Activation of respiratory muscles during respiratory muscle training.

It is unknown which respiratory muscles are mainly activated by respiratory muscle training. This study evaluated Inspiratory Pressure Threshold Loading (IPTL), Inspiratory Flow Resistive Loading (IFRL) and Voluntary Isocapnic Hyperpnea (VIH) with regard to electromyographic (EMG) activation of the sternocleidomastoid muscle (SCM), parasternal muscles (PARA) and the diaphragm (DIA) in randomized order. Surface EMG were analyzed at the end of each training session and normalized using the peak EMG recorded during maximum inspiratory maneuvers (Sniff nasal pressure: SnPna, maximal inspiratory mouth occlusion pressure: PImax). 41 healthy participants were included. Maximal activation was achieved for SCM by SnPna; the PImax activated predominantly PARA and DIA. Activations of SCM and PARA were higher in IPTL and VIH than for IFRL (p<0.05). DIA was higher applying IPTL compared to IFRL or VIH (p<0.05). IPTL, IFRL and VIH differ in activation of inspiratory respiratory muscles. Whereas all methods mainly stimulate accessory respiratory muscles, diaphragm activation was predominant in IPTL.

Resting limb muscle perfusion during inspiratory muscle loading in hypoxia and normoxia.

INTRODUCTION: Fatiguing of respiratory muscles reduces peripheral muscle perfusion. Further, acute hypoxia enhances respiratory muscle fatigue. This study investigated the effects of inspiratory muscle loading (IML) on resting locomotor muscle perfusion in hypoxia compared to normoxia. METHODS: Ten subjects completed two study days of fatiguing IML (blinded, randomized) in normobaric hypoxia (targeted oxygen saturation 80%) and normoxia, respectively. Contrast-enhanced ultrasound (CEUS) of the gastrocnemius muscle and popliteal doppler ultrasonography were used to monitor muscle perfusion. Based on CEUS and monitored cardiac output, perfusion surrogate parameters (CLPaer and CLPap) were established. RESULTS: Muscle perfusion declines early during IML in normoxia (CLPaer: -54±25%, p<0.01; CLPap: -58±32%, p<0.01) and hypoxia (CLPaer: -43±23%, p<0.01; CLPap: -41±20%, p<0.01). Hypoxia compared to normoxia increased cardiac output before (+23±19%, p<0.01 ANOVA) and during (+22±20%, p<0.01 ANOVA) IML, while local muscle perfusion during IML remained unchanged (CLPaer: p=0.41 ANOVA; CLPap: p=0.29 ANOVA). CONCLUSION: Acute hypoxia compared to normoxia does not affect locomotor muscle perfusion during fatiguing IML.

Activation of respiratory muscles during weaning from mechanical ventilation.

PURPOSE: Respiratory muscle dysfunction is a key component of weaning failure. Balancing respiratory muscle loading and unloading by applying different ventilation modes along with spontaneous breathing episodes are established weaning strategies. However, the effects of body positioning on the respiratory muscles during weaning remains unclear. MATERIALS AND METHODS: This study aimed at assessing respiratory drive by surface electromyography (EMG) of the diaphragm (EMGdia) and parasternal muscles (EMGpara) in tracheotomized patients during prolonged weaning in 3 randomized body positions-supine, 30° semirecumbent, and 80° sitting-during mechanical ventilation and spontaneous breathing. RESULTS: Nine patients were included for analysis. Cardiorespiratory parameters (heart rate, blood pressure, arterial oxygen saturation, dyspnea) did not change under each condition (all P>.05). EMGpara and EMGdia did not change under mechanical ventilation (both P>.05). EMGdia changed under spontaneous breathing from supine to sitting (0.45±0.26 vs 0.32±0.19; P=.012) and between semirecumbent to sitting (0.41±0.23 vs 0.32±0.19; P=.039), whereas EMGpara did not change. CONCLUSIONS: This is the first study to show that body positioning influences respiratory drive to the diaphragm in tracheotomized patients with prolonged weaning from mechanical ventilation during unassisted breathing. Sitting position reduces respiratory drive compared with semirecumbent and supine positioning and might therefore be favored during spontaneous breathing trials.

Diaphragmatic fatigue during inspiratory muscle loading in normoxia and hypoxia.

INTRODUCTION: Diaphragmatic fatigue (DF) occurs during strenuous loading of respiratory muscles (e.g., heavy-intensity whole-body exercise, normocapnic hyperpnea, inspiratory resistive breathing). DF develops early on during normoxia, without further decline toward task failure; however, its progression during inspiratory muscle loading in during hypoxia remains unclear. Therefore, the present study used volume-corrected transdiaphragmatic pressures during supramaximal magnetic phrenic nerve stimulation (Pdi,twc) to investigate the effect of hypoxia on the progression of diaphragmatic fatigue during inspiratory muscle loading. METHODS: Seventeen subjects completed two standardized rounds of inspiratory muscle loading (blinded, randomized) under the following conditions: (i) normoxia, and (ii) normobaric hypoxia (SpO2 80%), with Pdi,twc assessment every 45 s. RESULTS: In fatiguers (i.e., Pdi,twc reduction >10%, n=10), biometric approximation during normoxia is best represented by Pdi,twc=4.06+0.83 exp(-0.19 × x), in contrast to Pdi,twc=4.38-(0.05 × x) during hypoxia. CONCLUSION: Progression of diaphragmatic fatigue during inspiratory muscle loading assessed by Pdi,tw differs between normoxia and normobaric hypoxia: in the former, Pdi,tw follows an exponential decay, whereas during hypoxia, Pdi,tw follows a linear decline.

Walking with Non-Invasive Ventilation Does Not Prevent Exercise-Induced Hypoxaemia in Stable Hypercapnic COPD Patients.

BACKGROUND: Non-invasive positive pressure ventilation (NPPV) in addition to supplemental oxygen improves arterial oxygenation, walking distance and dyspnea when applied during exercise in stable hypercapnic COPD patients. The aim of the current study was to investigate whether NPPV without supplemental oxygen is capable of preventing severe exercise-induced hypoxemia in these patients when applied during walking. METHODS AND RESULTS: 15 stable hypercapnic COPD patients (FEV1 29.9 ± 15.9%) performed two 6-minute walk tests (6MWT) with a rollator in a randomized cross-over design: using either supplemental oxygen (2.4 ± 0.7 L/min) or NPPV (inspiratory/expiratory positive airway pressure of 28.2 ± 2.8 / 5.5 ± 1.5 mbar) without supplemental oxygen. RESULTS: 10 patients were able to complete both 6MWT. 6MWT with supplemental oxygen resulted in no changes for PO2 (pre: 67.3 ± 11.2 mmHg vs. post: 65.6 ± 12.0 mmHg, p = 0.72) whereas PCO2 increased (pre: 50.9 ± 8.1 mmHg vs. post: 54.3 ± 10.0 mmHg (p < 0.03). During 6MWT with NPPV PO2 significantly decreased from 66.8 ± 7.2 mmHg to 55.5 ± 10.6 mmHg (p < 0.02) whereas no changes occurred in PCO2 (pre: 50.6 ± 7.5 mmHg vs. post: 53.0 ± 7.1 mmHg; p = 0.17). Walking distance tended to be lower in 6MWT with NPPV compared to 6MWT with supplemental oxygen alone (318 ± 160 m vs. 377 ± 108 m; p = 0.08). CONCLUSION: The use of NPPV during walking without the application of supplemental oxygen does not prevent exercise-induced hypoxemia in patients with stable hypercapnic COPD.

The combination of exercise and respiratory training improves respiratory muscle function in pulmonary hypertension.

PURPOSE: Increased dyspnea and reduced exercise capacity in pulmonary arterial hypertension (PAH) can be partly attributed to impaired respiratory muscle function. This prospective study was designed to assess the impact of exercise and respiratory training on respiratory muscle strength and 6-min walking distance (6MWD) in PAH patients. METHODS: Patients with invasively confirmed PAH underwent 3 weeks of in-hospital exercise and respiratory training, which was continued at home for another 12 weeks. Medication remained constant during the study period. Blinded observers assessed efficacy parameters at baseline (I) and after 3 (II) and 15 weeks (III). Respiratory muscle function was assessed by twitch mouth pressure (TwPmo) during nonvolitional supramaximal magnetic phrenic nerve stimulation. RESULTS: Seven PAH patients (4 women; mean pulmonary artery pressure 45 ± 11 mmHg, median WHO functional class 3.1 ± 0.4, idiopathic/associated PAH n = 5/2) were included. The training program was feasible and well tolerated by all patients with excellent compliance. TwPmo was I: 0.86 ± 0.37 kPa, II: 1.04 ± 0.29 kPa, and III: 1.27 ± 0.44 kPa, respectively. 6MWD was I: 417 ± 51 m, II: 509 ± 39 m, and III: 498 ± 39 m, respectively. Both TwPmo (+0.41 ± 0.34 kPa, +56 ± 39 %) and 6MWD (+81 ± 30 m, +20 ± 9 %) increased significantly in the period between baseline and the final assessment (pairwise comparison: p = 0.012/<0.001; RM-ANOVA considering I, II, III: p = 0.037/<0.001). CONCLUSIONS: Exercise and respiratory training as an adjunct to medical therapy may be effective in patients with PAH to improve respiratory muscle strength and exercise capacity. Future, randomized, controlled trials should be carried out to further investigate these findings.

Respiratory muscle function during a six-week period of normocapnic hyperpnoea training.

Respiratory muscle endurance training (normocapnic hyperpnoea, RMET) improves maximal volitional ventilation (MVV) and respiratory muscle endurance while volitionally-assessed respiratory muscle strength remains unchanged (prior-to-post comparison). What remains unclear is how respiratory muscle function changes/adapts during a defined period of RMET in highly-trained subjects. This study assessed respiratory muscle function during a six-week period of RMET in 13 highly-trained, healthy subjects. Weekly-assessed twitch mouth pressure (prior/post 2.20 ± 0.41 kPa vs. 2.43 ± 0.61 kPa; p=0.14); twitch transdiaphragmatic pressure (prior/post 3.04 ± 0.58 kPa vs. 3.13 ± 0.48 kPa; p=0.58) and maximal inspiratory pressure (prior/post 12.6 ± 3.6 kPa vs. 13.9 ± 3.8 kPa; p=0.06) did not increase. MVV (prior/post 175 ± 18 l/min vs. 207 ± 30 l/min; p=0.001), sniff nasal pressure (prior/post 11.8 ± 2.8 kPa vs. 14.0 ± 2.9 kPa; p=0.003) and maximal expiratory pressure (prior/post 16.9 ± 5.8 kPa vs. 20.9 ± 4.9 kPa; p=0.006) each increased. In conclusion, non-volitionally assessed diaphragmatic strength does not increase during six weeks of RMET in highly-trained subjects, while expiratory muscle strength and MVV rose. Future studies should clarify if these findings apply when assessed during respiratory muscle strength rather than endurance training.

Biometric approximation of diaphragmatic contractility during sustained hyperpnea.

Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.

Characteristics of diaphragmatic fatigue during exhaustive exercise until task failure.

The diaphragm was postulated to fatigue relatively early during exhaustive whole body exercise without further loss in contractility as exercise proceeds towards task failure. Diaphragmatic contractility was investigated prior/during/after exhaustive whole body exercise until task failure by using lung volume corrected twitch transdiaphragmatic pressure (TwPdi(c)) during magnetic phrenic nerve stimulation (every 45s). Eleven cyclists exercised to exhaustion (workloads ≥85% maximal oxygen uptake; 20.7±9.8min). Individual post hoc calculation of TwPdi(c) was conducted (diaphragmatic contractility versus lung volume). Diaphragmatic fatigue (i.e. TwPdi reduction baseline/recovery ≥10%) occurred in 9/11 subjects (82% "fatiguers"; baseline/recovery TwPdi(c) -16±13%, p<0.01). Fatiguers TwPdi(c) was: baseline: 2.99±0.40kPa, exercise-onset: 2.98±0.41kPa, initial third: 2.80±0.67kPa, second third: 2.54±0.55kPa, final third-task failure: 2.51±0.44kPa, recovery: 2.50±0.52kPa. Diaphragmatic contractility and lung volume (rest) were strongly related (r(2)=0.98, mean TwPdi(c) gradient 0.78kPa/l). To conclude, diaphragmatic contractility (lung volume corrected) decreases relatively early (initial two thirds) during exhaustive exercise and remains preserved towards task failure. This confirms previous assumptions postulating that respiratory performance is sustained without further fatigue of the primary inspiratory muscle.