling exercise, fin swimming resulted in elevated or absent ventilatory threshold. Although VO(2)max did not differ in either condition, in fin swimming the maximal HR value was lower (-18%, p=0.0072), maximal VO(2)/HR higher (+20%, p=0.0325), and maximal VCO(2) lower (-17%, p=0.0071). We also measured significant reduction of VE, VT, and HR variations for the same VO(2) increase. This study suggests that the anaerobic muscle metabolism might be delayed in fin swimming. An attenuated chemoreflex drive to the heart and respiratory centres exerted by muscle metabolites might explain the depressed cardiopulmonary response to fin swimming.

Downregulation of uncoupling protein-3 in vivo is linked to changes in muscle mitochondrial energy metabolism as a result of capsiate administration.

Although it has been suggested that the skeletal muscle mitochondrial uncoupling protein-3 (UCP3) is involved in regulating energy expenditure, its role is still poorly understood. In the present study, we aimed at investigating noninvasively, using magnetic resonance techniques, metabolic changes occurring in exercising muscle as a result of capsiate treatment, which has been previously linked to UCP3 upregulation. We showed that capsiate ingestion strongly reduced UCP3 gene expression in rat gastrocnemius muscle. This large underexpression was accompanied by a significant increase in the rate of mitochondrial ATP production and phosphocreatine level both at rest and during muscle stimulation. Similarly, the stimulation-induced ATP fall and ADP accumulation were significantly less after capsiate administration than in untreated rats. The larger oxidative ATP production rate could not be explained by a proportional decrease in the anaerobic component, i.e., glycolysis and phosphocreatine breakdown. In addition, the mechanical performance was not affected by capsiate administration. Finally, the plasma free fatty acid (FFA) level increased in capsiate-treated rats, whereas no significant change was observed after muscle stimulation in the control group. Considering the corresponding enhanced UCP3 mRNA expression occurring in the control group after muscle stimulation, one can suggest that changes in FFA level and UCP3 mRNA expression are not mechanistically correlated. Overall, we have shown that capsiate administration induced a UCP3 downregulation coupled with an increased mitochondrial ATP synthesis, whereas the muscle force-generating capacity was unchanged. This suggests that a decrease in muscle efficiency and/or additional noncontractile ATP-consuming mechanisms result from UCP3 downregulation.

Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties.

This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.

Electromyographic signs of neuromuscular fatigue are concomitant with further increase in ventilation during static handgrip.

We questioned if a non-linear increase in ventilation defining a ventilatory threshold (V(Th)) accompanied the electromyographic (EMG) signs of neuromuscular fatigue. Indeed, the intramuscular accumulation of metabolites may activate the afferent nervous pathways responsible for both the 'muscle wisdom' phenomenon and the respiratory centre activation. During inframaximal (50%) handgrip sustained until exhaustion, minute ventilation (V(E)), V(E)/V(O2) and V(E)/V(CO2) ratios were measured simultaneously with surface EMG of the 'flexor digitorum' muscle. V(Th) was defined as a non-linear V(E) increase and/or an abrupt V(E)/V(O2) increase without any concomitant increase in the V(E)/V(CO2) ratio. Handgrip was repeated during complete arterial blood flow interruption in order to suppress any venous return from the exercising forearm. In both control and blood flow interruption conditions, an abrupt increase in the V(E)/V(O2) ratio was measured in the majority of trials (13 of 15 and 14 of 15, respectively) and the EMG signs of neuromuscular fatigue (a decline in median frequency and/or a non-linear increase in low-frequency EMG energies, E(L)) were concomitant with the V(Th) determination. Thus, V(Th) occurs during sustained static contraction and is concomitant with EMG signs of neuromuscular fatigue. Neurogenic factors seem to be responsible for the two responses which persist despite the absence of any release of metabolites in the circulation.

[Bioenergetic characteristics of the diaphragm after spinal cord injury]. / Caractéristiques bioénergétiques du diaphragme après une lésion spinale.

INTRODUCTION: C2 spinal cord hemisection interrupts descending bulbospinal respiratory axons coursing through the cervical spinal cord. One consequence of this type of spinal cord injury is the partial deafferentation of the ipsilateral phrenic nucleus, which renders the hemidiaphragm paralysed. The biochemical properties of the intact or denervated locomotor skeletal muscles have been studied extensively, whereas the biochemical properties of the diaphragm after a cervical spinal cord injury received relatively little attention. This seems unfortunate, given that the diaphragm is the most important mammalian respiratory muscle and is the only skeletal muscle considered essential for survival. Therefore, the purpose of this work was to analyse the bioenergetic characteristics of the diaphragm following a cervical spinal cord injury. METHODS: Segments of the crural diaphragm from rat were homogenised to determine the activities of a glycolytic enzyme, lactate dehydrogenase (LDH), and a Krebs cycle enzyme, citrate synthase (CS). RESULTS: Data show a significant decrease of the CS activity on the ipsilateral hemidiaphragm to the cervical hemisection. No change in the LDH is observed between the animal without or with a cervical spinal cord injury. CONCLUSIONS: These data suggested that the CS activity could be dependent of the nervous influx from the central respiratory rhythm generator and that LDH activity could be maintained by a peripheral respiratory activity or by the cross phrenic phenomenon activation. Biochemical data should be considered in subjects presenting respiratory deficiency induced by a cervical spinal cord injury. Furthermore, the diaphragmatic muscle metabolic activity could be used to evaluate the functional respiratory recovery observed spontaneously or experimentally after using repair strategies of the spinal cord.

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.