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BACKGROUND: Maximal respiratory pressure is used to assess the inspiratory and expiratory muscles strength by using maximal inspiratory pressure (PImax) and maximal expiratory pressure (PEmax). This study aimed to summarize and evaluate the reliability and validity of maximal respiratory pressure measurements. METHODS: This systematic review followed the Consensus-based Standards for the Selection of Health Measurement Instruments (COSMIN) recommendations and was reported by using the PRISMA checklist. Studies published before March 2023 were searched in PubMed and EMBASE databases. RESULTS: A total of 642 studies were identified by using the online search strategy and manual search (602 and 40, respectively). Twenty-three studies were included. The level of evidence for test-retest reliability was moderate for PImax and PEmax (intraclass correlation coefficient > 0.70 for both), inter-rater reliability was low for PImax and very low for PEmax (intraclass correlation coefficient > 0.70 for both), and the measurement error was very low for PImax and PEmax. In addition, concurrent validity presented a high level of evidence for PImax and PEmax (r > 0.80). CONCLUSIONS: Only concurrent validity of maximal respiratory pressure measured with the manometers evaluated in this review presented a high level of evidence. The quality of clinical studies by using maximal respiratory pressure would be improved if more high-quality studies on measurement properties, by following well established guidelines and the COSMIN initiative, were available.

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INTRODUCTION: Deficits in respiratory function of patients with Parkinson's disease contribute to aspiration pneumonia, one of the main causes of mortality in this population. The aim of this study was to evaluate the effects of functional training, bicycle exercise, and exergaming on respiratory function of elderly with Parkinson's disease. METHODS: A randomized clinical trial with single blinding was conducted in a public reference outpatient clinic for the elderly. The participants were randomly assigned to three groups. Group 1 was submitted to functional training (n = 18); group 2 performed bicycle exercise (n = 20), and group 3 trained with Kinect Adventures exergames (n = 20). The sessions performed lasted 8 weeks with a frequency of three 50-min sessions per week. The primary outcome was the forced expiratory volume in the first second; and the secondary outcomes were forced vital capacity, peak expiratory flow, and maximum inspiratory and expiratory pressures. RESULTS: The interventions performed did not improve the forced expiratory volume in the first second, forced vital capacity, and peak expiratory flow. However, group 2 improved (p = 0.03) maximum expiratory pressure (from 65.5cmH2O to 73.1cmH2O) (effect size 0.47), and group 3 increased (p = 0.03) maximum inspiratory pressure (from -61.3cmH2O to -71.6cmH2O) (effect size 0.53). CONCLUSIONS: No effect was found on lung volume, forced respiratory flow and capacity of the participants with Parkinson's disease submitted to three different modalities of motor training. However, bicycle exercise and exergaming have improved expiratory and inspiratory muscle strength, respectively. NCT02622737.

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AIMS: Stimulation of peripheral chemoreceptors, as during hypoxia, increases breathing and respiratory-related sympathetic bursting. Activation of catecholaminergic C1 neurones induces sympathoexcitation, while its ablation reduces the chemoreflex sympathoexcitatory response. However, no study has determined the respiratory phase(s) in which the pre-sympathetic C1 neurones are recruited by peripheral chemoreceptor and whether C1 neurone activation affects all phases of respiratory modulation of sympathetic activity. We addressed these unknowns by testing the hypothesis that peripheral chemoreceptor activation excites pre-sympathetic C1 neurones during inspiration and expiration. METHODS: Using the in situ preparation of rat, we made intracellular recordings from baroreceptive pre-sympathetic C1 neurones during peripheral chemoreflex stimulation. We optogenetically activated C1 neurones selectively and compared any respiratory-phase-related increases in sympathetic activity with that which occurs following stimulation of the peripheral chemoreflex. RESULTS: Activation of peripheral chemoreceptors using cytotoxic hypoxia (potassium cyanide) increased the firing frequency of C1 neurones and both the frequency and amplitude of their excitatory post-synaptic currents during the phase of expiration only. In contrast, optogenetic stimulation of C1 neurones activates inspiratory neurones, which secondarily inhibit expiratory neurones, but produced comparable increases in sympathetic activity across all phases of respiration. CONCLUSION: Our data reveal that the peripheral chemoreceptor-mediated expiratory-related sympathoexcitation is mediated through excitation of expiratory neurones antecedent to C1 pre-sympathetic neurones; these may be found in the Kölliker-Fuse nucleus. Despite peripheral chemoreceptor excitation of inspiratory neurones, these do not trigger C1 neurone-mediated increases in sympathetic activity. These studies provide compelling novel insights into the functional organization of respiratory-sympathetic neural networks.

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NEW FINDINGS: What is the central question of this study? Do mice submitted to sustained hypoxia present autonomic and respiratory changes similarly to rats? What is the main finding and its importance? Arterial pressure in the normal range, reduced baseline heart rate and tachypnoea were observed in behaving sustained hypoxia mice. Recordings in the in situ preparation of mice submitted to sustained hypoxia show an increase in cervical vagus nerve activity and a simultaneous reduction in thoracic sympathetic nerve activity correlated with changes in the respiratory cycle. Therefore, mice are an important model for studies on the modulation of sympathetic activity to the cardiovascular system and the vagus innervation of the upper airways due to changes in the respiratory network induced by sustained hypoxia. ABSTRACT: Short-term sustained hypoxia (SH) in rats induces sympathetic overactivity and hypertension due to changes in sympathetic-respiratory coupling. However, there are no consistent data about the effect of SH on mice due to the different protocols of hypoxia and difficulties associated with the handling of these rodents under different experimental conditions. In situ recordings of autonomic and respiratory nerves in SH mice have not been performed yet. Herein, we evaluated the effects of SH ( FiO2  = 0.1 for 24 h) on baseline mean arterial pressure (MAP), heart rate (HR), respiratory frequency (fR ) and responses to chemoreflex activation in behaving SH mice. A characterization of changes in cervical vagus (cVN), thoracic sympathetic (tSN), phrenic (PN) and abdominal (AbN) nerves in SH mice using the in situ working heart-brainstem preparation was also performed. SH mice presented normal MAP, significant reduction in baseline HR, increase in baseline fR , as well as increase in the magnitude of bradycardic response to chemoreflex activation. In in situ preparations, SH mice presented a reduction in PN discharge frequency, and increases in the time of expiration and incidence of late-expiratory bursts in AbN activity. Nerve recordings also indicated a significant increase in cVN activity and a significant reduction in tSN activity during expiration in SH mice. These findings make SH mice an important experimental model for better understanding how changes in the respiratory network may impact on the modulation of vagal control to the upper airways, as well as in the sympathetic activity to the cardiovascular system.

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NEW FINDINGS: What is the central question of this study? What is the carotid bodies' contribution to active inspiratory and expiratory response to exercise? What is the main finding and its importance? Removal of the carotid bodies reduced the active inspiratory and expiratory responses of diaphragm and abdominal internal oblique muscles, respectively, to high-intensity, but not to low-intensity, exercise in rats. Removal of the carotid bodies increased PaCO2 and decreased arterial pH in response to high-intensity exercise. The carotid bodies contribute to the inspiratory and expiratory adjustments to high-intensity exercise in rats. ABSTRACT: Exercise involves the interaction of several physiological processes, in which adjustments in pulmonary ventilation occur in response to increased O2 consumption, CO2 production and altered acid-base equilibrium. The peripheral chemoreceptors (carotid bodies; CBs) are sensitive to changes in the chemical composition of arterial blood, and their activation induces active inspiratory and expiratory responses. Herein, we tested the hypothesis that the CBs contribute to the active inspiratory and expiratory responses to exercise in rats. We performed electromyographic recordings of the diaphragm (DiaEMG ) and abdominal internal oblique (AbdEMG ) muscles in rats before and after bilateral removal of the CBs (CBX) during constant-load low-intensity and high-intensity progressive treadmill exercise. We also collected arterial blood samples for gaseous and pH analyses. Similar increases in DiaEMG frequency in both experimental conditions (before and after CBX) during low-intensity exercise were observed, without significant changes in the DiaEMG amplitude. During high-intensity exercise, lower responses of both DiaEMG frequency and DiaEMG amplitude were observed in rats after CBX. The AbdEMG phasic active expiratory response was not significant either before or after CBX during low-intensity exercise. However, CBX reduced the phasic active expiratory responses during high-intensity exercise. The blunted responses of inspiratory and expiratory adjustments to high-intensity exercise after CBX were associated with higher PaCO2 levels and lower arterial pH values. Our data show that in rats the CBs do not participate in the inspiratory and expiratory responses to low-intensity exercise, but are involved in the respiratory compensation against the metabolic acidosis induced by high-intensity exercise.

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The parafacial respiratory group (pFRG), located in the lateral aspect of the rostroventral lateral medulla, has been described as a conditional expiratory oscillator that emerges mainly in conditions of high metabolic challenges to increase breathing. The convergence of inhibitory and excitatory inputs to pFRG and the generation of active expiration may be more complex than previously thought. We hypothesized that the medullary raphe, a region that has long been described to be involved in breathing activity, is also responsible for the expiratory activity under hypercapnic condition. To test this hypothesis, we performed anatomical and physiological experiments in urethane-anesthetized adult male Wistar rats. Our data showed anatomical projections from serotonergic (5-HT-ergic) and GABAergic neurons of raphe magnus (RMg) and obscurus (ROb) to the pFRG region. Pharmacological inhibition of RMg or ROb with muscimol (60 pmol/30 nL) did not change the frequency or amplitude of diaphragm activity and did not generate active expiration. However, under hypercapnia (9-10% CO2), the inhibition of RMg or ROb increased the amplitude of abdominal activity, without changing the increased amplitude of diaphragm activity. Depletion of serotonergic neurons with saporin anti-SERT injections into ROb and RMg did not increase the amplitude of abdominal activity during hypercapnia. These results show that the presumably GABAergic neurons within the RMg and ROb may be the inhibitory source to modulate the activity of pFRG during hypercapnia condition.NEW & NOTEWORTHY Medullary raphe has been involved in the inspiratory response to central chemoreflex; however, these reports have never addressed the role of raphe neurons on active expiration induced by hypercapnia. Here, we showed that a subset of GABA cells within the medullary raphe directly project to the parafacial respiratory region, modulating active expiration under high levels of CO2.

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The purpose of this study was to evaluate the inspiratory and expiratory muscle strength of individuals affected by stroke and to compare it with the predicted values in the literature considering their corresponding age. Respiratory muscle strength was evaluated in 22 elderly people who had sequels of stroke, four with right hemiparesis, 16 with left hemiparesis and two with bilateral, of ages ranging from 34 to 82 years. The collected data were submitted to statistical analysis using a Mann-Whitney test to evaluate if there was a significant difference in the average data collected when compared with a mean of the predicted data in the literature. Fourteen men and eight women were evaluated, who obtained mean values of 71.85 cmH2O and 57.75 cmH2O, respectively, for a maximal inspiratory pressure (MIP), and when compared to the predicted values for men and women, 105.41 cmH2O (p-value 0.0019) and 80.57 cmH2O (p-value 0.00464) were significantly lower. For a maximal expiratory pressure (MEP), the mean value obtained for men was 62.28 cmH2O and 49.5 cmH2O for women, whereas the predicted values in the literature were 114.79 cmH2O (p-value < 0.0001) and 78, 46 cmH2O (p-value 0.0059), respectively. In the statistical analysis, it was possible to notice that the studied population did not reach the predicted age indexes and that there was a significant difference between the median columns. In conclusion, there is a weakness in the respiratory muscles of hemiparetic men and women due to stroke.

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Breathing results from the interaction of two distinct oscillators: the pre-Bötzinger Complex (preBötC), which drives inspiration; and the lateral parafacial region (pFRG), which drives active expiration. The pFRG is silent at rest and becomes rhythmically active during the stimulation of peripheral chemoreceptors, which also activates adrenergic C1 cells. We postulated that the C1 cells and the pFRG may constitute functionally distinct but interacting populations for controlling expiratory activity during hypoxia. We found in rats that: a) C1 neurons are activated by hypoxia and project to the pFRG region; b) active expiration elicited by hypoxia was blunted after blockade of ionotropic glutamatergic receptors at the level of the pFRG; and c) selective depletion of C1 neurons eliminated the active expiration elicited by hypoxia. These results suggest that C1 cells may regulate the respiratory cycle, including active expiration, under hypoxic conditions.

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OBJECTIVES: Using a method developed for this study, the objective was to perform a quantitative analysis of glottic aperture during the respiratory cycle in subjects suspected of having inducible laryngeal obstruction (ILO) and to compare results to healthy individuals. Correlations between glottic aperture and spirometric parameters were assessed. METHODS: Subjects with high clinical suspicion of ILO and atypical inspiratory findings in spirometry had the images of their laryngoscopy displayed alongside a respiratory flow chart and both were recorded simultaneously. This method allowed detailed analysis of the glottic aperture by measuring the angle of the anterior commissure during inspiration and expiration. Healthy volunteers who performed the same tests and agreed to provide data to this study were used as a control group. RESULTS: All 15 subjects with ILO and 16 healthy participants were evaluated successfully using the proposed method. Measures of the anterior commissure angle in the ILO versus control group were significantly different in all observed parameters and just three ILO subjects had an anterior commissure closure greater than 50% during the respiratory cycle. Inspired volume (FIF50 ) and mid-vital capacity ratio (FEF50 /FIF50 ) had a significant correlation with glottic aperture parameters when considering the evaluation of the subjects all together. CONCLUSION: The proposed method provided precise and quantitative analysis of glottic aperture during the respiratory cycle thus indicating that the usage of equipment that allows for such assessment should be encouraged. Also, the threshold of vocal cords closure accepted as indicative of ILO should be reconsidered, especially during the intercritical period of the disease. LEVEL OF EVIDENCE: 4 Laryngoscope, 130:E349-E356, 2020.

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NEW FINDINGS: What is the central question of this study? Does the parafacial respiratory group (pFRG), which mediates active expiration, recruit nasofacial and oral motoneurons to coordinate motor activities that engage muscles controlling airways in rats during active expiration. What is the main finding and its importance? Hypercapnia/acidosis or pFRG activation evoked active expiration and stimulated the motoneurons and nerves responsible for the control of nasofacial and oral airways patency simultaneously. Bilateral pFRG inhibition abolished active expiration and the simultaneous nasofacial and oral motor activities induced by hypercapnia/acidosis. The pFRG is more than a rhythmic oscillator for expiratory pump muscles: it also coordinates nasofacial and oral motor commands that engage muscles controlling airways. ABSTRACT: Active expiration is mediated by an expiratory oscillator located in the parafacial respiratory group (pFRG). Active expiration requires more than contracting expiratory muscles as multiple cranial nerves are recruited to stabilize the naso- and oropharyngeal airways. We tested the hypothesis that activation of the pFRG recruits facial and trigeminal motoneurons to coordinate nasofacial and oral motor activities that engage muscles controlling airways in rats during active expiration. Using a combination of electrophysiological and pharmacological approaches, we identified brainstem circuits that phase-lock active expiration, nasofacial and oral motor outputs in an in situ preparation of rat. We found that either high chemical drive (hypercapnia/acidosis) or unilateral excitation (glutamate microinjection) of the pFRG evoked active expiration and stimulated motoneurons (facial and trigeminal) and motor nerves responsible for the control of nasofacial (buccal and zygomatic branches of the facial nerve) and oral (mylohyoid nerve) motor outputs simultaneously. Bilateral pharmacological inhibition (GABAergic and glycinergic receptor activation) of the pFRG abolished active expiration and the simultaneous nasofacial and oral motor activities induced by hypercapnia/acidosis. We conclude that the pFRG provides the excitatory drive to phase-lock rhythmic nasofacial and oral motor circuits during active expiration in rats. Therefore, the pFRG is more than a rhythmic oscillator for expiratory pump muscles: it also coordinates nasofacial and oral motor commands that engage muscles controlling airways in rats during active expiration.

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OBJECTIVE: To evaluate the different components of the resistance of the respiratory system, respiratory muscle strength and to investigate the occurrence of expiratory flow limitation (EFL) in patients with morbid obesity (MO) when seated. METHODS: The sample was composed of MO (BMI≥40 kg/m2) and non-obese individuals (NO) with a BMI between 18 and 30 kg/m2. The protocol consisted of the anthropometric assessment and the following measures of respiratory function: spirometry, maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and impulse oscillometry. The group comparison was performed using T-test for unpaired samples. The correlations were evaluated by the Pearson test with a significance level of 5%. RESULTS: Fifty MO (age 40±10.4 years, 1.64±0.09 m, 138.8±33.6 kg and 50.7±8.9 kg/m2), and 30 NO (age 37.6±11.5 years, 1.67±0.09 m, 65.2±10.3 kg and 23.2±22 kg/m2) were evaluated. The MO showed higher values of total, peripheral, airways, tissue and central resistance when compared to the NO. No patient showed EFL. The waist circumference was associated with spirometric variables, MIP, and MEP. The waist-to-hip ratio was correlated to respiratory mechanics and spirometric variables, MIP, and MEP. CONCLUSION: Morbidly obese patients with no obstructive spirometric pattern show increased total, airway, peripheral, and tissue respiratory system resistance when compared to nonobese. These individuals, however, do not present with expiratory flow limitation and reduced respiratory muscles strength.

OBJETIVO: avaliar os diferentes componentes da resistência do sistema respiratório e a força muscular respiratória, bem como investigar a ocorrência de limitação de fluxo expiratório (LFE) de pacientes obesos mórbidos (OM) na posição sentada. MÉTODOS: a amostra foi composta de OM (IMC ≥ 40 kg/m2) e de indivíduos não obesos (NO) com IMC entre 18 e 30 kg/m2. O protocolo foi composto de: avaliação antropométrica e da função respiratória (espirometria, pressões inspiratória (PIM) e expiratória máximas (PEM) e oscilometria de impulso). Na comparação entre os grupos, foi utilizado o teste T para amostras não pareadas. As correlações foram avaliadas pelo teste de Pearson, e o nível de significância foi de 5%. RESULTADOS: Foram avaliados 50 OM (idade 40,0 ± 10,4 anos, 1,64 ± 0,09 m, 138,8 ± 33,6 kg e 50,7 ± 8,9 kg/m2), além de 30 NO (idade 37,6 ± 11,5 anos, 1,67 ± 0,09 m, 65,2 ± 10,3 kg e 23,2 ± 22 kg/m2). Os OM apresentaram maiores valores de resistência total, central, de vias aéreas, tecidual e periférica quando comparados aos NO. Nenhum paciente apresentou LFE. A circunferência abdominal se associou com variáveis espirométricas PIM e PEM. A relação cintura-quadril se correlacionou com variáveis de mecânica respiratória, além das espirométricas PIM e PEM. CONCLUSÕES: pacientes com obesidade mórbida e sem padrão espirométrico obstrutivo apresentam aumento nas resistências total, de vias aéreas, periférica e tecidual do sistema respiratório quando comparados a não obesos. Esses indivíduos, entretanto, não apresentam limitação de fluxo expiratório e redução da força muscular respiratória.

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BACKGROUND: Prolonged slow expiration (PSE) is a manual chest physical therapy technique routinely performed in clinical practice. However, the reliability and agreement of the technique have not been tested. OBJECTIVE: The objective of this study was to assess reliability and agreement between physical therapists during the application of PSE in infants with wheezing. DESIGN: This was a cross-sectional study. METHODS: Infants with a mean age of 59 weeks (SD = 26 weeks) were included in this study. Two physical therapists (physical therapist 1 and physical therapist 2) randomly performed 3 PSE sequences (A, B, and C). The expiratory reserve volume (ERV) was measured with a pneumotachograph connected to a face mask. ERV was used to evaluate the reproducibility of the technique between sequences and between physical therapist 1 and physical therapist 2. RESULTS: The mean ERV of the infants was 63 mL (SD = 21 mL). There was no statistically significant difference between the ERV values in the 3 sequences for physical therapist 1 (A: mean = 46.6 mL [SD = 17.8 mL]; B: mean = 45.7 mL [SD = 19.9 mL]; C: mean = 53.3 mL [SD = 26.3 mL]) and physical therapist 2 (A: mean = 43.5 mL [SD = 15.4 mL]; B: mean = 43.2 mL [SD = 18.3 mL]; C: mean = 44.8 mL [SD = 25.0 mL]). There was excellent reliability between the sequences for physical therapist 1 (ICC = 0.88 [95% CI = 0.63-0.95]) and physical therapist 2 (ICC = 0.82 [95% CI = 0.48-0.93]). Moderate agreement was observed between physical therapist 1 and physical therapist 2 (ICC = 0.67 [95% CI = 0.01-0.88]). According to Bland-Altman analysis, the mean difference between physical therapist 1 and physical therapist 2 was 4.1 mL (95% CI = -38.5 to 46.5 mL). LIMITATIONS: The data were collected in infants with wheezing who were not in crisis. This decreased lung mucus; however, it also reduced evaluation risks. CONCLUSIONS: PSE was a reproducible chest physical therapy technique between physical therapists.

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Active expiration (AE) is part of the breathing phase; it is conditional and occurs when we increase our metabolic demand, such as during hypercapnia, hypoxia, or exercise. The parafacial respiratory group (pFRG) is involved in AE. Data from the literature suggest that excitatory and the absence of inhibitory inputs to the pFRG are necessary to determine AE. However, the source of the inputs to the pFRG that trigger AE remains unclear. We show in adult urethane-anesthetized Wistar rats that the pharmacological inhibition of the medial aspect of the nucleus of the solitary tract (mNTS) or the rostral aspect of the pedunculopontine tegmental nucleus (rPPTg) is able to generate AE. In addition, direct inhibitory projection from the mNTS or indirect cholinergic projection from the rPPTg is able to contact pFRG to trigger AE. The inhibition of the mNTS or the rPPTg under conditions of high metabolic demand, such as hypercapnia (9-10% CO2), did not affect the AE. The present results suggest for the first time that inhibitory sources from the mNTS and a cholinergic pathway from the rPPTg, involving M2/M4 muscarinic receptors, could be important sources to modulate and sustain AE.

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NEW FINDINGS: What is the central question of this study? Chronic intermittent hypoxia (CIH) causes increased arterial pressure (AP), sympathetic overactivity and changes in expiratory modulation of sympathetic activity. However, changes in the short-term sleep-wake cycle pattern after CIH and their potential impact on cardiorespiratory parameters have not been reported previously. What is the main finding and its importance? Exposure to CIH for 10 days elevates AP in wakefulness and sleep but does not cause major changes in short-term sleep-wake cycle pattern. A higher incidence of muscular expiratory activity was observed in rats exposed to CIH only during wakefulness, indicating that active expiration is not required for the increase in AP in rats submitted to CIH. ABSTRACT: Chronic intermittent hypoxia (CIH) increases arterial pressure (AP) and changes sympathetic-respiratory coupling. However, the alterations in the sleep-wake cycle after CIH and their potential impact on cardiorespiratory parameters remain unknown. Here, we evaluated whether CIH-exposed rats present changes in their short-term sleep-wake cycle pattern and in cardiorespiratory parameters. Male Wistar rats (∼250 g) were divided into CIH and control groups. The CIH rats were exposed to 8 h day-1 of cycles of normoxia (fraction of inspired O2  = 0.208, 5 min) followed by hypoxia (fraction of inspired O2  = 0.06, 30-40 s) for 10 days. One day after CIH, electrocorticographic activity, cervical EMG, AP and heart rate were recorded for 3 h. Plethysmographic recordings were collected for 2 h. A subgroup of control and CIH rats also had the diaphragm and oblique abdominal muscle activities recorded. Chronic intermittent hypoxia did not alter the time for sleep onset, total time awake, durations of rapid eye movement (REM) and non-REM (NREM) sleep and number of REM episodes in the 3 h recordings. However, a significant increase in the duration of REM episodes was observed. The AP and heart rate were increased in all phases of the cycle in rats exposed to CIH. Respiratory frequency and ventilation were similar between groups in all phases, but tidal volume was increased during NREM and REM sleep in rats exposed to CIH. An increase in the incidence of active expiration during wakefulness was observed in rats exposed to CIH. The data show that CIH-related hypertension is not caused by changes in the sleep-wake cycle and suggest that active expiration is not required for the increase in AP in freely moving rats exposed to CIH.

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In a prospective study we describe the delivery of small tidal volumes to extremely low birth weight (ELBW) and very low birth weight (VLBW) infants using a volume-targeted ventilation mode (VTV). Tidal volume delivery was consistent for both ELBW and VLBW infants independent of gestational age, birth weight, and the target volume.

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Purpose: Evaluating the effects of interdialytic daily inspiratory muscle training (IMT) on respiratory muscle strength, chest wall regional volumes, diaphragmatic mobility and thickness, pulmonary function, functional capacity, and quality of life (QoL) in haemodialysis (HD) patients.Method: A randomised, and double-blind clinical trial composed of 24 chronic kidney disease patients undergoing HD. Patients were allocated into the IMT group (n = 12) or sham group (n = 12) and performed daily IMT twice per day with a load of 50% inspiratory muscle strength for the IMT group and 5 cmH2O for the sham group during 8 weeks. Respiratory muscle strength, diaphragm thickness and mobility, chest wall regional volumes, functional capacity, and QoL were measured.Results: At the end of the study, an increase in inspiratory and expiratory muscle strength was observed for both groups, but no significant difference was found between them. Changed volume distribution was also observed in the IMT group, with significantly increased inspiratory capacity in the pulmonary compartment compared to the sham group.Conclusions: Daily interdialytic IMT promoted a change in chest wall regional volumes, with an increase in the inspiratory capacity of the pulmonary rib cage. Both groups had increased inspiratory and expiratory muscle strength with daily respiratory exercise.Trial registration: www.ClinicalTrials.gov; study number: NCT02599987; name of trial registry: IMT in Patients with End-stage Renal Disease.Implications for rehabilitationMuscular impairment in chronic kidney disease patients results from a series of common alterations, affecting respiratory muscles.Patients with chronic kidney disease have low values of diaphragmatic thickness.The daily inspiratory muscle training (IMT) or breathing exercise over a period of 8 weeks provided increased respiratory muscle strength.The daily inspiratory muscle training presented a change in tri-compartment distribution of lung volume compared to the sham group, with increased inspiratory capacity of the pulmonary rib cage.

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RESUMO Objetivo avaliar os diferentes componentes da resistência do sistema respiratório e a força muscular respiratória, bem como investigar a ocorrência de limitação de fluxo expiratório (LFE) de pacientes obesos mórbidos (OM) na posição sentada. Métodos a amostra foi composta de OM (IMC ≥ 40 kg/m2) e de indivíduos não obesos (NO) com IMC entre 18 e 30 kg/m2. O protocolo foi composto de: avaliação antropométrica e da função respiratória (espirometria, pressões inspiratória (PIM) e expiratória máximas (PEM) e oscilometria de impulso). Na comparação entre os grupos, foi utilizado o teste T para amostras não pareadas. As correlações foram avaliadas pelo teste de Pearson, e o nível de significância foi de 5%. Resultados Foram avaliados 50 OM (idade 40,0 ± 10,4 anos, 1,64 ± 0,09 m, 138,8 ± 33,6 kg e 50,7 ± 8,9 kg/m2), além de 30 NO (idade 37,6 ± 11,5 anos, 1,67 ± 0,09 m, 65,2 ± 10,3 kg e 23,2 ± 22 kg/m2). Os OM apresentaram maiores valores de resistência total, central, de vias aéreas, tecidual e periférica quando comparados aos NO. Nenhum paciente apresentou LFE. A circunferência abdominal se associou com variáveis espirométricas PIM e PEM. A relação cintura-quadril se correlacionou com variáveis de mecânica respiratória, além das espirométricas PIM e PEM. Conclusões pacientes com obesidade mórbida e sem padrão espirométrico obstrutivo apresentam aumento nas resistências total, de vias aéreas, periférica e tecidual do sistema respiratório quando comparados a não obesos. Esses indivíduos, entretanto, não apresentam limitação de fluxo expiratório e redução da força muscular respiratória.

ABSTRACT Objective To evaluate the different components of the resistance of the respiratory system, respiratory muscle strength and to investigate the occurrence of expiratory flow limitation (EFL) in patients with morbid obesity (MO) when seated. Methods The sample was composed of MO (BMI≥40 kg/m2) and non-obese individuals (NO) with a BMI between 18 and 30 kg/m2. The protocol consisted of the anthropometric assessment and the following measures of respiratory function: spirometry, maximal inspiratory and expiratory pressures (MIP and MEP, respectively) and impulse oscillometry. The group comparison was performed using T-test for unpaired samples. The correlations were evaluated by the Pearson test with a significance level of 5%. Results Fifty MO (age 40±10.4 years, 1.64±0.09 m, 138.8±33.6 kg and 50.7±8.9 kg/m2), and 30 NO (age 37.6±11.5 years, 1.67±0.09 m, 65.2±10.3 kg and 23.2±22 kg/m2) were evaluated. The MO showed higher values of total, peripheral, airways, tissue and central resistance when compared to the NO. No patient showed EFL. The waist circumference was associated with spirometric variables, MIP, and MEP. The waist-to-hip ratio was correlated to respiratory mechanics and spirometric variables, MIP, and MEP. Conclusion Morbidly obese patients with no obstructive spirometric pattern show increased total, airway, peripheral, and tissue respiratory system resistance when compared to nonobese. These individuals, however, do not present with expiratory flow limitation and reduced respiratory muscles strength.

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The retrotrapezoid nucleus (RTN) contains chemosensitive cells that distribute CO2-dependent excitatory drive to the respiratory network. This drive facilitates the function of the respiratory central pattern generator (rCPG) and increases sympathetic activity. It is also evidenced that during hypercapnia, the late-expiratory (late-E) oscillator in the parafacial respiratory group (pFRG) is activated and determines the emergence of active expiration. However, it remains unclear the microcircuitry responsible for the distribution of the excitatory signals to the pFRG and the rCPG in conditions of high CO2. Herein, we hypothesized that excitatory inputs from chemosensitive neurons in the RTN are necessary for the activation of late-E neurons in the pFRG. Using the decerebrated in situ rat preparation, we found that lesions of neurokinin-1 receptor-expressing neurons in the RTN region with substance P-saporin conjugate suppressed the late-E activity in abdominal nerves (AbNs) and sympathetic nerves (SNs) and attenuated the increase in phrenic nerve (PN) activity induced by hypercapnia. On the other hand, kynurenic acid (100 mM) injections in the pFRG eliminated the late-E activity in AbN and thoracic SN but did not modify PN response during hypercapnia. Iontophoretic injections of retrograde tracer into the pFRG of adult rats revealed labeled phox2b-expressing neurons within the RTN. Our findings are supported by mathematical modeling of chemosensitive and late-E populations within the RTN and pFRG regions as two separate but interacting populations in a way that the activation of the pFRG late-E neurons during hypercapnia require glutamatergic inputs from the RTN neurons that intrinsically detect changes in CO2/pH.

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BACKGROUND: Pneumo-phono-articulatory coordination is often impaired in dysarthric patients. Because all speech is produced upon exhalation, adequate respiratory support and coordination are essential for communication. Nevertheless, studies investigating respiratory parameters for speech are scarce. The objectives of the present study were to analyze and compare the numbers of words and syllables (universal measurement) per exhalation among healthy and dysarthric speakers, in different speech tasks. DESIGN AND SETTING: A cross-sectional analytical study with a control group was conducted at the Department of Speech, Language and Hearing Sciences at UNIFESP. METHODS: The study sample consisted of 62 individuals: 31 dysarthric patients and 31 healthy individuals matched for sex, age and education level. All participants performed number counting and text reading tests in which the numbers of words and syllables per exhalation were recorded. All measurements obtained from the two groups were compared. RESULTS: Statistically significant differences between the dysarthric and healthy groups were found in the two tasks (counting of syllables and words per exhalation) (P < 0.001). In contrast, the performance of the dysarthric patients did not vary according to the task: reading and number counting in syllables/exhalation (P = 0.821) or words/exhalation (P = 0.785). CONCLUSIONS: The mean numbers of words and syllables per exhalation among dysarthric subjects did not vary according to the speech task used but they clearly showed differences between dysarthric patients and normal healthy subjects. The study also made it possible to obtain preliminary data on the average numbers of words and syllables per expiration produced by healthy individuals during their speech production.

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