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Hyperthermia stimulates ventilation in humans. This hyperthermia-induced hyperventilation may be mediated by the activation of peripheral chemoreceptors implicated in the regulation of respiration in reaction to various chemical stimuli, including reductions in arterial pH. Here, we investigated the hypothesis that during passive heating at rest, the increases in arterial pH achieved with sodium bicarbonate ingestion, which could attenuate peripheral chemoreceptor activity, mitigate hyperthermia-induced hyperventilation. We also assessed the effect of sodium bicarbonate ingestion on cerebral blood flow responses, which are associated with hyperthermia-induced hyperventilation. Twelve healthy men ingested sodium bicarbonate (0.3 g/kg body weight) or sodium chloride (0.208 g/kg). One hundred minutes after the ingestion, the participants were passively heated using hot-water immersion (42°C) combined with a water-perfused suit. Increases in esophageal temperature (an index of core temperature) and minute ventilation (V̇E) during the heating were similar in the two trials. Moreover, when V̇E is expressed as a function of esophageal temperature, there were no between-trial differences in the core temperature threshold for hyperventilation (38.0 ± 0.3 vs. 38.0 ± 0.4°C, P = 0.469) and sensitivity of hyperthermia-induced hyperventilation as assessed by the slope of the core temperature-V̇E relation (13.5 ± 14.2 vs. 15.8 ± 15.5 L/min/°C, P = 0.831). Furthermore, middle cerebral artery mean blood velocity (an index of cerebral blood flow) decreased similarly with heating duration in both trials. These results suggest that sodium bicarbonate ingestion does not mitigate hyperthermia-induced hyperventilation and the reductions in cerebral blood flow index in resting heated humans. NEW & NOTEWORTHY: Hyperthermia leads to hyperventilation and associated cerebral hypoperfusion, both of which may impair heat tolerance. This hyperthermia-induced hyperventilation may be mediated by peripheral chemoreceptors, which can be activated by reductions in arterial pH. However, our results suggest that sodium bicarbonate ingestion, which can increase arterial pH, is not an effective intervention in alleviating hyperthermia-induced hyperventilation and cerebral hypoperfusion in resting heated humans. [ABSTRACT FROM AUTHOR]

Childhood absence epilepsy is one of the most prevalent pediatric epilepsy syndromes, but diagnostic delay is common and consequential. Childhood absence epilepsy is diagnosed by history and physical examination including hyperventilation with electroencephalography (EEG) used to confirm the diagnosis. Hyperventilation produces generalized spike-wave discharges on EEG in >90% of patients with childhood absence epilepsy and provokes clinical absence seizures consisting of brief loss of consciousness typically within 90 seconds. Child neurologists report a high volume of referrals for children with "staring spells" that strain already limited health care resources. Resources are further strained by the use of EEG for monitoring antiseizure medication effectiveness with unclear benefit. In this review, we examine the safety and efficacy of hyperventilation activation as a tool for the diagnosis and management of childhood absence seizures. [ABSTRACT FROM AUTHOR]

Arterial carbon dioxide ( Pa CO 2 ) and posture influence the middle (MCAv) and posterior (PCAv) cerebral artery blood velocities, but there is paucity of data about their interaction and need for an integrated model of their effects, including dynamic cerebral autoregulation (dCA). In 22 participants (11 males, age 30.2 ± 14.3 yr), blood pressure (BP, Finometer), dominant MCAv and nondominant PCAv (transcranial Doppler ultrasound), end-tidal CO2 (EtCO2, capnography), and heart rate (HR, ECG) were recorded continuously. Two recordings (R) were taken when the participant was supine (R1, R2), two taken when the participant was sitting (R3, R4), and two taken when the participant was standing (R5, R6). R1, R3, and R5 consisted of 3 min of 5% CO2 through a mask and R2, R4, and R6 consisted of 3 min of paced hyperventilation. The effects of Pa CO 2 were expressed with a logistic curve model (LCM) for each parameter. dCA was expressed by the autoregulation index (ARI), derived by transfer function analysis. Standing shifted LCM to the left for MCAv (P < 0.001), PCAv (P < 0.001), BP (P = 0.03), and ARI (P = 0.001); downward for MCAv and PCAv (both P < 0.001), and upward for HR (P < 0.001). For BP, LCM was shifted downward by sitting and standing (P = 0.024). For ARI, the hypercapnic range of LCM was shifted upward during standing (P < 0.001). A more complete mapping of the combined effects of posture and arterial CO2 on the cerebral circulation and peripheral variables can be obtained with the LCM over a broad physiological range of EtCO2 values. NEW & NOTEWORTHY: Data from supine, sitting, and standing postures were measured. Modeling the data with logistic curves to express the effects of CO2 reactivity on middle cerebral artery blood velocity (MCAv), posterior cerebral artery blood velocity (PCAv), heart rate, blood pressure (BP), and the autoregulation index (ARI), provided a more comprehensive approach to study the interaction of arterial CO2 with posture than in previous studies. Above all, shifts of the logistic curve model with changes in posture have shown interactions with Pa CO 2 that have not been previously demonstrated. [ABSTRACT FROM AUTHOR]

Hyperventilation (HV) is an activation technique performed during clinical practices to trigger epileptiform activities, supporting the neurophysiological evaluation of patients with epilepsy. Although the role of HV has often been questioned, especially in the case of focal epilepsy, no studies have ever assessed how cortical structures respond to such a maneuver via intracranial EEG recordings. This work aims to fill this gap by evaluating the HV effects on the Stereo-EEG (SEEG) signals from a cohort of 10 patients with drug-resistant focal epilepsy. We extracted multiple quantitative metrics from the SEEG signals and compared the results obtained during HV, awake status, non-REM sleep, and seizure onset. Our findings show that the cortical connectivity, estimated via the phase transfer entropy (PTE) algorithm, strongly increases during the HV maneuver, similar to non-REM sleep. The opposite effect is observed during seizure onset, as ictal transitions involve the desynchronization of the brain structures within the epileptogenic zone. We conclude that HV promotes a conductive environment that may facilitate the propagation of epileptiform activities but is not sufficient to trigger seizures in focal epilepsy. [ABSTRACT FROM AUTHOR]

Background: Supramaximal constant work rate tests (CWR) elicit intense hyperventilation, thus potentially up-shifting ventilation (⩒E)-to-carbon dioxide (CO2) responses when compared to graded exercise tests (GXT) in athletes. We predicted higher ventilatory efficiency on supramaximal CWR using a new method, challenging the classic orthodox interpretation of an increased ⩒E-⩒CO2 as ventilatory inefficiency. This misinterpretation could make difficult to differentiate between physiological hyperventilation from heart disease conditions in athletes. Methods: On different days, a GXT and a CWR at 110% of the maximal velocity achieved in the GXT were performed. Twenty-seven athletes completed the two tests and were compared for usual (linear regression) and log-transformed new variables for ventilatory efficiency through paired t-Student statistics. Results: The ⩒E-⩒CO2 slope (31.4 ± 4.9 vs. 26.2 ± 3.4, p < .001), ⩒E-⩒CO2 intercept (7.2 ± 7.5 vs. 2.8 ± 4.2, p < .007), ⩒E/⩒CO2 nadir (33.0 ± 3.6 vs. 25.4 ± 2.2, p < .001), ⩒CO2-log⩒E slope (10.8 ± 2.9 vs. 6.9 ± 2.2 L*logL−1, p < .001), and η⩒E (36.0 ± 12 vs. 22.8 ± 8.1%, p < .001) values were all significantly higher in the CWR compared to the GXT. We registered a bi-modal nadir response for ⩒E/⩒CO2 on CWR for 22 out of 27 subjects for the first time. A weak association was observed between ⩒E/⩒CO2 nadir (coefficient of determination ~ 27%) and time to exhaustion. Conclusions: The new method allows us to improve the quantification and interpretation of ventilatory efficiency in athletes, avoiding misinterpretation due to the up-shifting elicited by the usual ⩒E-⩒CO2 slope and ⩒E/⩒CO2 nadir indices, which may be confounded with ventilatory inefficiency. This study suggests that ventilatory changes underpin better ventilatory efficiency during CWR. [ABSTRACT FROM AUTHOR]

The article discusses the damaging effects of stress overload and the therapeutic role of breathing practices. Topics include the reason that people get stressed, causes and types of stress, and neurobiology of the stress response. Also mentioned are the good, tolerable, and toxic stress and the importance of managing allostatic load and building stress resilience.

Postural control can be challenged by breathing. What is the effect of an acute increase in respiratory demand on postural control compared to quiet breathing? A systematic review was conducted. Electronic databases were systematically searched until October 18, 2022 on studies reporting changes in center of pressure (CoP) motion related to an acute manipulation of respiratory demand compared to quiet breathing during upright standing in healthy participants and/or participants with a clinical condition. Twenty-one studies in healthy participants showed that voluntary (not metabolic-induced) hyperventilation or inspiratory resistive loading significantly increased CoP motion, while breath-holding decreased CoP motion, compared to quiet breathing (p< 0.05). Manipulating respiratory rate or breathing patterns did not reveal consistent results. Four studies showed that people with low back pain showed similar CoP responses to increasing respiratory demand (p> 0.05), except for breathing at different rates, whereas they showed greater CoP motion during quiet breathing. The extent of postural disturbance depended on the breathing mode and how it was quantified (i.e., CoP coupled with breathing movement or overall CoP measures). Voluntary hyperventilation and inspiratory resistive loading increased postural sway. For voluntary hyperventilation, this could be explained by CoP motion being directly coupled to chest wall movements whereas metabolic-induced hyperventilation did not increase CoP motion or CoP coupling with breathing. Breath-holding decreased postural sway. Patients with low back pain show greater postural sways than pain-free individuals during quiet breathing, although they exhibit similar postural adaptations to respiratory-related challenges as controls. • Studies assessing the effect of breathing demand on postural control were reviewed • Voluntary (not metabolic-induced) hyperventilation increased postural sway • Inspiratory resistive loading increased postural sway • Breath-holding decreased postural sway • Patients with low back pain show similar responses to increasing breathing demand [ABSTRACT FROM AUTHOR]

Background. Mechanical ventilation is a critical intervention in neonatal intensive care units (NICUs), but it has been associated with increased mortality and morbidity, particularly through complications like hyperoxemia and hypocapnia. This study aims to identify the incidence of these conditions in ventilated neonates and correlate them with ventilator parameters and related complications. Materials and methods. This observational study was conducted on 100 neonates who were mechanically ventilated in the NICU of Abo-Rish El Monira Hospital, Cairo University, between March and September 2019. Participants were selected based on their requirement for mechanical ventilation during NICU admission. Data collection included perinatal history, ventilator parameters, and arterial blood gas results. Statistical analyses were performed using Pearson correlation, independent t-tests, and logistic regression analysis. Results. The incidence of hypocapnia was 82 %, while 77 % of neonates experienced arterial hyperoxemia. Hypocapnia was more frequent with prolonged mechanical ventilation, showing a significant positive correlation with the incidence (P 0.05). Mortality rates were higher among neonates with hypocapnia (67.1 %) and hyperoxemia (65 %). Conclusions. Hyperoxemia and hypocapnia are common complications of mechanical ventilation in the NICU settings, with hypocapnia showing a higher incidence. Both conditions are associated with increased mortality, particularly among neonates with lower gestational age and birth weight. Managing ventilator settings and monitoring blood gases are critical in reducing these complications.

Background Within the general epilepsy population, the incidence of Sudden Unexpected Death in Epilepsy (SUDEP) ranges from approximately 0.35 to 2.3 per 1,000 individuals per year.

The document explores the physiological challenges associated with artistic swimming, an Olympic sport that combines swimming, dance, weightlifting, cheerleading, and gymnastics. Athletes in artistic swimming perform routines involving vigorous exercise with prolonged breath-holds, leading to complex physiological responses and potential episodes of syncope (loss of consciousness). The text highlights the need for further research into the unique physiological demands of artistic swimming and the safety risks associated with prolonged breath-holding and autonomic conflict. [Extracted from the article]

This research letter published in the Clinical & Experimental Allergy journal discusses a study on the effects of pulmonary rehabilitation (PR) on individuals with severe asthma. The study found that PR was associated with improvements in asthma control, a reduction in severe exacerbations, and a decrease in glucocorticoid use. However, the study had limitations and further research is needed to confirm these findings. Overall, the study suggests that PR may be beneficial for individuals with severe asthma, but more research is necessary to determine its role in managing the condition. [Extracted from the article]

Dyspnea is a common yet poorly understood symptom of long COVID, affecting many patients. This brief report examines the role of dysfunctional breathing in persistent dyspnea among patients with mild post-COVID-19 using hyperventilation provocation tests (HVPT). In this case series, six patients with unexplained dyspnea and normal cardiopulmonary function underwent HVPT. Despite normal exercise testing results, all patients exhibited delayed PETCO2 recovery, indicative of a hyperventilation pattern consistent with chronic hyperventilation syndrome, without typical symptomatic manifestations. These findings suggest underlying post-COVID respiratory dysregulation, emphasizing the importance of targeted diagnostic and therapeutic approaches for persistent respiratory symptoms in long COVID patients. [ABSTRACT FROM AUTHOR]

This article provides information on the use of facemask noninvasive ventilation (NIV) in various clinical settings. NIV allows for positive airway pressure without the need for intubation, providing respiratory support while avoiding the negative effects of invasive mechanical ventilation. The article discusses the set-up and ventilatory settings for facemask NIV, as well as its indications and monitoring. It also highlights the limitations and contraindications of this technique. The information presented in the article is based on research and clinical experience. [Extracted from the article]

Current guidelines suggest a target of partial pressure of carbon dioxide (PaCO2) of 32–35 mmHg (mild hypocapnia) as tier 2 for the management of intracranial hypertension. However, the effects of mild hyperventilation on cerebrovascular dynamics are not completely elucidated. The aim of this study is to evaluate the changes of intracranial pressure (ICP), cerebral autoregulation (measured through pressure reactivity index, PRx), and regional cerebral oxygenation (rSO2) parameters before and after induction of mild hyperventilation. Single center, observational study including patients with acute brain injury (ABI) admitted to the intensive care unit undergoing multimodal neuromonitoring and requiring titration of PaCO2 values to mild hypocapnia as tier 2 for the management of intracranial hypertension. Twenty-five patients were included in this study (40% female), median age 64.7 years (Interquartile Range, IQR = 45.9–73.2). Median Glasgow Coma Scale was 6 (IQR = 3–11). After mild hyperventilation, PaCO2 values decreased (from 42 (39–44) to 34 (32–34) mmHg, p < 0.0001), ICP and PRx significantly decreased (from 25.4 (24.1–26.4) to 17.5 (16–21.2) mmHg, p < 0.0001, and from 0.32 (0.1–0.52) to 0.12 (-0.03–0.23), p < 0.0001). rSO2 was statistically but not clinically significantly reduced (from 60% (56–64) to 59% (54–61), p < 0.0001), but the arterial component of rSO2 (ΔO2Hbi, changes in concentration of oxygenated hemoglobin of the total rSO2) decreased from 3.83 (3–6.2) μM.cm to 1.6 (0.5–3.1) μM.cm, p = 0.0001. Mild hyperventilation can reduce ICP and improve cerebral autoregulation, with minimal clinical effects on cerebral oxygenation. However, the arterial component of rSO2 was importantly reduced. Multimodal neuromonitoring is essential when titrating PaCO2 values for ICP management. [ABSTRACT FROM AUTHOR]

Prior studies have identified variable effects of aging on neurovascular coupling (NVC). Carbon dioxide (CO2) affects both cerebral blood velocity (CBv) and NVC, but the effects of age on NVC under different CO2 conditions are unknown. Therefore, we investigated the effects of aging on NVC in different CO2 states during cognitive paradigms. Seventy-eight participants (18–78 yr), with well-controlled comorbidities, underwent continuous recordings of CBv by bilateral insonation of middle (MCA) and posterior (PCA) cerebral arteries (transcranial Doppler), blood pressure, end-tidal CO2, and heart rate during poikilocapnia, hypercapnia (5% CO2 inhalation), and hypocapnia (paced hyperventilation). Neuroactivation via visuospatial (VS) and attention tasks (AT) was used to stimulate NVC. Peak percentage and absolute change in MCAv/PCAv, were compared between CO2 conditions and age groups (≤30, 31–60, and >60 yr). For the VS task, in poikilocapnia, younger adults had a lower NVC response compared with older adults [mean difference (MD): −7.92% (standard deviation (SD): 2.37), P = 0.004], but comparable between younger and middle-aged groups. In hypercapnia, both younger [MD: −4.75% (SD: 1.56), P = 0.009] and middle [MD: −4.58% (SD: 1.69), P = 0.023] age groups had lower NVC responses compared with older adults. Finally, in hypocapnia, both older [MD: 5.92% (SD: 2.21), P = 0.025] and middle [MD: 5.44% (SD: 2.27), P = 0.049] age groups had greater NVC responses, compared with younger adults. In conclusion, the magnitude of NVC response suppression from baseline during hyper- and hypocapnia, did not differ significantly between age groups. However, the middle age group demonstrated a different NVC response while under hypercapnic conditions, compared with hypocapnia. NEW & NOTEWORTHY: This study describes the effects of age on neurovascular coupling under altered CO2 conditions. We demonstrated that both hypercapnia and hypocapnia suppress neurovascular coupling (NVC) responses. Furthermore, that middle age exhibits an NVC response comparable with younger adults under hypercapnia, and older adults under hypocapnia. [ABSTRACT FROM AUTHOR]

Background: TCF4 acts as a transcription factor that binds to the immunoglobulin enhancer Mu-E5/KE5 motif. Dominant variants in TCF4 are associated with the manifestation of Pitt-Hopkins syndrome, a rare disease characterized by severe mental retardation, certain features of facial dysmorphism and, in many cases, with abnormalities in respiratory rhythm (episodes of paroxysmal tachypnea and hyperventilation, followed by apnea and cyanosis). Frequently, patients also develop epilepsy, microcephaly, and postnatal short stature. Although TCF4 is expressed in skeletal muscle and TCF4 seems to play a role in myogenesis as demonstrated in mice, potential myopathological findings taking place upon the presence of dominant TCF4 variants are thus far not described in human skeletal muscle. Method: To address the pathological effect of a novel deletion affecting exons 15 and 16 of TCF4 on skeletal muscle, histological and immunofluorescence studies were carried out on a quadriceps biopsy in addition to targeted transcript studies and global proteomic profiling. Results: We report on muscle biopsy findings from a Pitt-Hopkins patient with a novel heterozygous deletion spanning exon 15 and 16 presenting with neuromuscular symptoms. Microscopic characterization of the muscle biopsy revealed moderate fiber type I predominance, imbalance in the proportion of fibroblasts co-expressing Vimentin and CD90, and indicate activation of the complement cascade in TCF4-mutant muscle. Protein dysregulations were unraveled by proteomic profiling. Transcript studies confirmed a mitochondrial vulnerability in muscle and confirmed reduced TCF4 expression. Conclusion: Our combined findings, for the first time, unveil myopathological changes as phenotypical association of Pitt-Hopkins syndrome and thus expand the current clinical knowledge of the disease as well as support data obtained on skeletal muscle of a mouse model. [ABSTRACT FROM AUTHOR]

Introduction: Current evidence indicates a modulating role of respiratory processes in cardiac interoception, yet whether altered breathing patterns influence heartbeat-evoked potentials (HEP) remains inconclusive. Methods: Here, we examined the effects of voluntary hyperventilation (VH) as part of a clinical routine examination on scalp-recorded HEPs in epilepsy patients (N = 80). Results: Using cluster-based permutation analyses, HEP amplitudes were compared across pre-VH and post-VH conditions within young and elderly subgroups, as well as for the total sample. No differences in the HEP were detected for younger participants or across the full sample, while an increased late HEP during pre-VH compared to post-VH was fond in the senior group, denoting decreased cardiac interoceptive processing after hyperventilation. Discussion: The present study, thus, provides initial evidence of breathingrelated HEP modulations in elderly epilepsy patients, emphasizing the potential of HEP as an interoceptive neural marker that could partially extend to the representation of pulmonary signaling. We speculate that aberrant CO2-chemosensing, coupled with disturbances in autonomic regulation, might constitute the underlying pathophysiological mechanism behind the obtained effect. Available databases involving patient records of routine VH assessment may constitute a valuable asset in disentangling the interplay of cardiac and ventilatory interoceptive information in various patient groups, providing thorough clinical data to parse, as well as increased statistical power and estimates of effects with higher precision through large-scale studies. [ABSTRACT FROM AUTHOR]

Introduction Traumatic brain injury (TBI) is the leading cause of combat casualties in modern war with an estimated 20% of casualties experiencing head injury. Since the release of the Brain Trauma Foundation's Guidelines for the Management of Severe Traumatic Brain Injury in 1995, recommendations for management of TBI have included the avoidance of routine hyperventilation. However, both published and anecdotal data suggest that many patients with TBI are inappropriately ventilated during transport, thereby increasing the risk of morbidity and mortality from secondary brain injury. Materials and Methods Enlisted Air Force personnel with prior emergency medical technician training completing a 3-week trauma course were evaluated on their ability to provide manual ventilation. Participants provided manual ventilation using either an in-situ endotracheal tube (ETT) or standard face mask on a standardized simulated patient manikin with TBI on the first and last days of the course. Manual ventilation was provided via a standard manual ventilator and a novel manual ventilator designed to limit tidal volume (VT) and respiratory rate (RR). Participants were given didactic and hands-on training on the third day of the course. Half of the participants were given simulator feedback during the hands-on training. All students provided 2 minutes of manual ventilation with each respirator. Data were collected on the breath-to-breath RR, VT, and peak airway pressures generated by the participant for each trial and were averaged for each trial. A minute ventilation (MV) was then derived from the calculated RR and VT. Results One hundred fifty-six personnel in the trauma course were evaluated in this study. Significant differences were found in the participant's performance with manual ventilation with the novel compared to the traditional ventilator. Before training, MV with the novel ventilator was less than with the traditional ventilator by 2.1 ± 0.4 L/min (P  = .0003) and 1.6 ± 0.5 L/min (P  = .0489) via ETT and face mask, respectively. This effect persisted after training with a difference between the devices of 1.8 ± 0.4 L/min (P  = .0069) via ETT. Both traditional education interventions (didactics with hands-on training) and simulator-based feedback did not make a significant difference in participant's performance in delivering MV. Conclusions The use of a novel ventilator that limits RR and VT may be useful in preventing hyperventilation in TBI patients. Didactic education and simulator-based feedback training may not have significant impact on improving ventilation practices in prehospital providers. [ABSTRACT FROM AUTHOR]

This document provides a comprehensive examination of the use of nitrogen anoxia as a method of execution in Alabama. The authors argue that this method is inherently inhumane and flawed from a physiological perspective. They discuss the respiratory physiology of nitrogen anoxia and its impact on the body until death, highlighting the vulnerability of the brain to oxygen deprivation. The article also addresses misinformation surrounding nitrogen-induced hypoxia as a form of capital punishment, emphasizing the importance of understanding the physiological effects of nitrogen inhalation. The authors express their opposition to the death penalty and advocate for challenging authority in matters of human health and life. [Extracted from the article]

Pain is a naturally occurring phenomenon that consistently inhibits exercise performance by imposing unconscious, neurophysiological alterations (e.g., corticospinal changes) as well as conscious, psychophysiological pressures (e.g., shared effort demands). Although several studies indicate that pain would elicit lower task outputs for a set intensity of perceived effort, no study has tested this. Therefore, this study investigated the impact of elevated muscle pain through a hypertonic saline injection on the power output, psychophysiological, cerebral oxygenation, and perceptual changes during fixed perceived effort exercise. Ten participants completed three visits (1 familiarization + 2 fixed perceived effort trials). Fixed perceived effort cycling corresponded to 15% above gas exchange threshold (GET) [mean rating of perceived effort (RPE) = 15 "hard"]. Before the 30-min fixed perceived effort exercise, participants received a randomized bilateral hypertonic or isotonic saline injection in the vastus lateralis. Power output, cardiorespiratory, cerebral oxygenation, and perceptual markers (e.g., affective valence) were recorded during exercise. Linear mixed-model regression assessed the condition and time effects and condition × time interactions. Significant condition effects showed that power output was significantly lower during hypertonic conditions [t107 = 208, P = 0.040, β = 4.77 W, 95% confidence interval (95% CI) [0.27 to 9.26 W]]. Meanwhile, all physiological variables (e.g., heart rate, oxygen uptake, minute ventilation) demonstrated no significant condition effects. Condition effects were observed for deoxyhemoglobin changes from baseline (t107 = −3.29, P = 0.001, β = −1.50 ΔμM, 95% CI [−2.40 to −0.61 ΔμM]) and affective valence (t127 = 6.12, P = 0.001, β = 0.93, 95% CI [0.63 to 1.23]). Results infer that pain impacts the self-regulation of fixed perceived effort exercise, as differences in power output mainly occurred when pain ratings were higher after hypertonic versus isotonic saline administration. NEW & NOTEWORTHY: This study identifies that elevated muscle pain through a hypertonic saline injection causes significantly lower power output when pain is experienced but does not seem to affect exercise behavior in a residual manner. Results provide some evidence that pain operates on a psychophysiological level to alter the self-regulation of exercise behavior due to differences between conditions in cerebral deoxyhemoglobin and other perceptual parameters. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Cabin decompression presents a threat in high-altitude-capable aircraft. A chamber study was performed to compare effects of rapid (RD) vs. gradual decompression and gauge impairment at altitude with and without hypoxia, as well as to assess recovery. METHODS: There were 12 participants who completed RD (1 s) and Gradual (3 min 12 s) ascents from 2743-7620 m (9000-25000 ft) altitude pressures while breathing air or 100% O2. Physiological indices included oxygen saturation (SPO2), heart rate (HR), respiration, end tidal O2 and CO2 partial pressures, and electroencephalography (EEG). Cognition was evaluated using SYNWIN, which combines memory, arithmetic, visual, and auditory tasks. The study incorporated ascent rate (RD, gradual), breathing gas (air, 100% O2) and epoch (ground-level, pre-breathe, ascent-altitude, recovery) as factors. RESULTS: Physiological effects in hypoxic "air" ascents included decreased SPO2 and end tidal O2 and CO2 partial pressures (hypocapnia), with elevated HR and minute ventilation (V̇ E); SPO2 and HR effects were greater after RD (-7.3% lower and +10.0 bpm higher, respectively). HR and V̇ E decreased during recovery. SYNWIN performance declined during ascent in air, with key metrics, including composite score, falling further (-75% vs. -50%) after RD. Broad cognitive impairment was not recorded on 100% O2, nor in recovery. EEG signals showed increased slow-wave activity during hypoxia. DISCUSSION: In hypoxic exposures, RD impaired performance more than gradual ascent. Hypobaria did not comprehensively impair performance without hypoxia. Lingering impairment was not observed during recovery, but HR and V̇ E metrics suggested compensatory slowing following altitude stress. Participants' cognitive strategy shifted as hypoxia progressed, with efficiency giving way to "satisficing," redistributing effort to easier tasks. [ABSTRACT FROM AUTHOR]

Background: Given the limited access to invasive vasospastic reactivity testing in Western Countries, there is a need to further develop alternative non‐invasive diagnostic methods for vasospastic angina (VSA). Hyperventilation testing (HVT) is defined as a class IIa recommendation to diagnose VSA by the Japanese Society of Cardiology. Methods: In this systematic review and meta‐analysis reported according to the PRISMA statement, we review the mechanisms, methods, modalities and diagnostic accuracy of non‐invasive HVT for the diagnostic of VSA. Results: A total of 106 articles published between 1980 and 2022 about VSA and HVT were included in the systematic review, among which 16 were included in the meta‐analysis for diagnostic accuracy. Twelve electrocardiogram‐HVT studies including 804 patients showed a pooled sensitivity of 54% (95% confidence intervals [CI]; 30%–76%) and a pooled specificity of 99% (95% CI; 88%–100%). Four transthoracic echocardiography‐HVT studies including 197 patients revealed a pooled sensitivity of 90% (95% CI; 82%–94%) and a pooled specificity of 98% (95% CI; 86%–100%). Six myocardial perfusion imaging‐HVT studies including 112 patients yielded a pooled sensitivity of 95% (95% CI; 63%–100%) and a pooled specificity of 78% (95% CI; 19%–98%). Non‐invasive HVT resulted in a low rate of adverse events, ventricular arrhythmias being the most frequently reported, and were resolved with the administration of nitroglycerin. Conclusions: Non‐invasive HVT offers a safe alternative with high diagnostic accuracy to diagnose VSA in patients with otherwise undiagnosed causes of chest pain. [ABSTRACT FROM AUTHOR]

Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease. [ABSTRACT FROM AUTHOR]

State-of-the-art therapy improves the five-year survival rate of patients under the age of 20 with cranial and craniospinal tumors by up to 74%. The urgency of dealing effectively with late treatment-associated cardiovascular complications is rising. Objective: We aimed to assess echocardiographic parameters and exercise performance in subjects with a history of complex treatment for cranial and craniospinal tumors in childhood. Methods: the study of 48 subjects who underwent cranial and craniospinal irradiation for CNS tumors in childhood and 20 healthy age- and sex-matched volunteers was conducted. The examination included hormone studies, cardiopulmonary exercise testing, and, in the main group, echocardiography (ECHO). Results: In five (10.4%) patients, ECHO changes were detected after complex anti-cancer treatment: thickening and calcification of the aortic valve leaflets (2%), and reduction in the systolic LV and RV function (8% and 6%, respectively). Irradiation of various areas was a significant predictor for reduced exercise tolerance, hyperventilation at rest and upon exertion, and an increased ventilatory equivalent for carbon dioxide. Low exercise tolerance was associated with a younger age at the time of treatment initiation. Significant differences were noted between the control group and the childhood cancer survivors with endocrine disorders. Conclusions: The obtained data confirm the importance of regular cardiovascular and endocrine monitoring of this group of cancer survivors. [ABSTRACT FROM AUTHOR]

In Canada, acupuncture is a regulated medical practice that involves inserting thin needles at specific points on the body to alleviate pain and other health conditions. Acupuncture is a controlled act in physiotherapy practice. Therefore, physiotherapists who incorporate acupuncture into their practice should have the necessary education and roster this controlled act with the regulatory college in their province. Although acupuncture can be helpful, potential complications can arise, ranging from minor bruising to life-threatening conditions such as pneumothorax and cardiac tamponade. This article provides information on the potential adverse effects of acupuncture and provides recommendations for physiotherapists regarding prevention and management of any incidents that may arise during treatment. [ABSTRACT FROM AUTHOR]

The aim of the study was to detect the relationship of isocapnic buffering phase values with the values of both aerobic and anaerobic power. A total of 14 athletes, five females and nine males, with ages between 18 and 25 volunteered to participate in the present study. At the beginning, the values of height, body mass, and body fat ratio of the volunteers were collected as required. Then, a maximal exercise test was applied to the volunteers and during the test, the values of maximal oxygen consumption capacity (VO2max), amount of oxygen consumed (VO2), amount of carbon dioxide produced (VCO2), ventilatory threshold, respiratory compensation point, and maximal heart rate were determined. Isocapnic buffering and hypocapnic hyperventilation phases were determined from the ventilatory threshold and respiratory compensation point values. One week after the maximal exercise test, the Wingate anaerobic test was applied to the volunteers and anaerobic power values were calculated. A significant relationship was found between the values of isocapnic buffering and hypocapnic hyperventilation, and the values of maximal heart rate (beats/min), ventilatory threshold VO2 (ml/kg/min), ventilatory threshold heart rate (beats/min), ventilatory threshold speed (km/hour), respiratory compensation point heart rate (beats/min), and respiratory compensation point speed (km/hour) in both male and female volunteers. The findings collected hereby indicate that as the VO2max levels of athletes increase, both their cardiopulmonary data and anaerobic power values and also their ability to resist the intensity of exercises applied after entering anaerobic threshold, increase. [ABSTRACT FROM AUTHOR]

The article discusses the prevalence of exercise-induced bronchoconstriction (EIB) in adolescent recreational athletes and the challenges in diagnosing and managing this condition. Screening strategies, such as the use of FeNO levels and the AQUA questionnaire, are highlighted as potential tools for early detection of EIB. The study emphasizes the need for better screening methods to identify athletes with EIB and ensure appropriate management. Additionally, the correlation between atopy, asthma, and EIB is explored, with findings suggesting that atopy may be linked to underlying Type 2 inflammation. [Extracted from the article]

Hypoxia during supramaximal exercise reduces aerobic metabolism with a compensatory increase in anaerobic metabolism without affecting exercise performance. A similar response is elicited by preexercise voluntary hypocapnic hyperventilation, but it remains unclear whether hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism during supramaximal exercise. To address that issue, 12 healthy subjects (8 males and 4 females) performed the 30-second Wingate anaerobic test (WAnT) after (1) spontaneous breathing in normoxia (control, ∼21% fraction of inspired O2 [FiO2]), (2) voluntary hypocapnic hyperventilation in normoxia (hypocapnia, ∼21% FiO2), (3) spontaneous breathing in hypoxia (hypoxia, ∼11% FiO2), or (4) voluntary hypocapnic hyperventilation in hypoxia (combined, ∼11% FiO2). Mean power output during the 30-second WAnT was similar among the control (561 [133] W), hypocapnia (563 [140] W), hypoxia (558 [131] W), and combined (560 [133] W) trials (P =.778). Oxygen uptake during the 30-second WAnT was lower in the hypocapnia (1523 [318] mL/min), hypoxia (1567 [300] mL/min), and combined (1203 [318] mL/min) trials than in the control (1935 [250] mL/min) trial, and the uptake in the combined trial was lower than in the hypocapnia or hypoxia trial (all P <.001). Oxygen deficit, an index of anaerobic metabolism, was higher in the hypocapnia (38.4 [7.3] mL/kg), hypoxia (37.8 [6.8] mL/kg), and combined (40.7 [6.9] mL/kg) trials than in the control (35.0 [6.8] mL/kg) trial, and the debt was greater in the combined trial than in the hypocapnia or hypoxia trial (all P <.003). Our results suggest that voluntary hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism without affecting exercise performance during the 30-second WAnT. [ABSTRACT FROM AUTHOR]

Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease.

Abstract Background SARS-CoV-2 infection has raised concerns about long-term health repercussions. Exercise ventilatory inefficiency (EVin) has emerged as a notable long-term sequela, potentially impacting respiratory and cardiovascular health. This study aims to assess the long-term presence of EVin after 34 months and its association with cardiorespiratory health in post-COVID patients. Methods In a longitudinal study on 32 selected post-COVID subjects, we performed two cardiopulmonary exercise tests (CPETs) at 6 months (T0) and 34 months (T1) after hospital discharge. The study sought to explore the long-term persistence of EVin and its correlation with respiratory and cardiovascular responses during exercise. Measurements included also V̇O2peak, end-tidal pressure of CO2 (PETCO2) levels, oxygen uptake efficiency slope (OUES) and other cardiorespiratory parameters, with statistical significance set at p

Background: SARS-CoV-2 infection has raised concerns about long-term health repercussions. Exercise ventilatory inefficiency (EVin) has emerged as a notable long-term sequela, potentially impacting respiratory and cardiovascular health. This study aims to assess the long-term presence of EVin after 34 months and its association with cardiorespiratory health in post-COVID patients. Methods: In a longitudinal study on 32 selected post-COVID subjects, we performed two cardiopulmonary exercise tests (CPETs) at 6 months (T0) and 34 months (T1) after hospital discharge. The study sought to explore the long-term persistence of EVin and its correlation with respiratory and cardiovascular responses during exercise. Measurements included also V̇O2peak, end-tidal pressure of CO2 (PETCO2) levels, oxygen uptake efficiency slope (OUES) and other cardiorespiratory parameters, with statistical significance set at p < 0.05. The presence of EVin at both T0 and T1 defines a persisting EVin (pEVin). Results: Out of the cohort, five subjects (16%) have pEVin at 34 months. Subjects with pEVin, compared to those with ventilatory efficiency (Evef) have lower values of PETCO2 throughout exercise, showing hyperventilation. Evef subjects demonstrated selective improvements in DLCO and oxygen pulse, suggesting a recovery in cardiorespiratory function over time. In contrast, those with pEvin did not exhibit these improvements. Notably, significant correlations were found between hyperventilation (measured by PETCO2), oxygen pulse and OUES, indicating the potential prognostic value of OUES and Evin in post-COVID follow-ups. Conclusions: The study highlights the clinical importance of long-term follow-up for post-COVID patients, as a significant group exhibit persistent EVin, which correlates with altered and potentially unfavorable cardiovascular responses to exercise. These findings advocate for the continued investigation into the long-term health impacts of COVID-19, especially regarding persistent ventilatory inefficiencies and their implications on patient health outcomes. [ABSTRACT FROM AUTHOR]

Pilomotor seizures are strongly associated with autoimmune encephalitis (AE), particularly anti‐LGI1 encephalitis. The carbonic anhydrase inhibitor acetazolamide may have special efficacy for treating AE‐associated pilomotor seizures. Six patients with AE (five anti‐LGI1, one seronegative) and temporal lobe pilomotor seizures (five with seizures inducible by hyperventilation) were treated with acetazolamide, administered in a cycling (2‐days‐ON, 4‐days‐OFF) regimen to offset tolerance. Seizures were assessed during epilepsy monitoring unit (EMU) recordings in four inpatients (one of whom also maintained an outpatient seizure diary chronicling 1203 seizures over 1079 days); two outpatients self‐reported seizure frequencies. The extended diary revealed an inverse correlation between acetazolamide and proportion of seizures/day: 6%, 2% (days 1, 2 ON); 3%, 13%, 31%, 45% (days 1, 2, 3, 4 OFF). This patient later developed focal status epilepticus upon wean of antiseizure medications during a seropositive AE relapse that was remarkably aborted with acetazolamide monotherapy. The other three EMU patients averaged.56 seizures/day ON, and 3.81 seizures/day OFF (p =.004). The two outpatients reported seizure reductions from 3–5/day to 2/week, and 15–20/day to none, respectively, after initiation of cycling acetazolamide. Likely related to cerebral CO2/pH sensitivity, acetazolamide can be unusually effective in controlling pilomotor seizures in AE, chronically or in acute settings. [ABSTRACT FROM AUTHOR]

Respiratory drive is defined as the intensity of respiratory centers output during the breath and is primarily affected by cortical and chemical feedback mechanisms. During the involuntary act of breathing, chemical feedback, primarily mediated through CO2, is the main determinant of respiratory drive. Respiratory drive travels through neural pathways to respiratory muscles, which execute the breathing process and generate inspiratory flow (inspiratory flow-generation pathway). In a healthy state, inspiratory flow-generation pathway is intact, and thus respiratory drive is satisfied by the rate of volume increase, expressed by mean inspiratory flow, which in turn determines tidal volume. In this review, we will explain the pathophysiology of altered respiratory drive by analyzing the respiratory centers response to arterial partial pressure of CO2 (PaCO2) changes. Both high and low respiratory drive have been associated with several adverse effects in critically ill patients. Hence, it is crucial to understand what alters the respiratory drive. Changes in respiratory drive can be explained by simultaneously considering the (1) ventilatory demands, as dictated by respiratory centers activity to CO2 (brain curve); (2) actual ventilatory response to CO2 (ventilation curve); and (3) metabolic hyperbola. During critical illness, multiple mechanisms affect the brain and ventilation curves, as well as metabolic hyperbola, leading to considerable alterations in respiratory drive. In critically ill patients the inspiratory flow-generation pathway is invariably compromised at various levels. Consequently, mean inspiratory flow and tidal volume do not correspond to respiratory drive, and at a given PaCO2, the actual ventilation is less than ventilatory demands, creating a dissociation between brain and ventilation curves. Since the metabolic hyperbola is one of the two variables that determine PaCO2 (the other being the ventilation curve), its upward or downward movements increase or decrease respiratory drive, respectively. Mechanical ventilation indirectly influences respiratory drive by modifying PaCO2 levels through alterations in various parameters of the ventilation curve and metabolic hyperbola. Understanding the diverse factors that modulate respiratory drive at the bedside could enhance clinical assessment and the management of both the patient and the ventilator. [ABSTRACT FROM AUTHOR]

Background: Despite being a prognostic predictor, cardiac autonomic dysfunction (AD) has not been well investigated in chronic obstructive pulmonary disease (COPD). We aimed to characterise computed tomography (CT), spirometry, and cardiopulmonary exercise test (CPET) features of COPD patients with cardiac AD and the association of AD with CT-derived vascular and CPET-derived ventilatory efficiency metrics. Methods: This observational cohort study included stable, non-severe COPD patients. They underwent clinical evaluation, spirometry, CPET, and CT. Cardiac AD was determined based on abnormal heart rate responses to exercise, including chronotropic incompetence (CI) or delayed heart rate recovery (HRR) during CPET. Results: We included 49 patients with FEV1 of 1.2–5.0 L (51.1–129.7%), 24 (49%) had CI, and 15 (31%) had delayed HRR. According to multivariate analyses, CI was independently related to reduced vascular volume (VV; VV ≤ median; OR [95% CI], 7.26 [1.56–33.91]) and low ventilatory efficiency (nadir VE/VCO2 ≥ median; OR [95% CI], 10.67 [2.23–51.05]). Similar results were observed for delayed HRR (VV ≤ median; OR [95% CI], 11.46 [2.03–64.89], nadir VE/VCO2 ≥ median; OR [95% CI], 6.36 [1.18–34.42]). Conclusions: Cardiac AD is associated with impaired pulmonary vascular volume and ventilatory efficiency. This suggests that lung blood perfusion abnormalities may occur in these patients. Further confirmation is required in a large population-based cohort. [ABSTRACT FROM AUTHOR]

Breath-holding preceded by either an overnight fast or hyperventilation has been shown to potentiate the risk of a hypoxic blackout. However, no study has explored the combined effects of fasting and hyperventilation on apneic performance and associated physiological responses. Nine nondivers (8 males) attended the laboratory on two separate occasions (≥48 h apart), both after a 12-h overnight fast. During each visit, a hyperoxic rebreathing trial was performed followed by three repeated maximal static apneas preceded by either normal breathing (NORM) or a 30-s hyperventilation (HYPER). Splenic volume, hematology, cardiovascular, and respiratory variables were monitored. There were no interprotocol differences at rest or during hyperoxic rebreathing for any variable (P ≥ 0.09). On nine occasions (8 in HYPER), the subjects reached our safety threshold (oxygen saturation 65%) and were asked to abort their apneas, with the preponderance of these incidents (6 of 9) occurring during the third repetition. Across the sequential attempts, longer apneas were recorded in HYPER [median(range), 220(123–324) s vs. 185(78–296) s, P ≤ 0.001], with involuntary breathing movements occurring later [134(65–234) s vs. 97(42–200) s, P ≤ 0.001] and end-apneic partial end-tidal pressures of oxygen (P ET O 2 ) being lower (P ≤ 0.02). During the final repetition, partial end-tidal pressure of carbon dioxide [(P ET CO 2 ), 6.53 ± 0.46 kPa vs. 6.01 ± 0.45 kPa, P = 0.005] was lower in HYPER. Over the serial attempts, preapneic tidal volume was gradually elevated [from apnea 1 to 3, by 0.26 ± 0.24 L (HYPER) and 0.28 ± 0.30 L (NORM), P ≤ 0.025], with a correlation noted with preapneic P ET CO 2 (r = −0.57, P < 0.001) and P ET O 2 (r = 0.76, P < 0.001), respectively. In a fasted state, preapnea hyperventilation compared with normal breathing leads to longer apneas but may increase the susceptibility to a hypoxic blackout. NEW & NOTEWORTHY: This study shows that breath-holds (apneas) preceded by a 12-h overnight fast coupled with a 30-s hyperventilation as opposed to normal breathing may increase the likelihood of a hypoxic blackout through delaying the excitation of hypercapnic ventilatory sensory chemoreflexes. Evidently, this risk is exacerbated over a series of repeated maximal attempts, possibly due to a shift in preapneic gas tensions facilitated by an unintentional increase in tidal volume breathing. [ABSTRACT FROM AUTHOR]