Respiratory Physiology & Neurobiology最新文献

Obstructive sleep apnea (OSA) is a breathing disorder in which airway obstruction during sleep leads to periodic bouts of inadequate (hypopneic) or absent (apneic) ventilation despite neurorespiratory effort. Repetitive apneic and hypopneic exposures can induce intermittent hypoxemia and lead to a host of maladaptive behavioral and physiological outcomes. Intermittent hypoxia treatment (IH), which consists of alternating exposure to hypoxic and normal air, can induce a long-lasting increase in breathing motor outputs called long term facilitation (LTF). IH models key aspects of the hypoxemia experienced during OSA and LTF might serve to prevent OSA or ameliorate its severity by stimulating ventilatory output during or after apnea/hypopnea. Ethanol consumption prior to sleep exacerbates existing OSA, but it is unknown how ethanol affects LTF expression. Thus, we hypothesized that ethanol treatment would attenuate LTF expression and the magnitude of the ventilatory response during acute hypoxic exposure. We administered either low-dose (0.8 g/kg) or high-dose (3 g/kg) ethanol or saline to adult female Sprague-Dawley rats through intraperitoneal injection and then measured subjects' ventilatory output by whole-body plethysmography during baseline, a 5 by 3-minute moderate IH protocol (hypoxia: F_iO₂ = 0.11, Normoxia: room air), and for one hour following the end of IH. Results indicate that low-dose ethanol abolishes LTF of respiratory rate and minute ventilation and trends suggest that low-dose ethanol might attenuate respiratory rate and minute ventilation during acute hypoxic exposure. While high-dose ethanol significantly diminished subjects' respiratory rate and minute ventilation during hypoxia, LTF expression was not significantly different between high-dose ethanol and saline-treated subjects. Overall, data indicate that ethanol exposure dramatically attenuates LTF expression following IH treatment and impairs ventilatory responses to hypoxia in a dose-dependent manner. Such findings inspire further consideration of ethanol's negative effects upon endogenous compensatory mechanisms for repeated hypoxic exposure, both in the context of OSA and beyond.

Transient receptor potential ankyrin-1 (TRPA1) is expressed in the trigeminal nerves in the nasal cavity. It detects irritant chemicals such as formalin and acrolein, induces respiratory depression to protect against further inhalation, and elicits avoidance behavior. Although tobacco smoke contains formalin, acrolein, and other irritant chemicals, the possible contribution of TRPA1 to protection against tobacco smoke has yet to be fully understood. In this study, we compared respiratory and behavioral responses to an aerosol of tobacco smoke between TRPA1 conditional knockout mice and the controls. We also compared the effect of aerosols from the smoke of traditional standard tobacco and a recently developed heated tobacco product. As expected, respiratory depression by tobacco aerosol was observed only in the TRPA1 intact mice and was associated with increased trigeminal activation. Meanwhile, mice did not avoid or even prefer tobacco aerosol in a TRPA1-independent manner, contrary to our expectations. Repeated exposure to tobacco aerosol resulted in lung inflammation in a TRPA1-independent manner. Aerosols from a heated tobacco product showed no significant effect as in traditional tobacco smoke. These results indicate that TRPA1 contributes to acute protection from tobacco smoke by inducing respiratory depression but not to the safety of the lungs in repeated exposure. Tobacco aerosol contains attractive substances for mice. Heated tobacco product aerosol contains less TRPA1 activating substances and less inflammation evoking than traditional tobacco smoke.

Objective: This study investigates the breathing patterns and immune status of guinea pigs raised under specific pathogen-free (SPF) conditions compared to conventionally bred (CON).

Methods: Breathing pattern parameters were assessed using whole-body plethysmography (WBP) during quiet breathing and saline nebulisation. Blood and bronchoalveolar lavage fluid (BALF) were analysed for white blood cell, neutrophil and eosinophil counts, and cytokine levels (TNF-α, IL-1β, IL-4).

Results: SPF guinea pigs exhibited higher tidal volume, expired volume, minute volume, and airflow parameters than CON guinea pigs. The immune analysis revealed lower white blood cell counts and IL-4 levels in SPF guinea pigs. These findings indicate that SPF guinea pigs have different respiratory and immune responses than CON guinea pigs.

Conclusion: The study highlights that the maturation processes affecting breathing pattern parameters in SPF guinea pigs differ significantly from those in CON guinea pigs. This suggests potential limitations of SPF animals in respiratory physiology research due to their different immune and respiratory responses.

High spinal cord injuries (SCIs) often result in persistent diaphragm paralysis and respiratory dysfunction. Chronic neuroinflammation within the damaged spinal cord after injury plays a prominent role in limiting functional recovery by impeding neuroplasticity. In this study, we aimed to reduce glucose metabolism that supports neuroinflammatory processes in an acute preclinical model of C2 spinal cord lateral hemisection in rats. We administered 2-deoxy-D-glucose (2-DG; 200 mg/kg/day s.c., for 7 days) and evaluated the effect on respiratory function and chondroitin sulfate proteoglycans (CSPGs) production around spinal phrenic motoneurons. Contrary to our initial hypothesis, our 2-DG treatment did not have any effect on diaphragm activity and CSPGs production in injured rats, although slight increases in tidal volume were observed. Unexpectedly, it led to deleterious effects in uninjured (sham) animals, characterized by increased ventilation and CSPGs production. Ultimately, our results seem to indicate that this 2-DG treatment paradigm may create a neuroinflammatory state in healthy animals, without affecting the already established spinal inflammation in injured rats.

Introduction: Transcranial direct current stimulation (tDCS) is a non-invasive technique with therapeutic potential, especially in respiratory muscle training (RMT) in pathological conditions such as chronic obstructive pulmonary disease and heart failure.

Objective: To evaluate the effect of bilateral cathodic tDCS on respiratory muscle strength and endurance in healthy young and elderly women.

Methods: An experimental, randomized study with 80 participants divided into young and old women, subdivided into intervention and sham control groups. The participants were evaluated by spirometry and dynamic muscle strength tests before and after the one session intervention. tDCS was applied with cathode electrodes positioned bilaterally in the motor area.

Results: The elderly women in the intervention group showed significant improvement in dynamic inspiratory muscle strength (S-Index) and dominant hand strength, with moderate to large effect sizes. The young women showed a significant increase only in the strength of the dominant hand, with no improvement in inspiratory muscle strength. There were no significant differences in ventilatory parameters, including Maximal Ventilatory Capacity, in any of the age groups.

Conclusion: Bilateral cathodic tDCS was effective in increasing dynamic inspiratory muscle strength and dominant hand strength in elderly women, with more pronounced effects compared to young women. The technique did not produce significant changes in maximal ventilatory capacity in any of the age groups, suggesting that the response to tDCS may vary with age, being more beneficial in elderly women.

Background/aim: Exertional breathlessness is a dominating symptom in cardiorespiratory disease, limiting exercise capacity. Multidimensional measurement has been proposed to capture breathlessness, but it is unknown whether it is useful to differentiate people with abnormal vs normal exertional breathlessness intensity.

Methods: This was a secondary analysis of a randomized controlled trial of outpatients aged ≥18 years performing a symptom-limited cycle incremental exercise test (IET). Breathlessness sensations at end of IET were identified using the multidimensional dyspnea profile (MDP) 30-min post-exercise and compared between people with abnormally high breathlessness (Borg 0-10 rating > upper limit of normal [ULN]) and people within normal ranges (≤ULN) in relation to the percentage of predicted peak power output defined by normative reference equations.

Results: Of 92 participants, 20 (22%) had abnormally high breathlessness. Compared with those with normal breathlessness (n=72 [78%]), the abnormal group reported higher symptom intensity at peak exercise (7.9 ± 1.7 vs 6.3 ± 1.4 Borg units; p<0.001) and had lower peak power output 129 ± 52W vs 167 ± 55W; p<0.001). Differences between those with normal, and abnormal exertional breathlessness regarding MDP ratings were not statistically significant (all p>0.05): overall unpleasantness, 4.1 ± 2.3 vs 4.7 ± 1.6; immediate perception, 10.9 ± 2.8 vs 11.5 ± 1.8; and emotional response, 4.1 ± 7.6 vs 3.2 ± 7.5. MDP ratings had no relation to peak power output.

Conclusion: Breathlessness dimensions are similar at the peak of a standardized IET and cannot differentiate between people with normal and abnormally high exertional breathlessness.

Central and Obstructive Sleep Apnea (CSA and OSA), Chronic Obstructive Pulmonary Disease (COPD), and Obesity Hypoventilation Syndrome (OHS) disrupt breathing patterns, posing significant health risks and reducing the quality of life. Bilevel Positive Airway Pressure (BiPAP) therapy offers adjustable inhalation and exhalation pressures, potentially enhancing treatment adaptability for the above diseases. This is the first-ever study that employs Computational Fluid Dynamics (CFD) to examine the biomechanical impacts of BiPAP under four settings: Inspiratory Positive Airway Pressure (IPAP)/Expiratory Positive Airway Pressure (EPAP) of 12/8, 16/6, and 18/8 cmH₂O, compared to a without-BiPAP scenario of zero-gauge pressure. Utilizing a computed-tomography-based respiratory tract model from the nasal cavity extending to the 13th generation, we analyzed parameters such as static pressure, shear stress, and airway wall normal force across different airway regions. Our results indicate that BiPAP, particularly at higher IPAP settings, effectively increases static pressure, thereby improving airway patency and potentially reducing the risk of airway collapse in both CSA and OSA. Lower EPAP, on the other hand, helps reduce the work of breathing during exhalation, which is particularly useful for patients who have difficulty exhaling against higher pressures or need to exhale CO₂ more effectively. This comparative analysis confirms that BiPAP not only maintains open airways but does so with an adjustable approach that can be used for the specific needs of patients with various respiratory dysfunctions, thereby offering a versatile and effective treatment option.

The central neural mechanism plays an important role in cardiopulmonary coupling. How the brain stem affects the cardiopulmonary coupling is relatively clear, but there are few studies on the cerebral cortex activity of cardiopulmonary coupling. We aim to study the response of the cerebral cortex for cardiopulmonary phase synchronization enhancement. The method of brain network was used and Pearson correlation analysis performed on the global attributes and phase synchronization time (CRPST) in the spontaneous, 2/2 and 4/4 breathing modes. Furthermore, calculated the phase lag index (PLI) among 21 lead EEG signals, and then analyzed the correlation between PLI and the parameters of cardiovascular and respiratory systems. Our results show that the global brain network characteristic parameters are significantly different in the three breath modes in the α (8-14 Hz) band. The global efficiency and feature path length are significantly positively correlated with the phase synchronization and PLI indexes are widely related to CRPST and respiratory depth in the spontaneous breathing mode, while the brain network parameters and PLI indexes are not correlated with CRPST and PLI mainly positively correlated with respiratory rate in the controlled breathing modes. The differences of brain networks in the three modes are mainly caused by the physiological factors of cardiopulmonary coupling. These show that enhanced cardiopulmonary phase synchronization with controlled breathing based on heartbeat has a significant effect on the cardiopulmonary system and maybe provide some ideas for regulating cardiopulmonary function in the future.

Well-trained individuals, compared to less well-trained individuals, exhibit a lower minute ventilation (V̇_E) and higher end-tidal partial pressure of CO₂ (P_ETCO₂) at a given work rate. This study investigated whether such breathing adaptations seen in well-trained individuals also applied to elite long-distance runners. Forty-one long-distance runners were categorized into high (Long-High, consisting of Tokyo-Hakone College Ekiden [relay marathon] runners and Olympic athletes, n=23), or low performance-level group (Long-Low, n=18) according to their race times. Ten Middle-distance runners (Middle) also participated in a comparison group. All subjects performed an incremental exercise test on a motorized treadmill until exhaustion. Maximum V̇O₂ and velocity were greater for the Long groups than the Middle group, however these measures were not distinguishable between the Long-High and the Long-Low groups. By contrast, V̇_E and P_ETCO₂ were able to identify the Long-High group. Submaximal V̇_E were lowest, whilst P_ETCO₂ especially at high running velocities were highest for the Long-High group. This study confirms that breathing patterns with lower V̇_E and higher P_ETCO₂ are relevant adaptation markers for assessing endurance race performance in elite long-distance runners.

Chronic hyperoxia during early postnatal development depresses breathing when neonatal rats are returned to room air and causes long-lasting attenuation of the hypoxic ventilatory response (HVR). In contrast, little is known about the control of breathing of juvenile or adult mammals after chronic exposure to moderate hyperoxia later in life. Therefore, Sprague-Dawley rats were exposed to 60 % O₂ for 7 days (juveniles) or for 4 and 14 days (adults) and ventilation was measured by whole-body plethysmography immediately after the exposure or following a longer period of recovery in room air. Hyperoxia-treated juvenile rats appeared to hypoventilate when returned to room air (11-13 % lower ventilation and CO₂ convection requirement relative to age-matched controls), but chronic hyperoxia did not alter normoxic ventilation in adult rats. In contrast, pre-treatment with chronic hyperoxia augmented the HVR in both juvenile rats (+41 %) and adult rats (+28-50 %). The hypercapnic ventilatory response (7 % CO₂) also tended to be augmented in adult rats after 14 days of hyperoxia, but this effect was not significant after accounting for variation in metabolic rate (i.e, CO₂ convection requirement). These findings confirm that chronic hyperoxia elicits age-specific respiratory plasticity in rats. These age-dependent differences are not caused by a lack of plasticity in adult-exposed rats; rather, there are qualitative differences in the plasticity that is expressed after chronic hyperoxia in neonates, juveniles, and adults as well as differences in its persistence.