Neuromechanical Coupling Research Articles

Surface electromyography to quantify neuro-respiratory drive and neuro-mechanical coupling in mechanically ventilated children

BackgroundThe patient’s neuro-respiratory drive, measured as electrical activity of the diaphragm (EAdi), quantifies the mechanical load on the respiratory muscles. It correlates with respiratory effort but requires a dedicated esophageal catheter. Transcutaneous (surface) monitoring of respiratory muscle electromyographic (sEMG) signals may be considered a suitable alternative to EAdi because of its non-invasive character, with the additional benefit that it allows for simultaneously monitoring of other respiratory muscles. We therefore sought to study the neuro-respiratory drive and timing of inspiratory muscles using sEMG in a cohort of children enrolled in a pediatric ventilation liberation trial. The neuro-mechanical coupling, relating the pressure generated by the inspiratory muscles to the sEMG signals of these muscles, was also calculated.MethodsThis is a secondary analysis of data from a randomized cross-over trial in ventilated patients aged < 5 years. sEMG recordings of the diaphragm and parasternal intercostal muscles (ICM), esophageal pressure tracings and ventilator scalars were simultaneously recorded during continuous spontaneous ventilation and pressure controlled-intermittent mandatory ventilation, and at three levels of pressure support. Neuro-respiratory drive, timing of diaphragm and ICM relative to the mechanical ventilator’s inspiration and neuro-mechanical coupling were quantified.ResultsTwenty-nine patients were included (median age: 5.9 months). In response to decreasing pressure support, both amplitude of sEMG (diaphragm: p = 0.001 and ICM: p = 0.002) and neuro-mechanical efficiency indices increased (diaphragm: p = 0.05 and ICM: p < 0.001). Poor correlations between neuro-respiratory drive and respiratory effort were found, with R2: 0.088 [0.021–0.152].ConclusionssEMG allows for the quantification of the electrical activity of the diaphragm and ICM in mechanically ventilated children. Both neuro-respiratory drive and neuro-mechanical efficiency increased in response to lower inspiratory assistance. There was poor correlation between neuro-respiratory drive and respiratory effort.Trial registrationClinicalTrials.gov ID NCT05254691. Registered 24 February 2022, registered retrospectively.

Model-Based Estimation of Inspiratory Effort Using Surface EMG.

The quantification of inspiratory patient effort in assisted mechanical ventilation is essential for the adjustment of ventilatory assistance and for assessing patient-ventilator interaction. The inspiratory effort is usually measured via the respiratory muscle pressure (P mus) derived from esophageal pressure (P es) measurements. As yet, no reliable non-invasive and unobtrusive alternatives exist to continuously quantify P mus. We propose a model-based approach to estimate P mus non-invasively during assisted ventilation using surface electromyographic (sEMG) measurements. The method combines the sEMG and ventilator signals to determine the lung elastance and resistance as well as the neuromechanical coupling of the respiratory muscles via a novel regression technique. Using the equation of motion, an estimate for P mus can then be calculated directly from the lung mechanical parameters and the pneumatic ventilator signals. The method was applied to data recorded from a total of 43 ventilated patients and validated against P es-derived P mus. Patient effort was quantified via the P mus pressure-time-product (PTP). The sEMG-derived PTP estimated using the proposed method was highly correlated to P es-derived PTP ([Formula: see text]), and the breath-wise deviation between the two quantities was [Formula: see text]. The estimated, sEMG-derived P mus is closely related to the P es-based reference and allows to reliably quantify inspiratory effort. The proposed technique provides a valuable tool for physicians to assess patients undergoing assisted mechanical ventilation and, thus, may support clinical decision making.

An Evolutionary Adolescent Idiopathic Scoliosis Etiology Spine-Limbs Links, Inspiration and Laterality as Basic Factors

Moving on an evolutionary sight, this article individualizes three basic human causative factors in adolescent idiopathic scoliosis developing inspiration, bipedal locomotion and lateralities. The integrative approach considers the neuromechanical coupling in respiration, introducing the concept of pneumofascial competition (section one) as the loop that occurs between inspired air and pleural fasciae and then global myofascia. Affordances (possibilities) and constraints of respiratory system match positions and movements of whole body, where the links between spine and periphery (limbs and head) play a determinant part: these connections, the one that involves the spinal transverse plane, are worked out in section two. Therefore, section two appears a decisive step in trying to solve some questions about human bipedal locomotion and its proficiency, again in a neuromechanical coupling view, with totally original considerations about the role of scapula and about the spine as a treble torsion spring. Finally, it is possible to trace out a new adolescent idiopathic scoliosis etiology (section three), adding a third factor: laterality. What is only human is the hyper stressed lateralization (s) by means of cultural requirements. The motor hyper specialization is another form of energy saving (automatism). Thus, all the article is about the evolutionary principle of costs minimizing. Adolescent idiopathic scoliosis is here seen as an evolutionary mismatch disease between human nature and human culture and every curve can be explained in an integrative way, where causes and effects develop a mutual self-powering cycle.

Expiratory Muscles, Neglected No More.

Expiratory Muscles, Neglected No More.

The Anticipation of Gravity in Human Ballistic Movement.

Stretch-shortening type actions are characterized by lengthening of the pre-activated muscle-tendon unit (MTU) in the eccentric phase immediately followed by muscle shortening. Under 1 g, pre-activity before and muscle activity after ground contact, scale muscle stiffness, which is crucial for the recoil properties of the MTU in the subsequent push-off. This study aimed to examine the neuro-mechanical coupling of the stretch-shortening cycle in response to gravity levels ranging from 0.1 to 2 g. During parabolic flights, 17 subjects performed drop jumps while electromyography (EMG) of the lower limb muscles was combined with ultrasound images of the gastrocnemius medialis, 2D kinematics and kinetics to depict changes in energy management and performance. Neuro-mechanical coupling in 1 g was characterized by high magnitudes of pre-activity and eccentric muscle activity allowing an isometric muscle behavior during ground contact. EMG during pre-activity and the concentric phase systematically increased from 0.1 to 1 g. Below 1 g the EMG in the eccentric phase was diminished, leading to muscle lengthening and reduced MTU stretches. Kinetic energy at take-off and performance were decreased compared to 1 g. Above 1 g, reduced EMG in the eccentric phase was accompanied by large MTU and muscle stretch, increased joint flexion amplitudes, energy loss and reduced performance. The energy outcome function established by linear mixed model reveals that the central nervous system regulates the extensor muscles phase- and load-specifically. In conclusion, neuro-mechanical coupling appears to be optimized in 1 g. Below 1 g, the energy outcome is compromised by reduced muscle stiffness. Above 1 g, loading progressively induces muscle lengthening, thus facilitating energy dissipation.

Noninvasive Assessment of Neuromechanical Coupling and Mechanical Efficiency of Parasternal Intercostal Muscle during Inspiratory Threshold Loading.

This study aims to investigate noninvasive indices of neuromechanical coupling (NMC) and mechanical efficiency (MEff) of parasternal intercostal muscles. Gold standard assessment of diaphragm NMC requires using invasive techniques, limiting the utility of this procedure. Noninvasive NMC indices of parasternal intercostal muscles can be calculated using surface mechanomyography (sMMGpara) and electromyography (sEMGpara). However, the use of sMMGpara as an inspiratory muscle mechanical output measure, and the relationships between sMMGpara, sEMGpara, and simultaneous invasive and noninvasive pressure measurements have not previously been evaluated. sEMGpara, sMMGpara, and both invasive and noninvasive measurements of pressures were recorded in twelve healthy subjects during an inspiratory loading protocol. The ratios of sMMGpara to sEMGpara, which provided muscle-specific noninvasive NMC indices of parasternal intercostal muscles, showed nonsignificant changes with increasing load, since the relationships between sMMGpara and sEMGpara were linear (R2 = 0.85 (0.75–0.9)). The ratios of mouth pressure (Pmo) to sEMGpara and sMMGpara were also proposed as noninvasive indices of parasternal intercostal muscle NMC and MEff, respectively. These indices, similar to the analogous indices calculated using invasive transdiaphragmatic and esophageal pressures, showed nonsignificant changes during threshold loading, since the relationships between Pmo and both sEMGpara (R2 = 0.84 (0.77–0.93)) and sMMGpara (R2 = 0.89 (0.85–0.91)) were linear. The proposed noninvasive NMC and MEff indices of parasternal intercostal muscles may be of potential clinical value, particularly for the regular assessment of patients with disordered respiratory mechanics using noninvasive wearable and wireless devices.

Isolating the energetic and mechanical consequences of imposed reductions in ankle and knee flexion during gait

BackgroundWeakness of ankle and knee musculature following injury or disorder results in reduced joint motion associated with metabolically expensive gait compensations to enable limb support and advancement. However, neuromechanical coupling between the ankle and knee make it difficult to discern independent roles of these restrictions in joint motion on compensatory mechanics and metabolic penalties.MethodsWe sought to determine relative impacts of ankle and knee impairment on compensatory gait strategies and energetic outcomes using an unimpaired cohort (N = 15) with imposed unilateral joint range of motion restrictions as a surrogate for reduced motion resulting from gait pathology. Participants walked on a dual-belt instrumented treadmill at 0.8 m s−1 using a 3D printed ankle stay and a knee brace to systematically limit ankle motion (restricted-ank), knee motion (restricted-knee), and ankle and knee motion (restricted-a + k) simultaneously. In addition, participants walked without any ankle or knee bracing (control) and with knee bracing worn but unrestricted (braced).ResultsWhen ankle motion was restricted (restricted-ank, restricted-a + k) we observed decreased peak propulsion relative to the braced condition on the restricted limb. Reduced knee motion (restricted-knee, restricted-a + k) increased restricted limb circumduction relative to the restricted-ank condition through ipsilateral hip hiking. Interestingly, restricted limb average positive hip power increased in the restricted-ank condition but decreased in the restricted-a + k and restricted-knee conditions, suggesting that locking the knee impeded hip compensation. As expected, reduced ankle motion, either without (restricted-ank) or in addition to knee restriction (restricted-a + k) yielded significant increase in net metabolic rate when compared with the braced condition. Furthermore, the relative increase in metabolic cost was significantly larger with restricted-a + k when compared to restricted-knee condition.ConclusionsOur methods allowed for the reproduction of asymmetric gait characteristics including reduced propulsive symmetry and increased circumduction. The metabolic consequences bolster the potential energetic benefit of targeting ankle function during rehabilitation.Trial registrationN/A.

The Inhibitory Tendon-Evoked Reflex Is Increased in the Torque-Enhanced State Following Active Lengthening Compared to a Purely Isometric Contraction.

Residual torque enhancement (rTE) is a history-dependent property of muscle, which results in an increase in steady-state isometric torque production following an active lengthening contraction as compared to a purely isometric (ISO) contraction at the same muscle length and level of activation. Once thought to be only an intrinsic property of muscle, recent evidence during voluntary contractions indicates a neuromechanical coupling between motor neuron excitability and the contractile state of the muscle. However, the mechanism by which this occurs has yet to be elucidated. The purpose of this study was to investigate inhibition arising from tendon-mediated feedback (e.g., Golgi tendon organ; GTO) through tendon electrical stimulation (TStim) in the ISO and rTE states during activation-matching and torque-matching tasks. Fourteen male participants (22 ± 2 years) performed 10 activation-matching contractions at 40% of their maximum tibialis anterior electromyography amplitude (5 ISO/5 rTE) and 10 torque-matching contractions at 40% of their maximum dorsiflexion torque (5 ISO/5 rTE). During both tasks, 10 TStim were delivered during the isometric steady state of all contractions, and the resulting tendon-evoked inhibitory reflexes were averaged and analyzed. Reflex amplitude increased by ~23% in the rTE state compared to the ISO state for the activation-matching task, and no differences were detected for the torque-matching task. The current data indicate an important relationship between afferent feedback in the torque-enhanced state and voluntary control of submaximal contractions. The history-dependent properties of muscle is likely to alter motor neuron excitability through modifications in tension- or torque-mediated afferent feedback arising from the tendon.

The relationship between leg stiffness, forces and neural control of the leg musculature during the stretch-shortening cycle is dependent on the anticipation of drop height.

This study aimed at investigating how prior knowledge of drop heights affects proactive and reactive motor control in drop jumps (DJ). In 22 subjects, the effect of knowledge of three different drop heights (20, 30, 40cm) during DJs was evaluated in seven conditions: three different drop heights were either known, unknown or cheated (announced 40cm, but actual drop height was 20cm). Peak ground reaction force (Fmax) to body weight (BW) ratio (Fmax/BW) and electromyographic (EMG) activities of three shank and five thigh muscles were assessed 150ms before and during ground contact (GC). Ankle, knee and hip joint kinematics were recorded in the sagittal plane. Leg stiffness, proactive and reactive EMG activity of the leg muscles diminished in unknown and cheat conditions for all drop heights (7-33% and 2-26%, respectively). Antagonistic co-activation increased in unknown (3-37%). At touchdown, increased flexion in knee (~ 5.3° ± 1.9°) and hip extension (~ 2° ± 0.6°) were observed in unknown, followed by an increased angular excursion in hip (~ 2.3° ± 0.2°) and knee joints (~ 5.6° ± 0.2°) during GC (p < 0.05). Correlations between changes in activation intensities, joint kinematics, leg stiffness and Fmax/BW (p < 0.05) indicate that anticipation changes the neuromechanical coupling of DJs. No dropouts were recorded. These findings underline that anticipation influences timing and adjustment of motor responses. It is argued that proactive and reactive modulations associated with diminished activation intensities in leg extensors are functionally relevant in explaining changes in leg stiffness and subsequent decline in performance.

Is non-normalized chest wall electromyogram activity a reliable index of respiratory neural drive? On the surface - yes!

Is non-normalized chest wall electromyogram activity a reliable index of respiratory neural drive? On the surface - yes!

Ipsilesional Mu Rhythm Desynchronization and Changes in Motor Behavior Following Post Stroke BCI Intervention for Motor Rehabilitation.

Loss of motor function is a common deficit following stroke insult and often manifests as persistent upper extremity (UE) disability which can affect a survivor’s ability to participate in activities of daily living. Recent research suggests the use of brain–computer interface (BCI) devices might improve UE function in stroke survivors at various times since stroke. This randomized crossover-controlled trial examines whether intervention with this BCI device design attenuates the effects of hemiparesis, encourages reorganization of motor related brain signals (EEG measured sensorimotor rhythm desynchronization), and improves movement, as measured by the Action Research Arm Test (ARAT). A sample of 21 stroke survivors, presenting with varied times since stroke and levels of UE impairment, received a maximum of 18–30 h of intervention with a novel electroencephalogram-based BCI-driven functional electrical stimulator (EEG-BCI-FES) device. Driven by spectral power recordings from contralateral EEG electrodes during cued attempted grasping of the hand, the user’s input to the EEG-BCI-FES device modulates horizontal movement of a virtual cursor and also facilitates concurrent stimulation of the impaired UE. Outcome measures of function and capacity were assessed at baseline, mid-therapy, and at completion of therapy while EEG was recorded only during intervention sessions. A significant increase in r-squared values [reflecting Mu rhythm (8–12 Hz) desynchronization as the result of attempted movements of the impaired hand] presented post-therapy compared to baseline. These findings suggest that intervention corresponds with greater desynchronization of Mu rhythm in the ipsilesional hemisphere during attempted movements of the impaired hand and this change is related to changes in behavior as a result of the intervention. BCI intervention may be an effective way of addressing the recovery of a stroke impaired UE and studying neuromechanical coupling with motor outputs.Clinical Trial Registration: ClinicalTrials.gov, identifier NCT02098265.

Noninvasive Assessment of Inspiratory Muscle Neuromechanical Coupling During Inspiratory Threshold Loading

Diaphragm neuromechanical coupling (NMC), which reflects the efficiency of conversion of neural activation to transdiaphragmatic pressure (Pdi), is increasingly recognized to be a useful clinical index of diaphragm function and respiratory mechanics in neuromuscular weakness and cardiorespiratory disease. However, the current gold standard assessment of diaphragm NMC requires invasive measurements of Pdi and crural diaphragm electromyography (oesEMGdi), which complicates the measurement of diaphragm NMC in clinical practice. This is the first study to compare invasive measurements of diaphragm NMC (iNMC) using the relationship between Pdi and oesEMGdi, with noninvasive assessment of NMC (nNMC) using surface mechanomyography (sMMGlic) and electromyography (sEMGlic) of lower chest wall inspiratory muscles. Both invasive and noninvasive measurements were recorded in twelve healthy adult subjects during an inspiratory threshold loading protocol. A linear relationship between noninvasive sMMGlic and sEMGlic measurements was found, resulting in little change in nNMC with increasing inspiratory load. By contrast, a curvilinear relationship between invasive Pdi and oesEMGdi measurements was observed, such that there was a progressive increase in iNMC with increasing inspiratory threshold load. Progressive recruitment of lower ribcage muscles, serving to enhance the mechanical advantage of the diaphragm, may explain the more linear relationship between sMMGlic and sEMGlic (both representing lower intercostal plus costal diaphragm activity) than between Pdi and crural oesEMGdi. Noninvasive indices of NMC derived from sEMGlic and sMMGlic may prove to be useful indices of lower chest wall inspiratory muscle NMC, particularly in settings that do not have access to invasive measures of diaphragm function.

Stimulus Prediction and Postural Reaction: Phase-Specific Modulation of Soleus H-Reflexes Is Related to Changes in Joint Kinematics and Segmental Strategy in Perturbed Upright Stance.

Anticipation determines the timing and efficiency of human motor performance. This study aimed to evaluate the effect of stimulus anticipation on proactive (prior to the event) and reactive (after the event) postural adjustments in response to perturbations. Postural set was manipulated by providing either (i) predictable, (ii) unpredictable, or (iii) cheated perturbations which require balance corrections to maintain postural stability. In 29 subjects, a protocol of anterior and posterior perturbations was applied for the conditions (i–iii). Center of pressure (COP) displacement, ankle, knee, and hip joint kinematics and electromyographic activity (EMG) of the soleus (SOL) and tibialis anterior (TA) muscles were recorded prior (PRE) and after posterior perturbations. SOL H-reflexes at the peak of the short-, medium- ,and long-latency responses (SLR, MLR, LLR) were assessed. For conditions (i to iii) EMG activity and COP differed prior to perturbation onset (p < 0.05). After perturbation, results demonstrated a progressively increased H-reflex amplitude in the MLR and LLR (p < 0.05), delayed muscle activities (p < 0.05), and shifted activation patterns, with muscles of the proximal segment being more involved in the compensatory postural response (p < 0.05). COP displacements and ankle, knee, and hip joint deflections progressively increased (p < 0.05). Neuromechanical coupling showed positive correlations for the anticipation-induced changes in EMG activity and H-reflex amplitude with that of COP displacement (p < 0.05). In conclusion, proactive and reactive postural responses indicated setting dependent modulations of segmental and phasic muscle activation. A shift to proximal muscle groups and facilitated late reflex responses compensating for cheated or unpredicted perturbations was found to recover a safe body equilibrium. In consideration of the phase-specific adaptation and its interrelationship to the kinematics, it suggested that changes in stimulus prediction challenged the central nervous system to appropriately counteract the higher postural challenges. The outcomes of this experiment are of functional relevance for experimental and training settings involving perturbation stimuli. These findings provide fundamental information of the mechanisms underlying postural adjustments in response to external perturbations.

Central contributions to torque depression: an antagonist perspective.

Torque depression (TD) is the reduction in steady-state isometric torque following active muscle shortening when compared to an isometric reference contraction at the same muscle length and activation level. Central nervous system excitability differs in the TD state. While torque production about a joint is influenced by both agonist and antagonist muscle activation, investigations of corticospinal excitability have focused on agonist muscle groups. Hence, it is unknown how the TD state affects spinal and supraspinal excitability of an antagonist muscle. Eight participants (~ 24y, three female) performed 14 submaximal dorsiflexion contractions at the intensity needed to maintain a level of integrated electromyographic activity in the soleus equivalent to 15% of that recorded during a maximum plantar flexion contraction. The seven contractions of the TD protocol included a 2s isometric phase at an ankle angle of 140°, a 1s shortening phase at 40°/s, and a 7s isometric phase at an angle of 100°. The seven isometric reference contractions were performed at an ankle angle of 100° for 10s. Motor evoked potentials (MEPs), cervicomedullary motor evoked potentials (CMEPs), and maximal M-waves (Mmax) were recorded from the soleus in both conditions. In the TD compared to isometric reference state, a 13% reduction in dorsiflexor torque was accompanied by 10% lower spinal excitability (normalized CMEP amplitude; CMEP/Mmax), and 17% greater supraspinal excitability (normalized MEP amplitude; MEP/CMEP) for the soleus muscle. These findings demonstrate a neuromechanical coupling following active muscle shortening and indicate that the underlying mechanisms of TD influence antagonist activation during voluntary force production.

Neuromechanical coupling within the human triceps surae and its consequence on individual force-sharing strategies.

Little is known about the factors that influence the coordination of synergist muscles that act across the same joint, even during single-joint isometric tasks. The overall aim of this study was to determine the nature of the relationship between the distribution of activation and the distribution of force-generating capacity among the three heads of the triceps surae [soleus (SOL), gastrocnemius medialis (GM) and gastrocnemius lateralis (GL)]. Twenty volunteers performed isometric plantarflexions, during which the activation of GM, GL and SOL was estimated using electromyography (EMG). Functional muscle physiological cross-sectional area (PCSA) was estimated using imaging techniques and was considered as an index of muscle force-generating capacity. The distribution of activation and PCSA among the three muscles varied greatly between participants. A significant positive correlation between the distribution of activation and the distribution of PCSA was observed when considering the two bi-articular muscles at intensities ≤50% of the maximal contraction (0.51<r<0.62). Specifically, the greater the PCSA of GM compared with GL, the stronger bias of activation to the GM. There was no significant correlation between monoarticular and biarticular muscles. A higher contribution of GM activation compared with GL activation was associated with lower triceps surae activation (-0.66<r<-0.42) and metabolic cost (-0.74<r<-0.52) for intensities ≥30% of the maximal contraction. Considered together, an imbalance of force between the three heads was observed, the magnitude of which varied greatly between participants. The origin and consequences of these individual force-sharing strategies remain to be determined.

The Dynamics of Voluntary Force Production in Afferented Muscle Influence Involuntary Tremor.

Voluntary control of force is always marked by some degree of error and unsteadiness. Both neural and mechanical factors contribute to these fluctuations, but how they interact to produce them is poorly understood. In this study, we identify and characterize a previously undescribed neuromechanical interaction where the dynamics of voluntary force production suffice to generate involuntary tremor. Specifically, participants were asked to produce isometric force with the index finger and use visual feedback to track a sinusoidal target spanning 5–9% of each individual's maximal voluntary force level. Force fluctuations and EMG activity over the flexor digitorum superficialis (FDS) muscle were recorded and their frequency content was analyzed as a function of target phase. Force variability in either the 1–5 or 6–15 Hz frequency ranges tended to be largest at the peaks and valleys of the target sinusoid. In those same periods, FDS EMG activity was synchronized with force fluctuations. We then constructed a physiologically-realistic computer simulation in which a muscle-tendon complex was set inside of a feedback-driven control loop. Surprisingly, the model sufficed to produce phase-dependent modulation of tremor similar to that observed in humans. Further, the gain of afferent feedback from muscle spindles was critical for appropriately amplifying and shaping this tremor. We suggest that the experimentally-induced tremor may represent the response of a viscoelastic muscle-tendon system to dynamic drive, and therefore does not fall into known categories of tremor generation, such as tremorogenic descending drive, stretch-reflex loop oscillations, motor unit behavior, or mechanical resonance. Our findings motivate future efforts to understand tremor from a perspective that considers neuromechanical coupling within the context of closed-loop control. The strategy of combining experimental recordings with physiologically-sound simulations will enable thorough exploration of neural and mechanical contributions to force control in health and disease.

Yoga-based pulmonary rehabilitation for the management of dyspnea in coal miners with chronic obstructive pulmonary disease: A randomized controlled trial

BackgroundCoal mine dust exposure causes chronic airflow limitation in coal miners resulting in dyspnea, fatigue, and eventually chronic obstructive pulmonary disease (COPD). Yoga can alleviate dyspnea in COPD by improving ventilatory mechanics, reducing central neural drive, and partially restoring neuromechanical coupling of the respiratory system. ObjectivesTo evaluate the effectiveness of Integrated Approach of Yoga Therapy (IAYT) in the management of dyspnea and fatigue in coal miners with COPD. Materials and methodsRandomized, waitlist controlled, single-blind clinical trial. Eighty-one coal miners (36–60 years) with stable Stages II and III COPD were recruited. The yoga group received an IAYT module for COPD that included asanas, loosening exercises, breathing practices, pranayama, cyclic meditation, yogic counseling and lectures 90 min/day, 6 days/week for 12 weeks. Measurements of dyspnea and fatigue on the Borg scale, exercise capacity by the 6 min walk test, peripheral capillary oxygen saturation (SpO2%), and pulse rate (PR) using pulse oximetry were made before and after the intervention. ResultsStatistically significant within group reductions in dyspnea (P < 0.001), fatigue (P < 0.001) scores, PR (P < 0.001), and significant improvements in SpO2% (P < 0.001) and 6 min walk distance (P < 0.001) were observed in the yoga group; all except the last were significant compared to controls (P < 0.001). ConclusionsFindings indicate that IAYT benefits coal miners with COPD, reducing dyspnea; fatigue and PR, and improving functional performance and peripheral capillary SpO2%. Yoga can now be included as an adjunct to conventional therapy for pulmonary rehabilitation programs for COPD patients.

Contribution of inter-muscular synchronization in the modulation of tremor intensity in Parkinson's disease.

BackgroundInvoluntary central oscillations at single and double tremor frequencies drive the peripheral neuromechanical system of muscles and joints to cause tremor in Parkinson’s disease (PD). The central signal of double tremor frequency was found to correlate more directly to individual muscle EMGs (Timmermann et al. 2003). This study is aimed at investigating what central components of oscillation contribute to inter-muscular synchronization in a group of upper extremity muscles during tremor in PD patients.Methods11 idiopathic, tremor dominant PD subjects participated in this study. Joint kinematics during tremor in the upper extremity was recorded along with EMGs of six upper arm muscles using a novel experimental apparatus. The apparatus provided support for the upper extremity on a horizontal surface with reduced friction, so that resting tremor in the arm can be recorded with a MotionMonitor II system. In each subject, the frequencies of rhythmic firings in upper arm muscles were determined using spectral analysis. Paired and pool-averaged coherence analyses of EMGs for the group of muscles were performed to correlate the level of inter-muscular synchronization to tremor amplitudes at shoulder and elbow. The phase shift between synchronized antagonistic muscle pairs was calculated to aid coherence analysis in the muscle pool.ResultsRecorded EMG revealed that rhythmic firings were present in most recorded muscles, which were either synchronized to form phase-locked bursting cycles at a subject specific frequency, or unsynchronized with a random phase distribution. Paired coherence showed a stronger synchronization among a subset of recorded arm muscles at tremor frequency than that at double tremor frequency. Furthermore, the number of synchronized muscles in the arm was positively correlated to tremor amplitudes at elbow and shoulder. Pool-averaged coherence at tremor frequency also showed a better correlation with the amplitude of resting tremor than that of double tremor frequency, indicating that the neuromechanical coupling in peripheral neuromuscular system was stronger at tremor frequency.ConclusionsBoth paired and pool-averaged coherences are more consistent indexes to correlate to tremor intensity in a group of upper extremity muscles of PD patients. The central drive at tremor frequency contributes mainly to synchronize peripheral muscles in the modulation of tremor intensity.

Neuromechanical coupling during mechanical ventilation: reverse-triggering vs others forms of asynchrony

The term “respiratory entrainment” refers to of coupling patterns between the rhythm neuronal and mechanical of ventilator to achieve satisfactory synchrony. Respiratory effort stimulated by the mechanical inspiratory flow or reverse trigger (RT), has been recently demonstrated [1]. This asynchrony is difficult to showed without additional signals as esophageal pressure or electrodiaphragmatic signal.

Diaphragmatic neuromechanical coupling and mechanisms of hypercapnia during inspiratory loading

We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading – the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9±4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.