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Given that there are both sex-based structural differences in the respiratory system and age-associated declines in pulmonary function, the purpose of this study was to assess the effects of age and sex on the metabolic cost of breathing (V̇ o 2RM) for exercise ventilations in healthy younger and older males and females. Forty healthy participants (10 young males 24 ± 3 yr; 10 young females 24 ± 3 yr; 10 older males 63 ± 3 yr, 10 older females 63 ± 6 yr) mimicked their exercise breathing patterns (voluntary hyperpnea) in the absence of exercise across a range of exercise intensities. At peak exercise, V̇ o 2RM represented a significantly greater fraction of peak oxygen consumption (V̇ o 2peak) in young females, 12.7 ± 4.0%, compared with young males, 10.7 ± 3.0% (P = 0.027), whereas V̇ o 2RM represented 13.5 ± 2.3% of V̇ o 2peak in older females and 13.2 ± 3.3% in older males. At relative ventilations, there was a main effect of age, with older males consuming a significantly greater fraction of V̇ o 2RM (6.6 ± 1.9%) than the younger males (4.4 ± 1.3%; P = 0.012), and older females consuming a significantly greater fraction of V̇ o 2RM (6.9 ± 2.5%) than the younger females (5.1 ± 1.4%; P = 0.004) at 65% V̇ e max. Furthermore, both younger and older males had significantly better respiratory muscle efficiency than their female counterparts at peak exercise (P = 0.011; P = 0.015). Similarly, younger participants were significantly more efficient than older participants (6.5 ± 1.5% vs. 5.5 ± 2.0%; P = 0.001). Normal age-related changes in respiratory function, in addition to sex-based differences in airway anatomy, appear to influence the ventilatory responses and the cost incurred to breathe during exercise. NEW & NOTEWORTHY: Here we show that at moderate and high-intensity exercise, older individuals incur a higher cost to breathe than their younger counterparts. However, as individuals age, the sex difference in the cost of breathing narrows. Collectively, our findings suggest that the normative age-related changes in respiratory structure and function, and sex differences in airway anatomy, appear to influence the ventilatory responses to exercise and the oxygen cost to breathe. [ABSTRACT FROM AUTHOR]

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]

Purpose: Ageing is associated with increased blood pressure (BP), reduced sleep, decreased pulmonary function and exercise capacity. The main purpose of this study was to test whether respiratory muscle endurance training (RMET) improves these parameters. Methods: Twenty-four active normotensive and prehypertensive participants (age: 65.8 years) were randomized and balanced to receive either RMET (N = 12) or placebo (PLA, N = 12). RMET consisted of 30 min of volitional normocapnic hyperpnea at 60% of maximal voluntary ventilation while PLA consisted of 1 inhalation day−1 of a lactose powder. Both interventions were performed on 4–5 days week−1 for 4–5 weeks. Before and after the intervention, resting BP, pulmonary function, time to exhaustion in an incremental respiratory muscle test (incRMET), an incremental treadmill test (IT) and in a constant-load treadmill test (CLT) at 80% of peak oxygen consumption, balance, sleep at home, and body composition were assessed. Data was analyzed with 2 × 2 mixed ANOVAs. Results: Compared to PLA, there was no change in resting BP (independent of initial resting BP), pulmonary function, IT performance, sleep, body composition or balance (all p > 0.05). Performance significantly increased in the incRMET (+ 6.3 min) and the CLT (+ 3.2 min), resulting in significant interaction effects (p < 0.05). Conclusion: In the elderly population, RMET might be used to improve respiratory and whole body endurance performance either as an adjunct to physical exercise training or as a replacement thereof for people not being able to intensively exercise even if no change in BP or sleep may be expected. [ABSTRACT FROM AUTHOR]

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This study examined the impact of aging on the elastic and resistive components of the work of breathing (Wb) during locomotor exercise at a given 1) ventilatory rate, 2) metabolic rate, and 3) operating lung volume. Eight healthy younger (25 ± 4 yr) and 8 older (72 ± 6 yr) participants performed incremental bicycle exercise, from which retrospective analyses identified similar ventilatory rates (approximately 40, 70, and 100 L·min-1), similar metabolic rates (VO2: approximately 1.2, 1.6, and 1.9 L·min-1), and similar lung volumes [inspiratory and expiratory reserve volumes (IRV/ERV: approximately 25/34%, 16/33%, and 13-34% of vital capacity]. Wb at each level was quantified by integrating the averaged esophageal pressure-volume loop, which was then partitioned into elastic and resistive components of inspiratory and expiratory work using the modified Campbell diagram. IRV was smaller in the older participants during exercise at ventilations of 70 and 100 L·min-1 and during exercise at the three metabolic rates (P < 0.05). Mainly because of a greater inspiratory elastic and resistive Wb in the older group (P < 0.05), total Wb was augmented by 40%-50% during exercise at matched ventilatory and matched metabolic rates. When examined during exercise evoking similar lung volumes, total Wb was not different between the groups (P = 0.86). Taken together, although aging exaggerates total Wb during locomotor exercise at a given ventilatory or a given metabolic rate, this difference is abolished during exercise at a given operating lung volume. These findings highlight the significance of operating lung volume in determining the age-related difference in Wb during locomotor exercise. [ABSTRACT FROM AUTHOR]

Transient increases in ventilation induced by arousal from sleep during Cheyne-Stokes respiration in heart failure patients are thought to contribute to sustaining and exacerbating the ventilatory oscillation. The only possibility to investigate the validity of this notion is to use observational data. This entails some significant challenges: (i) accurate identification of both arousal onset and offset; (ii) detection of short arousals (<3 s); (iii) breath-by-breath analysis of the interaction between arousals and ventilation; (iv) careful control for important confounding factors. In this paper we report how we have tackled these challenges by developing innovative computer-assisted methodologies. The identification of arousal onset and offset is performed by a hybrid approach that integrates visual scoring with computer-based automated analysis. We use a statistical detector to automatically discriminate between dominant theta–delta and dominant alpha activity at each instant of time. Moreover, a statistical detector is used to validate visual scoring of K complexes, delta waves or artifacts associated with an EEG frequency shift, as well as frequency shifts to beta activity. A high-resolution (250 ms) state-transition diagram providing continuous information on the sleep-wake state of the subject is finally obtained. Based on this information, arousals are automatically identified as any state change from sleep to wakefulness lasting ≥2 s. The assessment of the interaction between arousals and ventilation is performed using a breath-by-breath, case-control approach. The arousal-associated change in ventilation is measured as the normalized difference between minute ventilation in the case breath (i.e., with arousal) and that in the control breath (i.e., without arousal), controlling for sleep stage and chemical drive. The latter is estimated by using information from pulse oximetry at the finger. In the last part of the paper, we discuss main potential sources of error inherent in the described methodologies. [ABSTRACT FROM AUTHOR]

Transient increases in ventilation induced by arousal from sleep during Cheyne-Stokes respiration in heart failure patients are thought to contribute to sustaining and exacerbating the ventilatory oscillation. The only possibility to investigate the validity of this notion is to use observational data. This entails some significant challenges: (i) accurate identification of both arousal onset and offset; (ii) detection of short arousals (

Study Objectives: Arousals from sleep during the hyperpneic phases of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with heart failure are thought to cause ventilatory overshoot and a consequent longer apnea, thereby sustaining and exacerbating ventilatory instability. However, data supporting this model are lacking. We investigated the relationship between arousals, hyperpnea and post-hyperpnea apnea length during CSR-CSA.Methods: Breath-by-breath changes in ventilation associated with the occurrence of arousal were evaluated in 18 heart failure patients with CSR-CSA, apnea-hypopnea index ≥15/h and central apnea index ≥5/h. The change in apnea length associated with the presence of arousal during the previous hyperpnea was also evaluated. Potential confounding variables (chemical drive, sleep stage) were controlled for.Results: Arousals were associated with a large increase in ventilation at the beginning of the hyperpnea (+76 ± 35%, p < 0.0001), that rapidly declined during its crescendo phase. Around peak hyperpnea, the change in ventilation was −8 ± 26% (p = 0.14). The presence of arousal during the hyperpnea was associated with a median increase in the length of the subsequent apnea of +4.6% (Q1, Q2: −0.7%, 20.5%; range: −8.5%, 36.2%) (p = 0.021). The incidence of arousals occurring at the beginning of hyperpnea and mean ventilation in the region around its peak were independent predictors of the change in apnea length (p = 0.004 and p = 0.015, respectively; R2 = 0.78).Conclusions: Arousals from sleep during CSR-CSA in heart failure patients are associated with a rapidly decreasing ventilatory overshoot at the beginning of the hyperpnea, followed by a tendency toward a slight ventilatory undershoot around its peak. On average, arousals are also associated with a modest increase in post-hyperpnea apnea length; however, large increases in apnea length (>20%) occur in about a quarter of the patients.

Twenty 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. [ABSTRACT FROM AUTHOR]

IntroductionThe chronic effects of respiratory muscle training (RMT) on the cardiovascular system remain unclear. This investigation tested to which degree a single sessions of RMT with or without added vibration, which could enhance peripheral blood flow and vascular response, or a 4-week RMT program could result in changes in pulse wave velocity (PWV), blood pressure (systolic, SBP; diastolic, DBP) and other markers of cardiovascular health.MethodsSixteen young and healthy participants (8 m/8f) performed 15 min of either continuous normocapnic hyperpnea (RMET), sprint-interval-type hyperpnea (RMSIT) or a control session (quiet sitting). Sessions were performed once with and once without passive vibration of the lower limbs. To assess training-induced adaptations, thirty-four young and healthy participants (17 m/17f) were measured before and after 4 weeks (three weekly sessions) of RMET (n = 13, 30-min sessions of normocapnic hyperpnea), RMSIT [n = 11, 6 × 1 min (1 min break) normocapnic hyperpnea with added resistance] or placebo (n = 10).ResultsSBP was elevated from baseline at 5 min after each RMT session, but returned to baseline levels after 15 min, whereas DBP was unchanged from baseline following RMT. Carotid-femoral PWV (PWVCF) was elevated at 5 and 15 min after RMT compared to baseline (main effect of time, P = 0.001), whereas no changes were seen for carotid-radial PWV (PWVCR) or the PWVCF/PWVCR ratio. Vibration had no effects in any of the interventions. Following the 4-week training period, no differences from the placebo group were seen for SBP (P = 0.686), DBP (P = 0.233), PWVCF (P = 0.844), PWVCR (P = 0.815) or the PWVCF/PWVCR ratio (P = 0.389).Discussion/ConclusionAlthough 15 min of RMT sessions elicited transient increases in PWVCF and SBP, no changes were detected following 4 weeks of either RMET or RMSIT. Adding passive vibration of the lower limbs during RMT sessions did not provide additional value to the session with regards to vascular responses.

Introduction: The chronic effects of respiratory muscle training (RMT) on the cardiovascular system remain unclear. This investigation tested to which degree a single sessions of RMT with or without added vibration, which could enhance peripheral blood flow and vascular response, or a 4-week RMT program could result in changes in pulse wave velocity (PWV), blood pressure (systolic, SBP; diastolic, DBP) and other markers of cardiovascular health. Methods: Sixteen young and healthy participants (8 m/8f) performed 15 min of either continuous normocapnic hyperpnea (RMET), sprint-interval-type hyperpnea (RMSIT) or a control session (quiet sitting). Sessions were performed once with and once without passive vibration of the lower limbs. To assess training-induced adaptations, thirty-four young and healthy participants (17 m/17f) were measured before and after 4 weeks (three weekly sessions) of RMET (n = 13, 30-min sessions of normocapnic hyperpnea), RMSIT [ n = 11, 6 × 1 min (1 min break) normocapnic hyperpnea with added resistance] or placebo (n = 10). Results: SBP was elevated from baseline at 5 min after each RMT session, but returned to baseline levels after 15 min, whereas DBP was unchanged from baseline following RMT. Carotid-femoral PWV (PWVCF) was elevated at 5 and 15 min after RMT compared to baseline (main effect of time, P = 0.001), whereas no changes were seen for carotid-radial PWV (PWVCR) or the PWVCF/PWVCR ratio. Vibration had no effects in any of the interventions. Following the 4-week training period, no differences from the placebo group were seen for SBP (P = 0.686), DBP (P = 0.233), PWVCF (P = 0.844), PWVCR (P = 0.815) or the PWVCF/PWVCR ratio (P = 0.389). Discussion/Conclusion: Although 15 min of RMT sessions elicited transient increases in PWVCF and SBP, no changes were detected following 4 weeks of either RMET or RMSIT. Adding passive vibration of the lower limbs during RMT sessions did not provide additional value to the session with regards to vascular responses. [ABSTRACT FROM AUTHOR]

Prevalence of hypertension, subjective sleep complaints and snoring increases with age. Worse sleep and snoring, in turn, are independent risk factors to develop hypertension. Both respiratory muscle training (RMT) and intermittent hypoxia (IH) are suggested to have positive effects on these physiological and behavioral variables. This study therefore aimed to test the acute effects of a single bout of RMT, with and without IH, on resting blood pressure (BP) and sleep. Fourteen prehypertensive elderly performed a 60-min session of (a) intermittent voluntary normocapnic hyperpnea (HYP) alone, (b) HYP in combination with IH (HYP&IH) and (c) a sham intervention in randomized order. BP, hemodynamics, heart rate variability (HRV), cardiac baroreflex sensitivity (BRS) and pulse wave velocity (PWV) were assessed before and 15, 30 and 45 min after each intervention. Variables of sleep were assessed with actigraphy, pulse oximetry and with questionnaires during and after the night following each intervention. Neither HYP nor HYP&IH resulted in a decrease in BP. Repeated measures ANOVA revealed no significant interaction effect for systolic BP (p = 0.090), diastolic BP (p = 0.151), HRV parameters, BRS and PWV (all p > 0.095). Fragmentation index was lower after both HYP (−6.5 units) and HYP&IH (−8.4 units) compared to sham, p(ANOVA) = 0.046, although pairwise comparisons reveal no significant differences. There were no other significant effects for the remaining sleep variables. We conclude that one bout of intermittent hyperpnea, alone or in combination with IH, is not effective in lowering blood pressure or improving sleep in prehypertensive elderly.

Prevalence of hypertension, subjective sleep complaints and snoring increases with age. Worse sleep and snoring, in turn, are independent risk factors to develop hypertension. Both respiratory muscle training (RMT) and intermittent hypoxia (IH) are suggested to have positive effects on these physiological and behavioral variables. This study therefore aimed to test the acute effects of a single bout of RMT, with and without IH, on resting blood pressure (BP) and sleep. Fourteen prehypertensive elderly performed a 60-min session of (a) intermittent voluntary normocapnic hyperpnea (HYP) alone, (b) HYP in combination with IH (HYP&IH) and (c) a sham intervention in randomized order. BP, hemodynamics, heart rate variability (HRV), cardiac baroreflex sensitivity (BRS) and pulse wave velocity (PWV) were assessed before and 15, 30 and 45 min after each intervention. Variables of sleep were assessed with actigraphy, pulse oximetry and with questionnaires during and after the night following each intervention. Neither HYP nor HYP&IH resulted in a decrease in BP. Repeated measures ANOVA revealed no significant interaction effect for systolic BP (p = 0.090), diastolic BP (p = 0.151), HRV parameters, BRS and PWV (all p > 0.095). Fragmentation index was lower after both HYP (−6.5 units) and HYP&IH (−8.4 units) compared to sham, p (ANOVA) = 0.046, although pairwise comparisons reveal no significant differences. There were no other significant effects for the remaining sleep variables. We conclude that one bout of intermittent hyperpnea, alone or in combination with IH, is not effective in lowering blood pressure or improving sleep in prehypertensive elderly. [ABSTRACT FROM AUTHOR]

Swimmers have a high prevalence of exercise-induced bronchoconstriction (EIB), which may be associated with repeated exposure to chlorinated pool water. The eucapnic voluntary hyperpnea (EVH) test is used to diagnose EIB; however, it fails to replicate the environmental conditions experienced by swimmers. The relationship between the composition of the EVH inspired gas and the development of EIB from swim exercise remains unclear. Purpose: This study aimed to compare the bronchoconstrictive effect of a chlorinated inspirate EVH test and swim test to a laboratory-based EVH test in swimmers. Methods: Fifteen collegiate swimmers (n = 5 male, n = 10 female; 21 ± 2 yr) completed 3 d of testing in pseudorandom order; a standard EVH test (EVHL), a pool air EVH test (EVHCl), and a swimming test (Swim). Spirometry was measured at baseline, and 3, 5, 10, 15, and 20 min after each test. Results: EVHL elicited a forced expired volume in 1 s (FEV1) fall index of −9.7% ± 6.4% compared with −6.6% ± 9.2% and −3.0% ± 7.5% after EVHCl and Swim, respectively (P < 0.05). Using Bland–Altman analysis, we found good agreement between EVHL and EVHCl (bias = −2.8, r = 0.79; P < 0.05) with poor agreement between EVHL and Swim (bias = −6.7, r = 0.20) and between EVHCl and Swim (bias = −3.9, r = 0.50; both P < 0.05). Forced expired flow between 25% and 75% lung volume and peak expired flow were significantly reduced by the EVHL compared with the EVHCl and Swim tests (P < 0.05). Conclusions: EVHL elicits a greater forced expired volume in 1-s fall index compared with EVHCl and Swim. The unique aquatic environment of swimmers potentially protects against bronchoconstriction and should be considered in the determination of EIB. [ABSTRACT FROM AUTHOR]

The article present case study of a 26-year-old man ingested a packet of yellow "weight loss" tablets that he obtained online in an attempt to commit suicide with acute distress with profuse diaphoresis, hyperpnea and mottling. It further discusses the diagnosis of 2,4-dinitrophenol (DNP) poisoning; acceleration in hypercapnia points to an increase in metabolic production of carbon dioxide (CO2); and also mentions about uncouple oxidative phosphorylation (UOP).

More than a hundred years ago, it was first reported that increases in body temperature stimulate minute ventilation. Since then, the characteristics, mechanisms and physiological meaning of this ventilatory response to increasing body temperature, so-called hyperthermia-induced hyperventilation, have gradually been uncovered. For example, it is now known that hyperthermia-induced hyperventilation has a core temperature threshold, like heat-dissipating responses (sweating and cutaneous vasodilation); but several factors affecting heat-dissipating responses do not influence the ventilatory response to increasing body temperature. On the other hand, evidence from several studies suggests there may be some relation between hyperthermia-induced hyperventilation and heat-dissipating responses. In addition, more recent evidence indicates that hyperthermia-induced hyperventilation may be related to central fatigue, which is considered to be one of the reasons exercise performance is diminished in heat. In fact, it has been suggested that hyperthermia-induced hyperventilation causes cerebral blood perfusion to be reduced, which decreases cerebral oxygenation and heat removal. This review presents an overview of the characteristics of the ventilatory response to increasing body temperature and its effect on central fatigue.

Abstract Thermal hyperpnea, a pattern of breathing during hyperthermia that is characterized by an increase in tidal volume as well as breathing frequency, is known to lead to respiratory alkalosis. Thermal hyperpnea-induced respiratory alkalosis is linked to febrile seizures (FS). The heat-sensitive transient receptor potential vanilloid-1 (TRPV1) receptors are localized in, and implicated in the heat sensitivity of peripheral and central structures involved in the respiratory response to hyperthermia. We, therefore, hypothesize that TRPV1 activation increases susceptibility to experimental FS (EFS) in immature rats due to an exacerbated thermal hyperpnea. We found that peripheral, but not central TRPV1 activation had pro-convulsant effects. These pro-convulsant effects were associated with an increased rate of expired CO 2 due to an exaggerated ventilatory response to hyperthermia. The TRPV1 antagonist, AMG-9810, and TRPV1 deletion abolished the pro-convulsant effects, while exposure to 5% CO 2 , bilateral vagotomy and DREADD (designer receptor exclusively activated by designer drugs)-mediated inhibition of TRPV1-containing cells in the vagal nodose ganglia significantly attenuated these effects. These findings suggest that vagal TRPV1-driven thermal hyperpnea likely increases susceptibility to FS in immature rodents. This identifies a novel peripheral anatomical and molecular target that should be considered when developing therapeutics for FS. Highlights • Piperine has a proconvulsant effect in a rodent model of febrile seizures. • The proconvulsant effect of piperine is associated with thermal hyperpnea. • The proconvulsant effect of piperine is TRPV1 mediated. • The TRPV1-mediated proconvulsant effect of piperine involves the vagus nerve. [ABSTRACT FROM AUTHOR]

Upright hyperventilation occurs in ~25% of our patients with postural tachycardia syndrome (POTS). Poikilocapnic hyperventilation alone causes tachycardia. Here, we examined changes in respiration and hemodynamics comprising cardiac output (CO), systemic vascular resistance (SVR), and blood pressure (BP) measured during head-up tilt (HUT) in three groups: patients with POTS and hyperventilation (POTS-HV), patients with panic disorder who hyperventilate (Panic), and healthy controls performing voluntary upright hyperpnea (Voluntary-HV). Though all were comparably tachycardic during hyperventilation, POTS-HV manifested hyperpnea, decreased CO, increased SVR, and increased BP during HUT; Panic patients showed both hyperpnea and tachypnea, increased CO, and increased SVR as BP increased during HUT; and Voluntary-HV were hyperpneic by design and had increased CO, decreased SVR, and decreased BP during upright hyperventilation. Mechanisms of hyperventilation and hemodynamic changes differed among POTS-HV, Panic, and Voluntary- HV subjects. We hypothesize that the hyperventilation in POTS is caused by a mechanism involving peripheral chemoreflex sensitization by intermittent ischemic hypoxia. NEW & NOTEWORTHY Hyperventilation is common in postural tachycardia syndrome (POTS) and has distinctive cardiovascular characteristics when compared with hyperventilation in panic disorder or with voluntary hyperventilation. Hyperventilation in POTS is hyperpnea only, distinct from panic in which tachypnea also occurs. Cardiac output is decreased in POTS, whereas peripheral resistance and blood pressure (BP) are increased. This is distinct from voluntary hyperventilation where cardiac output is increased and resistance and BP are decreased and from panic where they are all increased. [ABSTRACT FROM AUTHOR]

Objective The interplay between arousals and respiratory events during Cheyne-Stokes respiration (CSR) with central sleep apnea (CSA) in heart failure (HF) patients is still not fully understood. We investigated the temporal relationship between arousals and CSR-CSA. Methods Episodes of CSR-CSA during sleep stages N1-N2 were analyzed in 22 HF patients with an apnea-hypopnea index ≥15/h, dominant CSA and central apnea index ≥5/h. For each CSR-CSA cycle (apnea + hyperpnea), we determined the onset (AR onset , relative to hyperpnea onset) and duration of detected arousals. Results Arousals (N = 2348) mostly occurred within the first half of the hyperpneic phase (42.6%, AR onset  = 10.6 ± 2.1 s; duration = 10.6 ± 5.2 s) or close to hyperpnea onset (21.5%, AR onset  = −0.1 ± 0.6 s; duration = 13.9 ± 5.4 s). Within-apnea arousals were less frequent (12.4%, AR onset  = −16.0 ± 4.7 s; duration = 3.8 ± 1.4 s). The proportion of CSR-CSA cycles without any hyperpnea-related arousal was 27.5 ± 18.2%. Hyperpnea-related arousability (total number of hyperpneic arousals/total duration of hyperpneas) and apnea-related arousability were 63.4 ± 21.0/h and 23.8 ± 16.9/h, respectively (p < 0.0001). Conclusion During CSR-CSA, a significant proportion of arousals occur at hyperpnea onset, indicating a low arousal threshold. Hyperpneic arousals are not essential for CSR-CSA. Arousability markedly increases during hyperpneas, likely due to the concurrent increase in chemoreceptor stimulation. Significance This study extends current knowledge on the interplay between sleep instability and respiratory events during CSR-CSA. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study? The lack of useful small‐animal models for studying exercise hyperpnoea makes it difficult to investigate the underlying mechanisms of exercise‐induced ventilatory abnormalities in various disease states. What is the main finding and its importance? We developed an anaesthetized‐rat model for studying exercise hyperpnoea, using a respiratory equilibrium diagram for quantitative characterization of the respiratory chemoreflex feedback system. This experimental model will provide an opportunity to clarify the major determinant mechanisms of exercise hyperpnoea, and will be useful for understanding the mechanisms responsible for abnormal ventilatory responses to exercise in disease models. Abstract: Exercise‐induced ventilatory abnormalities in various disease states seem to arise from pathological changes of respiratory regulation. Although experimental studies in small animals are essential to investigate the pathophysiological basis of various disease models, the lack of an integrated framework for quantitatively characterizing respiratory regulation during exercise prevents us from resolving these problems. The purpose of this study was to develop an anaesthetized‐rat model for studying exercise hyperpnoea for quantitative characterization of the respiratory chemoreflex feedback system. In 24 anaesthetized rats, we induced muscle contraction by stimulating bilateral distal sciatic nerves at low and high voltage to mimic exercise. We recorded breath‐by‐breath respiratory gas analysis data and cardiorespiratory responses while running two protocols to characterize the controller and plant of the respiratory chemoreflex. The controller was characterized by determining the linear relationship between end‐tidal CO2 pressure ( P ETC O 2) and minute ventilation ( V ̇ E), and the plant by the hyperbolic relationship between V ̇ E and P ETC O 2. During exercise, the controller curve shifted upward without change in controller gain, accompanying increased oxygen uptake. The hyperbolic plant curve shifted rightward and downward depending on exercise intensity as predicted by increased metabolism. Exercise intensity‐dependent changes in operating points ( V ̇ E and P ETC O 2) were estimated by integrating the controller and plant curves in a respiratory equilibrium diagram. In conclusion, we developed an anaesthetized‐rat model for studying exercise hyperpnoea, using systems analysis for quantitative characterization of the respiratory system. This novel experimental model will be useful for understanding the mechanisms responsible for abnormal ventilatory responses to exercise in disease models. [ABSTRACT FROM AUTHOR]

Exposure to high levels of hyperbaric oxygen (HBO2) can induce central nervous system oxygen toxicity in humans and animals, a phenomenon characterized by repeated tonic-clonic seizures. The risk of developing this type of convulsions represents the limiting factor in using HBO2 for a number of clinical and diving applications. Previously, using radio-telemetry in awake rats, a significant increase in the mean value of the ventilatory responses in rats to HBO2 approximately 5-8 min before onset of seizures has been observed. This response has been termed “hyperoxic hyperpnea,” and it has been hypothesized it may serve as a predictor of an impending seizure while breathing HBO2. The purpose of the present study was to apply soft computing methods to determine whether there is a direct correlation between the onset of hyperoxic hyperpnea (i.e., the ventilatory response as defined by tidal volume and respiratory frequency) and the onset of seizure. In our experiments, we used Multilayer Perceptron, Naive Bayes, J48, and U-BRAIN aimed at evidencing the correlation between the respiratory feature vectors and the onset of an impending seizure in unanesthetized, freely behaving rats breathing 4, 5 or 6 atmospheres absolute (ATA) of oxygen. This strategy was also aimed to finding a set of rules relating physiological parameters and convulsive phenomena through inductive inference. [ABSTRACT FROM AUTHOR]

It is unknown which respiratory muscles are mainly activated by respiratory muscle training. This study evaluated Inspiratory Pressure Threshold Loading (IPTL), Inspiratory Flow Resistive Loading (IFRL) and Voluntary Isocapnic Hyperpnea (VIH) with regard to electromyographic (EMG) activation of the sternocleidomastoid muscle (SCM), parasternal muscles (PARA) and the diaphragm (DIA) in randomized order. Surface EMG were analyzed at the end of each training session and normalized using the peak EMG recorded during maximum inspiratory maneuvers (Sniff nasal pressure: SnPna, maximal inspiratory mouth occlusion pressure: PImax). 41 healthy participants were included. Maximal activation was achieved for SCM by SnPna; the PImax activated predominantly PARA and DIA. Activations of SCM and PARA were higher in IPTL and VIH than for IFRL (p < 0.05). DIA was higher applying IPTL compared to IFRL or VIH (p < 0.05). IPTL, IFRL and VIH differ in activation of inspiratory respiratory muscles. Whereas all methods mainly stimulate accessory respiratory muscles, diaphragm activation was predominant in IPTL. [ABSTRACT FROM AUTHOR]

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes - V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min-1·°C-1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia. [ABSTRACT FROM AUTHOR]

New FindingsWhat is the central question of this study? By manipulating recovery intensity and exercise duration during high-intensity interval training (HIIT), we tested the hypothesis that fast inputs contribute more than metabolic stimuli to respiratory frequency (fR) regulation. What is the main finding and its importance? Respiratory frequency, but not tidal volume, responded rapidly and in proportion to changes in workload during HIIT, and was dissociated from some markers of metabolic stimuli in response to both experimental manipulations, suggesting that fast inputs contribute more than metabolic stimuli to fR regulation. Differentiating between fR and tidal volume may help to unravel the mechanisms underlying exercise hyperpnoea. Given that respiratory frequency (fR) has been proposed as a good marker of physical effort, furthering the understanding of how fR is regulated during exercise is of great importance. We manipulated recovery intensity and exercise duration during high-intensity interval training (HIIT) to test the hypothesis that fast inputs (including central command) contribute more than metabolic stimuli to fR regulation. Seven male cyclists performed an incremental test, a 10 and a 20 min continuous time trial (TT) as preliminary tests. Subsequently, recovery intensity and exercise duration were manipulated during HIIT (30 s work and 30 s active recovery) by performing four 10 min and one 20 min trial (recovery intensities of 85, 70, 55 and 30% of the 10 min TT mean workload; and 85% of the 20 min TT mean workload). The work intensity of the HIIT sessions was self-paced by participants to achieve the best performance possible. When manipulating recovery intensity, fR, but not tidal volume (VT), showed a fast response to the alternation of the work and recovery phases, proportional to the extent of workload variations. No association between fR and gas exchange responses was observed. When manipulating exercise duration, fR and rating of perceived exertion were dissociated from VT, carbon dioxide output and oxygen uptake responses. Overall, the rating of perceived exertion was strongly correlated with fR (r = 0.87; P < 0.001) but not with VT. These findings may reveal a differential control of fR and VT during HIIT, with fast inputs appearing to contribute more than metabolic stimuli to fR regulation. Differentiating between fR and VT may help to unravel the mechanisms underlying exercise hyperpnoea. [ABSTRACT FROM AUTHOR]

Objective: Sleep-disordered breathing (SDB) is highly prevalent in children with Down syndrome. Given the scarcity of resources and the presence of risk factors for SDB in this population, the objective of this study is to identify the clinical predictors of SDB, which would assist prioritization of children with Down syndrome for SDB evaluation.Methods: A retrospective cohort study was conducted on children enrolled in the Down syndrome clinic at CHEO who underwent polysomnography in 2004-2014. Total apnea-hypopnea index (AHI) or obstructive AHI (OAHI) > 5 events/hour was considered clinically significant. Associations between SDB and concurrent diagnoses, referral reasons, and sleep symptoms assessed by questionnaire were examined using Pearson's chi-square test or Fisher's exact test as appropriate. Univariate and multivariate logistic regression analyses were used to examine the predictors of SDB.Results: SDB was present in 42.9% of 119 children, with its highest prevalence at age 8 years. Symptoms were not significantly associated with AHI > 5 events/hour or OAHI > 5 events/hour. Gastroesophageal reflux was associated with lower odds of OAHI > 5 events/hour on univariate testing (odds ratio 0.16, 95% CI 0.04-0.72; p = 0.02) and multivariate analysis (odds ratio 0.05, 95% CI 0.0006-0.50; p = 0.002).Conclusions: SDB is highly prevalent at all ages in children with Down syndrome. Symptoms did not predict SDB in this population, although gastroesophageal reflux may mimic SDB, which indicates that clinicians should continue to perform ongoing surveillance for SDB throughout the lifespan of children with Down syndrome. [ABSTRACT FROM AUTHOR]

Whole-body warm-up exercises were shown to attenuate exercise-induced bronchoconstriction (EIB). Whether intense pre-exercise hyperpnea offers similar protection and whether this might negatively affect exercise performance is unknown. Nine subjects with EIB (25±5 yrs; forced expiratory volume in 1s [FEV1], 104±15% predicted) performed an exercise challenge (ECh) followed—after 30min—by a constant-load cycling test to exhaustion. The ECh was preceded by one of four conditions: by i) control warm-up (CON) or by 10min of normocapnic hyperpnea with partial rebreathing at either ii) 50% (WU50) or iii) variable intensity (8x 30s-80%/45s-30%; WU80/30), or at iv) 70% (WU70) of maximal voluntary ventilation. FEV1 was measured at baseline and in 5-min intervals until 15min after CON/warm-up and 30min after ECh. None of the warm-up conditions induced EIB. The maximal post-ECh decrease in FEV1 was -13.8±3.1% after CON, −9.3±5.0% after WU50 (p = 0.081 vs. CON), −8.6±7.5% after WU80/30 (p = 0.081 vs. CON) and −7.2±5.0% after WU70 (p = 0.006 vs. CON), and perception of respiratory exertion was significantly attenuated (all p≤0.048), with no difference between warm-up conditions. Only after CON, FEV1 remained significantly reduced up to the start of the cycling endurance test (−8.0±4.3%, p = 0.004). Cycling performance did not differ significantly between test days (CON: 13±7min; WU50: 14±9min; WU80/30: 13±9min; WU70: 14±7min; p = 0.582). These data indicate that intense hyperpnea warm-up is effective in attenuating EIB severity and accelerating lung function recovery while none of the warm-up condition do compromise cycling performance. [ABSTRACT FROM AUTHOR]

Previous research has shown an exaggeration in exercise hyperpnea 2 days after eccentric exercise (ECC). Enhancement in central command has been suggested as one candidate to account for this effect given that ECC-induced neuromuscular dysfunction increases relative exercise intensity, thus resulting in reinforcement of effort sense. The purpose of this study was, therefore, to elucidate whether the degree of alteration in effort sense caused by ECC affects exercise hyperpnea. Ten subjects performed 20-s single-arm extension-flexion exercises with weight strapped to the wrist, and ventilatory response was measured before (Pre) and 2 days after ECC (D2). Relative exercise intensity at Pre was 5 % of maximal voluntary contraction (MVC) of Pre, whereas that at D2 was 9 % MVC of D2 because of decline in muscle strength. Ventilatory responses were significantly exaggerated at D2 with a significant increase in effort sense. Although effort sense was significantly reduced during exercise at D2 when wrist weight was subtracted to match relative exercise intensity at Pre (5 % MVC of D2), ventilatory responses were still significantly higher than those of Pre. After the disappearance of post-ECC muscle damage, subjects performed the same exercise with weight added (9 % MVC of Pre) so that effort was equalized to match that of D2; however, no significant increase in ventilatory response was detected. The fact that the extent of change in effort sense caused by ECC-induced neuromuscular dysfunction did not affect ventilatory response at the onset of exercise after ECC may suggest that the exaggeration of ventilatory response after ECC is caused by mechanisms other than alteration of the central command. [ABSTRACT FROM AUTHOR]

Key points Hypoglycaemia is counteracted by release of hormones and an increase in ventilation and CO2 sensitivity to restore blood glucose levels and prevent a fall in blood pH., The full counter-regulatory response and an appropriate increase in ventilation is dependent on carotid body stimulation., We show that the hypoglycaemia-induced increase in ventilation and CO2 sensitivity is abolished by preventing adrenaline release or blocking its receptors., Physiological levels of adrenaline mimicked the effect of hypoglycaemia on ventilation and CO2 sensitivity., These results suggest that adrenaline, rather than low glucose, is an adequate stimulus for the carotid body-mediated changes in ventilation and CO2 sensitivity during hypoglycaemia to prevent a serious acidosis in poorly controlled diabetes., Abstract Hypoglycaemia in vivo induces a counter-regulatory response that involves the release of hormones to restore blood glucose levels. Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea that maintains arterial CO2 levels and prevents respiratory acidosis in the face of increased metabolism. It is unclear whether the carotid body is directly stimulated by low glucose or by a counter-regulatory hormone such as adrenaline. Minute ventilation was recorded during infusion of insulin-induced hypoglycaemia (8-17 mIU kg−1 min−1) in Alfaxan-anaesthetised male Wistar rats. Hypoglycaemia significantly augmented minute ventilation (123 ± 4 to 143 ± 7 ml min−1) and CO2 sensitivity (3.3 ± 0.3 to 4.4 ± 0.4 ml min−1 mmHg−1). These effects were abolished by either β-adrenoreceptor blockade with propranolol or adrenalectomy. In this hypermetabolic, hypoglycaemic state, propranolol stimulated a rise in [ABSTRACT FROM AUTHOR]

The purpose of this study was to elucidate the cardiovascular response during hyperpnoea in endurance-trained runners compared to sedentary controls. Twelve runners and ten sedentary individuals participated in this study. A maximal respiratory endurance test (MRET) was performed as follows: target minute ventilation was initially set at 30% of maximal voluntary ventilation (MVV 12 ) and was increased by 10% MVV 12 every 3 min. The test was terminated when the subject could no longer maintain the target ventilation. Heart rate and mean arterial blood pressure (MBP) were continuously measured. Respiratory endurance time during the MRET was longer in the runners than the controls. The change in MBP during the MRET was lower in the runners compared to the sedentary controls (runners: 100.2 ± 2.4 mmHg vs. controls: 109.1 ± 3.0 mmHg at 6 min of hyperpnoea). Therefore, the blood pressure response during hyperpnoea is blunted in endurance runners, suggesting that whole-body endurance exercise training attenuates the respiratory muscle-induced metaboreflex. [ABSTRACT FROM AUTHOR]

Respiratory Muscle Endurance (RME) is an alternative way to assess respiratory muscle impairment but normal values are lacking to use this test in a clinical perspective. Our objective was then to determine reference values of RME in healthy subjects. We recruited 161 healthy subjects (25–80 years old) who were distributed within 5 groups with a 10-year range. We measured vital capacity (VC) and maximal respiratory pressure (MIP, MEP). The RME test consisted of isocapnic hyperpnea at increasing levels of ventilation until exhaustion to determine Tlim (expressed in minutes and as percentage of maximal voluntary ventilation, MVV). A significant difference between age-groups was observed for both VC and MEP expressed as percentage of predicted value. Mean Tlim was 21.8 ± 5.9 min [95% confidence interval 20.9–22.8], 74.4 ± 15.9% of predicted MVV [95% CI 71.8–76.9]. Tlim was similar among age groups. Tolerance to the RME test was excellent. This study provides normal values of RME in a large age range of healthy subjects and demonstrates that RME is preserved in the elderly. [ABSTRACT FROM AUTHOR]

BACKGROUND: Climbing and trekking at altitude are common recreational and military activities. Physiological effects of altitude are hypoxia and hyperventilation. The hyperventilatory response to altitude may cause respiratory muscle fatigue and reduce sustained submaximal exercise. Voluntary isocapnic hyperpnea respiratory muscle training (VIHT) improves exercise endurance at sea level and at depth. The purpose of this study was to test the hypothesis that VI HT would improve exercise time at altitude [3600 m (11,811 ft)] compared to control and placebo groups. METHODS: Subjects pedaled an ergometer until exhaustion at simulated altitude in a hypobaric chamber while noninvasive arterial saturation (Sao2), ventilation (VE), and oxygen consumption (Vo2) were measured. RESULTS: As expected, Sao2 decreased to 88 ± 4% saturation at rest and to 81 ± 2% during exercise, and was not affected by VIHT. VIHT resulted in a 40% increase in maximal training VE compared to pre-VIHT. Exercise endurance significantly increased 44% after VIHT (P = <0.001). Vo2 (30 ± 3 ml • kg-1 • min-1) and heart rate (177 ± 10 bpm) did not change during exercise and were not affected by VIHT (P = 0.531). Pre-VIHT VE increased 21-27% during the initial 12 min of exercise, after which it decreased 17% at 17.7 ± 6.0 min. VE at altitude post-VIHT increased more (49%) for longer (21 min) and decreased less (11% at 25.4 ± 6.7 min). DISCUSSION: VIHT improved exercise time at altitude and sustained VE This suggests that VIHT reduced respiratory muscle fatigue and would be useful to trekkers and military personnel working at altitude. Heifer S, Quackenbush J, Fletcher M, Pendergast DR. Respiratory muscle training and exercise endurance at altitutde. Aerosp Med Hum Perform. 2016; 87(8)704-711. DISCUSSION: VIHT improved exercise time at altitude and sustained VE This suggests that VIHT reduced respiratory muscle fatigue and would be useful to trekkers and military personnel working at altitude. [ABSTRACT FROM AUTHOR]

Release of bronchoactive mediators from mast cells during exercise hyperpnea is a key factor in the pathophysiology of exercise-induced bronchoconstriction (EIB). Our aim was to investigate the effect of a standard, single dose of an inhaled β2-adrenoceptor agonist on mast cell activation in response to dry air hyperpnea in athletes with EIB. Twenty-seven athletes with EIB completed a randomized, double-blind, placebo-controlled, crossover study. Terbutaline (0.5 mg) or placebo was inhaled 15 min prior to 8 min of eucapnic voluntary hyperpnea (EVH) with dry air. Pre- and postbronchial challenge, urine samples were analyzed by enzyme immunoassay for 11β-prostaglandin F2α (11β-PGF2α). The maximum fall in forced expiratory volume in 1 s of 14 (12-20)% (median and interquartile range) following placebo was attenuated to 7 (5-9)% with the administration of terbutaline (P < 0.001). EVH caused a significant increase in 11β-PGF2α from 41 (27-57) ng/mmol creatinine at baseline to 58 (43-72) ng/mmol creatinine at its peak post-EVH following placebo (P = 0.002). The rise in 11β-PGF2α was inhibited with administration of terbutaline: 39 (28-44) ng/mmol creatinine at baseline vs. 40 (33-58) ng/mmol creatinine at its peak post-EVH (P = 0.118). These data provide novel in vivo evidence of mast cell stabilization following inhalation of a standard dose of terbutaline prior to bronchial provocation with EVH in athletes with EIB. [ABSTRACT FROM AUTHOR]

Cerebral blood flow (CBF) is temporally related to exercise-induced changes in partial pressure of end-tidal carbon dioxide (PETCO2); hyperoxia is known to enhance this relationship. We examined the hypothesis that preventing PETCO2 from rising (isocapnia) during submaximal exercise with and without hyperoxia [end-tidal PO2 (PETO2) = 300 mmHg] would attenuate the increases in CBF. Additionally, we aimed to identify the magnitude that breathing, per se, influences the CBF response to normoxic and hyperoxic exercise. In 14 participants, CBF (intra- and extracranial) measurements were measured during exercise [20, 40, 60, and 80% of maximum workload (Wmax)] and during rest while ventilation (VE) was volitionally increased to mimic volumes achieved during exercise (isocapnic hyperpnea). While VE was uncontrolled during poikilocapnic exercise, during isocapnic exercise and isocapnic hyperpnea, VE was increased to prevent PETCO2 from rising above resting values (~40 mmHg). Although PETCO2 differed by 2 ± 3 mmHg during normoxic poikilocapnic and isocapnic exercise, except for a greater poikilocapnic compared with isocapnic increase in blood velocity in the posterior cerebral artery at 60% Wmax, the between condition increases in intracranial (~12-15%) and extracranial (15-20%) blood flow were similar at each workload. The poikilocapnic hyperoxic increases in both intra- and extracranial blood-flow (~17-29%) were greater compared with poikilocapnic normoxia (~8-20%) at intensities >40% Wmax (P < 0.01). During both normoxic and hyperoxic conditions, isocapnia normalized both the intracranial and extracranial blood-flow differences. Isocapnic hyperpnea did not alter CBF. Our findings demonstrate a differential effect of PETCO2 on CBF during exercise influenced by the prevailing PETO2. [ABSTRACT FROM AUTHOR]

In humans, hyperthermia leads to activation of a set of thermoregulatory responses that includes cutaneous vasodilation and sweating. Hyperthermia also increases ventilation in humans, as is observed in panting dogs, but the physiological significance and characteristics of the hyperventilatory response in humans remain unclear. The relative contribution of respiratory heat loss to total heat loss in a hot environment in humans is small, and this hyperventilation causes a concomitant reduction in arterial CO2 pressure (hypocapnia), which can cause cerebral hypoperfusion. Consequently, hyperventilation in humans may not contribute to the maintenance of physiological homeostasis (i.e., thermoregulation). To gain some insight into the physiological significance of hyperthermia-induced hyperventilation in humans, in this review, we discuss 1) the mechanisms underlying hyperthermia-induced hyperventilation, 2) the factors modulating this response, and 3) the physiological consequences of the response. [ABSTRACT FROM AUTHOR]

Exercise endurance is reduced by heat. Among several factors that influence exercise performance is central fatigue, which appears to be caused by an increase in brain temperature. During prolonged exercise in heat, the core body temperature rises, and there is a corresponding and proportional increase in minute ventilation. It has been suggested that this hyperthermia-induced hyperventilation is related to central fatigue. Although hyperthermia-induced hyperventilation may have some relationship to heat-dissipating responses, it differs in several ways. For example, hyperthermia-induced hyperventilation causes a reduction in arterial CO2 pressure, which makes it different from thermal panting in animals. In fact, it has been suggested that hyperthermia-induced hyperventilation causes a reduction in cerebral perfusion, which reinforces the increase in brain temperature during exercise. This short review presents an overview of the characteristics of hyperthermia-induced hyperventilation and its effect on central fatigue.