Respiratory Physiology & Neurobiology最新文献

The respiratory muscle force determines the intensity of cough force. A greater cough force for cleaning the airways is essential for preventing and managing pneumonia. Body posture can affect the onset of aspiration pneumonia. However, the effects of body posture on the respiratory muscle and cough forces remain unclear. Thus, we aimed to explore the influence of the four body postures on respiratory muscle force, cough pressure, subjective ease of coughing, and pulmonary function in healthy individuals. Twenty healthy individuals were included in this study. Body postures were 0-degree supine, 30- and 60-degree semi-recumbent, and 90-degree sitting. The maximal inspiratory and expiratory pressures, maximal cough pressure, subjective ease of coughing, and pulmonary function, including peak expiratory flow, were evaluated. We set the measured values in the supine posture to 100% and showed the relative values. The 60-degree posture showed stronger inspiratory (125.1 ± 3.9%, mean ± standard error [SE]) and expiratory (116.4 ± 3.0%) muscle force, cough pressure, more subjective ease of coughing, and greater peak expiratory flow (113.4 ± 3.0%) than the supine posture. The sitting posture also showed greater inspiratory muscle force and peak expiratory flow than the supine posture. The correlation coefficient for the 60-degree posture showed that the maximal inspiratory pressure was moderately correlated with the maximal expiratory pressure (r = 0.512), cough pressure (r = 0.495), and peak expiratory flow (r = 0.558). The above findings suggest the advantage of keeping a 60-degree posture and avoiding the supine posture to generate a greater cough force in the prevention and management of pneumonia.

The tongue is a muscular hydrostat, with lingual movements occurring during breathing, chewing, swallowing, vocalization, vomiting, coughing and grooming/sexual activities. In the elderly, reduced lingual dysfunction and weakness contribute to increased risks of obstructive sleep apnea and aspiration pneumonia. In Fischer 344 (F344) rats, a validated model of aging, hypoglossal motor neuron death is apparent, although there is no information regarding tongue strength. The intrinsic tongue muscles, the superior and inferior longitudinal, transversalis and verticalis exist in an interdigitated state. Recently, we established a method to measure the specific force of individual intrinsic tongue muscle, accounting for the tissue bulk that is not in the direction of uniaxial force. In the longitudinal muscles of 6- (n = 10), 18- (n = 9) and 24-month-old (n = 12) female and male F344 rats, we assessed specific force, fatigability, fiber type dependent cross-sectional area (CSA) and overall CSA. Muscle force and fatigue was assessed ex vivo using platinum plate simulation electrodes. Tongue muscles were frozen in melting isopentane, and transverse sections cut at 10 µm. Muscle fiber type was classified based on immunoreactivity to myosin heavy chain (MyHC) isoform antibodies. In H&E stained muscle, CSA and uniaxial muscle contributions to total tongue bulk was assessed. We observed a robust ∼30% loss of longitudinal specific force, with reductions in overall longitudinal muscle fiber CSA and specific atrophy of type IIx/IIb fibers. It will be important to investigate the mechanistic underpinnings of hypoglossal motor neuron death and tongue muscle weakness to eventually provide therapies for age-associated lingual dysfunctions.

An anesthetized cat animal model was used to evaluate changes in cough and swallow after a small midline upper abdominal incision (laparotomy). Two additional conditions were tested: sealing the laparotomy with gentle suctioning via a small cannula, and subsequent closure of the abdominal wall with suture. These abdominal wall manipulations resulted in no changes in the cough reflex, but produced higher motor drive to pharyngeal musculature (thyropharyngeus and geniohyoid muscles) during swallow. Swallow-breathing coordination phase preference shifted towards swallow occurring more during the inspiratory phase. There were no significant changes in cough motor pattern, or cough and swallow number and temporal features. The respiratory changes were limited to reduced inspiratory motor drive to the diaphragm. The results are consistent with an important role of sensory feedback from the abdominal wall in regulation of swallow motor pattern. The level of reflex modulation may depend on the extent of injury and likely on its position in the abdomen.

Respiratory muscle endurance training reportedly has beneficial effects on whole-body endurance performance. We produced a novel high-intensity interval (HII) protocol and characterized the associated physiological responses and respiratory muscle fatigue. Peak oxygen uptake of respiratory muscle (V̇O2peakRM) was estimated during the respiratory incremental test. The HII session consisted of five 3-minute hyperpnea periods at 100%V̇O2peakRM interspersed with 2-minute periods at 40%V̇O2peakRM (25 min total). The high-intensity continuous (HIC) session involved a single time-to-end bout of hyperpnea at 100%V̇O2peakRM. The moderate-intensity continuous (MIC) session involved 25 min of hyperpnea at 60% of maximal voluntary ventilation. V̇O2RM was recorded continuously, and maximal inspiratory pressure (PImax) was assessed before and after the sessions. HII session: V̇O2RM gradually increased as the sets proceeded, whereas PImax decreased significantly. HIC session: V̇O2RM increased progressively, and the time to end was 6.5 ± 0.5 min. PImax decreased significantly. MIC session: V̇O2RM did not change for 25 min, and PImax remained unchanged. The duration of V̇O2RM at near- and supra-maximal levels in the HII session (10 ± 1 min) was longer than that in the HIC session (4 ± 1 min). The decrease in PImax was larger in the HII session (−12 ± 3 %) than MIC session (−4 ± 3 %). The HII protocol is characterized by a longer time to maximally stimulate the aerobic energy system of respiratory muscle than the HIC protocol and greater inspiratory muscle fatigue than the traditional MIC protocol. These results suggest that the HII protocol could enhance the efficacy of respiratory muscle training programs.

This study aimed to investigate whether Chronic Kidney Disease (CKD) influences O₂ supply including O₂ delivery and release to the active muscles during maximal physical exercise. Twelve CKD patients undergoing dialysis therapy (HD group) and twelve healthy adults (CTR group) performed an incremental exercise test to determine maximal oxygen uptake (VO_2peak). Throughout the exercise, near-infrared spectroscopy allowed the investigation of changes in oxyhemoglobin (∆O₂Hb), deoxyhemoglobin (∆HHb), and total hemoglobin (∆THb) in the vastus lateralis muscle. VO_2peak was significantly lower in HD group. In addition, HD patients had impaired changes in muscular oxygenation (∆HHb and ∆O₂Hb) and blood volume (∆THb) during the exercise (p < 0.05). Moreover, a positive correlation was observed between VO_2peak and muscle blood volume (∆THb) in both groups (p < 0.05). This study provides the first evidence that HD patients displayed lower VO_2peak and blunted muscular deoxyhemoglobin increase during exercise. This result supports the hypothesis of an increase in oxygen affinity and/or mitochondrial dysfunction in this population.

Background

Exercise-induced rhinitis (EIR) is a poorly understood phenomenon that may be related to increased inspiratory airflow. Characterization of the development of EIR is important to understand contributing factors.

Objective

To characterize how different nasal morphologies respond to airflow-related variables during rapid/deep inspiratory conditions.

Methods

Subject-specific nasal airways were reconstructed from radiographic images. Unilateral airways were classified as Standard, Notched, or Elongated accord to their distinct nasal vestibule morphology. Computational fluid dynamics simulations were performed at various airflow rates.

Results

For all simulated flow rates, average resistance at the nasal vestibule, airflow velocity and wall sheer stress were highest in Notched. Average mucosal heat flux was highest in Standard. Notched phenotypes showed lower mean percent increases from 10 L/min to 50 L/min in all computed variables.

Conclusion

Resistance values and airflow velocities depicted a more constricted nasal vestibule in the Notched phenotypes, while perception of nasal mucosal cooling (heat flux) favored the Standard phenotypes. Different nasal phenotypes may predispose to EIR.

This study examined the effect of breath-hold (BH) training on apnoeic performance in novice BH divers (NBH:n = 10) and compared them with data from elite BH divers (EBH:n = 11). Both groups performed 5-maximal BHs (PRE). The NBH group repeated this protocol after two weeks of BH training (POST). The NBH group during BH efforts significantly increased red blood cell concentration (4.56 ± 0.16Mio/μl) by 5.06%, hemoglobin oxygen saturation steady state duration (110.32 ± 29.84 s) by 15.48%, and breath-hold time (BHT:144.19 ± 47.35 s) by 33.77%, primarily due to a 59.70% increase in struggle phase (71.85 ± 30.89 s), in POST. EBH group exhibited longer BHT (283.95 ± 36.93 s) and struggle-phase (150.10 ± 34.69 s) than NBH (POST). Elite divers recorded a higher peak MAP (153.18 ± 12.28 mmHg) compared to novices (PRE:123.70 ± 15.65 mmHg, POST:128.30 ± 19.16 mmHg), suggesting that a higher peak MAP is associated with a better BHT. The concurrent abrupt increase of diaphragmatic activity and MAP, seen only in the EBH group, suggests a potential interaction. Additionally, apnoea training increases red blood cells concentration in repeated apnoea efforts and increases BH stamina.

Chronic hypoxia (CH) from birth attenuates the acute hypoxic ventilatory response (HVR) in rats and other mammals, but CH is often reported to augment the HVR in adult mammals. To test the hypothesis that this transition – from blunting to augmenting the HVR – occurs in the third or fourth postnatal week in rats, juvenile and adult rats were exposed to normobaric CH (12% O₂) for 7 days and the HVR was assessed by whole-body plethysmography. No transition was observed, however, and the acute HVR was reduced by 61 – 85% across all ages studied. The failure to observe an augmented HVR in adult rats could not be explained by the substrain of Sprague Dawley rats used, the duration of the CH exposure, the order in which test gases were presented, the level of hypoxia used for CH and to assess the HVR, or the effects of CH on the metabolic response to hypoxia and the hypercapnic ventilatory response. A literature survey revealed several distinct patterns of ventilatory acclimatization to hypoxia (VAH) in adult rats, with most studies (77%) revealing a decrease or no change in the acute HVR after CH. In conclusion, the effects of CH on respiratory control are qualitatively similar across age groups, at least within the populations of Sprague Dawley rats used in the present study, and there does not appear to be one “typical” pattern for VAH in adult rats.

Objective

Evidence suggest that the renin-angiotensin system (RAS) is activated in people with asthma, although its pathophysiological role is unclear. Angiotensin-converting enzyme 2 (ACE2) is the major enzyme that converts angiotensin II to angiotensin 1–7 (Ang-1–7), and is also known as a receptor of SARS-CoV-2. The current study was conducted to identify the change in RAS-related gene expression in airways of a murine asthma model.

Methods

The ovalbumin (OA)-sensitized mice were repeatedly challenged with aerosolized OA to induce asthmatic reaction. Twenty-four hours after the last antigen challenge, the main bronchial smooth muscle (BSM) tissues were isolated.

Results

The KEGG pathway analysis of differentially expressed genes in our published microarray data revealed a significant change in the RAS pathway in the antigen-challenged mice. Quantitative RT-PCR analyses showed significant increases in the angiotensin II-generating enzymes (Klk1, Klk1b3 and Klk1b8) and a significant decrease in Ace2. Surprisingly, ELISA analyses revealed a significant increase in Ang-1–7 levels in bronchoalveolar lavage (BAL) fluids of the antigen-challenged animals, while no significant change in angiotensin II was observed. Application of Ang-1–7 to the isolated BSMs had no effect on their isometrical tension.

Conclusion

The expression of Ace2 was downregulated in the BSMs of OA-challenged mice, while Klk1, Klk1b3 and Klk1b8 were upregulated. Despite the downregulation of ACE2, the level of its enzymatic product, Ang-1–7, was increased in the inflamed airways, suggesting the existence of an unknown ACE2-independent pathway for Ang-1–7 production. The functional role of Ang-1–7 in the airways remains unclear.