Browsing by Author "Poulin, Marc J."
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Item Open Access Cerebral blood flow responses to sustained alterations in end-tidal PO2 and PCO2 in humans(2004) Vantanajal, Jimmy S.; Poulin, Marc J.The techniques of transcranial Doppler ultrasound and dynamic end-tidal forcing were used to study the dynamics of the middle cerebral artery peak flow velocity (V P) (i.e. index of cerebral blood flow) response to 60 min of sustained isocapnic hypoxia, isocapnic hyperoxia, euoxic hypocapnia, and euoxic hypercapnia in humans. Each protocol involved two 60-min interventions, with a 60-min recovery period between tests. Peak flow velocity increased significantly during hypoxia (14.7%) and decreased during hyperoxia (11.8%). During hypercapnia, VP increased significantly (33.6%) and remained elevated. There was no evidence of adaptation during these protocols. However, a significant adaptation was observed during hypocapnia. After an initial decrease (39%), VP increased significantly and stabilized at 25.2% below baseline. This adaptive component was found to be significantly faster during the second intervention. There were no significant differences between the first and second intervention for the remaining protocols.Item Open Access Cerebrovascular responses to submaximal exercise in women with COPD(BioMed Central, 2014-06-05) Hartmann, Sara E.; Leigh, Richard; Poulin, Marc J.Item Open Access Effect of Acute, Subacute, and Repeated Exposure to High Altitude (5050 m) on Psychomotor Vigilance(Frontiers in Physiology, 2018-01) Pun, Matiram; Hartmann, Sara E.; Furian, Michael; Dyck, Adrienna M.; Muralt, Lara; Lichtblau, Mona; Bader, Patrick R.; Ulrich, Silvia; Bloch, Konrad E.; Rawling, Jean M.; Poulin, Marc J.Aim: High altitude (HA) hypoxia may affect cognitive performance and sleep quality. Further, vigilance is reduced following sleep deprivation. We investigated the effect on vigilance, actigraphic sleep indices, and their relationships with acute mountain sickness (AMS) during very HA exposure, acclimatization, and re-exposure. Methods: A total of 21 healthy altitude-naive individuals (25 ± 4 years; 13 females) completed 2 cycles of altitude exposure separated by 7 days at low altitude (LA, 520 m). Participants slept at 2900 m and spent the day at HA, (5050 m). We report acute altitude exposure on Day 1 (LA vs. HA1) and after 6 days of acclimatization (HA1 vs. HA6). Vigilance was quantified by reaction speed in the 10-min psychomotor vigilance test reaction speed (PVT-RS). AMS was evaluated using the Environmental Symptoms Questionnaire Cerebral Score (AMS-C score). Nocturnal rest/activity was recorded to estimate sleep duration using actigraphy. Results: In Cycle 1, PVT-RS was slower at HA1 compared to LA (4.1 ± 0.8 vs. 4.5 ± 0.6 s-1, respectively, p = 0.029), but not at HA6 (4.6 ± 0.7; p > 0.05). In Cycle 2, PVT-RS at HA1 (4.6 ± 0.7) and HA6 (4.8 ± 0.6) were not different from LA (4.8 ± 0.6, p > 0.05) and significantly greater than corresponding values in Cycle 1. In both cycles, AMS scores were higher at HA1 than at LA and HA6 (p < 0.05). Estimated sleep durations (TST) at LA, 1st and 5th nights were 431.3 ± 28.7, 418.1 ± 48.6, and 379.7 ± 51.4 min, respectively, in Cycle 1 and they were significantly reduced during acclimatization exposures (LA vs. 1st night, p > 0.05; LA vs. 5th night, p = 0.012; and 1st vs. 5th night, p = 0.054). LA, 1st and 5th nights TST in Cycle 2 were 477.5 ± 96.9, 430.9 ± 34, and 341.4 ± 32.2, respectively, and we observed similar deteriorations in TST as in Cycle 1 (LA vs. 1st night, p > 0.05; LA vs. 5th night, p = 0.001; and 1st vs. 5th night, p < 0.0001). At HA1, subjects who reported higher AMS-C scores exhibited slower PVT-RS (r = -0.56; p < 0.01). Subjects with higher AMS-C scores took longer time to react to the stimuli during acute exposure (r = 0.62, p < 0.01) during HA1 of Cycle 1. Conclusion: Acute exposure to HA reduces the PVT-RS. Altitude acclimatization over 6 days recovers the reaction speed and prevents impairments during subsequent altitude re-exposure after 1 week spent near sea level. However, acclimatization does not lead to improvement in total sleep time during acute and subacute exposures.Item Open Access Effect of age, sex and aerobic exercise on cerebrovascular regulation in older adults: Results from the Brain in Motion Study(2019-09-17) Wyer, Leanna; Poulin, Marc J.; Phillips, Aaron Alexander; McDonough, Meghan H.; Longman, Richard StewartBackground: By 2024, 20% of Canada’s population will be 65 and older. Aging is associated with progressive declines in cerebrovascular and cognitive function and an increased prevalence of age-related diseases such as Alzheimer’s Disease (AD). Physical activity has been associated with improvements in cerebrovascular function and cognitive performance, and may help to prevent and/or delay AD. However, the underlying time-course by which enhanced physical activity may be protective for brain health and differences between men and women is poorly understood. Objective: To determine the influence of age and sex on the cerebrovascular responses to submaximal exercise and euoxic hypercapnia in older adults. Furthermore, this study assessed the effects of a 6-month aerobic exercise intervention on cerebrovascular measures and evaluated outcomes after three and six months of exercise. Design: 202 participants aged 66.5 ± 6.5 years (mean ± SD, 101 females) completed the aerobic exercise intervention. Measurements took place pre-, mid- and post-intervention including demographic information, maximal aerobic capacity (VO2max) and cerebrovascular function. Linear mixed models adjusted for covariates were used to measure the physiological responses to submaximal exercise and euoxic hypercapnia pre-intervention and the changes in middle cerebral artery peak blood flow velocity (VP), mean arterial pressure (MAP) and cerebrovascular resistance (CVRi) and conductance (CVCi) indices after three and six months of aerobic exercise. Results: Pre-intervention, both age and sex were significant predictors of VP (p=0.002; p<0.010), CVRi (p<0.001; p=0.029), and CVCi (p<0.001; p=0.004) during exercise. Compared to rest, acute exercise led to increases in VP, CVRi and MAP and decreases in CVCi (p<0.001). Three months of aerobic exercise led to increases in VP (p=0.005) and CVCi (p=0.021) and decreases in CVRi (p=0.002) in women only, with no further changes observed after an additional three months of exercise. Conclusion: Male sex and increasing age were associated with lower VP, CVCi and higher CVRi. Three months of aerobic exercise led to improvements in cerebrovascular measures in women that were maintained in the latter three months of the intervention in healthy, older adults. Such results have important implications for the role of physical activity in improving health outcomes and the differences observed with aging and sex.Item Open Access Effect of Selective and Nonselective Cyclooxygenase Enzyme Inhibition on Arterial Blood Pressure and Cerebral Blood Flow with Exposure to Intermittent Hypoxia in Humans(2013-04-23) Pun, Matiram; Poulin, Marc J.Background: Intermittent hypoxia (IH) simulating obstructive sleep apnea raises blood pressure (BP) and impairs cerebral blood flow response. The pathophysiology of intermittent hypoxia-mediated increase in BP involves multiple mechanisms but the role of cyclooxygenase (COX) catalyzed vasoactive prostaglandins (PG) is unclear. Methods: A placebo controlled double-blind randomized cross-over trial was designed using nonselective COX inhibitor indomethacin (50 mg tid/po), selectively COX-2 inhibitor celecoxib (200 mg bid/po) comparing with placebo. Healthy males ingested either of drugs for 4 days and physiological measurements were taken on 5th day with an acute isocapnic-hypoxia challenge pre- and post 6 hrs of IH exposure. Urinary PGs were assayed pre- and post- IH exposure. Results: After 4 days of drug, INDO increased BP compared to PLBO and CLBX; and lowered CBF compared to PLBO (air and baseline breathing). Mean arterial pressure gain with INDO increased followed by CLBX in response to acute isocapnic hypoxia and it was driven by increased gains in both systolic BP and diastolic BP (statistically not significant). CBF gain was blunted with CLBX while it was similar between INDO and PLBO although they were not statistically significant. With 6 hrs of IH (post-IH), CBF gain remained blunted with CLBX but was augmented with INDO (statistically not significant). CVC gain was lower with CLBX (statistically not significant). Both drugs lowered vasodilator and vasoconstrictor PGs compared to PLBO. Pre-IH PGI2:TxA2 was higher with INDO compared to PLBO (p < 0.001) and CLBX (p < 0.001). Conclusion: Indomethacin perturbs cardio- and cerebrovascular homeostasis in more robust manner as compared to placebo and celecoxib after 4 days of ingestion.Item Open Access Effects of aging and aerobic fitness on cerebrovascular regulation and cognition in postmenopausal women(2008) Brown, Allison; Poulin, Marc J.Item Open Access Effects of aging on the association between cerebrovascular responses to visual stimulation, hypercapnia and arterial stiffness(Frontiers, 2014-02-19) Fluck, Daniela; Beaudin, Andrew E.; Steinback, Craig D.; Kumparpillai, Gopukumar; Shobha, Nandavar; McCreary, Cheryl R.; Peca, Stefano; Smith, Eric E.; Poulin, Marc J.Item Open Access Item Open Access Effects of intermittent hypoxia on cardiovascular and cerebrovascular function: implications for obstructive sleep apnoea(2009) Foster, Glen Edward; Poulin, Marc J.; Hanly, Patrick J.Intermittent hypoxia is thought to be an important contributor to the increased risk of cardiovascular and cerebrovascular disease observed in patients with obstructive sleep apnoea (OSA). This thesis reports findings from three major experiments designed to examine the relationship between OSA, intermittent hypoxia, and vascular function. In Study 1, the cerebral vascular response to hypoxia was assessed in newly diagnosed patients with OSA, both before and after 4-6 weeks of continuous positive airway pressure (CP AP). The cerebral blood flow response to hypoxia was found to be significantly reduced in patients with OSA and treatment with CPAP normalized this response. An attenuated cerebral blood flow response to hypoxia may contribute to an increased risk for cerebral vascular disease. In Study 2, the cardiovascular and cerebrovascular responses to acute hypoxia were assessed following exposure to prolonged bouts of intermittent hypoxia in healthy human subjects. The results from this study demonstrate that intennittent hypoxia can enhance the presser response to hypoxia and increase resting arterial pressure. Furthermore, the cerebral vascular response to hypoxia and the production of nitric oxide were reduced with intermittent hypoxia. These findings suggest that intennittent hypoxia affects blood pressure and cerebrovascular regulation which is, therefore, likely to contribute to the pathogenesis of cardiovascular and cerebrovascular disease in OSA patients. Study 3 was designed to assess the importance of the angiotensin-II type-I receptor in the cardiovascular response to a single six-hour bout of intermittent hypoxia. Healthy human subjects took part in a double blind, placebo-controlled, and randomized, crossover study. The results demonstrate the importance of the type-I angiotensin-II receptor in mediating the hypertensive response associated with intennittent hypoxia. Taken together, the results from these three studies provide evidence to support the hypothesis that intermittent hypoxia exposure similar to that experienced by OSA patients can contribute to changes in cardiovascular and cerebrovascular regulation. Ultimately, these regulatory changes may be precursors to the development of cardiovascular and cerebrovascular disease in OSA.Item Open Access Effects on Cognitive Functioning of Acute, Subacute and Repeated Exposures to High Altitude(Frontiers, https://www.frontiersin.org, 2018-08-21) Pun, Matiram; Guadagni, Veronica; Aitken, Julie; Furian, Michael; Lichtblau, Mona; Ulrich, Silvia; Bettauer, Kaitlyn M.; Drogos, Lauren L.; Hartmann, Sara E.; Bader, Patrick R.; Rawling, Jean M.; Protzner, Andrea B.; Bloch, Konrad Ernst; Giesbrecht, Barry L.; Poulin, Marc J.; Rawling, Jean M.Objective: Neurocognitive functions are affected by high altitude, however the altitude effects of acclimatization and repeated exposures are unclear. We investigated the effects of acute, subacute and repeated exposure to 5,050 m on cognition among altitude-naïve participants compared to control subjects tested at low altitude. Methods: Twenty-one altitude-naïve individuals (25.3 ± 3.8 years, 13 females) were exposed to 5,050 m for 1 week (Cycle 1) and re-exposed after a week of rest at sea-level (Cycle 2). Baseline (BL, 520 m), acute (Day 1, HA1) and acclimatization (Day 6, HA6, 5,050 m) measurements were taken in both cycles. Seventeen control subjects (24.9 ± 2.6 years, 12 females) were tested over a similar period in Calgary, Canada (1,103 m). The Reaction Time (RTI), Attention Switching Task (AST), Rapid Visual Processing (RVP) and One Touch Stockings of Cambridge (OTS) tasks were administered and outcomes were expressed in milliseconds/frequencies. Lake Louise Score (LLS) and blood oxygen saturation (SpO2) were recorded. Results: In both cycles, no significant changes were found with acute exposure on the AST total score, mean latency and SD. Significant changes were found upon acclimatization solely in the altitude group, with improved AST Mean Latency [HA1 (588 ± 92) vs. HA6 (526 ± 91), p < 0.001] and Latency SD [HA1 (189 ± 86) vs. HA6 (135 ± 65), p < 0.001] compared to acute exposure, in Cycle 1. No significant differences were present in the control group. When entering Acute SpO2 (HA1-BL), Acclimatization SpO2 (HA6-BL) and LLS score as covariates for both cycles, the effects of acclimatization on AST outcomes disappeared indicating that the changes were partially explained by SpO2 and LLS. The changes in AST Mean Latency [ΔBL (-61.2 ± 70.2) vs. ΔHA6 (-28.0 ± 58), p = 0.005] and the changes in Latency SD [ΔBL (-28.4 ± 41.2) vs. ΔHA6 (-0.2235 ± 34.8), p = 0.007] across the two cycles were smaller with acclimatization. However, the percent changes did not differ between cycles. These results indicate independent effects of altitude across repeated exposures. Conclusions: Selective and sustained attention are impaired at altitude and improves with acclimatization.The observed changes are associated, in part, with AMS score and SpO2. The gains in cognition with acclimatization during a first exposure are not carried over to repeated exposures.Item Open Access Factors influencing acute mountain sickness in Nepal trekkers(2007) Johannson, Linda Diane; Poulin, Marc J.Item Open Access Impact of a 6-month aerobic exercise intervention on oxidative stress in sedentary older adults(2018-12-17) Rytz, Chantal Louise; Poulin, Marc J.; Pialoux, Vincent; Hogan, David B.Background: Reactive oxygen species (ROS) play integral roles in cell signalling and systemic processes and are tightly controlled through workings of antioxidants. An imbalance in this relationship can lead to oxidative stress. Completion of regular exercise can mitigate oxidative stress, strengthen antioxidant capacity and improve oxidative stress- associated conditions, such as metabolic syndrome (MetS) and decreased cerebrovascular function. However, there is limited knowledge as to how the aging population with and without MetS compare in terms of changes in markers of oxidative stress and antioxidant profiles with an aerobic exercise intervention, and the effect these changes in have on cerebrovascular function. Objective: We aimed to assess the effects of a 6-month aerobic exercise intervention on markers of oxidative stress and antioxidant capacity in older, sedentary yet healthy adults, and to determine how MetS status affected these exercise-induced changes. Further, as an exploratory measure, we aimed to assess the association between changes in markers of oxidative stress and antioxidant capacity and measures of cerebrovascular function. Design: Blood samples from 206 participants (mean age=66.8 ± SE=6.4 years, 104 females) pre-, midway, and post-intervention were assessed for markers of oxidative stress (advanced oxidation protein products [AOPP; malondialdehyde [MDA]; 3-nitrotyrosine [3-NT]) and antioxidant capacity (superoxide dismutase [SOD]; uric acid [UA]; ferric- reducing ability of ṗ lasma [FRAP]; nitric oxide metabolites [NOx]; catalase). Maximal aerobic capacity (VO2max), anthropometric and demographic information was also collected. Repeated measures linear mixed models adjusted for covariates were used to evaluate changes in markers of oxidative stress and antioxidant capacity across the exercise intervention. Factors represented by changes in markers of oxidative stress and antioxidant status were used in a linear regression analysis to assess the potential association between oxidative stress and cerebrovascular function. Results: There was a significant effect of the exercise intervention on decreasing levels of AOPP (p=0.004) however, neither MetS status (p=0.214) nor sex (p=0.437) modified the effect. Individuals with MetS had significantly higher levels of AOPP (p<0.001), MDA (p<0.001), FRAP (p=0.03) and UA (p=0.003) compared to those without. Men possessed significantly higher levels of AOPP (p=0.001), FRAP (p<0.001), catalase (p=0.013) and UA (p<0.001) compared to women. Interestingly, the effect of MetS status on FRAP and 3-NT was highly dependent on sex. Further, exercise-induced changes in measures of oxidative stress and antioxidant status were significantly associated with post-intervention measures of cerebrovascular function at rest and submaximal exercise. Conclusion: These results indicate that MetS may blunt exercise-induced improvements in oxidative stress and that changes in markers of oxidative stress and antioxidant status may impact exercise-induced cerebrovascular improvements in older, healthy adults.Item Open Access Impact of Intermittent Hypoxia on Human Cardiorespiratory and Cerebrovascular Function(2016) Beaudin, Andrew Edward; Poulin, Marc J.; Hanly, Patrick J.; Wilson, Richard J. A.; Anderson, Todd J.; Thompson, Roger J.; Horner, Richard L.Obstructive sleep apnoea (OSA) is a chronic sleep disorder characterized by intermittent hypoxia (IH) exposure during sleep and is an independent risk factor for cardiovascular and cerebrovascular disease. IH in untreated OSA is advanced as the principal pathway leading to the greater risk of vascular disease associated with OSA. Additionally, IH is implicated in the propagation of OSA severity by increasing ventilatory instability, in part, by enhancing ventilatory chemosensitivity. Therefore, the focus of this thesis was to investigate the mechanisms through which IH functions and the role of IH in disrupting vascular and ventilatory regulation in OSA. The molecular pathways through which IH disrupts vascular and ventilatory regulation are poorly understood, but IH-induced inflammation is believed to be a primary contributor. Using a human experimental model of IH during wakefulness and a clinical population of untreated OSA patients, Study 1 investigated the role of cyclooxygenase (COX)-1 and COX-2 derived prostanoids (mediators of the inflammatory response and vascular regulation) in IH-induced alterations in cardiovascular and cerebrovascular regulation. Additionally, Study 2 examined the role of inflammation in IH-induced respiratory plasticity. Study 3 investigated the effects of nocturnal oxygen therapy (to remove IH) and continuous positive airway pressure (CPAP; gold standard OSA treatment) on cardiorespiratory and cerebrovascular responses to hypoxia in newly diagnosed OSA patients. Finally, Study 4 assessed the feasibility of adapting our human IH model to sleep while incorporating the ability to assess cardiovascular and cerebrovascular responses to hypoxia and hypercapnia during sleep. Studies 1-3 add substantial knowledge to this important area of research. Specifically, they reveal that 1) cyclooxygenase (COX)-1 and COX-2 differentially regulate blood pressure and cerebrovascular responses to acute and chronic IH; 2) inflammation does not contribute to IH-induced respiratory plasticity following an acute (6h) IH exposure; and 3) both nocturnal oxygen and CPAP treatment of OSA may lower blood pressure during isocapnic-euoxia and the hypoxic ventilatory response, but neither modality effects vascular responses to hypoxia. Lastly, Study 4 showed it is feasible to apply our human IH model to sleep and to concurrently assess vascular responses to hypoxia and hypercapnia during sleep.Item Open Access Objective subjective genotype dataset(2020-09-09) Tyndall, Amanda V.; Poulin, Marc J.Item Open Access Regulation of cerebral blood flow and ventilation by oxygen and carbon dioxide in women(2003) Debert, Chantel T.; Poulin, Marc J.Item Open Access Respiration-induced changes in heart rate in humans(2004) Melashenko, Lara D.; Giles, Wayne R.; Poulin, Marc J.Item Open Access Stability dataset(2015) Poulin, Marc J.; Argourd, Laurie; Tyndall, AmandaItem Open Access The Brain in Motion II Study: study protocol for a randomized controlled trial of an aerobic exercise intervention for older adults at increased risk of dementia(2021-06-14) Krüger, Renata L.; Clark, Cameron M.; Dyck, Adrienna M.; Anderson, Todd J.; Clement, Fiona; Hanly, Patrick J.; Hanson, Heather M.; Hill, Michael D.; Hogan, David B.; Holroyd-Leduc, Jayna; Longman, R. S.; McDonough, Meghan; Pike, G. B.; Rawling, Jean M.; Sajobi, Tolulope; Poulin, Marc J.Abstract Background There remains no effective intervention capable of reversing most cases of dementia. Current research is focused on prevention by addressing risk factors that are shared between cardiovascular disease and dementia (e.g., hypertension) before the cognitive, functional, and behavioural symptoms of dementia manifest. A promising preventive treatment is exercise. This study describes the methods of a randomized controlled trial (RCT) that assesses the effects of aerobic exercise and behavioural support interventions in older adults at increased risk of dementia due to genetic and/or cardiovascular risk factors. The specific aims are to determine the effect of aerobic exercise on cognitive performance, explore the biological mechanisms that influence cognitive performance after exercise training, and determine if changes in cerebrovascular physiology and function persist 1 year after a 6-month aerobic exercise intervention followed by a 1-year behavioural support programme (at 18 months). Methods We will recruit 264 participants (aged 50–80 years) at elevated risk of dementia. Participants will be randomly allocated into one of four treatment arms: (1) aerobic exercise and health behaviour support, (2) aerobic exercise and no health behaviour support, (3) stretching-toning and health behaviour support, and (4) stretching-toning and no health behaviour support. The aerobic exercise intervention will consist of three supervised walking/jogging sessions per week for 6 months, whereas the stretching-toning control intervention will consist of three supervised stretching-toning sessions per week also for 6 months. Following the exercise interventions, participants will receive either 1 year of ongoing telephone behavioural support or no telephone support. The primary aim is to determine the independent effect of aerobic exercise on a cognitive composite score in participants allocated to this intervention compared to participants allocated to the stretching-toning group. The secondary aims are to examine the effects of aerobic exercise on a number of secondary outcomes and determine whether aerobic exercise-related changes persist after a 1-year behavioural support programme (at 18 months). Discussion This study will address knowledge gaps regarding the underlying mechanisms of the pro-cognitive effects of exercise by examining the potential mediating factors, including cerebrovascular/physiological, neuroimaging, sleep, and genetic factors that will provide novel biologic evidence on how aerobic exercise can prevent declines in cognition with ageing. Trial registration ClinicalTrials.gov NCT03035851 . Registered on 30 January 2017