Two-way Non-rebreathing Valves Research Articles

Effect of Breathing Room Air Through a Two-Way Non-Rebreathing Valve on HRV in BI and NBI College-Aged Students

Behavioral inhibition (BI) is a temperament associated with increased vulnerability to stress compared to non-behaviorally inhibited (NBI) individuals. Heart-rate variability (HRV) analysis to assess physiological stress has been growing in popularity due to its association with crucial physiological functions, including cardiac activity, autonomic nervous system activity, and physiologic stress. Previous studies in our lab have demonstrated that HRV in female college-age students expressing a BI temperament is significantly lower than in NBI individuals while breathing room air through a two-way non-rebreathing valve. These findings suggested that the parasympathetic nervous system is partially inhibited at rest in BI females; however, it is unknown if the parasympathetic nervous system in these individuals is inhibited prior to or after breathing through a breathing valve. Our current study will address this question by measuring HRV in BI and NBI individuals while breathing room air for 15 minutes without a breathing valve and for 10 minutes with a two-way breathing valve. Raw electrocardiogram signals will be collected throughout the study protocol and will be used to calculate HRV, which will be measured using a BIOPAC data acquisition system during the experiment. BI individuals will be identified through a series of self-reported questionnaires. Our preliminary results indicate that BI individuals have a lower HRV and are stressed throughout the duration of the study. Thank you to Carthage College's Biology and Neuroscience Department for allowing this research project to be conducted. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Comparison of physical properties of voluntary coughing, huffing and swallowing in healthy subjects.

Coughing, huffing and swallowing protect the airway from aspiration. This study was conducted to compare the physical properties of voluntary coughing, huffing and swallowing in healthy subjects. Ten healthy men were asked to huff, cough and swallow repeatedly. Electromyograms (EMGs) were recorded from the left side of the external oblique (EO), sternocleidomastoid, suprahyoid (SH) and thyrohyoid muscles. Airflow was recorded using a face mask with two-way non-rebreathing valves. The expiratory velocity of huffing and coughing and the SH EMG of all actions presented high intraclass correlation coefficients (> 0.8). The inspiratory and expiratory velocities did not differ significantly between coughing and huffing. The expiratory acceleration of coughing was significantly higher than that of huffing, whereas the expiratory volume of coughing was significantly smaller than that of huffing. The EO EMG of coughing and huffing were significantly larger than that of swallowing. The EO EMG activity during the expiratory phase was significantly higher than that of the other phases of both coughing and huffing. The SH EMG of coughing and huffing were significantly smaller than that of swallowing. Correlation analysis revealed that the expiratory velocity of coughing was strongly positively correlated with that of huffing. The expiratory volume of huffing was significantly positively correlated with hand grip strength. These results suggest that EO and SH muscle activities during huffing or coughing differ those during swallowing, and huffing and coughing may work similarly in expiratory function.

Oro-nasal Mask Versus Two-way Non-rebreathing Valves For Maximal Aerobic Capacity Testing In Astronauts

Oro-nasal Mask Versus Two-way Non-rebreathing Valves For Maximal Aerobic Capacity Testing In Astronauts

Breathing valve resistance alters physiological responses during a graded exercise test.

To determine the impact of breathing valve resistance on peak aerobic capacity ([Formula: see text]) and running economy (RE) in endurance-trained and recreationally active individuals. Ten endurance-trained males (ETM), 10 endurance-trained females (ETF), 10 recreationally active males (RAM), and 10 recreationally active females (RAF) participated in this study. On two separate occasions, subjects performed identicalgraded exercise treadmill protocols using either a Hans Rudolph 2700 (high resistance) or a Daniels' (low resistance) two-way non-rebreathing valve. Parameters obtained from these protocols included energy expenditure (EE), ventilation ([Formula: see text]), heart rate, respiratory exchange ratio, RE, [Formula: see text], and time to exhaustion (TTE). When using the Daniels' valve, all groups had lower submaximal EE (- 2.4, - 3.4, - 2.7, and - 2.0% for ETM, ETF, RAM, and RAF) and better RE (- 2.7, - 3.5, - 1.9, and - 1.8% for ETM, ETF, RAM and RAF) across all submaximal speeds. Only the ET groups had lower submaximal [Formula: see text] (4.6 and 3.8% for ETM and ETF) when using the Daniels' valve. TTE increased when using the Daniels' valve for all groups (6.0, 10.9, 6.2 and 9.8% for ETM, ETF, RAM and RAF), but [Formula: see text] was unaltered. Compared to the Daniels' valve, the Hans Rudolph 2700 valve altered the assessment of RE, submaximal EE, and TTE regardless of fitness level or sex, but did not change [Formula: see text]. Therefore, airflow resistance of a breathing valve must be considered when assessing and comparing EE, RE and TTE in the applied and research settings.

Tiotropium bromide exerts anti-inflammatory effects during resistive breathing, an experimental model of severe airway obstruction.

IntroductionResistive breathing (RB), a hallmark of obstructive airway diseases, is characterized by strenuous contractions of the inspiratory muscles that impose increased mechanical stress on the lung. RB is shown to induce pulmonary inflammation in previous healthy animals. Tiotropium bromide, an anticholinergic bronchodilator, is also shown to exert anti-inflammatory effects. The effect of tiotropium on RB-induced pulmonary inflammation is unknown.MethodsAdult rats were anesthetized, tracheostomized and breathed spontaneously through a two-way non-rebreathing valve. Resistances were connected to the inspiratory and/or expiratory port, to produce inspiratory resistive breathing (IRB) of 40% or 50% Pi/Pi,max (40% and 50% IRB), expiratory resistive breathing (ERB) of 60% Pe/Pe,max (60% ERB) or combined resistive breathing (CRB) of both 40% Pi/Pi,max and 60% Pe/Pe,max (40%/60% CRB). Tiotropium aerosol was inhaled prior to RB. After 6 h of RB, mechanical parameters of the respiratory system were measured and bronchoalveolar lavage (BAL) was performed. IL-1β and IL-6 protein levels were measured in lung tissue. Lung injury was estimated histologically.ResultsIn all, 40% and 50% IRB increased macrophage and neutrophil counts in BAL and raised IL-1β and IL-6 lung levels, tissue elasticity, BAL total protein levels and lung injury score. Tiotropium attenuated BAL neutrophil number, IL-1β, IL-6 levels and lung injury score increase at both 40% and 50% IRB. The increase in macrophage count and protein in BAL was only reversed at 40% IRB, while tissue elasticity was not affected. In all, 60% ERB raised BAL neutrophil count and total protein and reduced macrophage count. IL-1β and IL-6 levels and lung injury score were increased. Tiotropium attenuated these alterations, except for the decrease in macrophage count and the increase in total protein level. In all, 40%/60% CRB increased macrophage and neutrophil count in BAL, IL-1β and IL-6 levels, tissue elasticity, total protein in BAL and histological injury score. Tiotropium attenuated the aforementioned alterations.ConclusionTiotropium inhalation attenuates RB-induced pulmonary inflammation.

Use of a two-way non-rebreathing valve to simplify the measurement of twitch mouth pressure using an inspiratory pressure trigger and the establishment of an optimal trigger threshold for healthy subjects and COPD patients

ObjectiveControlled twitch mouth pressure (Tw Pmo) via the use of a two-way non-rebreathing valve is a new method to assess diaphragm contractility. The optimal trigger threshold was confirmed. DesignWe sought to determine the optimal trigger threshold for 17 healthy subjects (29±4 years) and 17 COPD patients (64±10 years). The Tw Pmo, twitch oesophageal pressure (Tw Pes) and twitch transdiaphragmatic pressure (Tw Pdi) in response to phrenic nerve stimulation were measured using an inspiratory pressure trigger at −1, −2, −3, −4, −5 and −6cmH2O. ResultsThe lung volume did not change during triggering at different trigger thresholds using a two-way non-rebreathing valve. The highest correlation between Tw Pmo and Tw Pes in healthy subjects and COPD patients occurred for a −2cmH2O trigger threshold (r=0.939 and r=0.869, P<0.0001). The narrowest limits of agreement for Tw Pmo and Tw Pes both occurred at −2cmH2O in healthy subjects, with a bias (range) of −0.4cmH2O (−1.85 to 1.41), and in COPD patients, with a bias (range) of 0.16cmH2O (−1.36–1.67). ConclusionsWe conclude that the measurement of Tw Pmo using a two-way non-rebreathing valve is of clinical value to investigate the suspected diaphragm contractility. The highest trigger threshold for clinical applications was −2cmH2O.

MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress

Inspiratory resistive breathing (IRB) induces cytokine expression in the diaphragm. The mechanism of this cytokine induction remains elusive. The roles of MAPKs and NF-κB and the impact of oxidative stress in IRB-induced cytokine upregulation in the diaphragm were studied. Wistar rats were subjected to IRB (50% of maximal inspiratory pressure) via a two-way nonrebreathing valve for 1, 3, or 6 h. Additional groups of rats subjected to IRB for 6 h were randomly assigned to receive either solvent or N-acetyl-cysteine (NAC) or inhibitors of NF-κB (BAY-11-7082), ERK1/2 (PD98059), and P38 MAPK (SB203580) to study the effect of oxidative stress, NF-κB, and MAPKs in IRB-induced cytokine upregulation in the diaphragm. Quietly breathing animals served as controls. IRB upregulated cytokine (IL-6, TNF-α, IL-10, IL-2, IL-1β) protein levels in the diaphragm and resulted in increased activation of MAPKs (P38, ERK1/2) and NF-κB. Inhibition of NF-κB and ERK1/2 blunted the upregulation of all cytokines except that of IL-6, which was further increased. P38 inhibition attenuated all cytokine (including IL-6) upregulation. Both P38 and ERK1/2 inhibition decreased NF-κB/p65 subunit phosphorylation. NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-κB/p65 phosphorylation. In conclusion, IRB-induced cytokine upregulation in the diaphragm is under the regulatory control of MAPKs and NF-κB. IL-6 is regulated differently from all other cytokines through a P38-dependent and NF-κB independent pathway. Oxidative stress is a stimulus for IRB-induced cytokine upregulation in the diaphragm.

Alterations in cerebral blood flow and cerebrovascular reactivity during 14 days at 5050 m

Upon ascent to high altitude, cerebral blood flow (CBF) rises substantially before returning to sea-level values. The underlying mechanisms for these changes are unclear. We examined three hypotheses: (1) the balance of arterial blood gases upon arrival at and across 2 weeks of living at 5050 m will closely relate to changes in CBF; (2) CBF reactivity to steady-state changes in CO2 will be reduced following this 2 week acclimatisation period, and (3) reductions in CBF reactivity to CO2 will be reflected in an augmented ventilatory sensitivity to CO2. We measured arterial blood gases, middle cerebral artery blood flow velocity (MCAv, index of CBF) and ventilation () at rest and during steady-state hyperoxic hypercapnia (7% CO2) and voluntary hyperventilation (hypocapnia) at sea level and then again following 2–4, 7–9 and 12–15 days of living at 5050 m. Upon arrival at high altitude, resting MCAv was elevated (up 31 ± 31%; P < 0.01; vs. sea level), but returned to sea-level values within 7–9 days. Elevations in MCAv were strongly correlated (R2= 0.40) with the change in ratio (i.e. the collective tendency of arterial blood gases to cause CBF vasodilatation or constriction). Upon initial arrival and after 2 weeks at high altitude, cerebrovascular reactivity to hypercapnia was reduced (P < 0.05), whereas hypocapnic reactivity was enhanced (P < 0.05 vs. sea level). Ventilatory response to hypercapnia was elevated at days 2–4 (P < 0.05 vs. sea level, 4.01 ± 2.98 vs. 2.09 ± 1.32 l min−1 mmHg−1). These findings indicate that: (1) the balance of arterial blood gases accounts for a large part of the observed variability (∼40%) leading to changes in CBF at high altitude; (2) cerebrovascular reactivity to hypercapnia and hypocapnia is differentially affected by high-altitude exposure and remains distorted during partial acclimatisation, and (3) alterations in cerebrovascular reactivity to CO2 may also affect ventilatory sensitivity.

Inspiratory Resistive Breathing Induces Acute Lung Injury

Resistive breathing is associated with large negative intrathoracic pressures. Increased mechanical stress induces high-permeability pulmonary edema and lung inflammation. To determine the effects of resistive breathing on the healthy lung. Anesthetized rats breathed through a two-way nonrebreathing valve. The inspiratory line was connected to a resistance setting peak inspiratory tracheal pressure at 50% of maximum (inspiratory resistive breathing), while 100% oxygen was supplied to prevent hypoxemia. Quietly breathing animals (100% oxygen) served as controls. Lung injury was evaluated after 3 and 6 hours of resistive breathing. After both 3 and 6 hours of resistive breathing, lung permeability was increased, as assessed by (99m)Tc-diethylenetriaminepentaacetic acid scintigraphy and Evans blue dye extravasation. Tissue elasticity, measured on the basis of static pressure-volume curves and by the low-frequency forced oscillation technique, was also increased. After both 3 and 6 hours of resistive breathing, gravimetric measurements revealed the presence of pulmonary edema and analysis of bronchoalveolar lavage showed increased total protein content, whereas the total cell count was elevated only after 6 hours of resistive breathing. Cytokine levels were assessed in bronchoalveolar lavage fluid and lung tissue by ELISA and were increased after 6 hours compared with controls. Western blot analysis showed early activation of Src kinase via phosphorylation (at 30 min), and Erk1/2 and IκBα (nuclear factor-κB inhibitor) were phosphorylated at 3 and 6 hours. Pathology revealed the presence of lung injury after resistive breathing. Resistive breathing induces acute lung injury and inflammation.

Postexercise oxygen consumption and substrate use after resistance exercise in women.

This study investigated the acute effects of 45 min of resistance exercise (RE) on excess postexercise oxygen consumption (EPOC) and substrate oxidation 120 min after exercise in moderately trained women. Ten RE trained women (age = 29 +/- 3 yr; ht = 168 +/- 8.3 cm; wt = 59 +/- 5.7 kg; VO2max = 38.3 +/- 4.7 mL.kg-1.min-1) underwent two trials: control sitting and RE. Subjects acted as their own controls in a random counterbalanced design. A 2-d nonexercise period was established between testing trials. Oxygen consumption (VO2) and respiratory exchange ratio (RER) were measured continuously by indirect calorimetry before, during, and after exercise and on a separate control day. RE consisted of 3 sets of 10 exercises at 10-repetition maximum with a 1-min rest period between each set. Fingertip samples of blood lactate concentration [BL] were collected immediately postexercise and every 30 min thereafter until [BL] returned to resting baseline values after exercise. The overall 2-h EPOC was 6.2-L (RE = 33.4 +/- 5.1 L vs control = 27.2 +/- 0.3 L), corresponding to an 18.6% elevation over the control period. RER was significantly (P < 0.01) below the control RER from minute 30 to minute 120 postexercise (RE = 0.75 +/- 0.01 vs control = 0.85 +/- 0.01). During the last 30 min of recovery, VO2 and [BL] had returned to control/baseline values and fat oxidation was significantly (P < 0.0001) higher (29.2 vs 16.3 kcal) after RE compared with the control trial. These data indicate that in young RE trained women, acute RE produces a modest increase in VO2 during a 2-h recovery period and an increase in fat oxidation.

Effect of tidal volume on the output and particle size distribution of hypertonic saline from an ultrasonic nebulizer

The purpose of the present study was to measure the output and particle size distribution of hypertonic saline from an ultrasonic nebulizer over the range of tidal volumes (VT) used in an epidemiological survey of asthma in children. A Starling pump was used to generate different VTs from 250 to 500 ml, at different respiratory rates of 12 and 20 breaths.min-1, to cover the normal range of respiratory pattern of children aged 7-14 yrs. The Starling pump was connected to a Timeter Compuneb Ultrasonic Nebulizer Model MP 500 with 24 cm of corrugated aerosol tubing, ID 2.2 cm, and a two-way non-rebreathing valve. Nebulizer output was measured by weighing the nebulizer chamber plus tubing and valve before and after each nebulization. To measure particle size distribution, a Malvern Particle Sizer M 3.0 (laser diffraction) was used, with a special adapter attached between valve and Starling pump. Nebulizer output increased linearly from 1.6 to 2.5 ml.min-1 for VT 250 to 500 ml, with little influence by the respiratory frequency. Furthermore, we found that in the range of VT = 300-500 ml the mass median aerodynamic diameter (MMAD) was 2.61 microns, with 100% of the particles less than 5 microns, whereas at VT = 150-250 ml the MMAD was 8.89 microns, with 90% larger than 5 microns. As output from this ultrasonic nebulizer correlates linearly with tidal volumes, size correction may not be necessary in hypertonic saline challenge tests in children. Above a VT of 300 ml, the MMAD is in the respirable range, with 100% of particles less than 5 microns.(ABSTRACT TRUNCATED AT 250 WORDS)