Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults.

Passive hyperthermia causes cerebral hypoperfusion primarily from heat-induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro-inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water-perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet-poor plasma via cells expressing CD62E (activated endothelial cells), CD31+ /CD42b- (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan-leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P-values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+ /CD42b- (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2 /pH-mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. KEY POINTS: The hyperthermia-induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow. We tested the hypothesis that the respiratory-induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow. At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross-brain microvesicle kinetics. However, when core temperature was increased by 2°C with CO2 /pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2 /pH-mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia. These new findings suggest that the heat-induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain.

Sodium bicarbonate reduces ventilation without altering core temperature threshold or sensitivity of hyperthermia-induced hyperventilation in exercising humans.

Hyperthermia stimulates ventilation (hyperthermia-induced hyperventilation). In exercising humans, once the core temperature reaches ∼37°C, minute ventilation (V̇e) increases linearly with rising core temperature, and the slope of the relation between V̇e and core temperature reflects the sensitivity of the response. We previously reported that sodium bicarbonate ingestion reduces V̇e during prolonged exercise in the heat without affecting the sensitivity of hyperthermia-induced hyperventilation. Here, we hypothesized that reductions in V̇e associated with sodium bicarbonate ingestion reflect elevation of the core temperature threshold for hyperthermia-induced hyperventilation. Thirteen healthy young males ingested sodium bicarbonate (0.3 g/kg body wt) (NaHCO3 trial) or sodium chloride (0.208 g/kg body wt) (NaCl trial), after which they performed a cycle exercise at 50% of peak oxygen uptake in the heat (35°C and 50% relative humidity) following a pre-cooling. The pre-cooling enabled detection of an esophageal temperature (Tes: an index of core temperature) threshold for hyperthermia-induced hyperventilation. The Tes thresholds for increases in V̇e were similar between the two trials (P = 0.514). The slopes relating V̇E to Tes also did not differ between trials (P = 0.131). However, V̇e was lower in the NaHCO3 than in the NaCl trial in the range of Tes = 36.8-38.4°C (P = 0.007, main effect of trial). These results suggest that sodium bicarbonate ingestion does not alter the core temperature threshold or sensitivity of hyperthermia-induced hyperventilation during prolonged exercise in the heat; instead, it downshifts the exercise hyperpnea.

Biofeedback Training to Increase P co2 in Asthma With Elevated Anxiety: A One-Stop Treatment of Both Conditions?

OBJECTIVE: Anxiety is highly prevalent in individuals with asthma. Asthma symptoms and medication can exacerbate anxiety, and vice versa. Unfortunately, treatments of comorbid anxiety and asthma are largely lacking. A problematic feature common to both conditions is hyperventilation. It adversely affects lung function and symptoms in asthma and anxiety. We examined whether a treatment to reduce hyperventilation, shown to improve asthma symptoms, also improves anxiety in asthma patients with high anxiety. METHOD: One hundred twenty English- or Spanish-speaking adult patients with asthma were randomly assigned to either Capnometry-Assisted Respiratory Training (CART) to raise P co2 or feedback to slow respiratory rate (SLOW). Although anxiety was not an inclusion criterion, 21.7% met clinically relevant anxiety levels on the Hospital Anxiety and Depression Scale (HADS). Anxiety (HADS-A) and depression (HADS-D) scales, anxiety sensitivity (Anxiety Sensitivity Index [ASI]), and negative affect (Negative Affect Scale of the Positive Affect Negative Affect Schedule) were assessed at baseline, posttreatment, 1-month follow-up, and 6-month follow-up. RESULTS: In this secondary analysis, asthma patients with high baseline anxiety showed greater reductions in ASI and PANAS-N in CART than in SLOW ( p values ≤ .005, Cohen d values ≥ 0.58). Furthermore, at 6-month follow-up, these patients also had lower ASI, PANAS-N, and HADS-D in CART than in SLOW ( p values ≤ .012, Cohen d values ≥ 0.54). Patients with low baseline anxiety did not have differential outcomes in CART than in SLOW. CONCLUSIONS: For asthma patients with high anxiety, our brief training designed to raise P co2 resulted in significant and sustained reductions in anxiety sensitivity and negative affect compared with slow-breathing training. The findings lend support for P co2 as a potential physiological target for anxiety reduction in asthma. TRIAL REGISTRATION: Clinicaltrials.gov Identifier: NCT00975273 .

Pulmonary ventilation and gas exchange during prolonged exercise in humans: Influence of dehydration, hyperthermia and sympathoadrenal activity.

NEW FINDINGS: What is the central question of the study? Ventilation increases during prolonged intense exercise, but the impact of dehydration and hyperthermia, with associated blunting of pulmonary circulation, and independent influences of dehydration, hyperthermia and sympathoadrenal discharge on ventilatory and pulmonary gas exchange responses remain unclear. What is the main finding and its importance? Dehydration and hyperthermia led to hyperventilation and compensatory adjustments in pulmonary CO2 and O2 exchange, such that CO2 output increased and O2 uptake remained unchanged despite the blunted circulation. Isolated hyperthermia and adrenaline infusion, but not isolated dehydration, increased ventilation to levels similar to combined dehydration and hyperthermia. Hyperthermia is the main stimulus increasing ventilation during prolonged intense exercise, partly via sympathoadrenal activation. ABSTRACT: The mechanisms driving hyperthermic hyperventilation during exercise are unclear. In a series of retrospective analyses, we evaluated the impact of combined versus isolated dehydration and hyperthermia and the effects of sympathoadrenal discharge on ventilation and pulmonary gas exchange during prolonged intense exercise. In the first study, endurance-trained males performed two submaximal cycling exercise trials in the heat. On day 1, participants cycled until volitional exhaustion (135 ± 11 min) while experiencing progressive dehydration and hyperthermia. On day 2, participants maintained euhydration and core temperature (Tc ) during a time-matched exercise (control). At rest and during the first 20 min of exercise, pulmonary ventilation ( V ̇ E ${\skew2\dot V_{\rm{E}}}$ ), arterial blood gases, CO2 output and O2 uptake were similar in both trials. At 135 ± 11 min, however, V ̇ E ${\skew2\dot V_{\rm{E}}}$ was elevated with dehydration and hyperthermia, and this was accompanied by lower arterial partial pressure of CO2 , higher breathing frequency, arterial partial pressure of O2 , arteriovenous CO2 and O2 differences, and elevated CO2 output and unchanged O2 uptake despite a reduced pulmonary circulation. The increased V ̇ E ${\skew2\dot V_{\rm{E}}}$ was closely related to the rise in Tc and circulating catecholamines (R2  ≥ 0.818, P ≤ 0.034). In three additional studies in different participants, hyperthermia independently increased V ̇ E ${\skew2\dot V_{\rm{E}}}$ to an extent similar to combined dehydration and hyperthermia, whereas prevention of hyperthermia in dehydrated individuals restored V ̇ E ${\skew2\dot V_{\rm{E}}}$ to control levels. Furthermore, adrenaline infusion during exercise elevated both Tc and V ̇ E ${\skew2\dot V_{\rm{E}}}$ . These findings indicate that: (1) adjustments in pulmonary gas exchange limit homeostatic disturbances in the face of a blunted pulmonary circulation; (2) hyperthermia is the main stimulus increasing ventilation during prolonged intense exercise; and (3) sympathoadrenal activation might partly mediate the hyperthermic hyperventilation.

Effects of visual feedback of thoracoabdominal motion on oxygen consumption during hyperventilation - Pilot study.

INTRODUCTION: Respiratory muscle oxygen consumption increases with the work of breathing. We hypothesized that reducing excessive respiratory muscle activity during exercise may improve exercise tolerance. METHOD: We developed a device to provide real-time visual feedback of thoracoabdominal movement and used it to examine the influence of visual feedback of thoracoabdominal movement during diaphragmatic breathing on oxygen consumption in eight healthy men. While sitting on a wheelchair with the backrest reclined at 60°, oxygen consumption per body weight (VO2/BW), minute ventilation (VE), tidal volume (VT), and breathing frequency (fR) were measured, breath-by-breath, using an expired-gas analyzer. The breathing pattern was analyzed by inductance plethysmography, with transducer bands over the chest and abdomen recording thoracoabdominal movements. RESULTS: There was no significant difference in RatioTH-ABD and the ventilatory parameters between diaphragmatic breathing and diaphragmatic breathing with visual feedback. The average VO2/BW during diaphragmatic breathing with visual feedback was 0.6 ml/kg lower than that during diaphragmatic breathing without visual feedback (p<0.05). CONCLUSION: When visual feedback was used during diaphragmatic breathing, the RatioTH-ABD remained essentially unchanged, but VO2/BW decreased significantly. This suggests that visual feedback of thoracoabdominal movement during diaphragmatic breathing may reduce respiratory muscle oxygen consumption.

Acute thoracoabdominal and hemodynamic responses to tapered flow resistive loading in healthy adults.

We investigated the acute physiological responses of tapered flow resistive loading (TFRL) at 30, 50 and 70 % maximal inspiratory pressure (PImax) in 12 healthy adults to determine an optimal resistive load. Increased end-inspiratory rib cage and decreased end-expiratory abdominal volumes equally contributed to the expansion of thoracoabdominal tidal volume (captured by optoelectronic plethysmography). A significant decrease in end-expiratory thoracoabdominal volume was observed from 30 to 50 % PImax, from 30 to 70 % PImax, and from 50 to 70 % PImax. Cardiac output (recorded by cardio-impedance) increased from rest by 30 % across the three loading trials. Borg dyspnoea increased from 2.36 ±â€¯0.20 at 30 % PImax, to 3.45 ±â€¯0.21 at 50 % PImax, and 4.91 ±â€¯0.25 at 70 % PImax. End-tidal CO2 decreased from rest during 30, 50 and 70 %PImax (26.23 ±â€¯0.59, 25.87 ±â€¯1.02 and 24.30 ±â€¯0.82 mmHg, respectively). Optimal intensity for TFRL is at 50 % PImax to maximise global respiratory muscle and cardiovascular loading whilst minimising hyperventilation and breathlessness.

Voluntary hypocapnic hyperventilation lasting 5†min and 20†min similarly reduce aerobic metabolism without affecting power outputs during Wingate anaerobic test.

AbstractTwenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise performance during the Wingate anaerobic test (WAnT). Thus, pre-exercise hypocapnic hyperventilation may be a useful means of stressing the anaerobic energy system during training, ultimately improving anaerobic exercise performance. However, it remains unclear whether a shorter (e.g., 5 min) pre-exercise hypocapnic hyperventilation is sufficient to reduce the aerobic metabolic rate during high-intensity exercise. We therefore compared the effects of 5-min and 20-min pre-exercise hypocapnic hyperventilation on aerobic metabolism during the 30-s WAnT. Ten healthy young males and one female performed the WAnT following 20 min of spontaneous breathing (control trial) or 5 or 20 min of voluntary hypocapnic hyperventilation. Both the 5-min and 20-min hyperventilation reduced end-tidal CO2 partial pressure (an index of arterial CO2 partial pressure) to ∼23 mmHg, whereas it remained unchanged during the spontaneous breathing. The peak, mean and minimum power outputs during the WAnT did not differ among the three trials. Oxygen uptake during the WAnT was lower in both the 5-min (1493 ± 257 mL min-1) and 20-min (1397 ± 447 mL min-1) hyperventilation trials than during the control trial (1847 ± 286 mL min-1), and was similar in the two hyperventilation trials. These results suggest that 5 min of pre-exercise hypocapnic hyperventilation reduces aerobic metabolism during the 30-s WAnT to a level similar to that seen with the 20-min hyperventilation. Moreover, exercise performance was unaffected, which implies anaerobic metabolism was enhanced.

Breathing exercises for adults with asthma.

BACKGROUND: Breathing exercises have been widely used worldwide as a non-pharmacological therapy to treat people with asthma. Breathing exercises aim to control the symptoms of asthma and can be performed as the Papworth Method, the Buteyko breathing technique, yogic breathing, deep diaphragmatic breathing or any other similar intervention that manipulates the breathing pattern. The training of breathing usually focuses on tidal and minute volume and encourages relaxation, exercise at home, the modification of breathing pattern, nasal breathing, holding of breath, lower rib cage and abdominal breathing. OBJECTIVES: To evaluate the evidence for the efficacy of breathing exercises in the management of people with asthma. SEARCH METHODS: To identify relevant studies we searched The Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL and AMED and performed handsearching of respiratory journals and meeting abstracts. We also consulted trials registers and reference lists of included articles. The most recent literature search was on 4 April 2019. SELECTION CRITERIA: We included randomised controlled trials of breathing exercises in adults with asthma compared with a control group receiving asthma education or, alternatively, with no active control group. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed study quality and extracted data. We used Review Manager 5 software for data analysis based on the random-effects model. We expressed continuous outcomes as mean differences (MDs) with confidence intervals (CIs) of 95%. We assessed heterogeneity by inspecting the forest plots. We applied the Chi2 test, with a P value of 0.10 indicating statistical significance, and the I2 statistic, with a value greater than 50% representing a substantial level of heterogeneity. The primary outcome was quality of life. MAIN RESULTS: We included nine new studies (1910 participants) in this update, resulting in a total of 22 studies involving 2880 participants in the review. Fourteen studies used Yoga as the intervention, four studies involved breathing retraining, one the Buteyko method, one the Buteyko method and pranayama, one the Papworth method and one deep diaphragmatic breathing. The studies were different from one another in terms of type of breathing exercise performed, number of participants enrolled, number of sessions completed, period of follow-up, outcomes reported and statistical presentation of data. Asthma severity in participants from the included studies ranged from mild to moderate, and the samples consisted solely of outpatients. Twenty studies compared breathing exercise with inactive control, and two with asthma education control groups. Meta-analysis was possible for the primary outcome quality of life and the secondary outcomes asthma symptoms, hyperventilation symptoms, and some lung function variables. Assessment of risk of bias was impaired by incomplete reporting of methodological aspects of most of the included studies. We did not include adverse effects as an outcome in the review. Breathing exercises versus inactive control For quality of life, measured by the Asthma Quality of Life Questionnaire (AQLQ), meta-analysis showed improvement favouring the breathing exercises group at three months (MD 0.42, 95% CI 0.17 to 0.68; 4 studies, 974 participants; moderate-certainty evidence), and at six months the OR was 1.34 for the proportion of people with at least 0.5 unit improvement in AQLQ, (95% CI 0.97 to 1.86; 1 study, 655 participants). For asthma symptoms, measured by the Asthma Control Questionnaire (ACQ), meta-analysis at up to three months was inconclusive, MD of -0.15 units (95% CI -2.32 to 2.02; 1 study, 115 participants; low-certainty evidence), and was similar over six months (MD -0.08 units, 95% CI -0.22 to 0.07; 1 study, 449 participants). For hyperventilation symptoms, measured by the Nijmegen Questionnaire (from four to six months), meta-analysis showed less symptoms with breathing exercises (MD -3.22, 95% CI -6.31 to -0.13; 2 studies, 118 participants; moderate-certainty evidence), but this was not shown at six months (MD 0.63, 95% CI -0.90 to 2.17; 2 studies, 521 participants). Meta-analyses for forced expiratory volume in 1 second (FEV1) measured at up to three months was inconclusive, MD -0.10 L, (95% CI -0.32 to 0.12; 4 studies, 252 participants; very low-certainty evidence). However, for FEV1 % of predicted, an improvement was observed in favour of the breathing exercise group (MD 6.88%, 95% CI 5.03 to 8.73; five studies, 618 participants). Breathing exercises versus asthma education For quality of life, one study measuring AQLQ was inconclusive up to three months (MD 0.04, 95% CI -0.26 to 0.34; 1 study, 183 participants). When assessed from four to six months, the results favoured breathing exercises (MD 0.38, 95% CI 0.08 to 0.68; 1 study, 183 participants). Hyperventilation symptoms measured by the Nijmegen Questionnaire were inconclusive up to three months (MD -1.24, 95% CI -3.23 to 0.75; 1 study, 183 participants), but favoured breathing exercises from four to six months (MD -3.16, 95% CI -5.35 to -0.97; 1 study, 183 participants). AUTHORS' CONCLUSIONS: Breathing exercises may have some positive effects on quality of life, hyperventilation symptoms, and lung function. Due to some methodological differences among included studies and studies with poor methodology, the quality of evidence for the measured outcomes ranged from moderate to very low certainty according to GRADE criteria. In addition, further studies including full descriptions of treatment methods and outcome measurements are required.

Breathlessness and dysfunctional breathing in patients with postural orthostatic tachycardia syndrome (POTS): The impact of a physiotherapy intervention.

Postural orthostatic tachycardia syndrome (POTS) is a chronic, multifactorial syndrome with complex symptoms of orthostatic intolerance. Breathlessness is a prevalent symptom, however little is known about the aetiology. Anecdotal evidence suggests that breathless POTS patients commonly demonstrate dysfunctional breathing/hyperventilation syndrome (DB/HVS). There are, however, no published data regarding DB/HVS in POTS, and whether physiotherapy/breathing retraining may improve patients' breathing pattern and symptoms. The aim of this study was to explore the potential impact of a physiotherapy intervention involving education and breathing control on DB/HVS in POTS. A retrospective observational cohort study of all patients with POTS referred to respiratory physiotherapy for treatment of DB/HVS over a 20-month period was undertaken. 100 patients (99 female, mean (standard deviation) age 31 (12) years) with a clinical diagnosis of DB/HV were referred, of which data was available for 66 patients pre - post intervention. Significant improvements in Nijmegen score, respiratory rate and breath hold time (seconds) were observed following treatment. These data provide a testable hypothesis that breathing retraining may provide breathless POTS patients with some symptomatic relief, thus improving their health-related quality of life. The intervention can be easily protocolised to ensure treatment fidelity. Our preliminary findings provide a platform for a subsequent randomised controlled trial of breathing retraining in POTS.

Assessing and responding to anxiety and panic in the Emergency Department.

Anxiety and panic symptoms are widespread in the general population. The physical manifestations of anxiety and panic commonly account for people presenting to Emergency Departments (EDs). It is therefore important for ED clinicians to be informed of the numerous causes of anxiety and panic and equipped to respond effectively. This paper describes the underlying pathophysiology of the physical symptoms of anxiety and panic and differential diagnoses to consider. Organic conditions that are associated with symptoms of anxiety and panic are highlighted. Brief interventions are tabled for ED clinicians to use when explaining symptoms, and to promote individual self-management.

Effects of GB34 acupuncture on hyperventilation-induced carbon dioxide reactivity and cerebral blood flow velocity in the anterior and middle cerebral arteries of normal subjects.

OBJECTIVES: To determine whether acupuncture at GB34 affects cerebral blood flow (CBF) via the anterior cerebral arteries (ACAs) and middle cerebral arteries (MCAs). METHODS: This study included 10 healthy young male volunteers. CBF velocity and cerebrovascular reactivity (CVR) were measured using transcranial Doppler sonography (TCD). The changes in hyperventilation-induced carbon dioxide (CO2) reactivity and modified blood flow velocity at 40 mm Hg (CV40) were observed for both ACAs and MCAs before and after GB34 acupuncture treatment. Blood pressure and heart rate were also measured before and after GB34 acupuncture treatment. RESULTS: The CO2 reactivity of the ipsilateral MCA significantly increased after GB34 acupuncture treatment, compared with that at baseline (P=0.007). In contrast, the CO2 reactivity of both ACAs and the contralateral MCA remained unchanged. The CV40 of both ACAs and MCAs did not change after GB34 acupuncture treatment and neither did the mean arterial blood pressure and heart rate. CONCLUSIONS: GB34 acupuncture treatment increased CO2 reactivity specifically in the ipsilateral MCA, but had no effect on either the ACAs or the contralateral MCA. These data suggest that GB34 acupuncture treatment improves the vasodilatory potential of the cerebral vasculature to compensate for fluctuations caused by changes in external conditions and could potentially be useful for the treatment of disorders of the ipsilateral MCA circulation.

The Effect of a Brief Mindfulness Training on Distress Tolerance and Stress Reactivity.

Poor distress tolerance (DT) is considered an underlying facet of anxiety, depression, and a number of other psychological disorders. Mindfulness may help to increase DT by fostering an attitude of acceptance or nonjudgment toward distressing experiences. Accordingly, the present study examined the effects of a brief mindfulness training on tolerance of different types of distress, and tested whether trait mindfulness moderates the effect of such training. Undergraduates (n = 107) naïve to mindfulness completed a measure of trait mindfulness and underwent a series of stress tasks (cold pressor, hyperventilation challenge, neutralization task) before and after completing a 15-minute mindfulness training or a no-instruction control in which participants listened to relaxing music. Participants in the mindfulness condition demonstrated greater task persistence on the hyperventilation task compared to the control group, as well as a decreased urge to neutralize the effects of writing an upsetting sentence. No effect on distress ratings during the tasks were found. Overall trait mindfulness did not significantly moderate task persistence, but those with lower scores on the act with awareness facet of mindfulness demonstrated greater relative benefit of mindfulness training on the hyperventilation challenge. Mediation analyses revealed significant indirect effects of mindfulness training on cold pressor task persistence and urges to neutralize through the use of the nonjudge and nonreact facets of mindfulness. These results suggest that a brief mindfulness training can increase DT without affecting the subjective experience of distress.

Dysfunctional breathing: what do we know?

Dysfunctional breathing (DB) is a respiratory condition characterized by irregular breathing patterns that occur either in the absence of concurrent diseases or secondary to cardiopulmonary diseases. Although the primary symptom is often dyspnea or "air hunger", DB is also associated with nonrespiratory symptoms such as dizziness and palpitations. DB has been identified across all ages. Its prevalence among adults in primary care in the United Kingdom is approximately 9.5%. In addition, among individuals with asthma, a positive diagnosis of DB is found in a third of women and a fifth of men. Although DB has been investigated for decades, it remains poorly understood because of a paucity of high-quality clinical trials and validated outcome measures specific to this population. Accordingly, DB is often underdiagnosed or misdiagnosed, given the similarity of its associated symptoms (dyspnea, tachycardia, and dizziness) to those of other common cardiopulmonary diseases such as COPD and asthma. The high rates of misdiagnosis of DB suggest that health care professionals do not fully understand this condition and may therefore fail to provide patients with an appropriate treatment. Given the multifarious, psychophysiological nature of DB, a holistic, multidimensional assessment would seem the most appropriate way to enhance understanding and diagnostic accuracy. The present narrative review was developed as a means of summarizing the available evidence about DB, as well as improving understanding of the condition by researchers and practitioners.

Respiratory mechanics and cerebral blood flow during heat-induced hyperventilation and its voluntary suppression in passively heated humans.

We investigated whether heat-induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot-water immersion and a water-perfused garment covering their upper body (both 41°C) until esophageal temperature (Tes ) reached 39°C or volitional termination. In each trial, participants breathed normally (normal-breathing) or voluntarily controlled minute ventilation (VE ) at a level equivalent to that observed after 5 min of heating (controlled-breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end-expiratory and inspiratory lung volumes were measured. During normal-breathing, VE increased as Tes rose above 38.0 ± 0.3°C, whereas controlled-breathing diminished the increase in VE (VE at Tes  = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min-1 during normal- and controlled-breathing, respectively, P < 0.001). During normal-breathing, end-tidal CO2 pressure and MCAV decreased with rising Tes , but controlled-breathing diminished these reductions (at Tes  = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec-1 , both P < 0.001). The work of breathing correlated positively with changes in VE (P < 0.001) and was lower during controlled- than normal-breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min-1 , respectively, at heating termination, P = 0.013). End-expiratory and inspiratory lung volumes did not differ between trials (P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat-induced hyperventilation increases the work of breathing without affecting end-expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing.

Out of thin air: Hyperventilation-triggered seizures.

Voluntary hyperventilation triggers seizures in the vast majority of people with absence epilepsy. The mechanisms that underlie this phenomenon remain unknown. Herein, we review observations - many made long ago - that provide insight into the relationship between breathing and absence seizures.

Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans.

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual's predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (-9 to -13 l/min) than at rest (-2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15-20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.

Dysfunctional breathing: what do we know? / Disfunção respiratória: o que sabemos?

ABSTRACT Dysfunctional breathing (DB) is a respiratory condition characterized by irregular breathing patterns that occur either in the absence of concurrent diseases or secondary to cardiopulmonary diseases. Although the primary symptom is often dyspnea or "air hunger", DB is also associated with nonrespiratory symptoms such as dizziness and palpitations. DB has been identified across all ages. Its prevalence among adults in primary care in the United Kingdom is approximately 9.5%. In addition, among individuals with asthma, a positive diagnosis of DB is found in a third of women and a fifth of men. Although DB has been investigated for decades, it remains poorly understood because of a paucity of high-quality clinical trials and validated outcome measures specific to this population. Accordingly, DB is often underdiagnosed or misdiagnosed, given the similarity of its associated symptoms (dyspnea, tachycardia, and dizziness) to those of other common cardiopulmonary diseases such as COPD and asthma. The high rates of misdiagnosis of DB suggest that health care professionals do not fully understand this condition and may therefore fail to provide patients with an appropriate treatment. Given the multifarious, psychophysiological nature of DB, a holistic, multidimensional assessment would seem the most appropriate way to enhance understanding and diagnostic accuracy. The present narrative review was developed as a means of summarizing the available evidence about DB, as well as improving understanding of the condition by researchers and practitioners.

RESUMO A disfunção respiratória (DR) é um quadro respiratório caracterizado por padrões respiratórios irregulares que ocorrem na ausência de doenças concomitantes ou secundariamente a doenças cardiopulmonares. Embora o principal sintoma seja frequentemente dispneia ou "fome por ar", a DR também está associada a sintomas não respiratórios, como vertigem e palpitações. A DR pode ser identificada em todas as idades. Sua prevalência entre adultos na atenção primária no Reino Unido é de aproximadamente 9,5%. Além disso, entre indivíduos com asma, um diagnóstico positivo de DR é encontrado em um terço das mulheres e um quinto dos homens. Embora a DR tenha sido investigada por décadas, ela permanece pouco compreendida devido a uma escassez de ensaios clínicos de alta qualidade e de variáveis de desfecho validadas especificamente para essa população. Assim, a DR é frequentemente subdiagnosticada ou diagnosticada incorretamente, devido à similaridade de seus sintomas associados (dispneia, taquicardia e vertigem) aos de outras doenças cardiopulmonares comuns, como DPOC e asma. As altas taxas de diagnóstico incorreto de DR sugerem que os profissionais de saúde não entendam completamente esse quadro e possam, portanto, não fornecer aos pacientes um tratamento adequado. Dada à natureza multifatorial e psicofisiológica da DR, uma avaliação holística e multidimensional parece ser a maneira mais apropriada de melhorar a compreensão e a precisão do diagnóstico. A presente revisão foi desenvolvida como um meio de resumir as evidências disponíveis sobre DB, bem como de melhorar a compreensão do quadro por pesquisadores e profissionais.

Respiratory Muscle Training Effects on Performance in Hypo- and Hyperbaria.

INTRODUCTION: Performing at high altitude and scuba diving impose functional limitations to the respiratory system and impair exercise performance compared to normobaria. At altitude, the partial pressure of oxygen is reduced, which decreases arterial oxygen saturation and exercise performance. Falling arterial oxygen saturation results in hyperventilation and increased pulmonary ventilation. Diving poses unique effects on the respiratory system. The work of breathing is increased from marked increased airway resistance, static lung load, and hydrostatic pressure from the water on the thoracic wall. Both altitude and diving increase the work and energy cost of breathing, resulting in respiratory muscle fatigue. Respiratory muscle training (RMT) has been employed to target the deleterious effects on the respiratory system and exercise capacity. Although the literature is sparse, RMT has been reported to decrease the work and energy cost of breathing and improve pulmonary ventilation, respiratory muscle strength, pulmonary function, and exercise capacity. This narrative review summarizes what is currently known about RMT for exercise performance at altitude and in diving, including potential mechanisms and outlines gaps in the literature.Hess H, Hostler D. Respiratory muscle training effects on performance in hypo- and hyperbaria. Aerosp Med Hum Perform. 2018; 89(11):996-1001.

Respiratory muscle training positively affects vasomotor response in young healthy women.

Vasomotor response is related to the capacity of the vessel to maintain vascular tone within a narrow range. Two main control mechanisms are involved: the autonomic control of the sympathetic neural drive (global control) and the endothelial smooth cells capacity to respond to mechanical stress by releasing vasoactive factors (peripheral control). The aim of this study was to evaluate the effects of respiratory muscle training (RMT) on vasomotor response, assessed by flow-mediated dilation (FMD) and heart rate variability, in young healthy females. The hypothesis was that RMT could enhance the balance between sympathetic and parasympathetic neural drive and reduce vessel shear stress. Thus, twenty-four women were randomly assigned to either RMT or SHAM group. Maximal inspiratory mouth pressure and maximum voluntary ventilation were utilized to assess the effectiveness of the RMT program, which consisted of three sessions of isocapnic hyperventilation/ week for eight weeks, (twenty-four training sessions). Heart rate variability assessed autonomic balance, a global factor regulating the vasomotor response. Endothelial function was determined by measuring brachial artery vasodilation normalized by shear rate (%FMD/SR). After RMT, but not SHAM, maximal inspiratory mouth pressure and maximum voluntary ventilation increased significantly (+31% and +16%, respectively). Changes in heart rate variability were negligible in both groups. Only RMT exhibited a significant increase in %FMD/SR (+45%; p<0.05). These data suggest a positive effect of RMT on vasomotor response that may be due to a reduction in arterial shear stress, and not through modulation of sympatho-vagal balance.