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Aidan Bradford – One of the best experts on this subject based on the ideXlab platform.

  • Oxidative Stress Impairs Upper Airway Muscle Endurance in an Animal Model of Sleep-Disordered Breathing
    Advances in experimental medicine and biology, 2008
    Co-Authors: Mark Dunleavy, Aidan Bradford, Ken D. O'halloran
    Abstract:

    Obstructive sleep apnoea is characterised by intermittent hypohypoxia due to recurrent obstructions of the pharyngeal Airway during sleep. We have shown that chronic intermittent hypohypoxia impairs respiratory Muscle function and CNS control of upper Airway patency. In this study, we tested the hypothesis that disruption of an endogenous antioxidant defence system exacerbates the effects of intermittent hypohypoxia on upper Airway Muscle contractile function. Thirty-two male Wistar rats were placed in restrainers with their heads in hoods in which the ambient oxygen concentration could be modified by controlling the gas supply to the hoods. Sixteen rats were exposed to alternating equal periods of hypoxia and normoxia, twice per minute, 8 hours per day for 1 week. The remaining 16 animals were exposed to normoxia continuously under identical experimental conditions. In both groups, half the animals received daily injections of buthionine sulfoxamine (BSO), an inhibitor of the rate-limiting enzyme in glutathione synthesis. The other half received daily vehicle injections. At the end of the 1-week treatment period, the sternohyoid Muscles were removed and fatigue characteristics were determined in vitro. Intermittent hypohypoxia was associated with a decrease in sternohyoid Muscle endurance, an effect that was exacerbated by treatment with BSO. In separate experiments, daily treatment with the antioxidant N-acetyl cysteine blocked the deleterious effects of intermittent hypohypoxia on respiratory Muscle function. We suggest that oxidative stress contributes to impaired upper Airway Muscle endurance in our animal model and that endogenous glutathione may be especially important in limiting free radical-induced Muscle dysfunction. Our results may have particular relevance to respiratory disorders associated with recurrent hypoxia, such as the sleep apnoea/hypopnoea syndrome.

  • Does episodic hypoxia affect upper Airway dilator Muscle function? Implications for the pathophysiology of obstructive sleep apnoea.
    Respiratory physiology & neurobiology, 2005
    Co-Authors: Aidan Bradford, Michelle Mcguire, Ken D. O'halloran
    Abstract:

    Obstructive sleep apnoea (OSA) is characterised by repetitive collapse of the upper Airway during sleep owing to a sleep-related decrement in upper Airway Muscle activity with consequent failure of the pharyngeal dilator Muscles to oppose the collapsing pressure that is generated by the diaphragm and accessory Muscles during inspiration. The causes of upper Airway obstruction during sleep are multi-factorial but there is evidence implicating intrinsic upper Airway Muscle function and impaired central regulation of the upper Airway Muscles in the pathophysiology of OSA. The condition is associated with episodic hypoxia due to recurrent apnoea. However, despite its obvious importance very little is known about the effects of episodic hypoxia on upper Airway Muscle function. In this review, we examine the evidence that chronic intermittent hypohypoxia can affect upper Airway Muscle structure and function and impair CNS control of the pharyngeal dilator Muscles. We review the literature and discuss results from our laboratory showing that episodic hypoxia/asphyxia reduces upper Airway Muscle endurance and selectively impairs pharyngeal dilator EMG responses to physiological stimulation. Our observations lead us to speculate that episodic hypoxia–a consequence of periodic Airway occlusion–is responsible for progression of OSA through impairment of the neural control systems that regulate upper Airway patency and through altered respiratory Muscle contractile function, leading to the establishment of a vicious cycle of further Airway obstruction and hypoxic insult that chronically exacerbates and perpetuates the condition. We conclude that chronic intermittent hypohypoxia/asphyxia contributes to the pathophysiology of sleep-disordered breathing.

  • Effects of chronic intermittent asphyxia on haematocrit, pulmonary arterial pressure and skeletal Muscle structure in rats
    Experimental physiology, 2003
    Co-Authors: Aidan Bradford
    Abstract:

    Sleep-disordered breathing in humans is a common condition associated with serious cardiovascular and other abnormalities. The prevalence and pathogenesis of increased haematocrit and pulmonary hypertension is controversial and it has been suggested that these changes only occur in patients who also have daytime continuous hypoxaemia. The hypothesis tested here is that the chronic intermittent hypohypoxia and asphyxia associated with sleep-disordered breathing causes erythropoiesis and pulmonary hypertension and that this occurs in the absence of periods of continuous hypoxia. In humans and animals with obstructive sleep apnoea, there are abnormalities of upper Airway Muscle structure that have been ascribed to increased load placed on these Muscles. An alternative hypothesis is that chronic intermittent hypohypoxia and asphyxia cause changes in upper Airway Muscle structure and function. To test these hypotheses, rats were exposed to intermittent hypohypoxia and asphyxia for 8 h per day for 5 weeks. This caused an increase in haematocrit, right ventricular weight and pulmonary arterial pressure. There were only slight changes in diaphragm, upper Airway and limb Muscle structure and force production but in general, Muscle fatigability was increased. In conclusion chronic intermittent hypohypoxia and asphyxia cause an increase in haematocrit and pulmonary arterial pressure in the absence of periods of continuous hypoxia. Chronic intermittent hypohypoxia and asphyxia have little effect on skeletal Muscle structure and force production but increase Muscle fatigue. Increased upper Airway Muscle fatigue could lead to a vicious cycle of further compromise in upper Airway patency and further hypoxia and asphyxia.

David P White – One of the best experts on this subject based on the ideXlab platform.

  • desipramine improves upper Airway collapsibility and reduces osa severity in patients with minimal Muscle compensation
    European Respiratory Journal, 2016
    Co-Authors: Luigi Tarantomontemurro, Danny J Eckert, Scott A. Sands, Bradley A. Edwards, Ali Azarbarzin, Melania Marques, Camila Maria De Melo, David P White
    Abstract:

    We recently demonstrated that desipramine reduces the sleep-related loss of upper Airway dilator Muscle activity and reduces pharyngeal collapsibility in healthy humans without obstructive sleep apnoea (OSA). The aim of the present physiological study was to determine the effects of desipramine on upper Airway collapsibility and apnoea-hypopnea index (AHI) in OSA patients.A placebo-controlled, double-blind, randomised crossover trial in 14 OSA patients was performed. Participants received treatment or placebo in randomised order before sleep. Pharyngeal collapsibility (critical collapsing pressure of the upper Airway (Pcrit)) and ventilation under both passive (V’0,passive) and active (V’0,active) upper Airway Muscle conditions were evaluated with continuous positive Airway pressure (CPAP) manipulation. AHI was quantified off CPAP.Desipramine reduced active Pcrit (median (interquartile range) -5.2 (4.3) cmH2O on desipramine versus -1.9 (2.7) cmH2O on placebo; p=0.049) but not passive Pcrit (-2.2 (3.4) versus -0.7 (2.1) cmH2O; p=0.135). A greater reduction in AHI occurred in those with minimal Muscle compensation (defined as V’0,active-V’0,passive) on placebo (r=0.71, p=0.009). The reduction in AHI was driven by the improvement in Muscle compensation (r=0.72, p=0.009).In OSA patients, noradrenergic stimulation with desipramine improves pharyngeal collapsibility and may be an effective treatment in patients with minimal upper Airway Muscle compensation.

  • upper Airway collapsibility pcrit and pharyngeal dilator Muscle activity are sleep stage dependent
    Sleep, 2016
    Co-Authors: Jayne C Carberry, Amy S Jordan, David P White, Andrew Wellman, Danny J Eckert
    Abstract:

    STUDY OBJECTIVES An anatomically narrow/highly collapsible upper Airway is the main cause of obstructive sleep apnea (OSA). Upper Airway Muscle activity contributes to Airway patency and, like apnea severity, can be sleep stage dependent. Conversely, existing data derived from a small number of participants suggest that upper Airway collapsibility, measured by the passive pharyngeal critical closing pressure (Pcrit) technique, is not sleep stage dependent. This study aimed to determine the effect of sleep stage on Pcrit and upper Airway Muscle activity in a larger cohort than previously tested. METHODS Pcrit and/or Muscle data were obtained from 72 adults aged 20-64 y with and without OSA.Pcrit was determined via transient reductions in continuous positive Airway pressure (CPAP) during N2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. Genioglossus and tensor palatini Muscle activities were measured: (1) awake with and without CPAP, (2) during stable sleep on CPAP, and (3) in response to the CPAP reductions used to quantify Pcrit. RESULTS Pcrit was 4.9 ± 1.4 cmH2O higher (more collapsible) during REM versus SWS (P = 0.012), 2.3 ± 0.6 cmH2O higher during REM versus N2 (P < 0.001), and 1.6 ± 0.7 cmH2O higher in N2 versus SWS (P = 0.048). Muscle activity decreased from wakefulness to sleep and from SWS to N2 to REM sleep for genioglossus but not for tensor palatini. Pharyngeal Muscle activity increased by ∼50% by breath 5 following CPAP reductions. CONCLUSIONS Upper Airway collapsibility measured via the Pcrit technique and genioglossus Muscle activity vary with sleep stage. These findings should be taken into account when performing and interpreting “passive” Pcrit measurements.

  • Enhanced upper-Airway Muscle responsiveness is a distinct feature of overweight/obese individuals without sleep apnea.
    American journal of respiratory and critical care medicine, 2014
    Co-Authors: Scott A. Sands, Danny J Eckert, Amy S Jordan, Atul Malhotra, Bradley A. Edwards, Robert L. Owens, James P. Butler, Richard J. Schwab, Stephen H. Loring, David P White
    Abstract:

    Rationale: Body habitus is a major determinant of obstructive sleep apnea (OSA). However, many individuals do not have OSA despite being overweight/obese (body mass index > 25 kg/m2) for reasons that are not fully elucidated.Objectives: To determine the key physiologic traits (upper-Airway anatomy/collapsibility, upper-Airway Muscle responsiveness, chemoreflex control of ventilation, arousability from sleep) responsible for the absence of OSA in overweight/obese individuals.Methods: We compared key physiologic traits in 18 overweight/obese subjects without apnea (apnea–hypopnea index < 15 events per hour) with 25 overweight/obese matched patients with OSA (apnea–hypopnea index ≥ 15 events per hour) and 11 normal-weight nonapneic control subjects. Traits were measured by repeatedly lowering continuous positive Airway pressure to subtherapeutic levels for 3 minutes during non-REM sleep.Measurements and Main Results: Overweight/obese subjects without apnea exhibited a less collapsible Airway than overweight/…

John Trinder – One of the best experts on this subject based on the ideXlab platform.

  • Common drive to the upper Airway Muscle genioglossus during inspiratory loading.
    Journal of neurophysiology, 2015
    Co-Authors: Michael J Woods, Amy S Jordan, Christian L Nicholas, John G Semmler, Julia K. M. Chan, John Trinder
    Abstract:

    Common drive is thought to constitute a central mechanism by which the efficiency of a motor neurneuron pool is increased. This study tested the hypothesis that common drive to the upper Airway Muscle

  • The effect of sleep onset on upper Airway Muscle activity in patients with sleep apnoea versus controls
    The Journal of Physiology, 2005
    Co-Authors: Robert B. Fogel, David P White, Atul Malhotra, John Trinder, Darci Kleverlaan, Jill Raneri, Karen Schory, Robert J. Pierce
    Abstract:

    Pharyngeal dilator Muscles are important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that during wakefulness, the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) is greater in patients with OSA compared with controls. Further, EMG activity decreases at sleep onset, and the decrement is greater in apnoea patients than in healthy controls. In addition, it is known that the prevalence of OSA is greater in middle-aged compared with younger men. Thus, we had two goals in this study. First we compared upper Airway Muscle activity between young and middle-aged healthy men compared with men with OSA. We also explored the mechanisms responsible for the decrement in Muscle activity at sleep onset in these groups. We investigated Muscle activity, ventilation , and upper Airway resistance (UAR) during wakefulness and sleep onset (transition from α to θ EEG activity) in all three groups. Measurements were obtained during basal breathing (BB) and nasal continuous positive Airway pressure (CPAP) was applied to reduce negative pressure-mediated Muscle activation). We found that during wakefulness there was a gradation of GGEMG and UAR (younger < older < OSA) and that Muscle activity was reduced by the application of nasal CPAP (to a greater degree in the OSA patients). Although CPAP eliminated differences in UAR during wakefulness and sleep, GGEMG remained greater in the OSA patients. During sleep onset, a greater initial fall in GGEMG was seen in the OSA patients followed by subsequent Muscle recruitment in the third to fifth breaths following the α to θ transition. On the CPAP night, and GGEMG still fell further in the OSA patients compared with control subjects. CPAP prevented the rise in UAR at sleep onset along with the associated recruitment in GGEMG. Differences in TPEMG among the groups were not significant. These data suggest that the middle-aged men had upper Airway function midway between that of young normal men and the abnormal Airway of those with OSA. Furthermore it suggests that the initial sleep onset reduction in upper Airway Muscle activity is due to loss of a ‘wakefulness’ stimulus, rather than to loss of responsiveness to negative pressure, and that this wakefulness stimulus may be greater in the OSA patient than in healthy controls.

  • Control of upper Airway Muscle activity in younger versus older men during sleep onset.
    The Journal of physiology, 2003
    Co-Authors: Robert B. Fogel, David P White, Atul Malhotra, Robert J. Pierce, Jill K. Edwards, Judy Dunai, Darci Kleverlaan, John Trinder
    Abstract:

    Pharyngeal dilator Muscles are clearly important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) are decreased at sleep onset, and that this decrement in Muscle activity is greater in the apnoea patient than in healthy controls. We have also previously shown this decrement to be greater in older men when compared with younger ones. In order to explore the mechanisms responsible for this decrement in Muscle activity nasal continuous positive Airway pressure (CPAP) was applied to reduce negative pressure mediated Muscle activation. We then investigated the effect of sleep onset (transition from predominantly alpha to predominantly theta EEG activity) on ventilation, upper Airway Muscle activation and upper Airway resistance (UAR) in middle-aged and younger healthy men. We found that both GGEMG and TPEMG were reduced by the application of nasal CPAP during wakefulness, but that CPAP did not alter the decrement in activity in either Muscle seen in the first two breaths following an alpha to theta transition. However, CPAP prevented both the rise in UAR at sleep onset that occurred on the control night, and the recruitment in GGEMG seen in the third to fifth breaths following the alpha to theta transition. Further, GGEMG was higher in the middle-aged men than in the younger men during wakefulness and was decreased more in the middle-aged men with the application of nasal CPAP. No differences were seen in TPEMG between the two age groups. These data suggest that the initial sleep onset reduction in upper Airway Muscle activity is due to loss of a ‘wakefulness’ stimulus, rather than to loss of responsiveness to negative pressure. In addition, it suggests that in older men, higher wakeful Muscle activity is due to an anatomically more collapsible upper Airway with more negative pressure driven Muscle activation. Sleep onset per se does not appear to have a greater effect on upper Airway Muscle activity as one ages.

Ken D. O'halloran – One of the best experts on this subject based on the ideXlab platform.

  • Sex, stress and sleep apnoea: Decreased susceptibility to upper Airway Muscle dysfunction following intermittent hypoxia in females
    Respiratory physiology & neurobiology, 2016
    Co-Authors: Ken D. O'halloran, Philip Lewis, Fiona B. Mcdonald
    Abstract:

    Abstract Obstructive sleep apnoea syndrome (OSAS) is a devastating respiratory control disorder more common in men than women. The reasons for the sex difference in prevalence are multifactorial, but are partly attributable to protective effects of oestrogen. Indeed, OSAS prevalence increases in post-menopausal women. OSAS is characterized by repeated occlusions of the pharyngeal Airway during sleep. Dysfunction of the upper Airway Muscles controlling Airway calibre and collapsibility is implicated in the pathophysiology of OSAS, and sex differences in the neuro-mechanical control of upper Airway patency are described. It is widely recognized that chronic intermittent hypohypoxia (CIH), a cardinal feature of OSAS due to recurrent apnoea, drives many of the morbid consequences characteristic of the disorder. In rodents, exposure to CIH-related redox stress causes upper Airway Muscle weakness and fatigue, associated with mitochondrial dysfunction. Of interest, in adults, there is female resilience to CIH-induced Muscle dysfunction. Conversely, exposure to CIH in early life, results in upper Airway Muscle weakness equivalent between the two sexes at 3 and 6 weeks of age. Ovariectomy exacerbates the deleterious effects of exposure to CIH in adult female upper Airway Muscle, an effect partially restored by oestrogen replacement therapy. Intriguingly, female advantage intrinsic to upper Airway Muscle exists with evidence of substantially greater loss of performance in male Muscle during acute exposure to severe hypoxic stress. Sex differences in upper Airway Muscle physiology may have relevance to human OSAS. The oestrogen–oestrogen receptor α axis represents a potential therapeutic target in OSAS, particularly in post-menopausal women.

  • Evidence of hypoxic tolerance in weak upper Airway Muscle from young mdx mice
    Respiratory physiology & neurobiology, 2015
    Co-Authors: David P. Burns, Ken D. O'halloran
    Abstract:

    Duchenne muscmuscular dystrophy (DMD) is a genetic disease characterised by deficiency in the protein dystrophin. The respiratory system is weakened and patients suffer from sleep disordered breathing and hypoventilation culminating in periods of hypoxaemia. We examined the effects of an acute (6h) hypoxic stress on sternohyoid Muscle function (representative pharyngeal dilator). 8 week old male, wild-type (WT; C57BL/10ScSnJ; n=18) and mdx (C57BL/10ScSn-Dmd(mdx)/J; n=16) mice were exposed to sustained hypoxia (FIO2=0.10) or normoxia. Muscle functional properties were examined ex vivo. Additional WT (n=5) and mdx (n=5) sternohyoid Muscle was exposed to an anoxic challenge. Sternohyoid dysfunction was observed in mdx mice with significant reductions in force and power. Following exposure to the acute in vivo hypoxic stress, WT sternohyoid Muscle showed evidence of functional impairment (reduced force, work and power). Conversely, mdx sternohyoid showed an apparent tolerance to the acute hypoxic stress. This tolerance was not maintained for mdx following a severe hypoxic stress. A dysfunctional upper Airway Muscle phenotype is present at 8 weeks of age in the mdx mouse, which may have implications for the control of Airway patency in DMD. Hypoxic tolerance in mdx respiratory Muscle is suggestive of adaptation to chronic hypoxia, which could be present due to respiratory morbidity. We speculate a role for hypoxia in mdx respiratory Muscle morbidity.

  • Chronic nitric oxide synthase inhibition does not impair upper Airway Muscle adaptation to chronic intermittent hypoxia in the rat.
    Progress in brain research, 2014
    Co-Authors: Fiona B. Mcdonald, Deirdre Edge, Ken D. O'halloran
    Abstract:

    Abstract Nitric oxide (NO) is an important modulator of striated Muscle function. Nitric oxide synthase (NOS) expression and activity is altered by hypoxia and NO is implicated in respiratory Muscle remodeling following chronic sustained hypoxia. We sought to determine if NO is implicated in upper Airway dilator Muscle adaptation to chronic intermittent hypohypoxia (CIH). Thirty-two adult male Wistar rats (284 ± 13, mean ± SD) were exposed to alternating bouts of hypoxia (90 s; 5% O 2 at the nadir) and normoxia (210 s; 21% O 2 ) for 12 cycles per hour, 8 h/day for 3 weeks. Sham animals were exposed to normoxia in parallel. Half of the animals in both groups received the nNOS inhibitor— l -NNA (2 mM) in the drinking water throughout the study ( N  = 8 for all groups). Sternohyoid (pharyngeal dilator) Muscle contractile and endurance properties were determined ex vivo . Sternohyoid Muscle myosin heavy chain (MHC) isoform composition and cross-sectional area was determined by fluorescence microscopy. Chronic nNOS blockade did not alter sternohyoid Muscle peak force or force–frequency relationship in sham or CIH-treated animals. In contrast, chronic nNOS blockade significantly decreased sternohyoid Muscle endurance with equivalent effects in sham and CIH-treated rats. Our results suggest that NO is an important modulator of sternohyoid Muscle endurance. However, our data provide no evidence to suggest that NO is implicated in upper Airway Muscle adaptation to CIH.

Atul Malhotra – One of the best experts on this subject based on the ideXlab platform.

  • Enhanced upper-Airway Muscle responsiveness is a distinct feature of overweight/obese individuals without sleep apnea.
    American journal of respiratory and critical care medicine, 2014
    Co-Authors: Scott A. Sands, Danny J Eckert, Amy S Jordan, Atul Malhotra, Bradley A. Edwards, Robert L. Owens, James P. Butler, Richard J. Schwab, Stephen H. Loring, David P White
    Abstract:

    Rationale: Body habitus is a major determinant of obstructive sleep apnea (OSA). However, many individuals do not have OSA despite being overweight/obese (body mass index > 25 kg/m2) for reasons that are not fully elucidated.Objectives: To determine the key physiologic traits (upper-Airway anatomy/collapsibility, upper-Airway Muscle responsiveness, chemoreflex control of ventilation, arousability from sleep) responsible for the absence of OSA in overweight/obese individuals.Methods: We compared key physiologic traits in 18 overweight/obese subjects without apnea (apnea–hypopnea index < 15 events per hour) with 25 overweight/obese matched patients with OSA (apnea–hypopnea index ≥ 15 events per hour) and 11 normal-weight nonapneic control subjects. Traits were measured by repeatedly lowering continuous positive Airway pressure to subtherapeutic levels for 3 minutes during non-REM sleep.Measurements and Main Results: Overweight/obese subjects without apnea exhibited a less collapsible Airway than overweight/…

  • enhanced upper Airway Muscle responsiveness is a distinct feature of overweight obese individuals without sleep apnea
    American Journal of Respiratory and Critical Care Medicine, 2014
    Co-Authors: Scott A. Sands, Danny J Eckert, Amy S Jordan, Atul Malhotra, Bradley A. Edwards, Robert L. Owens, James P. Butler, Stephen H. Loring, Richard Schwab, David P White
    Abstract:

    Rationale: Body habitus is a major determinant of obstructive sleep apnea (OSA). However, many individuals do not have OSA despite being overweight/obese (body mass index > 25 kg/m2) for reasons that are not fully elucidated.Objectives: To determine the key physiologic traits (upper-Airway anatomy/collapsibility, upper-Airway Muscle responsiveness, chemoreflex control of ventilation, arousability from sleep) responsible for the absence of OSA in overweight/obese individuals.Methods: We compared key physiologic traits in 18 overweight/obese subjects without apnea (apnea–hypopnea index < 15 events per hour) with 25 overweight/obese matched patients with OSA (apnea–hypopnea index ≥ 15 events per hour) and 11 normal-weight nonapneic control subjects. Traits were measured by repeatedly lowering continuous positive Airway pressure to subtherapeutic levels for 3 minutes during non-REM sleep.Measurements and Main Results: Overweight/obese subjects without apnea exhibited a less collapsible Airway than overweight/…

  • neostigmine but not sugammadex impairs upper Airway dilator Muscle activity and breathing
    BJA: British Journal of Anaesthesia, 2008
    Co-Authors: Amy S Jordan, Matthias Eikermann, S Zaremba, Atul Malhotra, Carl E Rosow, Nancy L Chamberlin
    Abstract:

    Background Cholinesterase inhiinhibitor-based reversal agents, given in the absence of neuromuscular block, evoke a partial upper Airway obstruction by decreasing skeletal upper Airway Muscle function. Sugammadex reverses neuromuscular block by encapsulating rocuronium. However, its effects on upper Airway integrity and breathing are unknown.