Effects of postural changes and vestibular lesions on diaphragm and rectus abdominis activity in awake cats.

Changes in posture can affect the resting length of the diaphragm, requiring alterations in the activity of both the abdominal muscles and the diaphragm to maintain stable ventilation. To determine the role of the vestibular system in regulating respiratory muscle discharges during postural changes, spontaneous diaphragm and rectus abdominis activity and modulation of the firing of these muscles during nose-up and ear-down tilt were compared before and after removal of labyrinthine inputs in awake cats. In vestibular-intact animals, nose-up and ear-down tilts from the prone position altered rectus abdominis firing, whereas the effects of body rotation on diaphragm activity were not statistically significant. After peripheral vestibular lesions, spontaneous diaphragm and rectus abdominis discharges increased significantly (by approximately 170%), and augmentation of rectus abdominis activity during nose-up body rotation was diminished. However, spontaneous muscle activity and responses to tilt began to recover after a few days after the lesions, presumably because of plasticity in the central vestibular system. These data suggest that the vestibular system provides tonic inhibitory influences on rectus abdominis and the diaphragm and in addition contributes to eliciting increases in abdominal muscle activity during some changes in body orientation.     

Effect of diaphragm fatigue on neural respiratory drive.

To test the hypothesis that diaphragm fatigue leads to an increase in neural respiratory drive, we measured the esophageal diaphragm electromyogram (EMG) during CO(2) rebreathing before and after diaphragm fatigue in six normal subjects. The electrode catheter was positioned on the basis of the amplitude and polarity of the diaphragm compound muscle action potential recorded simultaneously from four pairs of electrodes during bilateral anterior magnetic phrenic nerve stimulation (BAMPS) at functional residual capacity. Two minutes of maximum isocapnic voluntary ventilation (MIVV) were performed in six subjects to induce diaphragm fatigue. A maximal voluntary breathing against an inspiratory resistive loading (IRL) was also performed in four subjects. The reduction of transdiaphragmatic pressure elicited by BAMPS was 22% (range 13-27%) after 2 min of MIVV and was similar, 20% (range 13-26%), after IRL. There was a linear relationship between minute ventilation (VE) and the root mean square (RMS) of the EMG during CO(2) rebreathing before and after fatigue. The mean slope of the linear regression of RMS on VE was similar before and after diaphragm fatigue: 2.80 +/- 1.31 vs. 3.29 +/- 1.40 for MIVV and 1.51 +/- 0.31 vs 1.55 +/- 0.31 for IRL, respectively. We conclude that the esophageal diaphragm EMG can be used to assess neural drive and that diaphragm fatigue of the intensity observed in this study does not affect respiratory drive.     

Ventilatory response to hypoxia in unanesthetized newborn kittens

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.     

Function of external respiration in patients with systemic scleroderma (according to roentgenopneumopolygraphic data)

External respiratory function was investigated in 33 patients with systemic scleroderma+ using roentgenopneumopolygraphy (RPPG). Respiratory changes consisted in diffuse and regional ventilation disturbance (after emphysematous, hypoventilation or mixed type), disorders of respiratory kinetics of the diaphragm, ribs and mediastinum. External respiratory functional disturbance showed direct correlation with the patients' age, period of disease and a degree of pathological activity. The type of external respiratory functional disturbance was unchanged during observation over time. The use of exercise testing showed the presence of signs of latent ventilation insufficiency in most of the patients.     

Near-maximal voluntary hyperpnea and ventilatory muscle function

Because of its potential relevance to heavy exercise we studied the ventilatory muscle function of five normal subjects before, during, and after shortterm near-maximal voluntary normocapnic hyperpnea. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made at four levels of ventilation: 76, 79, and 86% maximal voluntary ventilation (MVV) and at MVV. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made. The pressure-stimulation frequency relationship of the diaphragm obtained by unilateral transcutaneous phrenic nerve stimulation was studied in two subjects before and after hyperpnea. Decreases in maximal inspiratory (PImax) and transdiaphragmatic (Pdimax) strength were recorded posthyperpnea at 76 and 79% MVV. Decreases in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm EMG occurred in association with decreases in Pdimax. Analysis of the pressure-time product (P X dt) for the inspiratory and expiratory muscles individually indicated the increasing contribution of expiratory muscle force to the attainment of higher levels of ventilation. Demonstrable ventilatory muscle fatigue may limit endurance at high levels of ventilation.     

Metabolic and functional adaptation of the diaphragm to training with resistive loads

To study the metabolic and functional changes that occur during training with inspiratory flow resistive loads, a chronically instrumented unanesthetized sheep preparation was used. Sheep were exposed to resistances ranging from 50 to 100 cmH2O.l-1.s, for 2-4 h/day, 5-6 days/wk, for a total of 3 wk. Load intensity was adjusted to maintain arterial Po2 (PaO2) above 60 Torr and arterial PCO2 (PaCO2) below 45 Torr. Training produced significant (P less than 0.05) increases in citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, and cytochrome oxidase in the costal and crural diaphragm of the trained sheep (n = 9) compared with control sheep (n = 7). Phosphofructokinase did not increase. In the quadriceps, citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, and phosphofructokinase did not change with training but cytochrome oxidase increased significantly (P less than 0.01). Function of the diaphragm was assessed in a subset of five sheep exposed to the same severe load 1 wk before and 2 days after the final training session. After training, sheep had a lower PaCO2 (10-40%), generated a higher transdiaphragmatic pressure (20-40%), and could sustain this level of transdiaphragmatic pressure for 0.5-2 h longer. The respiratory duty cycle was 10-15% lower, whereas minute ventilation and tidal volume were 20-30% higher in the posttraining test. We conclude that 1) training with inspiratory flow resistive loads improves the performance of the respiratory neuromuscular system and 2) the shift in enzyme profile of the diaphragm is at least in part responsible for this improvement.     

State and chemical drive modulate respiratory variability.

The quantification of respiratory variability may provide insight into the integrative control of breathing. To test the hypothesis that sleep and/or increased chemical drive modifies respiratory variability, six male adult Sprague-Dawley rats were instrumented with diaphragm electromyographic (EMG) electrodes and exposed to 0, 2.5, and 5.0% CO2 with a balance of room air during wakefulness and behaviorally determined sleep. Respiratory interval (Ttot), peak diaphragm EMG, and ventilation index (peak diaphragm EMG/Ttot) were calculated for 1,024 sequential breaths. The variability of breathing was quantified with a measurement of signal complexity, the approximate entropy, and two autocorrelation measurements, the autoregressive power spectrum slope and the detrended fluctuation analysis slope. Elevated chemical drive and/or sleep significantly modulated the variability of ventilation index and Ttot. There were also significant interactions between state and CO2 drive in all respiratory parameters. We conclude that state (sleep or wakefulness) and increased chemical drive affect respiratory variability differentially.     

Respiratory responses in reversible diaphragm paralysis

The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.     

Abdominal distension alters regional pleural pressures and chest wall mechanics in pigs in vivo

Abdominal distension (AD) occurs in pregnancy and is also commonly seen in patients with ascites from various causes. Because the abdomen forms part of the "chest wall," the purpose of this study was to clarify the effects of AD on ventilatory mechanics. Airway pressure, four (vertical) regional pleural pressures, and abdominal pressure were measured in five anesthetized, paralyzed, and ventilated upright pigs. The effects of AD on the lung and chest wall were studied by inflating a liquid-filled balloon placed in the abdominal cavity. Respiratory system, chest wall, and lung pressure-volume (PV) relationships were measured on deflation from total lung capacity to residual volume, as well as in the tidal breathing range, before and 15 min after abdominal pressure was raised. Increasing abdominal pressure from 3 to 15 cmH2O decreased total lung capacity and functional residual capacity by approximately 40% and shifted the respiratory system and chest wall PV curves downward and to the right. Much smaller downward shifts in lung deflation curves were seen, with no change in the transdiaphragmatic PV relationship. All regional pleural pressures increased (became less negative) and, in the dependent region, approached 0 cmH2O at functional residual capacity. Tidal compliances of the respiratory system, chest wall, and lung were decreased 43, 42, and 48%, respectively. AD markedly alters respiratory system mechanics primarily by "stiffening" the diaphragm/abdomen part of the chest wall and secondarily by restricting lung expansion, thus shifting the lung PV curve as seen after chest strapping. The less negative pleural pressures in the dependent lung regions suggest that nonuniformities of ventilation could also be accentuated and gas exchange impaired by AD.     

Diaphragm muscle weakness in an experimental porcine intensive care unit model

In critically ill patients, mechanisms underlying diaphragm muscle remodeling and resultant dysfunction contributing to weaning failure remain unclear. Ventilator-induced modifications as well as sepsis and administration of pharmacological agents such as corticosteroids and neuromuscular blocking agents may be involved. Thus, the objective of the present study was to examine how sepsis, systemic corticosteroid treatment (CS) and neuromuscular blocking agent administration (NMBA) aggravate ventilator-related diaphragm cell and molecular dysfunction in the intensive care unit. Piglets were exposed to different combinations of mechanical ventilation and sedation, endotoxin-induced sepsis, CS and NMBA for five days and compared with sham-operated control animals. On day 5, diaphragm muscle fibre structure (myosin heavy chain isoform proportion, cross-sectional area and contractile protein content) did not differ from controls in any of the mechanically ventilated animals. However, a decrease in single fibre maximal force normalized to cross-sectional area (specific force) was observed in all experimental piglets. Therefore, exposure to mechanical ventilation and sedation for five days has a key negative impact on diaphragm contractile function despite a preservation of muscle structure. Post-translational modifications of contractile proteins are forwarded as one probable underlying mechanism. Unexpectedly, sepsis, CS or NMBA have no significant additive effects, suggesting that mechanical ventilation and sedation are the triggering factors leading to diaphragm weakness in the intensive care unit.     

Effects of the beta(2)-agonist clenbuterol on respiratory and limb muscles of weaning rats

The aim of this study was to analyze the effects of chronic administration of the beta(2)-agonist clenbuterol (1.5 mg x kg(-1) x day(-1) for 4 wk in the drinking water) on respiratory (diaphragm and parasternal intercostal) and hindlimb (tibialis and soleus) muscles in young rats during postnatal development (21 to 49 postnatal days). The treatment resulted in very little stimulation of muscle growth. Significant slow-to-fast transitions in the expression of myosin heavy chain isoforms and significant increases in the myofibrillar ATPase activity were found in the diaphragm and soleus, whereas tibialis anterior and intercostal muscles did not show any significant fiber-type alteration. Decrease of oxidative enzyme activities and increase of glycolytic enzyme activities were also observed. It is concluded that whereas the growth stimulation is age dependent and only detectable in adult rats, the fiber-type transformation is also present in weaning rats and particularly evident in the soleus and diaphragm. The fiber-type transformation caused by clenbuterol might lead to an enhancement of contractile performance and also to a reduced resistance to fatigue.     

Effect of hyperinflation on inspiratory function of the diaphragm.

The inspiratory efficiency of the diaphragm during unilateral and bilateral phrenic stimulation (UEPS and BEPS) with constant stimulus was studied in seven dogs from FRC to 120% TLC. Alveolar pressures (PAl) were recorded during relaxation, BEPS and UEPS at each lung volume in the closed respiratory system. From the PAl-lung volume curves, tidal volume (VT), and pressure developed by the diaphragm (Pmus) were derived. Results are summarized below. a) Hyperinflation impaired the inspiratory efficiency of the diaphragm which behaved as an expiratory muscle beyond the lung volume of 103.7% TLC (Vinef). b) The diaphragm during UEPS became expiratory at the same Vinef as during (BEPS. C) The VT-lung volume relationship was linear during BEPS, allowing simple quantitation of VT loss with hyperinflation and prediction of Vinef. d) With only one phrenic nerve stimulated, the functional loss is less pronounced in VT than in Pmus, as compared to BEPS, indicating that the respiratory system was more compliant during UEPS than BEPS. This compliance difference from UEPS to BEPS diminished with severe hyperinflation.     

Regional ventilation during spontaneous breathing and mechanical ventilation in dogs

We evaluated the effects of the different patterns of chest wall deformation that occur with different body positions and modes of breathing on regional lung deformation and ventilation. Using the parenchymal marker technique, we determined regional lung behavior during mechanical ventilation and spontaneous breathing in five anesthetized recumbent dogs. Regional lung behavior was related to the patterns of diaphragm motion estimated from X-ray projection images obtained at functional residual capacity (FRC) and end inspiration. Our results indicate that 1) in the prone and supine positions, FRC was larger during mechanical ventilation than during spontaneous breathing; 2) there were significant differences in the patterns of diaphragm motion and regional ventilation between mechanical ventilation and spontaneous breathing in both body positions; 3) in the supine position only, there was a vertical gradient in lung volume at FRC; 4) in both positions and for both modes of breathing, regional ventilation was nonlinearly related to changes in lobar and overall lung volumes; and 5) different patterns of diaphragm motion caused different sliding motions and differential rotations of upper and lower lobes. Our results are inconsistent with the classic model of regional ventilation, and we conclude that the distribution of ventilation is determined by a complex interaction of lung and chest wall shapes and by the motion of the lobes relative to each other, all of which help to minimize distortion of the lung parenchyma.     

Respiratory effects of bombesin at the level of pre-Botzinger complex in rats

Respiratory effects of 0.1 pM - .1 mM bombesin microinjected to the pre-Botzinger complex were studied in anaesthetised rats. Bombesin induced an increase in minute ventilation, respiratory frequency, a decrease in expiratory duration and shortening of inter-burst intervals on the EMG of diaphragm and external intercostal muscles. The responses to bombesin characterised by short latency, quick development (with the maximum in 3-minutes after microinjection) and found to be reversible. The effects of bombesin on membrane potential, input resistance and pattern of spontaneous activity ofpre-Botzinger neurons were investigated in brainstem slices. 1 nM bombesin introduced into the perfusion solution in most cases (68%) induced membrane depolarisation, an increase in input resistance and in spike activity of spontaneously active cells. The data obtained suggest that the respiratory effects ofbombesin at the level ofpre-Botzinger complex are caused by its action on the membrane of neurons.     

Effect of head-down tilt on respiratory responses and human inspiratory muscle activity

The effect of a head-down tilt on the responses of the external respiration system and the functional capacity of the diaphragm and parasternal muscles were investigated in 11 healthy subjects. A 30-min head-down tilt posture (−30° relative to the horizontal) significantly increased the inspiratory time, decreased the respiration rate and the inspiratory and expiratory flow rates; and increased the airway resistance compared to these values in the vertical posture. There were no significant changes in tidal volume or minute ventilation. The electromyograms (EMGs) of the diaphragm and parasternal muscles showed that the constant values of tidal volume and minute ventilation during head-down tilt could be provided by an increase in the electric activity of the thoracic inspiratory muscles. It was established that the contribution of the thoracic inspiratory muscles increased, while the diaphragms’ contribution decreased, during patient, spontaneous breathing. The maximal inspiratory effort (Muller’s maneuver) during a head-down tilt evoked the opposite EMG-activity pattern: the contribution of inspiratory thoracic muscles was decreased and the diaphragm EMG activity was increased compared to the vertical posture. These results suggest that coordinated modulations in inspiratory muscle activity make it possible to preserve the functional reserve of human inspiratory muscles during a short-term head-down tilt.     

罗库溴铵和顺式阿曲库铵持续输注对机械通气SD 大鼠膈肌功能 的影响

目的:比较罗库溴铵或顺式阿曲库铵24h持续输注对机械通气SD大鼠膈肌功能的影响.方法:雄性SD大鼠随机分为四组:一组作为对照组,另外三组用来进行24h的机械通气.其中一组为罗库溴铵组持续输注罗库溴铵,一组顺式阿曲库铵和一组生理盐水.结果:24h机械通气后,与生理盐水组相比,罗库溴铵组的膈肌最大强直张力下降29％,膈肌MuRF-1的mRNA水平增加30％,calpain活性增加约57％,而等效剂量的顺式阿曲库铵组则没有明显改变.结论:与顺式阿曲库铵相比,罗库溴铵可引起Calpain活性的增强和泛素-蛋白酶体系统的激活,对膈肌功能的损害和蛋白水解活性的增强作用更明显.     

Ventilatory effects of stimulation of phrenic afferents

The diaphragm, a ventilatory muscle, has abundant sensory innervation. The effects of phrenic afferent activation on ventilation have been varied. In this study the proximal end of the phrenic nerve was electrically stimulated, and the effects on ventilation were measured in supine dogs anesthetized with either alpha-chloralose or pentobarbital sodium. We found a maximum increase in ventilation of 45 +/- 4% in the alpha-chloralose group and an increase in mean arterial blood pressure of 18 +/- 4%. This response was obtained at high stimulus intensities (60 times twitch threshold). Stimulation of the proximal end of the gastrocnemius nerve produced a similar ventilatory response (61 +/- 10%) but at lower stimulus intensities. During pentobarbital sodium anesthesia both the hyperventilation and the pressor response were produced; however, ventilation was increased by an increase in respiratory frequency. The reflex was abolished by sectioning of the cervical dorsal roots (C4-C7). Proximal cold blockade of the nerve abolished the response at a perineural temperature of 1.35 +/- 0.64 degrees C. The main effect of activation of phrenic afferents was an increase in ventilation and blood pressure that was mediated by unmyelinated fibers and possibly thin myelinated fibers. This response is similar to skeletal muscle afferent activation and may play a role in ventilatory drive during such conditions as exercise and respiratory muscle fatigue.     

Effect of nasal continuous or intermittent positive airway pressure on nonnutritive swallowing in the newborn lamb.

The present study was aimed at investigating the effects of nasal continuous positive airway pressure (nCPAP; 6 cmH2O) or intermittent positive pressure ventilation (nIPPV; 10/4 cmH2O) on nonnutritive swallowing (NNS) and on the coordination between NNS and phases of the respiratory cycle, while taking into account the potential effects of states of alertness. Twelve full-term lambs were chronically instrumented at 48 h after birth for polysomnographic recordings, including NNS, diaphragm electromyographic activity, respiratory movements, pulse oximetry, and states of alertness. Studies in control conditions, with nCPAP and nIPPV, were performed in random order in nonsedated lambs at 4, 5, and 6 days of life. Results demonstrate that nCPAP significantly decreased overall NNS frequency, more specifically isolated NNS during quiet sleep and bursts of NNS in active sleep. In comparison, the effects of nIPPV on NNS frequency were more variable, with an inhibition of NNS only in wakefulness and an increase in isolated NNS frequency in active sleep. In addition, neither nCPAP nor nIPPV disrupted the coordination between NNS and phases of the respiratory cycle. In conclusion, nCPAP inhibits NNS occurrence in newborn lambs. Clinical relevance of this novel finding is related to the importance of NNS for clearing the upper airways from secretions and gastric content frequently regurgitated in the neonatal period.     

Adverse effects of myasthenia gravis on rat phrenic diaphragm contractile performance.

Myasthenia gravis has variable effects on the respiratory system, ranging from no abnormalities to life-threatening respiratory failure. Studies characterized diaphragm muscle contractile performance in rat autoimmune myasthenia gravis. Rats received monoclonal antibody that recognizes acetylcholine receptor determinants (or inactive antibody); 3 days later, phrenic nerve and diaphragm were studied in vitro. Myasthenic rats segregated into two groups, those with normal vs. impaired limb muscle function when tested in intact animals ("mild" and "severe" myasthenic). Baseline diaphragm twitch force was reduced for both severe (P < 0.01) and mild (P < 0.05) myasthenic compared with control animals (twitch force: normal 1,352 +/- 140, mild myasthenic 672 +/- 99, severe myasthenic 687 +/- 74 g/cm2). However, only severe myasthenic diaphragm had impaired diaphragm endurance, based on significantly (P < 0.05) accelerated rate of peak force decline during the initial period of stimulation (0.02 + 0.02, 0.03 +/- 0.01, and 0.09 +/- 0.01%/pulse for normal, mild myasthenic, and severe myasthenic, respectively, during continuous stimulation) and intratrain fatigue (up to 30.5 +/- 7.4% intratrain force drop in severe myasthenic vs. none in normal and mild myasthenic, P < 0.01). Furthermore, compared with continuous stimulation, intermittent stimulation had a protective effect on force of severe myasthenic diaphragm (force after 2,000 pulses was 31.4 +/- 2.0% of initial during intermittent stimulation vs. 13.0 +/- 2.1% of initial during continuous stimulation, P < 0.01) but not on normal diaphragm. These data indicate that baseline force and fatigue may be affected to different extents by varying severity of myasthenia gravis and furthermore provide a mechanism by which alterations in breathing pattern may worsen respiratory muscle function in neuromuscular diseases.     

Reorganization of Respiratory Descending Pathways following Cervical Spinal Partial Section Investigated by Transcranial Magnetic Stimulation in the Rat

High cervical spinal cord injuries lead to permanent respiratory deficits. One preclinical model of respiratory insufficiency in adult rats is the C2 partial injury which causes unilateral diaphragm paralysis. This model allows the investigation of a particular population of respiratory bulbospinal axons which cross the midline at C3-C6 spinal segment, namely the crossed phrenic pathway. Transcranial magnetic stimulation (TMS) is a non-invasive technique that can be used to study supraspinal descending respiratory pathways in the rat. Interestingly, a lateral C2 injury does not affect the amplitude and latency of the largest motor-evoked potential recorded from the diaphragm (MEPdia) ipsilateral to the injury in response to a single TMS pulse, compared to a sham animal. Although the rhythmic respiratory activity on the contralateral diaphragm is preserved at 7 days post-injury, no diaphragm activity can be recorded on the injured side. However, a profound reorganization of the MEPdia evoked by TMS can be observed. The MEPdia is reduced on the non-injured rather than the injured side. This suggests an increase in ipsilateral phrenic motoneurons excitability. Moreover, correlations between MEPdia amplitude and spontaneous contralateral diaphragmatic activity were observed. The larger diaphragm activity correlated with a larger MEPdia on the injured side, and a smaller MEPdia on the non-injured side. This suggests, for the first time, the occurrence of a functional neuroplasticity process involving changes in motoneuron excitability balance between the injured and non-injured sides at a short post-lesional delay.