Mouth Occlusion Pressure Research Articles

Predicting parameters of airway dynamics generated from inspiratory and expiratory plethysmographic airway loops, differentiating subtypes of chronic obstructive diseases

BackgroundThe plethysmographic shift volume–flow loop (sRaw-loop) measured during tidal breathing allows the determination of several lung function parameters such as the effective specific airway resistance (sReff), calculated from the ratio...

APOE4, Age, and Sex Regulate Respiratory Plasticity Elicited by Acute Intermittent Hypercapnic-Hypoxia.

Acute intermittent hypoxia (AIH) shows promise for enhancing motor recovery in chronic spinal cord injuries and neurodegenerative diseases. However, human trials of AIH have reported significant variability in individual responses. Identify individual factors (eg, genetics, age, and sex) that determine response magnitude of healthy adults to an optimized AIH protocol, acute intermittent hypercapnic-hypoxia (AIHH). In 17 healthy individuals (age = 27 ± 5 yr), associations between individual factors and changes in the magnitude of AIHH (15, 1-min O2 = 9.5%, CO2 = 5% episodes) induced changes in diaphragm motor-evoked potential (MEP) amplitude and inspiratory mouth occlusion pressures (P0.1) were evaluated. Single nucleotide polymorphisms (SNPs) in genes linked with mechanisms of AIH induced phrenic motor plasticity (BDNF, HTR2A, TPH2, MAOA, NTRK2) and neuronal plasticity (apolipoprotein E, APOE) were tested. Variations in AIHH induced plasticity with age and sex were also analyzed. Additional experiments in humanized (h)ApoE knock-in rats were performed to test causality. AIHH-induced changes in diaphragm MEP amplitudes were lower in individuals heterozygous for APOE4 (i.e., APOE3/4) compared to individuals with other APOE genotypes (P = 0.048) and the other tested SNPs. Males exhibited a greater diaphragm MEP enhancement versus females, regardless of age (P = 0.004). Additionally, age was inversely related with change in P0.1 (P = 0.007). In hApoE4 knock-in rats, AIHH-induced phrenic motor plasticity was significantly lower than hApoE3 controls (P < 0.05). APOE4 genotype, sex, and age are important biological determinants of AIHH-induced respiratory motor plasticity in healthy adults. AIH is a novel rehabilitation strategy to induce functional recovery of respiratory and non-respiratory motor systems in people with chronic spinal cord injury and/or neurodegenerative disease. Figure 5 Since most AIH trials report considerable inter-individual variability in AIH outcomes, we investigated factors that potentially undermine the response to an optimized AIH protocol, AIHH, in healthy humans. We demonstrate that genetics (particularly the lipid transporter, APOE), age and sex are important biological determinants of AIHH-induced respiratory motor plasticity.

The effectiveness of the respiratory muscles in children with oncohematological diseases after hematopoietic stem cell transplantation

The article analyzes the effectiveness of the respiratory muscles by measuring inspiratory mouth occlusion pressure at 0.1 seconds during quiet breathing (P0.1) and maximum voluntary ventilation maneuver (P0.1 max ) in children with acute leukemia and acquired idiopathic aplastic anemia after allogeneic hematopoietic stem cell transplantation (HSCT). We carried out a comparative analysis of the Р0.1 and Р0.1 max values measured before HSCТ and on days +30, +90, +180 and +360. In a group of patients with acquired idiopathic aplastic anemia, we revealed a significant decrease in these values starting from day +30, followed by a recovery to baseline values by one year of follow-up. In children with acute leukemia, effectiveness of the respiratory muscles was increased after 360 days of transplantation as a result of the aggravation of impaired ventilation. This method for measuring airway occlusion pressure can be used in a comprehensive assessment of the functional state of the respiratory system for the timely diagnosis of pulmonary complications after HSCT. The study was approved by the Independent Ethics Committee and the Scientific Council of the Dmitry Rogachev National Medical Research Center of Pediatric Hematology, Oncology and Immunology of Ministry of Healthcare of the Russian Federation.

Respiratory phenotypes in ALS as determined by respiratory questions of the ALSFRS-R and their relation to respiratory tests.

Respiratory insufficiency and its complications are the main cause of death in amyotrophic lateral sclerosis (ALS). Respiratory symptoms are scored in questions Q10 (dyspnoea) and Q11 (orthopnoea) of the revised ALS functional rating scale (ALSFRS-R). The association of respiratory test alterations with respiratory symptoms is unclear. Patients with ALS and progressive muscular atrophy were included. We recorded retrospectively demographic data, ALSFRS-R, forced vital capacity (FVC), maximal inspiratory (MIP) and expiratory (MEP) pressures, mouth occlusion pressure at 100ms (P0.1), nocturnal oximetry (SpO2 mean), arterial blood gases, phrenic nerve amplitude (PhrenAmpl). Three groups were categorized: G1- normal Q10 and Q11; G2- abnormal Q10; G3- abnormal Q10 and Q11 or only abnormal Q11. A binary logistic regression model explored independent predictors. We included 276 patients (153 men, onset-age 62.6±11.0yrs, disease duration 13.0±9.6mo, spinal-onset 182) with mean survival 40.1±26.0mo. Gender, onset-region and disease duration were similar in G1 (n=149), G2 (n=78) and G3 (n=49). Time to NIV was shorter in G3 (p<0.001), but survival was similar. ALSFRS-R subscores were significantly different (G1>G2>G3, p<0.001), except for lower limb subscore (p=0.077). G2 and G3 patients were older than G1 (p<0.001), had lower FVC, MIP, MEP, PhrenAmpl and SpO2 mean. Independent predictors for G2 were MIP and SpO2 mean; for G3 was only PhrenAmpl. These three distinct ALS phenotypic respiratory categories represent progressive stages of ventilatory dysfunction, supporting ALSFRS-R clinical relevance. Orthopnea is a severe symptom that should prompt NIV, being phrenic nerve response an independent predictor. Early NIV promotes similar survival for G2 and G3.

Acute intermittent hypercapnic-hypoxia elicits central neural respiratory motor plasticity in humans.

Acute intermittent hypoxia (AIH) elicits long-term facilitation (LTF) of respiration. Although LTF is observed when CO2 is elevated during AIH in awake humans, the influence of CO2 on corticospinal respiratory motor plasticity is unknown. Thus, we tested the hypotheses that acute intermittent hypercapnic-hypoxia (AIHH): (1) enhances cortico-phrenic neurotransmission (reflecting volitional respiratory control); and (2) elicits ventilatory LTF (reflecting automatic respiratory control). Eighteen healthy adults completed four study visits. Day 1 consisted of anthropometry and pulmonary function testing. On Days 2, 3 and 4, in a balanced alternating sequence, participants received: AIHH, poikilocapnic AIH, and normocapnic-normoxia (Sham). Protocols consisted of 15, 60s exposures with 90s normoxic intervals. Transcranial (TMS) and cervical (CMS) magnetic stimulation were used to induce diaphragmatic motor-evoked potentials and compound muscle action potentials, respectively. Respiratory drive was assessed via mouth occlusion pressure (P0.1 ), and minute ventilation measured at rest. Dependent variables were assessed at baseline and 30-60min after exposures. Increases in TMS-evoked diaphragm potential amplitudes were observed following AIHH vs. Sham (+28±41%, P=0.003), but not after AIH. No changes were observed in CMS-evoked diaphragm potential amplitudes. Mouth occlusion pressure also increased after AIHH (+21±34%, P=0.033), but not after AIH. Ventilatory LTF was not observed after any treatment. We demonstrate that AIHH elicits central neural mechanisms of respiratory motor plasticity and increases resting respiratory drive in awake humans. These findings may have important implications for neurorehabilitation after spinal cord injury and other neuromuscular disorders compromising breathing. KEY POINTS: The occurrence of respiratory long-term facilitation following acute exposure to intermittent hypoxia is believed to be dependent upon CO2 regulation - mechanisms governing the critical role of CO2 have seldom been explored. We tested the hypothesis that acute intermittent hypercapnic-hypoxia (AIHH) enhances cortico-phrenic neurotransmission in awake healthy humans. The amplitude of diaphragmatic motor-evoked potentials induced by transcranial magnetic stimulation was increased after AIHH, but not the amplitude of compound muscle action potentials evoked by cervical magnetic stimulation. Mouth occlusion pressure (P0.1 , an indicator of neural respiratory drive) was also increased after AIHH, but not tidal volume or minute ventilation. Thus, moderate AIHH elicits central neural mechanisms of respiratory motor plasticity, without measurable ventilatory long-term facilitation in awake humans.

Respiratory Muscle Function Tests and Diaphragm Ultrasound Predict Nocturnal Hypoventilation in Slowly Progressive Myopathies.

Introduction: In slowly progressive myopathies, diaphragm weakness early manifests through sleep-related hypoventilation as reflected by nocturnal hypercapnia. This study investigated whether daytime tests of respiratory muscle function and diaphragm ultrasound predict hypercapnia during sleep.Methods: Twenty-seven patients with genetic myopathies (myotonic dystrophy type 1 and 2, late-onset Pompe disease, facioscapulohumeral dystrophy; 48 ± 11 years) underwent overnight transcutaneous capnometry, spirometry, measurement of mouth occlusion pressures, and diaphragm ultrasound.Results: Sixteen out of 27 patients showed nocturnal hypercapnia (peak ptcCO2 ≥ 50 mmHg for ≥ 30 min or increase in ptcCO2 by 10 mmHg or more from the baseline value). In these patients, forced vital capacity (FVC; % predicted) and maximum inspiratory pressure (MIP; % of lower limit or normal or LLN) were significantly reduced compared to normocapnic individuals. Nocturnal hypercapnia was predicted by reduction in FVC of <60% [sensitivity, 1.0; area under the curve (AUC), 0.82] and MIP (%LLN) <120% (sensitivity, 0.83; AUC, 0.84), the latter reflecting that in patients with neuromuscular disease, pretest likelihood of abnormality is per se higher than in healthy subjects. Diaphragm excursion velocity during a sniff maneuver excluded nocturnal hypercapnia with high sensitivity (0.90) using a cutoff of 8.0 cm/s.Conclusion: In slowly progressive myopathies, nocturnal hypercapnia is predicted by FVC <60% or MIP <120% (LLN). As a novelty, nocturnal hypercapnia can be excluded with acceptable sensitivity by diaphragm excursion velocity >8.0 cm/s on diaphragm ultrasound.

Single-session effects of acute intermittent hypoxia on breathing function after human spinal cord injury

After spinal cord injury (SCI) respiratory complications are a leading cause of morbidity and mortality. Acute intermittent hypoxia (AIH) triggers spinal respiratory motor plasticity in rodent models, and repetitive AIH may have the potential to restore breathing capacity in those with SCI. As an initial approach to provide proof of principle for such effects, we tested single-session AIH effects on breathing function in adults with chronic SCI. 17 adults (13 males; 34.1 ± 14.5 years old; 13 motor complete SCI; >6 months post injury) completed two randomly ordered sessions, AIH versus sham. AIH consisted of 15, 1-min episodes (hypoxia: 10.3% O2; sham: 21% O2) interspersed with room air breathing (1.5 min, 21% oxygen); no attempt was made to regulate arterial CO2 levels. Blood oxygen saturation (SpO2), maximal inspiratory and expiratory pressures (MIP; MEP), forced vital capacity (FVC), and mouth occlusion pressure within 0.1 s (P0.1) were assessed. Outcomes were compared using nonparametric Wilcoxon's tests, or a 2 × 2 ANOVA. Baseline SpO2 was 97.2 ± 1.3% and was unchanged during sham experiments. During hypoxic episodes, SpO2 decreased to 84.7 ± 0.9%, and returned to baseline levels during normoxic intervals. Outcomes were unchanged from baseline post-sham. Greater increases in MIP were evident post AIH vs. sham (median values; +10.8 cmH2O vs. -2.6 cmH2O respectively, 95% confidence interval (−18.7) – (−4.3), p = .006) with a moderate Cohen's effect size (0.68). P0.1, MEP and FVC did not change post-AIH. A single AIH session increased maximal inspiratory pressure generation, but not other breathing functions in adults with SCI. Reasons may include greater spared innervation to inspiratory versus expiratory muscles or differences in the capacity for AIH-induced plasticity in inspiratory motor neuron pools. Based on our findings, the therapeutic potential of AIH on breathing capacity in people with SCI warrants further investigation.

CO 2 Effects on Intermittent Hypoxia‐Induced Respiratory Motor Plasticity in Humans: In Progress Study

Intermittent hypoxia (IH) elicits respiratory motor plasticity (known as ventilatory long-term facilitation [LTF]) in humans and other mammals. However, awake humans exhibit ventilatory LTF only when CO2 levels are raised slightly above eupneic levels in a sustained or intermittent fashion during the IH protocol. In this ongoing study, we seek to determine the effect of CO2 on IH-induced respiratory motor plasticity by examining multiple, distinct mechanisms contributing to the ventilatory response during and following acute intermittent hypercapnic hypoxia (IHH). We hypothesized that IHH elicits a prolonged increase in cortico-diaphragmatic conduction, resting neural drive to breathe, and respiratory motor output versus poikilocapnic IH and a normoxic, normocapnic control (CTRL). Five healthy young adults (age = 32 ± 5 years; 3 female) completed four study visits. Day 1 consisted of general subject characterization. On Days 2, 3 and 4 (separated by ≥72 h), subjects were randomly assigned to receive either: IHH (PETO2 = 55 ± 4 Torr, PETCO2 = 44 ± 3 Torr), IH (PETO2 = 55 ± 3 Torr, PETCO2 = 37 ± 2 Torr), or CTRL (PETO2 = 107 ± 3 Torr, PETCO2 = 36 ± 2 Torr). Protocols consisted of 15 episodes of 60 s exposure with 90 s breathing ambient room air. Cardiovascular responses (heart rate, blood pressure and oxygen saturation) were monitored throughout. Cortico-diaphragmatic conduction was quantified by recording motor evoked potentials (MEPs) using transcranial magnetic stimulation and surface EMG electrodes. Resting neural drive to breathe was assessed using the mouth occlusion pressure technique (i.e. P0.1). Respiratory motor output was measured as minute ventilation () during resting isocapnic conditions (PETCO2 maintained within 1 mmHg of baseline) and adjusted based on the rate of metabolic CO2 production (/). Dependent variables were assessed at baseline, and 30-60 min post. Following IHH, IH and CTRL, the mean change in MEP amplitude was +34 ± 48%, +9 ± 21%, and +2 ± 22%; the mean change in P0.1 was +26 ± 17%, +15 ± 16%, and +7 ± 16%; and the mean change in was +0.3 ± 1.0 L·min-1, +0.3 ± 1.1 L·min-1, and +0.3 ± 0.8 L·min-1. When adjusted for , the mean change in / was -0.5 ± 1.0, +0.4 ± 1.8, and -0.2 ± 1.1. Based on these preliminary data in 5 subjects, we suggest that IHH elicits greater increases in cortico-diaphragmatic conduction and resting neural drive to breathe vs. poikilocapnic IH and CTRL. Conversely, our IHH protocol does not elicit ventilatory LTF. We reason that measures such as MEP amplitude and P0.1 are less sensitive to behavioral influences vs. , and may provide unique insights into mechanisms of IH-induced respiratory motor plasticity in awake healthy humans.

Heart Failure Results in Inspiratory Muscle Dysfunction Irrespective of Left Ventricular Ejection Fraction

Background: Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) results from both cardiac dysfunction and skeletal muscle weakness. Respiratory muscle dysfunction with restrictive ventilation disorder may be present irrespective of left ventricular ejection fraction and might be mediated by circulating pro-inflammatory cytokines. Objective: To determine lung and respiratory muscle function in patients with HFrEF/HFpEF and to determine its associations with exercise intolerance and markers of systemic inflammation. Methods: Adult patients with HFrEF (n = 22, 19 male, 61 ± 14 years) and HFpEF (n = 8, 7 male, 68 ± 8 years) and 19 matched healthy control subjects underwent spirometry, measurement of maximum mouth occlusion pressures, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. New York Heart Association (NYHA) class and 6-min walking distance (6MWD) were used to quantify exercise intolerance. Levels of circulating interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using ELISAs. Results: Compared with controls, both patient groups showed lower forced vital capacity (FVC) (p < 0.05), maximum inspiratory pressure (PI_max), maximum expiratory pressure (PE_max) (p < 0.05), diaphragm thickening ratio (p = 0.01), and diaphragm strength (twitch transdiaphragmatic pressure in response to supramaximal cervical magnetic phrenic nerve stimulation) (p = 0.01). In patients with HFrEF, NYHA class and 6MWD were both inversely correlated with FVC, PI_max, and PE_max. In those with HFpEF, there was an inverse correlation between amino terminal pro B-type natriuretic peptide levels and FVC (r = −0.77, p = 0.04). In all HF patients, IL-6 and TNF-α were statistically related to FVC. Conclusions: Irrespective of left ventricular ejection fraction, HF is associated with respiratory muscle dysfunction, which is associated with increased levels of circulating IL-6 and TNF-α.

Mouth occlusion pressure at 100ms (P0.1) as a respiratory biomarker in amyotrophic lateral sclerosis

Introduction Airway pressure in the first 100ms of an occluded inspiration (P0.1) evaluates the respiratory center activity, increasing in the presence of respiratory muscle weakness. It is uncertain if its activity can compensate for respiratory muscles weakness in amyotrophic lateral sclerosis (ALS). Methods: Consecutive ALS patients with P0.1 evaluated at first visit were included. Depending on P0.1 percentile, patients were divided in three groups: G1 (<25th percentile); G2 (25th–74th percentiles); G3 (≥75th percentile); two subgroups were further considered: SG0 (<10th percentile); SG1 (>90th percentile). Body mass index (BMI), functional ALS rating scale and its subscores, respiratory function tests, including forced vital capacity, maximal inspiratory (MIP) and expiratory pressures, percentage of P0.1 (%P0.1), blood gas analyses, phrenic nerve motor amplitude (MeanPhrenAmpl) were compared. P0.1/MIP and %P0.1 predictors were explored by linear and multinomial logistic regression analyses. p < 0.05 was considered as significant. Results: From the 497 patients included, 124 were in G1 and G3 each, 249 in G2, 49 in SG0 and SG1 each. G1 included more men, with higher BMI (p < 0.001). G3 had older women, with predominant bulbar phenotype (p < 0.001). Lower respiratory function (p < 0.05) was present in both groups. SG0 (%P0.1 < 51.73%, P0.1/MIP = 1.48 ± 1.02) had more spinal-onset men (p < 0.001) with lower MeanPhrenAmpl (p < 0.004). SG1 (P0.1 > 147.12, P0.1/MIP = 7.92 ± 4.62) predominantly included older patients (p = 0.033), women (p = 0.012), with lower MeanPhrenAmpl (p = 0.039). Discussion: ALS patients with respiratory failure can show high or low P01 values, related to phenotype. Possible central drive reactivity and exhaustion, and the role of respiratory-metabolic-renal buffering system should be further addressed.

Inspiratory muscle dysfunction and restrictive lung function impairment in congenital heart disease: Association with immune inflammatory response and exercise intolerance

BackgroundIn adult patients with congenital heart disease (ACHD), both underlying disease and lung restriction contribute to exercise intolerance. In ACHD the yet incompletely understood mechanism underlying restricted ventilation may be inspiratory muscle weakness. Therefore, this study comprehensively evaluated inspiratory muscle function in ACHD and associations with systemic inflammation and the clinical severity of exercise intolerance. Methods30 ACHD patients (21 men, 35 ± 12 years) and 30 healthy controls matched for age, gender and body mass index underwent spirometry, measurement of mouth occlusion pressures, and diaphragm ultrasound. Six-minute walking distance (6MWD) and New York Heart Association functional class were used to quantify exercise intolerance. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) levels were measured using enzyme-linked immunosorbent assays. ResultsACHD patients showed lower forced vital capacity (FVC), and maximum inspiratory (PImax) and expiratory (PEmax) pressures compared with controls (all p < 0.05). On ultrasound, ACHD patients showed a lower diaphragm thickening ratio (2.3 ± 0.5 vs. 2.8 ± 0.9, p < 0.01) and lower diaphragm excursion velocity during a voluntary sniff maneuver (5.7 ± 2.2 vs. 7.6 ± 2.0 cm/s, p < 0.01). Respiratory parameters, such as FVC (r = 0.53; p < 0.01) and PImax (r = 0.43; p = 0.02), correlated with 6MWD. Furthermore, amino terminal pro B-type natriuretic peptide levels were inversely correlated with FVC (r = −0.54; p < 0.01). Circulating pro-inflammatory cytokines were markedly increased, and IL-6 was correlated with 6MWD, dyspnea, and biomarkers of heart, lung and inspiratory muscle function (all p < 0.05). ConclusionsOur findings show that diaphragm dysfunction is present in ACHD and relates to restrictive ventilation disorder and exercise intolerance, possibly mediated by increased IL-6 levels.

Respiratory Muscle and Lung Function in Lung Allograft Recipients: Association with Exercise Intolerance

Background: In lung transplant recipients (LTRs), restrictive ventilation disorder may be present due to respiratory muscle dysfunction that may reduce exercise capacity. This might be mediated by pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Objective: We investigated lung respiratory muscle function as well as circulating pro-inflammatory cytokines and exercise capacity in LTRs. Methods: Fifteen LTRs (6 female, age 56 ± 14 years, 63 ± 45 months post-transplantation) and 15 healthy controls matched for age, sex, and body mass index underwent spirometry, measurement of mouth occlusion pressures, diaphragm ultrasound, and recording of twitch transdiaphragmatic (twPdi) and gastric pressures (twPgas) following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. Exercise capacity was quantified using the 6-min walking distance (6MWD). Plasma IL-6 and TNF-α were measured using enzyme-linked immunosorbent assays. Results: Compared with controls, patients had lower values for forced vital capacity (FVC; 81 ± 30 vs.109 ± 18% predicted, p = 0.01), maximum expiratory pressure (100 ± 21 vs.127 ± 17 cm H₂O, p = 0.04), diaphragm thickening ratio (2.2 ± 0.4 vs. 3.0 ± 1.1, p = 0.01), and twPdi (10.4 ± 3.5 vs. 17.6 ± 6.7 cm H₂O, p = 0.01). In LTRs, elevation of TNF-α was related to lung function (13 ± 3 vs. 11 ± 2 pg/mL in patients with FVC ≤80 vs. >80% predicted; p < 0.05), and lung function (forced expiratory volume after 1 s) was closely associated with diaphragm thickening ratio (r = 0.81; p < 0.01) and 6MWD (r = 0.63; p = 0.02). Conclusion: There is marked restrictive ventilation disorder and respiratory muscle weakness in LTRs, especially inspiratory muscle weakness with diaphragm dysfunction. Lung function impairment relates to elevated levels of circulating TNF-α and diaphragm dysfunction and is associated with exercise intolerance.

The Relationship Between Airway Occlusion Pressure and Severity of liver Cirrhosis in Candidates for Liver Transplantation.

BACKGROUND End-stage cirrhosis is an irreversible condition, and liver transplantation is the only treatment option in for the affected patients. Respiratory problems and abnormal breathing are common findings among these patients. In this study, for the first time, we examined the relationship between the severity of liver cirrhosis and respiratory drive measured by mouth occlusion pressure (P0.1). METHODS This was a cross-sectional study conducted on 50 candidates for liver transplantation who were referred to the pulmonary clinic of Imam Khomeini Hospital for pre-operative pulmonary evaluations. Arterial blood gas analysis (ABG), pulmonary function tests, and measurement of P0.1 were performed for all patients. The severity of liver disease was assessed using the Model for End-Stage Liver Disease (MELD) score. RESULTS The median P0.1 was 5 cm H2 O. P0.1 was negatively associated with PaCO2 (r = -0.466, p = 0.001) and HCO3 - (r = -0.384, p = 0.007), and was positively correlated with forced expiratory volume at 1s (FEV1 )/ forced vital capacity (FVC) (r = 0.282, p = 0.047). There was a strong correlation between P0.1 and MELD score (r = 0.750, p < 0.001). Backward multivariate linear regression revealed that a higher MELD score and lower PaCO2 were associated with increased P0.1. CONCLUSION High levels of P0.1 and strong direct correlation between P0.1 and MELD score observed in the present study are suggestive of the presence of abnormal increased respiratory drive in candidates for liver transplantation, which is closely related to their disease severity.

Interval exercise induces milder respiratory responses compared to continuous exercise

ABSTRACTThe purpose of this study was to explore the respiratory response of acute interval and continuous exercise (CE) of low and high intensity. Fourteen recreational athletes (7 men and 7 women; VO2max = 35.7 ± 6.1 mlkg–1min–1) performed a bout of continuous and a bout of interval exercise (IE) both consisted of 5-min cycling at low intensity [80% of the power output (W) of the predetermined gas exchange threshold (GET) (80%WGET)] and 5-min cycling at high intensity {WGET plus the work rate corresponding to 50% of the difference between peak power output (PPO) at oxygen uptake (VO2max) test and the WGET [WGET + 0.50 Δ(PPO – WGET)]}. CE compared to IE induced significant higher heart rate and ventilation as well as significant higher levels of mouth occlusion pressure for 0.1 s (P0.1) (P < 0.05) during low and high intensities. Our results indicate that CE stimulates respiration more than IE when the exercise is performed at the same relative intensity.

Effect of continuous positive airway pressure on respiratory drive in patients with obstructive sleep apnea

ObjectivePatients with obstructive sleep apnea (OSA) have an altered control of breathing during wakefulness. Thus far, whether and how treatment with continuous positive airway pressure (CPAP) may restore these abnormalities has been poorly understood. The aim of this study was to investigate the long-term effects of CPAP on the breathing pattern, ventilatory drive (VDr), and chemoreceptor sensitivity in OSA patients. Patients and methodsThis was a prospective, observational study, carried out in an academic sleep outpatient clinic. A total of 62 patients with OSA (mean age [SD], 51 [11] years) underwent polysomnography (PSG), breathing pattern assessment, mouth occlusion pressure, ventilatory response to hypoxemia (Ve/SaO2), and hypercapnia (Ve/PETCO2) before and after CPAP titration and during 12-month follow-up. A total of 48 age-matched healthy subjects served as controls. Patients with good (≥6 h/night) and poor (<6 h/night) compliance with CPAP were also compared. ResultsAt baseline, VDr as well as thoracic and inspiratory impedances were greater in patients with OSA compared with controls and were reduced by CPAP treatment, starting from the night of titration (P < 0.01), especially in patients with good compliance with CPAP. Baseline Ve/SaO2 was higher in OSA patients (P < 0.05) and was progressively normalized during CPAP treatment (P < 0.001). The pathophysiological changes were mainly due to a reduction in tidal volume. The remaining breathing pattern parameters were unaltered by CPAP treatment and were similar between groups. ConclusionIn OSA patients, the mechanics of breathing are inefficient because of an imbalance of the VDr. Regular CPAP treatment improves the efficiency of the respiratory system and normalizes the hypoxemic stimulus.

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.

The pulmonary effects of exspiratory muscle training in patients with heart failure of ischemic ethiology

Aim: To objectify the effect of at-home-performed expiratory muscle training (EMT) with a Threshold PEP® trainer on functional lung capacity, mouth occlusion pressures, chest expansion, dyspnea and fatigue in patients with systolic heart failure.

Effect of Aerobic Exercise Training on Ventilatory Efficiency and Respiratory Drive in Obese Subjects.

Obese patients show a decline in exercise capacity and diverse degrees of dyspnea in association with mechanical abnormalities, increased ventilatory requirements secondary to the increased metabolic load, and a greater work of breathing. Consequently, obese patients may be particularly predisposed to the development of respiratory muscle fatigue during exercise. The aim of this study was to assess inspiratory muscle performance during incremental exercise in 19 obese male subjects (body mass index 41 ± 6 kg/m2) after aerobic exercise training using the noninvasive, inspiratory muscle tension-time index (TT0.1). Measurements performed included anthropometric parameters, lung function assessed by spirometry, rate of perceived breathlessness with the modified Borg dyspnea scale (0-10), breathing pattern, maximal exercise capacity, and inspiratory muscle performance with a breath-by-breath automated exercise metabolic system during an incremental exercise test. TT0.1 was calculated using the equation, TT0.1 = P0.1/PImax × TI/Ttot (where P0.1 represents mouth occlusion pressure, PImax is maximal inspiratory pressure, and TI/Ttot is the duty cycle). At rest, there was no statistically significant difference for spirometric parameters and cardiorespiratory parameters between pre- and post-training. At maximal exercise, the minute ventilation, the rate of exchange ratio, the rate of perceived breathlessness, and the respiratory muscle performance parameters were not significantly different pre- and post-training; in contrast, tidal volume (P = .037, effect size = 1.51), breathing frequency (P = .049, effect size = 0.97), power output (P = .048, effect size = 0.79), peak oxygen uptake (P = .02, effect size = 0.92) were significantly higher after training. At comparable work load, training induces lower minute ventilation, mouth occlusion pressure, ratio of occlusion pressure to maximal inspiratory pressure, TT0.1, and rate of perceived breathlessness. Aerobic exercise at ventilatory threshold can induce significant improvement in respiratory muscle strength, maximal exercise capacity, and inspiratory muscle performance and decreased dyspnea perception in obese subjects.

Positive airway pressure therapy in heart failure patients: Long-term effects on lung function

PurposeThe prevalence of sleep-disordered breathing (SDB) in patients with heart failure (HF) is high. Positive airway pressure (PAP) is first-choice therapy, but recent data indicates that PAP therapy may increase mortality in HF patients with reduced ejection fraction (HF-REF) and predominant central sleep apnea (CSA). This study investigated long-term effects of PAP therapy on pulmonary function, including respiratory muscle strength. All patients underwent multichannel cardiorespiratory polysomnography (PSG) and comprehensive lung function testing at baseline and follow-up (mean 588±43days). Results350 patients (mean age 68±10.7years, 88% male) were included, inspiratory vital capacity, 3.3±0.9 vs 3.2±0.8L; forced expiratory volume in 1s, 2.5±0.7 vs 2.4±0.7L; lung diffusion capacity, 6.2±1.9 vs 5.9±1.8mmol/min/kPa; correction for hemoglobin, 1.1±0.02 vs 1.1±0.3mmol/min/kPa/L; and mouth occlusion pressure, 0.42±0.11 vs 0.4±0.12kPa. ConclusionsPAP therapy had no negative nor positive impact on lung function, including respiratory muscle strength, in stable HF-REF patients with SDB, and is therefore safe from a respiratory perspective.

Daytime hypercapnia in patients with obstructive sleep apnea hypopnea syndrome in Han and Uygur nationality

Objective: To evaluate the incidence and factors related to daytime hypercapnia in Han and Uygur patients with obstructive sleep apnea hypopnea syndrome (OSAHS). Methods: There were 221 patients with OSAHS (include 179 Han patients and 42 Uygur patients) in Sleep Center of Department of Respiratory and Critical Care Medicine of Karamay Central Hospital from 2015, Jan to Dec. All the patients underwent polysomnography (PSG), nocturnal oximetry, daytime blood gas analysis, pulmonary function test and Mouth occlusion pressure (P0.1) results were recorded. The features of hypercapnia was analyzed for patients with OSAHS, and linear regression analysis was used to evaluate the arterial carbon dioxide partial pressure (PaCO2) levels and related factors. Results: Daytime hypercapnia occurred in 16.7% (37/221) of the 221 patients with OSAHS. Compare with no hypercapnia groups, the body mass [(31.6±5.6) vs (27.9±1.7) kg/m2], sleep apnea index (AHI) [(40.9±26.3) vs (32.2±20.1) times/h], the percentage of time spent at oxygen saturation below 90 (SIT90) [(38.6±31.9)% vs (23.9±23.6)%], P0.1 [(3.08±2.86) vs (2.03±1.20) mmHg, 1 mmHg=0.133 kPa] were higher in hypercapnia groups, but the mean nocturnal arterial oxygen saturation (MSaO2) [(86.0±15.5)% vs (92.0±3.0)%], the nadir arterial oxygen saturation (LSaO2) [(68.9±13.0)% vs (75.3±9.9)%] and arterial partial pressure of oxygen (PaO2) [(74.5±23.0) vs (86.1±14.8) were lower in hypercapnia groups (all P<0.05). Compare with Han patients with OSAHS, MSaO2 and LSaO2 was lower, PaCO2 and P0.1 was higher in Uygur patients (all P<0.05). Conclusions: Uygur OSAHS patients with hypercapnia have a higher daytime PaCO2 than the Han counterparts. BMI, AHI, MSaO2, P0.1 level are all related with daytime hypercapnia in OSAHS.