Publications by authors named "Andrew E Beaudin"

25 Publications

  • Page 1 of 1

Cognitive Function in a Sleep Clinic Cohort of Patients with Obstructive Sleep Apnea.

Ann Am Thorac Soc 2020 Nov 4. Epub 2020 Nov 4.

University of Calgary, Medicine, Calgary, Alberta, Canada.

Obstructive sleep apnea (OSA) is associated with an increased risk of mild cognitive impairment (MCI) within the general population. However, MCI risk in sleep-clinic populations of OSA patients is poorly characterized. To determine the prevalence of MCI in a sleep-clinic population of OSA patients and which patients are at the greatest risk for this complication. Adults (n=1084) referred to three academic sleep centers for suspected OSA who had home sleep apnea testing or in-laboratory polysomnography were recruited. Patients completed sleep and medical history questionnaires, the Montreal Cognitive Assessment Test (MoCA) of global cognition, Rey Auditory Verbal Learning Test (RAVLT) of memory and WAIS-IV Digit-Symbol Coding (DSC) subtest of information processing speed. A MoCA score<26 (range 0-30) was operationally defined as MCI. MCI was present in 47.9% of our entire patient cohort; increasing to >55.3% in patients with moderate and severe OSA. Patients with a MoCA<26 were predominantly older males with more severe OSA, hypoxemia and vascular comorbidities. Moderate and severe OSA were independently associated with >70% higher odds for MCI compared to patients with no OSA (p=0.003). Memory and information processing speed was lower than age-matched normal values (p<0.001) with lower MoCA and DSC scores associated with a higher oxygen desaturation index and nocturnal hypoxemia. Cognitive impairment is highly prevalent in patients referred to sleep clinics for suspected OSA, occurring predominantly in older males with moderate-to-severe OSA and concurrent vascular comorbidities. Moderate-to-severe OSA is an independent risk factor for MCI.
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http://dx.doi.org/10.1513/AnnalsATS.202004-313OCDOI Listing
November 2020

Symptom subtypes and cognitive function in a clinic-based OSA cohort: a multi-centre Canadian study.

Sleep Med 2020 10 11;74:92-98. Epub 2020 May 11.

Department of Medicine, Respiratory and Critical Care Divisions, University of British Columbia, Vancouver, BC, Canada; Canadian Sleep and Circadian Network, Canada. Electronic address:

Background: Distinct symptom subtypes are found in patients with OSA. The association between these subtypes and neurocognitive function is unclear.

Objective: The purposes of this study were to assess whether OSA symptom subtypes are present in a cohort of Canadian patients with suspected OSA and evaluate the relationship between subtypes and neurocognitive function.

Methods: Patients with suspected OSA who completed a symptom questionnaire and underwent testing for OSA were included. Symptom subtypes were identified using latent class analysis. Associations between subtypes and neurocognitive outcomes (Montreal Cognitive Assessment [MoCA], Rey Auditory Verbal Learning Test [RAVLT], Wechsler Adult Intelligence Scale [WAIS-IV], Digit-Symbol Coding subtest [DSC]) were assessed using analysis of covariance (ANCOVA), controlling for relevant covariates.

Results: Four symptom subtypes were identified in patients with OSA (oxygen desaturation index ≥5 events/hour). Three were similar to prior studies, including the Excessively Sleepy (N=405), Disturbed Sleep (N=382) and Minimally Symptomatic (N=280), and one was a novel subtype in our sample defined as Excessively Sleepy with Disturbed Sleep (N=247). After covariate adjustment, statistically significant differences among subtypes (p=0.037) and among subtypes and patients without OSA (p=0.044) were observed in DSC scores; the Minimally Symptomatic subtype had evidence of higher DSC scores than all other groups, including non-OSA patients. No differences were seen in MoCA or RAVLT.

Conclusions: Results support the existence of previously identified OSA symptom subtypes of excessively sleepy, disturbed sleep and minimally symptomatic in a clinical sample from Canada. Subtypes were not consistently associated with neurocognitive function across multiple instruments.
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http://dx.doi.org/10.1016/j.sleep.2020.05.001DOI Listing
October 2020

Cross-sectional and longitudinal differences in peak skeletonized white matter mean diffusivity in cerebral amyloid angiopathy.

Neuroimage Clin 2020 26;27:102280. Epub 2020 May 26.

Departments of Clinical Neurosciences and Radiology, Hotchkiss Brain Institute, University of Calgary, Seaman Family MR Research Centre, Foothills Medical Centre, Alberta Health Sciences, Calgary, Alberta, Canada.

Objectives: To test the hypotheses that peak skeletonized mean diffusivity (PSMD), a measure of cerebral white matter microstructural disruption, is 1) increased in patients with cerebral amyloid angiopathy (CAA) compared to normal control (NC), mild cognitive impairment (MCI), and Alzheimer's disease (AD); 2) associated with neuropsychological test performance among CAA patients; and 3) increased more quickly over one year in CAA than in AD, MCI, and NC.

Methods: Ninety-two participants provided a medical history, completed a neuropsychological assessment, and had a magnetic resonance (MR) exam including diffusion tensor imaging (DTI) from which PSMD was calculated. A 75-minute neuropsychological test battery was used to derive domain scores for memory, executive function, and processing speed. Multivariable analyses controlling for age and sex (and education, for cognitive outcomes) were used to test the study hypotheses.

Results: PSMD was higher in the CAA group (mean 4.97 × 10 mm/s) compared to NC (3.25 × 10 mm/s), MCI (3.62 × 10 mm/s) and AD (3.89 × 10 mm/s) groups (p < .01). Among CAA patients, higher PSMD was associated with slower processing speed (estimated -0.22 standard deviation (SD) change in processing speed z score per SD increase in PSMD, 95% CI -0.42 to -0.03, p = .03), higher WMH volume [β = 0.74, CI 0.48 to 1.00], and higher CAA SVD score [β = 0.68, CI 0.24 to 1.21] but was not associated with MMSE, executive function, memory, CMB count, or cortical thickness. PSMD increased over 1-year in all groups (p < .01) but without rate differences between groups (p = .66).

Conclusions: PSMD, a simple marker of diffuse global white matter heterogeneity, is increased in CAA. Our findings further support a role for white matter disruption in causing cognitive impairment in CAA.
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http://dx.doi.org/10.1016/j.nicl.2020.102280DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284130PMC
May 2020

Vascular responses to hypoxia are not impaired in obstructive sleep apnoea patients free of overt cardiovascular disease.

Exp Physiol 2019 04 27;104(4):580-600. Epub 2019 Feb 27.

Department of Physiology & Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

New Findings: What is the central question of this study? Does treatment of obstructive sleep apnoea (OSA) with nocturnal oxygen or continuous positive airway pressure (CPAP) improve hypoxic vascular responses, which are reportedly impaired in OSA? What is the main finding and its importance? Cerebrovascular and cardiovascular hypoxic responses were not impaired in OSA patients free of overt cardiovascular disease and known risk factors, and were not altered by nocturnal oxygen or CPAP treatment. We conclude that this OSA patient phenotype has normal vascular responses to hypoxia and is unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.

Abstract: Cerebral blood flow (CBF) and cardiovascular responses to hypoxia are reportedly impaired in obstructive sleep apnoea (OSA) patients and corrected by continuous positive airway pressure (CPAP), beneficial effects that are ascribed to correction of OSA-related intermittent hypoxia (IH). However, CPAP corrects both IH and ancillary OSA features (i.e. intermittent hypercapnia, sympathetic activation, blood pressure surges, negative intrathoracic pressure swings and sleep fragmentation). Whether correction of these ancillary OSA features contribute to CPAP's beneficial effects on vascular hypoxic responses is unknown. Nocturnal oxygen corrects OSA-induced IH, but apnoeas and ancillary features persist. Thus, we examined the effects of nocturnal oxygen and CPAP on cerebrovascular and cardiovascular hypoxic responses in untreated OSA patients. Responses were assessed in 52 OSA patients free of overt cardiovascular disease and known risk factors at baseline, after 2 weeks of nocturnal oxygen (n = 26) or no treatment (n = 26), and after ∼4 weeks of CPAP treatment (n = 40). Twenty-two age-matched controls were assessed at baseline and follow-up visits. Resting, isocapnic euoxia mean blood pressure was decreased following nocturnal oxygen (-3.6 ± 6.0 mmHg; P = 0.006) and CPAP (-4.5 ± 7.5 mmHg; P < 0.001) while cerebrovascular conductance was increased with CPAP (P = 0.001). However, these changes were not different from controls. Unexpectedly, OSA patients and controls had similar hypoxic vascular responses at baseline that were not changed by either nocturnal oxygen or CPAP. We conclude that OSA patients free of overt cardiovascular disease and known risk factors did not have impaired cerebrovascular or cardiovascular responses to hypoxia and are unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.
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http://dx.doi.org/10.1113/EP086845DOI Listing
April 2019

Plasma Exosomes and Improvements in Endothelial Function by Angiotensin 2 Type 1 Receptor or Cyclooxygenase 2 Blockade following Intermittent Hypoxia.

Front Neurol 2017 22;8:709. Epub 2017 Dec 22.

Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, University of Chicago, Chicago, IL, United States.

Intermittent hypoxia (IH) is associated with increased endothelial dysfunction and cardiovascular disorders. Exosomes released in biological fluids may act as vehicles for propagating such damage, modifying the functional phenotype of endothelial cells. Drug interventions, however, may provide protection for the endothelium, in spite of exosomal activity. Using an experimental human model of IH, we investigated whether the beneficial effects of two drugs, celecoxib (CEL) and losartan (LOS), on IH-induced vascular dysfunction was mediated exosomes or independent of IH-induced exosomal cargo alterations. We hypothesized that the beneficial effects of CEL and LOS on IH-induced vascular dysfunction would be mediated modifications of exosomal properties by the drugs, rather than by direct effects of the drugs on the endothelium. Ten male volunteers were exposed to IH (single exposure of 6 h) while receiving LOS, CEL, or placebo (P) for 4 days before IH exposures, and plasma samples were obtained from which exosomes were isolated, and incubated with naïve human endothelial cell cultures either not treated or pretreated with LOS, CEL, or P. Functional reporter assays (monolayer impedance, monocyte adhesion, and eNOS phosphorylation) revealed that the degree of exosome-induced endothelial dysfunction was similar among IH-exposed subjects independent of drug treatment. However, pretreatment of naïve endothelial cells with LOS or CEL before addition of exosomes from IH-exposed subjects afforded significant protection. Thus, the cardiovascular protective impact of LOS and CEL appears to be mediated by their direct effects on endothelial cells, rather than modulation of exosomal cargo.
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http://dx.doi.org/10.3389/fneur.2017.00709DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743928PMC
December 2017

New insights into cerebral small vessel disease and vascular cognitive impairment from MRI.

Curr Opin Neurol 2018 Feb;31(1):36-43

Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.

Purpose Of Review: We review recent MRI research that addresses two important challenges in cerebral small vessel disease (SVD) research: early diagnosis, and linking SVD with cognitive impairment. First, we review studies of MRI measurements of blood flow and blood-brain barrier integrity. Second, we review MRI studies identifying neuroimaging correlates of SVD-related cognitive dysfunction, focusing on brain connectivity and white matter microarchitecture. This research is placed in context through discussion of recent recommendations for management of incidentally discovered SVD, and neuroimaging biomarker use in clinical trials.

Recent Findings: Cerebral perfusion, cerebrovascular reactivity (CVR), blood-brain barrier permeability, and white matter microarchitecture are measurable using MRI, and are altered in SVD. Lower cerebral blood flow predicts a higher future risk for dementia, whereas decreased CVR occurs at early stages of SVD and is associated with future white matter hyperintensity growth. Two new approaches to analyzing diffusion tensor imaging (DTI) data in SVD patients have emerged: graph theory-based analysis of networks of DTI connectivity between cortical nodes, and analysis of histograms of mean diffusivity of the hemispheric white matter.

Summary: New, advanced quantitative neuroimaging techniques are not ready for routine radiological practice but are already being employed as monitoring biomarkers in the newest generation of trials for SVD.
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http://dx.doi.org/10.1097/WCO.0000000000000513DOI Listing
February 2018

Human cerebral blood flow control during hypoxia: focus on chronic pulmonary obstructive disease and obstructive sleep apnea.

J Appl Physiol (1985) 2017 Nov 10;123(5):1350-1361. Epub 2017 Aug 10.

Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada;

The brain is a vital organ that relies on a constant and adequate blood flow to match oxygen and glucose delivery with the local metabolic demands of active neurons. Thus exquisite regulation of cerebral blood flow (CBF) is particularly important under hypoxic conditions to prevent a detrimental decrease in the partial pressure of oxygen within the brain tissues. Cerebrovascular sensitivity to hypoxia, assessed as the change in CBF during a hypoxic challenge, represents the capacity of cerebral vessels to respond to, and compensate for, a reduced oxygen supply, and has been shown to be impaired or blunted in a number of conditions. For instance, this is observed with aging, and in clinical conditions such as untreated obstructive sleep apnea (OSA) and in healthy humans exposed to intermittent hypoxia. This review will ) provide a brief overview of cerebral blood flow regulation and results of pharmacological intervention studies which we have performed to better elucidate the basic mechanisms of cerebrovascular regulation in humans; and ) present data from studies in clinical and healthy populations, using a translational physiology approach, to investigate human CBF control during hypoxia. Results from studies in patients with chronic obstructive pulmonary disease and OSA will be presented to identify the effects of the disease processes on cerebrovascular sensitivity to hypoxia. Data emerging from experimental human models of intermittent hypoxia during wakefulness will also be reviewed to highlight the effects of intermittent hypoxia on the brain.
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http://dx.doi.org/10.1152/japplphysiol.00352.2017DOI Listing
November 2017

Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation.

Exp Physiol 2017 07 27;102(7):743-763. Epub 2017 Jun 27.

Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

New Findings: What is the topic of this review? This review examines the notion that obstructive sleep apnoea (OSA) and intermittent hypoxia (IH) have hormetic effects on vascular health. What advances does it highlight? Clinical (OSA patient) and experimental animal and human models report that IH is detrimental to vascular regulation. However, mild IH and, by extension, mild OSA also have physiological and clinical benefits. This review highlights clinical and experimental animal and human data linking OSA and IH to vascular disease and discusses how hormetic effects of OSA and IH relate to OSA severity, IH intensity and duration, and patient/subject age. Obstructive sleep apnoea (OSA) is associated with increased risk of cardiovascular and cerebrovascular disease, a consequence attributed in part to chronic intermittent hypoxia (IH) resulting from repetitive apnoeas during sleep. Although findings from experimental animal, and human, models have shown that IH is detrimental to vascular regulation, the severity of IH used in many of these animal studies [e.g. inspired fraction of oxygen (FI,O2) = 2-3%; oxygen desaturation index = 120 events h ] is considerably greater than that observed in the majority of patients with OSA. This may also explain disparities between animal and recently developed human models of IH, where IH severity is, by necessity, less severe (e.g. FI,O2 = 10-12%; oxygen desaturation index = 15-30 events h ). In this review, we highlight the current knowledge regarding the impact of OSA and IH on cardiovascular and cerebrovascular regulation. In addition, we critically discuss the recent notion that OSA and IH may have hormetic effects on vascular health depending on conditions such as OSA severity, IH intensity and duration, and age. In general, data support an independent causal link between OSA and vascular disease, particularly for patients with severe OSA. However, the data are equivocal for older OSA patients and patients with mild OSA, because advanced age and short-duration, low-intensity IH have been reported to provide a degree of protection against IH and ischaemic events such as myocardial infarction and stroke, respectively. Overall, additional studies are needed to investigate the beneficial/detrimental effects of mild OSA on the various vascular beds.
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http://dx.doi.org/10.1113/EP086051DOI Listing
July 2017

Effects of continuous positive airway pressure and isocapnic-hypoxia on cerebral autoregulation in patients with obstructive sleep apnoea.

J Physiol 2016 12;594(23):7089-7104

Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

Key Points: Altered cerebral autoregulation (CA) in obstructive sleep apnoea (OSA) patients may contribute to increased stroke risk in this population; the gold standard treatment for OSA is continuous positive airway pressure, which improves cerebrovascular regulation and may decrease the risk of stroke. Isocapnic-hypoxia impairs CA in healthy subjects, but it remains unknown in OSA whether impaired CA is further exacerbated by isocapnic-hypoxia and whether it is improved by treatment with continuous positive airway pressure. During normoxia, CA was altered in the more severe but not in the less severe OSA patients, while, in contrast, during isocapnic-hypoxia, CA was similar between groups and tended to improve in patients with more severe OSA compared to normoxia. From a clinical perspective, one month of continuous positive airway pressure treatment does not improve CA. From a physiological perspective, this study suggests that sympathetic overactivity may be responsible for altered CA in the more severe OSA patients.

Abstract: Cerebral autoregulation (CA) impairment may contribute to the increased risk of stroke associated with obstructive sleep apnoea (OSA). It is unknown if impaired CA is further exacerbated by isocapnic-hypoxia and whether it is improved by treatment of OSA with continuous positive airway pressure (CPAP). CA was assessed during wakefulness in 53 OSA patients (50.3 ± 9.3 years) and 21 controls (49.8 ± 8.6 years) at baseline and following a minimum of 1 month of effective CPAP therapy (OSA patients, n = 40). Control participants (n = 21) performed a follow-up visit to control for time effects within OSA patients between baseline and the post-CPAP visit. Beat-by-beat middle cerebral artery blood flow velocity and mean arterial blood pressure (MBP), and breath-by-breath end-tidal partial pressure of CO (P ET ,CO2) were monitored. CA was determined during normoxia and isocapnic-hypoxia using transfer function (phase and gain) and coherence analysis (including multiple and partial coherence (using MBP and P ET ,CO2 as inputs)) in the very low frequency range (0.03-0.07 Hz). OSA patients were divided into two subgroups (less severe and more severe) based upon the median respiratory disturbance index (RDI). During normoxia, the more severe OSA patients (RDI 45.9 ± 10.3) exhibited altered CA compared to controls and the less severe OSA patients (RDI 24.5 ± 5.9). In contrast, during isocapnic-hypoxia, CA was similar between groups. CPAP had no effect on CA. In conclusion, CA is altered in the more severe OSA patients during normoxia but not during isocapnic-hypoxia and CPAP treatment does not impact CA.
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http://dx.doi.org/10.1113/JP272967DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5134415PMC
December 2016

Effect on Intermittent Hypoxia on Plasma Exosomal Micro RNA Signature and Endothelial Function in Healthy Adults.

Sleep 2016 Dec 1;39(12):2077-2090. Epub 2016 Dec 1.

Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Science Division, University of Chicago, Chicago, IL.

Study Objective: Intermittent hypoxia (IH) is associated with increased risk of cardiovascular disease. Exosomes are secreted by most cell types and released in biological fluids, including plasma, and play a role in modifying the functional phenotype of target cells. Using an experimental human model of IH, we investigated potential exosome-derived biomarkers of IH-induced vascular dysfunction.

Methods: Ten male volunteers were exposed to room air (D0), IH (6 h/day) for 4 days (D4) and allowed to recover for 4 days (D8). Circulating plasma exosomes were isolated and incubated with human endothelial monolayer cultures for impedance measurements and RNA extracted and processed with messenger RNA (mRNA) arrays to identify gene targets. In addition, immunofluorescent assessments of endothelial nitric oxide synthase () mRNA expression, ICAM-1 cellular distribution were conducted.

Results: Plasma exosomal micro RNAs (miRNAs) were profiled. D4 exosomes, primarily from endothelial sources, disrupted impedance levels compared to D0 and D8. ICAM-1 expression was markedly upregulated in endothelial cells exposed to D4 exosomes along with significant reductions in expression. Microarray approaches identified a restricted and further validated signature of exosomal miRNAs in D4 exosomes, and mRNA arrays revealed putative endothelial gene target pathways.

Conclusions: In humans, intermittent hypoxia alters exosome cargo in the circulation which promotes increased permeability and dysfunction of endothelial cells . A select number of circulating exosomal miRNAs may play important roles in the cardiovascular dysfunction associated with OSA by targeting specific effector pathways.
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http://dx.doi.org/10.5665/sleep.6302DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5103796PMC
December 2016

What role for hypercapnia in obstructive sleep apnea?

J Appl Physiol (1985) 2016 07;121(1):362

Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Canada.

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http://dx.doi.org/10.1152/japplphysiol.00377.2016DOI Listing
July 2016

Human intermittent hypoxia-induced respiratory plasticity is not caused by inflammation.

Eur Respir J 2015 Oct 11;46(4):1072-83. Epub 2015 Jun 11.

Dept of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada Dept of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada

Ventilatory instability, reflected by enhanced acute hypoxic (AHVR) and hypercapnic (AHCVR) ventilatory responses is a fundamental component of obstructive sleep apnoea (OSA) pathogenesis. Intermittent hypoxia-induced inflammation is postulated to promote AHVR enhancement in OSA, although the role of inflammation in intermittent hypoxia-induced respiratory changes in humans has not been examined. Thus, this study assessed the role of inflammation in intermittent hypoxia-induced respiratory plasticity in healthy humans.In a double-blind, placebo-controlled, randomised crossover study design, 12 males were exposed to 6 h of intermittent hypoxia on three occasions. Prior to intermittent hypoxia exposures, participants ingested (for 4  days) either placebo or the nonsteroidal anti-inflammatory drugs indomethacin (nonselective cyclooxygenase (COX) inhibitor) and celecoxib (selective COX-2 inhibitor). Pre- and post-intermittent hypoxia resting ventilation, AHVR, AHCVR and serum concentration of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α were assessed.Pre-intermittent hypoxia resting ventilation, AHVR, AHCVR and TNF-α concentrations were similar across all three conditions (p≥0.093). Intermittent hypoxia increased resting ventilation and the AHVR similarly across all conditions (p=0.827), while the AHCVR was increased (p=0.003) and TNF-α was decreased (p=0.006) with only selective COX-2 inhibition.These findings indicate that inflammation does not contribute to human intermittent hypoxia-induced respiratory plasticity. Moreover, selective COX-2 inhibition augmented the AHCVR following intermittent hypoxia exposure, suggesting that selective COX-2 inhibition could exacerbate OSA severity by increasing ventilatory instability.
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http://dx.doi.org/10.1183/09031936.00007415DOI Listing
October 2015

Studying cerebral hemodynamics and metabolism using simultaneous near-infrared spectroscopy and transcranial Doppler ultrasound: a hyperventilation and caffeine study.

Physiol Rep 2015 Apr;3(4)

Department of Radiology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada Faculty of Medicine, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada

Caffeine is one of the most widely consumed psycho-stimulants in the world, yet little is known about its effects on brain oxygenation and metabolism. Using a double-blind, placebo-controlled, randomized cross-over study design, we combined transcranial Doppler ultrasound (TCD) and near-infrared spectroscopy (NIRS) to study caffeine's effect on middle cerebral artery peak blood flow velocity (Vp), brain tissue oxygenation (StO2), total hemoglobin (tHb), and cerebral oxygen metabolism (CMRO2) in five subjects. Hyperventilation-induced hypocapnia served as a control to verify the sensitivity of our measurements. During hypocapnia (~16 mmHg below resting values), Vp decreased by 40.0 ± 2.4% (95% CI, P < 0.001), while StO2 and tHb decreased by 2.9 ± 0.3% and 2.6 ± 0.4%, respectively (P = 0.003 and P = 0.002, respectively). CMRO2, calculated using the Fick equation, was reduced by 29.3 ± 9% compared to the isocapnic-euoxia baseline (P < 0.001). In the pharmacological experiments, there was a significant decrease in Vp, StO2, and tHb after ingestion of 200 mg of caffeine compared with placebo. There was no significant difference in CMRO2 between caffeine and placebo. Both showed a CMRO2 decline compared to baseline showing the importance of a placebo control. In conclusion, this study showed that profound hypocapnia impairs cerebral oxidative metabolism. We provide new insight into the effects of caffeine on cerebral hemodynamics. Moreover, this study showed that multimodal NIRS/TCD is an excellent tool for studying brain hemodynamic responses to pharmacological interventions and physiological challenges.
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http://dx.doi.org/10.14814/phy2.12378DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425980PMC
April 2015

Cyclooxygenases 1 and 2 differentially regulate blood pressure and cerebrovascular responses to acute and chronic intermittent hypoxia: implications for sleep apnea.

J Am Heart Assoc 2014 May 9;3(3):e000875. Epub 2014 May 9.

Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.

Background: Obstructive sleep apnea (OSA) is associated with increased risk of cardiovascular and cerebrovascular disease resulting from intermittent hypoxia (IH)-induced inflammation. Cyclooxygenase (COX)-formed prostanoids mediate the inflammatory response, and regulate blood pressure and cerebral blood flow (CBF), but their role in blood pressure and CBF responses to IH is unknown. Therefore, this study's objective was to determine the role of prostanoids in cardiovascular and cerebrovascular responses to IH.

Methods And Results: Twelve healthy, male participants underwent three, 6-hour IH exposures. For 4 days before each IH exposure, participants ingested a placebo, indomethacin (nonselective COX inhibitor), or Celebrex(®) (selective COX-2 inhibitor) in a double-blind, randomized, crossover study design. Pre- and post-IH blood pressure, CBF, and urinary prostanoids were assessed. Additionally, blood pressure and urinary prostanoids were assessed in newly diagnosed, untreated OSA patients (n=33). Nonselective COX inhibition increased pre-IH blood pressure (P ≤ 0.04) and decreased pre-IH CBF (P=0.04) while neither physiological variable was affected by COX-2 inhibition (P ≥ 0.90). Post-IH, MAP was elevated (P ≤ 0.05) and CBF was unchanged with placebo and nonselective COX inhibition. Selective COX-2 inhibition abrogated the IH-induced MAP increase (P=0.19), but resulted in lower post-IH CBF (P=0.01). Prostanoids were unaffected by IH, except prostaglandin E2 was elevated with the placebo (P=0.02). Finally, OSA patients had elevated blood pressure (P ≤ 0.4) and COX-1 formed thromboxane A2 concentrations (P=0.02).

Conclusions: COX-2 and COX-1 have divergent roles in modulating vascular responses to acute and chronic IH. Moreover, COX-1 inhibition may mitigate cardiovascular and cerebrovascular morbidity in OSA.

Clinical Trial Registration Url: www.clinicaltrials.gov. Unique identifier: NCT01280006.
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http://dx.doi.org/10.1161/JAHA.114.000875DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4309085PMC
May 2014

Effects of aging on the association between cerebrovascular responses to visual stimulation, hypercapnia and arterial stiffness.

Front Physiol 2014 19;5:49. Epub 2014 Feb 19.

Department of Physiology and Pharmacology, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary Calgary, AB, Canada ; Faculty of Kinesiology, University of Calgary Calgary, AB, Canada ; The Libin Cardiovascular Institute of Alberta, Faculty of Medicine, University of Calgary Calgary, AB, Canada.

Aging is associated with decreased vascular compliance and diminished neurovascular- and hypercapnia-evoked cerebral blood flow (CBF) responses. However, the interplay between arterial stiffness and reduced CBF responses is poorly understood. It was hypothesized that increased cerebral arterial stiffness is associated with reduced evoked responses to both, a flashing checkerboard visual stimulation (i.e., neurovascular coupling), and hypercapnia. To test this hypothesis, 20 older (64 ± 8 year; mean ± SD) and 10 young (30 ± 5 year) subjects underwent a visual stimulation (VS) and a hypercapnic test. Blood velocity through the posterior (PCA) and middle cerebral (MCA) arteries was measured concurrently using transcranial Doppler ultrasound (TCD). Cerebral and systemic vascular stiffness were calculated from the cerebral blood velocity and systemic blood pressure waveforms, respectively. Cerebrovascular (MCA: young = 76 ± 15%, older = 98 ± 19%, p = 0.004; PCA: young = 80 ± 16%, older = 106 ± 17%, p < 0.001) and systemic (young = 59 ± 9% and older = 80 ± 9%, p < 0.001) augmentation indices (AI) were higher in the older group. CBF responses to VS (PCA: p < 0.026) and hypercapnia (PCA: p = 0.018; MCA: p = 0.042) were lower in the older group. A curvilinear model fitted to cerebral AI and age showed AI increases until ~60 years of age, after which the increase levels off (PCA: R (2) = 0.45, p < 0.001; MCA: R (2) = 0.31, p < 0.001). Finally, MCA, but not PCA, hypercapnic reactivity was inversely related to cerebral AI (MCA: R (2) = 0.28, p = 0.002; PCA: R (2) = 0.10, p = 0.104). A similar inverse relationship was not observed with the PCA blood flow response to VS (R (2) = 0.06, p = 0.174). In conclusion, older subjects had reduced neurovascular- and hypercapnia-mediated CBF responses. Furthermore, lower hypercapnia-mediated blood flow responses through the MCA were associated with increased vascular stiffness. These findings suggest the reduced hypercapnia-evoked CBF responses through the MCA, in older individuals may be secondary to vascular stiffening.
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http://dx.doi.org/10.3389/fphys.2014.00049DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928624PMC
March 2014

Neurovascular decoupling is associated with severity of cerebral amyloid angiopathy.

Neurology 2013 Nov 4;81(19):1659-65. Epub 2013 Oct 4.

From the Department of Radiology, Seaman Family MR Centre (S.P., C.R.M., R.F., B.G.G., E.E.S.), Departments of Clinical Neurosciences (E.D., G.K., N.S., K.S., A.C., N.P., M.J.P., R.F., B.G.G., E.E.S.), Physiology and Pharmacology (C.D.S., A.B., D.F., M.J.P.), and Community Health Sciences (G.H.F., E.E.S.), University of Calgary, Canada; Institute of Human Movement Sciences and Sport (D.F.), ETH Zurich, Switzerland; Hotchkiss Brain Institute (M.J.P., R.F., B.G.G., E.E.S.), and Faculty of Kinesiology (M.J.P.), University of Calgary; Foothills Medical Centre, Alberta Health Services, Canada.

Objectives: We used functional MRI (fMRI), transcranial Doppler ultrasound, and visual evoked potentials (VEPs) to determine the nature of blood flow responses to functional brain activity and carbon dioxide (CO2) inhalation in patients with cerebral amyloid angiopathy (CAA), and their association with markers of CAA severity.

Methods: In a cross-sectional prospective cohort study, fMRI, transcranial Doppler ultrasound CO2 reactivity, and VEP data were compared between 18 patients with probable CAA (by Boston criteria) and 18 healthy controls, matched by sex and age. Functional MRI consisted of a visual task (viewing an alternating checkerboard pattern) and a motor task (tapping the fingers of the dominant hand).

Results: Patients with CAA had lower amplitude of the fMRI response in visual cortex compared with controls (p = 0.01), but not in motor cortex (p = 0.22). In patients with CAA, lower visual cortex fMRI amplitude correlated with higher white matter lesion volume (r = -0.66, p = 0.003) and more microbleeds (r = -0.78, p < 0.001). VEP P100 amplitudes, however, did not differ between CAA and controls (p = 0.45). There were trends toward reduced CO2 reactivity in the middle cerebral artery (p = 0.10) and posterior cerebral artery (p = 0.08).

Conclusions: Impaired blood flow responses in CAA are more evident using a task to activate the occipital lobe than the frontal lobe, consistent with the gradient of increasing vascular amyloid severity from frontal to occipital lobe seen in pathologic studies. Reduced fMRI responses in CAA are caused, at least partly, by impaired vascular reactivity, and are strongly correlated with other neuroimaging markers of CAA severity.
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http://dx.doi.org/10.1212/01.wnl.0000435291.49598.54DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812103PMC
November 2013

Ventilatory responses to exercise and CO2 after menopause in healthy women: effects of age and fitness.

Respir Physiol Neurobiol 2012 Oct 28;184(1):1-8. Epub 2012 Jun 28.

Department of Physiology & Pharmacology, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada.

The extent to which aging affects respiratory control in postmenopausal women remains relatively unknown. In a cross-sectional study of 39 postmenopausal women (50-79 years), we examined the influence of age and fitness on the ventilatory responses to hypercapnia (HCVR; +8 mmHg) and exercise (ΔV˙(E)/ΔV˙CO2) above and below the anaerobic threshold (AT). Data were analyzed using the full cohort, by age (younger postmenopausal: YPM, 50-64 years; and older postmenopausal: OPM, 65-79 years) and fitness as per our previous work (Active: V˙O2max ≥90% age-predicted values; and Sedentary: V˙O2max <90% age-predicted values). Although age did not affect the sensitivity of HCVR, Active women had significantly lower HCVR gain compared to sedentary women (Sedentary: 2.12±0.80; Active: 1.57±0.73, p=0.02). In contrast, age, but not fitness, was inversely related to ΔV˙(E)/ΔV˙CO2 above AT (YPM: 46.8±11.5; OPM: 34.8±6.9, p<0.01) which may be explained, at least in part, by age-related declines in lung function. HCVR and ΔV˙(E)/ΔV˙CO2 were not correlated.
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http://dx.doi.org/10.1016/j.resp.2012.06.020DOI Listing
October 2012

Central chemoreflex ventilatory responses in humans following passive heat acclimation.

Respir Physiol Neurobiol 2012 Jan 29;180(1):97-104. Epub 2011 Oct 29.

Laboratory for Exercise and Environmental Physiology, Department of Biomedical Physiology and Kinesiology, Simon Fraser University, 8888 University Drive, Burnaby, BC, Canada V5A 1S6.

Since there is temperature dependence of pulmonary ventilation (V˙(E)) in response to the normal modulators (i.e. [Formula: see text] , [Formula: see text] ), it was asked in this study if passive heat acclimation (HA) modifies the human central chemoreflex ventilatory response to CO(2). Nine males performed normothermic- and hyperthermic modified Read re-breathing tests before and after HA. Heat acclimation consisted of 2hday(-1) exposures to 50°C and 20% RH for 10 consecutive days and each exposure elevated rectal temperature to between 38.5 and 39.0°C. Ventilatory recruitment thresholds (VRTs) and central chemosensitivity were assessed before and after HA during normothermia with an oesophageal temperature (T(es)) of ∼37°C and in hyperthermia when T(es) was 38.5-39.0°C. Results showed VRT and central chemosensitivities were unaltered by HA (p≥0.375) and hyperthermia increased pre- (p=0.010) but not post-acclimation (p=0.332) central chemosensitivity. Additionally, during hyperthermia V˙(E) became progressively greater (p=0.027) relative to corresponding normothermic values in the re-breathing tests. In conclusion, the ventilatory response to hyperoxic CO(2) was unaltered by heat Acclimation State.
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http://dx.doi.org/10.1016/j.resp.2011.10.014DOI Listing
January 2012

Losartan abolishes oxidative stress induced by intermittent hypoxia in humans.

J Physiol 2011 Nov 19;589(Pt 22):5529-37. Epub 2011 Sep 19.

Department of Physiology and Pharmacology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.

The aim of this study was to assess the role of the type 1 angiotensin II (AT(1)) receptor in the increase of oxidative stress and NO metabolism during a single 6 h exposure to intermittent hypoxia (IH). Nine healthy young men were exposed, while awake, to sham IH, IH with placebo medication, and IH with the AT(1) receptor antagonist, losartan, using a double-blind, placebo-controlled, randomized, crossover study design. In addition to blood pressure, oxidative stress, peroxynitrite activity, uric acid, global antioxidant status and the end-products of NO (NOx) metabolism were measured in plasma before and after 6 h of IH. Oxidative stress and peroxynitrite activity increased and NOx decreased during IH with placebo. In contrast, neither sham IH nor IH with losartan affected these parameters. With respect to each condition, blood pressure had the same profile as oxidative stress. These results demonstrate that blockade of AT(1) receptors prevented the increase in oxidative stress and peroxynitrite activity and the decrease in NO metabolism induced by IH. Finally, this study suggests that the renin-angiotensin system may participate in the overproduction of reactive oxygen species associated with IH by upregulation of the actions of angiotensin II.
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http://dx.doi.org/10.1113/jphysiol.2011.218156DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240889PMC
November 2011

Cerebral and myocardial blood flow responses to hypercapnia and hypoxia in humans.

Am J Physiol Heart Circ Physiol 2011 Oct 1;301(4):H1678-86. Epub 2011 Jul 1.

Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.

In humans, cerebrovascular responses to alterations in arterial Pco(2) and Po(2) are well documented. However, few studies have investigated human coronary vascular responses to alterations in blood gases. This study investigated the extent to which the cerebral and coronary vasculatures differ in their responses to euoxic hypercapnia and isocapnic hypoxia in healthy volunteers. Participants (n = 15) were tested at rest on two occasions. On the first visit, middle cerebral artery blood velocity (V(P)) was assessed using transcranial Doppler ultrasound. On the second visit, coronary sinus blood flow (CSBF) was measured using cardiac MRI. For comparison with V(P), CSBF was normalized to the rate pressure product [an index of myocardial oxygen consumption; normalized (n)CSBF]. Both testing sessions began with 5 min of euoxic [end-tidal Po(2) (Pet(O(2))) = 88 Torr] isocapnia [end-tidal Pco(2) (Pet(CO(2))) = +1 Torr above resting values]. Pet(O(2)) was next held at 88 Torr, and Pet(CO(2)) was increased to 40 and 45 Torr in 5-min increments. Participants were then returned to euoxic isocapnia for 5 min, after which Pet(O(2)) was decreased from 88 to 60, 52 and 45 Torr in 5-min decrements. Changes in V(P) and nCSBF were normalized to isocapnic euoxic conditions and indexed against Pet(CO(2)) and arterial oxyhemoglobin saturation. The V(P) gain for euoxic hypercapnia (%/Torr) was significantly higher than nCSBF (P = 0.030). Conversely, the V(P) gain for isocapnic hypoxia (%/%desaturation) was not different from nCSBF (P = 0.518). These findings demonstrate, compared with coronary circulation, that the cerebral circulation is more sensitive to hypercapnia but similarly sensitive to hypoxia.
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http://dx.doi.org/10.1152/ajpheart.00281.2011DOI Listing
October 2011

Intermittent hypoxia increases arterial blood pressure in humans through a Renin-Angiotensin system-dependent mechanism.

Hypertension 2010 Sep 12;56(3):369-77. Epub 2010 Jul 12.

Department of Physiology and Pharmacology and Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada.

Intermittent hypoxia (IH) is believed to contribute to the pathogenesis of hypertension in obstructive sleep apnea through mechanisms that include activation of the renin-angiotensin system. The objective of this study was to assess the role of the type I angiotensin II receptor in mediating an increase in arterial pressure associated with a single 6-hour IH exposure. Using a double-blind, placebo-controlled, randomized, crossover study design, we exposed 9 healthy male subjects to sham IH, IH with placebo medication, and IH with the type I angiotensin II receptor antagonist losartan. We measured blood pressure, cerebral blood flow, and ventilation at baseline and after exposure to 6 hours of IH. An acute isocapnic hypoxia experimental protocol was conducted immediately before and after exposure to IH. IH with placebo increased resting mean arterial pressure by 7.9+/-1.6 mm Hg, but mean arterial pressure did not increase with sham IH (1.9+/-1.5 mm Hg) or with losartan IH (-0.2+/-2.4 mm Hg; P<0.05). Exposure to IH prevented the diurnal decrease in the cerebral blood flow response to hypoxia, independently of the renin-angiotensin system. Finally, in contrast to other models of IH, the acute hypoxic ventilatory response did not change throughout the protocol. IH increases arterial blood pressure through activation of the type I angiotensin II receptor, without a demonstrable impact on the cerebrovascular or ventilatory response to acute hypoxia.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.110.152108DOI Listing
September 2010

Effects of exposure to intermittent hypoxia on oxidative stress and acute hypoxic ventilatory response in humans.

Am J Respir Crit Care Med 2009 Nov 27;180(10):1002-9. Epub 2009 Aug 27.

Departments of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada.

Rationale: Periodic occlusion of the upper airway in patients with obstructive sleep apnea leads to chronic intermittent hypoxia, which increases the acute hypoxic ventilatory response (AHVR). Animal studies suggest that oxidative stress may modulate AHVR by increasing carotid body sensitivity to hypoxia. This has not been shown in humans.

Objectives: To determine whether 4 days of exposure to chronic intermittent hypoxia increases AHVR and oxidative stress and to determine the strength of the association between oxidative stress and AHVR.

Methods: After two normoxic control days (Day -4 and Day 0), 10 young healthy men were exposed awake to 4 days (Days 1-4) of intermittent hypoxia for 6 hours per day.

Measurements And Main Results: AHVR, assessed using an isocapnic hypoxia protocol, was determined as the slope of the linear regression between ventilation and oxygen desaturation. Oxidative stress was evaluated by measuring plasma DNA, lipid and protein oxidation, uric acid and antioxidant status by measuring alpha-tocopherol, total vitamin C, and antioxidant enzymatic activities. Between baseline and Day 4, there were significant increases in AHVR, DNA oxidation, uric acid, and vitamin C, whereas antioxidant enzymatic activities and alpha-tocopherol were unchanged. There were strong correlations between the changes in AHVR and DNA oxidation (r = 0.88; P = 0.002).

Conclusions: Chronic intermittent hypoxia increases oxidative stress by increasing production of reactive oxygen species without a compensatory increase in antioxidant activity. This human study shows that reactive oxygen species overproduction modulates increased AHVR. These mechanisms may be responsible for increased AHVR in patients with obstructive sleep apnea.
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http://dx.doi.org/10.1164/rccm.200905-0671OCDOI Listing
November 2009

Adaptation of exercise ventilation during an actively-induced hyperthermia following passive heat acclimation.

Am J Physiol Regul Integr Comp Physiol 2009 Sep 3;297(3):R605-14. Epub 2009 Jun 3.

Laboratory for Exercise and Environmental Physiology, Dept. of Biomedical Physiology and Kinesiology, Simon Fraser Univ., 8888 Univ. Dr., Burnaby, BC, Canada, V5A 1S6.

Hyperthermia-induced hyperventilation has been proposed to be a human thermolytic thermoregulatory response and to contribute to the disproportionate increase in exercise ventilation (VE) relative to metabolic needs during high-intensity exercise. In this study it was hypothesized that VE would adapt similar to human eccrine sweating (E(SW)) following a passive heat acclimation (HA). All participants performed an incremental exercise test on a cycle ergometer from rest to exhaustion before and after a 10-day passive exposure for 2 h/day to either 50 degrees C and 20% relative humidity (RH) (n = 8, Acclimation group) or 24 degrees C and 32% RH (n = 4, Control group). Attainment of HA was confirmed by a significant decrease (P = 0.025) of the esophageal temperature (T(es)) threshold for the onset of E(SW) and a significantly elevated E(SW) (P < or = 0.040) during the post-HA exercise tests. HA also gave a significant decrease in resting T(es) (P = 0.006) and a significant increase in plasma volume (P = 0.005). Ventilatory adaptations during exercise tests following HA included significantly decreased T(es) thresholds (P < or = 0.005) for the onset of increases in the ventilatory equivalents for O(2) (VE/VO(2)) and CO(2) (VE/VCO(2)) and a significantly increased VE (P < or = 0.017) at all levels of T(es). Elevated VE was a function of a significantly greater tidal volume (P = 0.003) at lower T(es) and of breathing frequency (P < or = 0.005) at higher T(es). Following HA, the ventilatory threshold was uninfluenced and the relationships between VO(2) and either VE/VO(2) or VE/VCO(2) did not explain the resulting hyperventilation. In conclusion, the results support that exercise VE following passive HA responds similarly to E(SW), and the mechanism accounting for this adaptation is independent of changes of the ventilatory threshold or relationships between VO(2) with each of VE/VO(2) and VE/VCO(2).
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http://dx.doi.org/10.1152/ajpregu.90672.2008DOI Listing
September 2009

Effects of ovarian hormones and aging on respiratory sinus arrhythmia and breathing patterns in women.

Clin Auton Res 2008 Jun 6;18(3):134-44. Epub 2008 May 6.

Department of Physiology and Biophysics, Faculty of Medicine, Heritage Medical Research Building, Room 212, University of Calgary, 3330 Hospital Drive NW, T2N 4N1 Calgary, AB, Canada.

We investigated the effect of ovarian hormones and aging on breathing pattern [pulmonary minute ventilation (V(E))], tidal volume (V(T)), breathing frequency (F(b)), and respiratory sinus arrhythmia (RSA) in women. Recordings of V(E) and electrocardiogram (ECG) were obtained from 23 healthy women (10 premenopausal, 13 postmenopausal) under resting, isocapnic hypoxia (IH), and euoxic hypercapnia (EH) conditions. Premenopausal women were tested on three different days, each day corresponding to a specific phase of the menstrual cycle (follicular, mid-cycle, and luteal); postmenopausal women (PMW) were tested on 1 day only. On each test day, subjects were challenged with IH and EH. The order of the two tests was randomized and separated by at least 1 hour. Due to the low F (b) of several PMW, the band limits for RSA analysis had to be adjusted. The spectral coherence between respiratory flow and ECG RR-interval was used to determine the spectral band. Within the spectral band, there was a consistent phase relationship between the two variables where high values of spectral coherence indicate a well-defined phase relationship between respiratory flow and RR-interval variability. The main findings in this study for RSA are fourfold. First, RSA did not change with different levels of ovarian hormones (progesterone, serum 17beta-estradiol) during the menstrual cycle. Second, RSA was not influenced by hormone replacement therapy. Third, RSA did not change with age. Fourth, RSA did not change with IH and EH-induced changes in breathing patterns. Finally, high individual variability of average RR-interval change per breath was found.
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http://dx.doi.org/10.1007/s10286-008-0473-0DOI Listing
June 2008