Philip N Ainslie

University of British Columbia - Vancouver, Vancouver, British Columbia, Canada

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Publications (208)695.44 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The cerebral pressure-flow relationship can be quantified as a high-pass filter, where slow oscillations are buffered (<0.20 Hz) and faster oscillations are passed through relatively unimpeded. During moderate intensity exercise previous studies have reported paradoxical transfer function analysis (TFA) findings (altered phase or intact gain). This study aimed to determine if these previous findings accurately represent this relationship. Both younger (20-30 years; n=10) and older (62-72 years; n=9) adults were examined. To enhance the signal-to-noise ratio, large oscillations in blood pressure (via oscillatory lower body negative pressure - OLBNP) that were induced during steady-state moderate intensity supine exercise (~45-50% of heart rate reserve). Beat-to-beat blood pressure, cerebral blood velocity, and end-tidal PCO2 were monitored. Very low (VLF: 0.02-0.07 Hz) and low frequency (LF: 0.07-0.20 Hz) range spontaneous data was quantified. Driven OLBNP point-estimates were sampled at 0.05 and 0.10 Hz. The OLBNP maneuvers augmented coherence to >0.97 at 0.05 Hz and >0.98 at 0.10 Hz in both age-groups. The OLBNP protocol conclusively revealed the cerebrovascular system functions as a high-pass filter during exercise throughout aging. It was also discovered that the older adults had elevations [+71%] in normalized gain (+0.46 ± 0.36 %/%: 0.05 Hz) and reductions [-34%] in phase (-0.24 ± 0.22 radians: 0.10 Hz). There were also age-related phase differences between resting and exercise conditions. It is speculated that these age-related changes in the TFA metrics are mediated by alterations in vasoactive factors, sympathetic tone or the mechanical buffering of the compliance vessels.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00667.2015 · 3.06 Impact Factor
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    ABSTRACT: One of the most effective ways of engaging students of physiology and medicine is through laboratory demonstrations and case studies which combine (a) the use of equipment, (b) problem solving, (c) visual representations, and (d) manipulation and interpretation of data. Depending on the measurements made and the type of test, laboratory demonstrations have the added benefit of being able to show multiple organ system integration. Many research techniques can also serve as effective demonstrations of integrative human physiology. The “Duffin” hyperoxic rebreathing test is often used in research settings as a test of central respiratory chemosensitivity and cerebrovascular reactivity to carbon dioxide (CO2). We aim to demonstrate the utility of the hyperoxic rebreathing test for both respiratory and cerebrovascular responses to increases in CO2, and illustrate the integration of the respiratory and cerebrovascular systems. Methods such as spirometry, respiratory gas analysis, and transcranial Doppler ultrasound are described, and raw data traces can be adopted for discussion in a tutorial setting. If educators have these instruments available, instructions on how to carry out the test are provided so students can collect their own data. In either case, data analysis and quantification are discussed, including principles of linear regression, calculation of slope, coefficient of determination (R2), and the differences between plotting absolute vs. normalized data. Utilizing the hyperoxic rebreathing test as a demonstration of the complex interaction and integration between the respiratory and cerebrovascular systems provides senior undergraduate, graduate and medical students with an advanced understanding of integrative nature of human physiology.
    AJP Advances in Physiology Education 11/2015; In Press. · 0.94 Impact Factor
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    ABSTRACT: Transient reduction in vascular function following systemic large muscle group exercise has previously been reported in humans. The mechanisms responsible are currently unknown. We hypothesised that sympathetic nervous system activation, induced by cycle ergometer exercise, would contribute to post-exercise reductions in flow-mediated dilation (FMD). Ten healthy male subjects (28 ± 5years) undertook two 30 minute sessions of cycle exercise at 75% HRmax. Prior to exercise, individuals ingested either a placebo or an α1 -adrenoreceptor blocker (Prazosin; ). Central hemodynamics, brachial artery shear rate (SR) and blood flow profiles were assessed throughout each exercise bout and in response to brachial artery FMD, measured prior to-, immediately after, and 60-minutes post-exercise. Cycle exercise increased both mean and antegrade SR (P < 0.001) with retrograde SR also elevated under both conditions (P < 0.001). Pre-exercise FMD was similar on both occasions, and significantly reduced (27%) immediately following exercise in the placebo condition (t-test, P = 0.03). In contrast, FMD increased (37%) immediately following exercise in the Prazosin condition (t-test, P = 0.004, interaction effect P = 0.01). Post-exercise FMD remained different between conditions after correction for baseline diameters preceding cuff deflation and also post-deflation shear rate. No differences in FMD or other variables were evident 60-minutes following recovery. Our results indicate that sympathetic vasoconstriction competes with endothelium-dependent dilator activity to determine post-exercise arterial function. These findings have implications for understanding the chronic impacts of interventions, such as exercise training, which affect both sympathetic activity and arterial shear stress. This article is protected by copyright. All rights reserved.
    The Journal of Physiology 10/2015; DOI:10.1113/JP270946 · 5.04 Impact Factor
  • Ali M McManus · Philip N Ainslie · Daniel J Green · Ryan G Simair · Kurt Smith · Nia Lewis ·
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    ABSTRACT: New findings: What is the central question of this study? Children are spending more than 60% of their waking day sedentary. The consequences of excessive sedentary behaviour are not well understood in the child, but there is growing evidence that with increasing sedentary time, cardiovascular risk in childhood also increases. What is the main finding and its importance? Our findings show that a 3 h period of uninterrupted sitting causes a profound (33%) reduction in vascular function in young girls. Importantly, we also demonstrate that breaking up sitting with regular exercise breaks can prevent this. Excessive sedentary behaviour has serious clinical and public health implications; however, the physiological changes that accompany prolonged sitting in the child are not completely understood. Herein, we examined the acute effect a prolonged period of sitting has upon superficial femoral artery function in 7- to 10-year-old girls and the impact of interrupting prolonged sitting with exercise breaks. Superficial femoral artery endothelium-dependent flow-mediated dilatation, total shear rate, anterograde and retrograde shear rates and oscillatory shear index were assessed before and after two experimental conditions: a 3 h uninterrupted period of sitting (SIT) and a 3 h period of sitting interrupted each hour with 10 min of moderate-intensity exercise (EX). A mixed-model analysis of variance was used to compare between-condition and within-condition main effects, controlling for the within-subject nature of the experiment by including random effects for participant. Superficial femoral artery endothelium-dependent flow-mediated dilatation decreased significantly from pre- to post-SIT (mean difference 2.2% flow-mediated dilatation; 95% confidence interval = 0.60-2.94%, P < 0.001). This relative decline of 33% was abolished in the EX intervention. Shear rates were not significantly different within conditions. Our data demonstrate the effectiveness of short but regular exercise breaks in offsetting the detrimental effects of uninterrupted sitting in young girls.
    Experimental physiology 09/2015; 100(11). DOI:10.1113/EP085355 · 2.67 Impact Factor

  • European Respiratory Journal 09/2015; 46(suppl 59):OA300. DOI:10.1183/13993003.congress-2015.OA300 · 7.64 Impact Factor
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    Mike Stembridge · Philip N Ainslie · Rob Shave ·
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    ABSTRACT: High-altitude exposure challenges the cardiovascular system to maintain oxygen delivery to the mitochondria under conditions of hypoxic stress. Following acclimatisation (3-5 days), stroke volume (SV) falls to below sea-level values but heart rate remains elevated, such that cardiac output is maintained compared to sea level. The decrease in SV has been a topic of research for over 40 years, but the underlying mechanisms are incompletely understood. Impaired systolic contractile function secondary to reduced coronary arterial oxygen tension has been investigated as a potential cause for the decrease in SV. However, despite in vitro evidence of impaired cardiac contractile force in severe hypoxia, the majority of studies to date have reported enhanced in vivo ventricular systolic function at rest and during exercise in humans up to and above 5000 m. However, the elevated function observed at rest has recently been suggested to reduce the functional reserve available during exercise. While in vivo systolic function appears enhanced at high altitude, a decrease in left ventricular end-diastolic volume (EDV) and altered filling patterns of both ventricles has been observed. The reduction in ventricular filling will undoubtedly affect SV, and four potential mechanisms have been proposed to explain the reduction in left ventricular filling. In this article, both historical and recent reports of systolic function at high altitude will be reviewed, and evidence supporting and refuting each of the four mechanisms underpinning reduced left ventricular filling will be discussed.
    09/2015; DOI:10.1080/17461391.2015.1071876
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    ABSTRACT: The purpose of this study was to determine the impact of peripheral chemoreflex inhibition with low-dose dopamine on maximal apnea time, and the related hemodynamic and cerebrovascular responses in elite apnea divers. In a randomized order, participants performed a maximal apnea while receiving either I.V. 2µg・kg(-1)・min(-1) dopamine or volume matched saline (placebo). The chemoreflex and hemodynamic response to dopamine was also assessed during hypoxia (arterial O2 tension, [PaO2]~35mmHg) and mild hypercapnia (arterial CO2 tension [PaCO2]~46mmHg) that mimicked the latter parts of apnea. Outcome measures included apnea duration, arterial blood gases (radial), heart rate (HR, ECG), mean arterial pressure (MAP, intra-arterial), middle (MCAv) and posterior (PCAv) cerebral artery blood velocity (transcranial ultrasound), internal carotid (ICA) and vertebral (VA) artery blood flow (ultrasound), and the chemoreflex responses. Although dopamine depressed the ventilatory response by 27±41% (vs. placebo; p=0.01), the maximal apnea duration was increased by only 5±8% (p=0.02). The PaCO2 and PaO2 at apnea breakpoint were similar (p>0.05). Compared to placebo, dopamine increased HR and decreased MAP during both apnea and chemoreflex test (p all<0.05). At rest, dopamine compared to placebo dilated the ICA (3.0±4.1%, p=0.05) and VA (6.6±5.0%, p<0.01). During apnea and chemoreflex test, conductance of the cerebral vessels (ICA, VA, MCAv, PCAv) was increased with dopamine; however, flow (ICA and VA) was similar. At least in elite apnea divers, the small increase in apnea time and similar PaO2 at breakpoint (~31mmHg) suggest the apnea breakpoint is more related to PaO2, rather than peripheral chemoreflex drive to breathe. Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
    AJP Regulatory Integrative and Comparative Physiology 08/2015; DOI:10.1152/ajpregu.00271.2015 · 3.11 Impact Factor
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    ABSTRACT: We examined the between-day reproducibility of active (squat-stand maneuvers) and passive (oscillatory lower body negative pressure [OLBNP] maneuvers) driven oscillations in blood pressure. These relationships were examined in both younger (n=10; 25 ± 3 years) and older (n=9; 66 ± 4 years) adults. Each testing protocol incorporated rest (5-minutes), followed by driven maneuvers at 0.05 (5-minuntes) and 0.10 Hz (5-minuntes) to increase blood pressure variability and improve assessment of the pressure-flow dynamics using linear transfer function analysis. Beat-to-beat blood pressure, middle cerebral artery velocity, and end-tidal PCO2 were monitored. The pressure-flow relationship was quantified in the very low (0.02-0.07 Hz) and low (0.07-0.20 Hz) frequencies (spontaneous data) and at 0.05 and 0.10 Hz (driven maneuvers point estimates). Although there were no between age-differences, very few spontaneous and OLBNP transfer function metrics met the criteria for acceptable reproducibility as reflected in between-day within-subject coefficient of variation (CoV) of <20%. Combined CoV data: LF coherence (15.1 ± 12.2%), LF gain (15.1 ± 12.2%) and LF normalized gain (18.5 ± 10.9%). OLBNP data: 0.05 Hz coherence (12.1 ± 15.%), 0.10 Hz coherence (4.7 ± 7.8%). In contrast, the squat-stand maneuvers revealed that all metrics (coherence: 0.6 ± 0.5%, 0.3 ± 0.5%; gain: 17.4 ± 12.3%, 12.7 ± 11.0%; normalized gain: 16.7 ± 10.9%, 15.7 ± 11.0%; and phase: 11.6 ± 10.2%, 17.3 ± 10.8%) at 0.05 and 0.10 Hz, respectively, were considered biologically acceptable for reproducibility. These findings have important implications for the reliable assessment and interpretation of cerebral-pressure flow dynamics in humans. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 07/2015; 119(5):jap.00264.2015. DOI:10.1152/japplphysiol.00264.2015 · 3.06 Impact Factor
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    Kate N Thomas · Nia C S Lewis · Brigid G Hill · Philip N Ainslie ·
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    ABSTRACT: Duplex ultrasound is evolving technology that allows the assessment of volumetric blood flow in the carotid and vertebral arteries during a range of interventions along the spectrum of health and chronic disease. Duplex ultrasound can provide high-resolution diameter and velocity information in real-time, and is non-invasive with minimal risks or contra-indications. However, this ultrasound approach is a specialized technique requiring intensive training and stringent control of multiple complex settings; results are highly operator-dependent, and analysis approaches are inconsistent. Importantly, therefore, methodological differences can invalidate comparisons between different imaging modalities and studies; such methodological errors therefore have potential to discredit study findings completely. The task of this review is to provide the first comprehensive, user-friendly technical guideline for the application of duplex ultrasound in measuring extracranial blood flow in human research. An update on recent developments in the use of edge-detection software for offline analysis is highlighted, and suggestions for future directions in this field are provided. These recommendations are presented in an attempt to standardize measurements across research groups and hence ultimately will improve the accuracy and reproducibility of measuring extracranial blood flow both within-subjects and between groups. Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
    AJP Regulatory Integrative and Comparative Physiology 07/2015; 309(7):ajpregu.00211.2015. DOI:10.1152/ajpregu.00211.2015 · 3.11 Impact Factor
  • Anthony R Bain · Lars Nybo · Philip N Ainslie ·
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    ABSTRACT: This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.
    Comprehensive Physiology 07/2015; 5(3):1345-1380. DOI:10.1002/cphy.c140066 · 4.74 Impact Factor
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    ABSTRACT: Following exercise a reduction in mean arterial pressure (MAP) is often experienced and is referred to as post-exercise hypotension (PEH). Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise-intensity mediated effect on PEH. We examined the effect of exercise intensity on time to presyncope, induced via combined head-up tilt and lower body negative pressure following one-hour cycling at 30 and 70% of heart rate range (HRR). Healthy participants (n = 8, mean±SD: 28 ± 5 y) completed orthostatic testing to presyncope before and following exercise. Beat-to-beat middle cerebral artery blood flow velocity (MCAv), MAP and cerebral oxygenation (NIRS) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95 ± 6 and 147 ± 5 b∙min(-1) for 30% and 70% HRR, respectively, with average power outputs 103 ± 22 and 221 ± 45 watts, respectively. Time to presyncope occurred 32% faster following the 70% HRR trial (952 ± 484 s vs. 1418 ± 435 s, p = 0.004). Both before and following exercise, presyncope occurred at the same reduction in MCAv (grouped mean -30 ± 11 cm∙s(-1) ), MAP (-18 ± 13 mm Hg), total oxygenation index (-6 ± 2%) and partial pressure of end tidal CO2 (PET CO2 , -16 ± 8 mm Hg, all P > 0.1). At presyncope following exercise the MCAv response was related more to the change in PET CO2 from the baseline preceding orthostatic testing (R(2) = 0.50, P = 0.01) than to the hypotension (R(2) = 0.12, P = 0.17). Presyncope both before and following exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Experimental physiology 06/2015; 100(8). DOI:10.1113/EP085143 · 2.67 Impact Factor
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    ABSTRACT: We sought to characterize and quantify the performance of a portable dynamic end-tidal forcing (DEF) system in controlling the partial pressure of arterial CO2 (PaCO2) and O2 (PaO2) at low- (LA; 344m) and high-altitude (HA; 5050m) during an isooxic CO2 test, and an isocapnic O2 test, commonly used to measure ventilatory and vascular reactivity in humans (n=9). The isooxic CO2 tests involved step changes in the partial pressure of end-tidal carbon dioxide (PETCO2) of -10, -5, 0, +5 and +10 mmHg from baseline. The isocapnic O2 test consisted of a 10-min hypoxic step (PETO2=47mmHg) from baseline at LA, and a 5-min euoxic step (PETO2=100mmHg) from baseline at HA. At both altitudes, PETO2 and PETCO2 were controlled within narrow limits (<1mmHg from target) during each protocol. During the isooxic CO2 test at LA, PETCO2 consistently overestimated PaCO2 (P<0.01) at both baseline (2.1±0.5mmHg) and hypercapnia (+5mmHg: 2.1±0.7mmHg; +10mmHg: 1.9±0.5mmHg). This Pa-PETCO2 gradient was approximately two-fold greater at HA (P<0.05). At baseline at both altitudes, PETO2 overestimated PaO2 by a similar extent (LA: 6.9±2.1mmHg; HA: 4.5±0.9mmHg; both P<0.001). This overestimation persisted during isocapnic hypoxia at LA (6.9±0.6mmHg), and during isocapnic euoxia at HA (3.8±1.2mmHg). Step-wise multiple regression analysis, on the basis of the collected data, revealed that it may be possible to predict an individual's arterial blood gases during DEF. Future research is needed to validate these prediction algorithms, and determining the implications of end-tidal-to-arterial gradients in the assessment of ventilatory and/or vascular reactivity. Copyright © 2014, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
    AJP Regulatory Integrative and Comparative Physiology 03/2015; 308(11):ajpregu.00425.2014. DOI:10.1152/ajpregu.00425.2014 · 3.11 Impact Factor
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    ABSTRACT: Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and following 10 days at 5050 m. In contrast to SL, LV end-diastolic volume was ~19% lower at rest (p=0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (~17%; 60±10 vs. 70±8 ml) despite higher LV twist (43%), apical rotation (115%) and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 ml vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely due to the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, whilst hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted. Copyright © 2014, Journal of Applied Physiology.
    Journal of Applied Physiology 03/2015; DOI:10.1152/japplphysiol.00995.2014 · 3.06 Impact Factor
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    ABSTRACT: We examined the impact of progressive hypotension with and without hypocapnia on regional extracranial cerebral blood flow and intra-cranial velocities. Participants underwent progressive lower-body negative pressure until pre-syncope to inflict hypotension. End-tidal carbon dioxide was clamped at baseline levels (isocapnic trial) or uncontrolled (poikilocapnic trial). Middle and posterior cerebral artery blood velocities (transcranial Doppler), heart rate, blood pressure and end-tidal carbon dioxide were obtained continuously. Measurements of internal carotid artery and vertebral artery blood flow were also obtained. Overall, blood pressure was reduced by ~20% from baseline in both trials (P<0.001). In the isocapnic trial, end-tidal carbon dioxide was successfully clamped at baseline with hypotension, whereas in the poikilocapnic trial it was reduced by 11.1 mm Hg (P<0.001) with hypotension. The decline in the internal carotid artery blood-flow with hypotension was comparable between trials (-139 ± 82 ml; ~30%; P<0.0001); however, the decline in the vertebral artery blood flow was -28 ± 22 ml/min (~21%) greater in the poikilocapnic trial compared with the isocapnic trial (P=0.002). Regardless of trial, the blood flow reductions in internal carotid artery (-26 ± 14%) and vertebral artery (-27 ± 14%) were greater than the decline in middle cerebral artery (-21 ± 15%) and posterior middle cerebral artery velocities (-19 ± 10%), respectively (P≤0.01). Significant reductions in the diameter of both the ICA (~5%) and VA (~7%) contributed to the decline in cerebral perfusion with systemic hypotension, independent of hypocapnia. In summary, our findings indicate that blood flow in the VA, unlike the ICA, is sensitive to changes hypotension and hypocapnia. We show for the first time that the decline in global CBF with hypotension is influenced by arterial constriction in the ICA and VA. Additionally, our findings suggest TCD measures of blood flow velocity may modestly underestimate changes in CBF during hypotension with and without hypocapnia, particularly in the posterior circulation.
    Clinical Science 02/2015; 129(2). DOI:10.1042/CS20140751 · 5.60 Impact Factor
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    ABSTRACT: The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial-jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H(+) relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.Journal of Cerebral Blood Flow & Metabolism advance online publication, 18 February 2015; doi:10.1038/jcbfm.2015.4.
    Journal of Cerebral Blood Flow & Metabolism 02/2015; 35(5). DOI:10.1038/jcbfm.2015.4 · 5.41 Impact Factor
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    ABSTRACT: Transfer function analysis (TFA) is a frequently used method to assess dynamic cerebral autoregulation (CA) using spontaneous oscillations in blood pressure (BP) and cerebral blood flow velocity (CBFV). However, controversies and variations exist in how research groups utilise TFA, causing high variability in interpretation. The objective of this study was to evaluate between-centre variability in TFA outcome metrics. 15 centres analysed the same 70 BP and CBFV datasets from healthy subjects (n = 50 rest; n = 20 during hypercapnia); 10 additional datasets were computer-generated. Each centre used their in-house TFA methods; however, certain parameters were specified to reduce a priori between-centre variability. Hypercapnia was used to assess discriminatory performance and synthetic data to evaluate effects of parameter settings. Results were analysed using the Mann-Whitney test and logistic regression. A large non-homogeneous variation was found in TFA outcome metrics between the centres. Logistic regression demonstrated that 11 centres were able to distinguish between normal and impaired CA with an AUC>0.85. Further analysis identified TFA settings that are associated with large variation in outcome measures. These results indicate the need for standardisation of TFA settings in order to reduce between-centre variability and to allow accurate comparison between studies. Suggestions on optimal signal processing methods are proposed.
    Medical Engineering & Physics 01/2015; in press:2014. · 1.83 Impact Factor
  • A. Gardner · G. L. Iverson · P. van Donkelaar · P. N. Ainslie · P. Stanwell ·
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    ABSTRACT: Sport-related concussion has been referred to as a functional rather than a structural injury with neurometabolic and microstructural alterations reported in several studies. Accordingly, conventional neuroimaging techniques, such as computed tomography (CT) and structural magnetic resonance imaging (MRI), have limited value beyond ruling out structural injury such as a contusion or hemorrhage. This chapter presents a review of three neuroimaging techniques that offer insight into the connectivity and neurometabolic consequences of concussion. A number of studies have now been published using magnetic resonance spectroscopy (MRS), diffusion tensor imaging (DTI)/diffusion-weighted imaging, and transcranial Doppler ultrasound (TCD) with varying findings. The results of these studies will be presented, together with current and possible future application of these techniques within the field of sport-related concussion.
    01/2015: pages 1; Oxford University Press.

  • Tairyoku kagaku. Japanese journal of physical fitness and sports medicine 01/2015; 64(1):112-112. DOI:10.7600/jspfsm.64.112 · 0.08 Impact Factor
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    ABSTRACT: Background: The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin saturation (SpO2) at HA would correlate better than HVR at SL to PASP at HA. Methods: In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min·-%SpO2-1) and resting PASP using echocardiography. Both resting SpO2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks (n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa; n=21). Results: Compared to SL, SpO2 decreased from 98.6 to 80.5% (P<0.001), while PASP increased from 21.7 to 34.0mmHg (P<0.001) after 2-3 weeks at 5050m. Isocapnic HVR at SL was not related to SpO2 or PASP at any time point at 5050m (all P>0.05). Sherpa had lower PASP (P<0.01) than lowlanders on days 4-8 despite similar SpO2. Upon correction for hematocrit, Sherpa PASP was not different from lowlanders at SL, but lower than lowlanders at all HA time points. At 5050m, whilst SpO2 was not related to PASP in lowlanders at any point (all R2=<0.05; P>0.50), there was a weak relationship in the Sherpa (R2=0.16; P=0.07). Conclusion: We conclude that neither HVR at SL nor resting SpO2 at HA correlates with elevations in PASP at HA.
    Chest 12/2014; 148(1). DOI:10.1378/chest.14-1992 · 7.48 Impact Factor
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    ABSTRACT: Traumatic brain injury influences regulation of cerebral blood flow in animal models and in human studies. We reviewed the use of transcranial Doppler ultrasound (US) to monitor cerebrovascular reactivity following sport-related concussion. A narrative and systematic review of articles published in the English language, from December 1982 to October 2013. Articles were retrieved via numerous databases using relevant key terms. Observational, cohort, correlational, cross-sectional and longitudinal studies were included. Three publications met the criteria for inclusion; these provided data from 42 athletes and 33 controls. All three studies reported reductions in cerebrovascular reactivity via transcranial Doppler US. These initial results support the use of cerebrovascular reactivity as a research tool for identifying altered neurophysiology and monitoring recovery in adult athletes. Larger cross-sectional, prospective and longitudinal studies are required to understand the sensitivity and prognostic value of cerebrovascular reactivity in sport-related concussion. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
    British Journal of Sports Medicine 12/2014; 49(16). DOI:10.1136/bjsports-2014-093901 · 5.03 Impact Factor

Publication Stats

3k Citations
695.44 Total Impact Points


  • 2010-2015
    • University of British Columbia - Vancouver
      Vancouver, British Columbia, Canada
  • 2009-2015
    • University of British Columbia - Okanagan
      • • School of Health and Exercise Sciences
      • • Faculty of Health and Social Development
      Kelowna, British Columbia, Canada
    • University of Lincoln
      Lincoln, England, United Kingdom
  • 2013
    • Laval University
      Quebec City, Quebec, Canada
  • 2012
    • University of Wales
      Cardiff, Wales, United Kingdom
    • Government of British Columbia, Canada
      Vancouver, British Columbia, Canada
  • 2005-2012
    • University of Otago
      • Department of Physiology
      Taieri, Otago Region, New Zealand
  • 2003-2010
    • The University of Calgary
      • Faculty of Medicine
      Calgary, Alberta, Canada
  • 2002
    • Liverpool John Moores University
      • Research Institute for Sport and Exercise Sciences (RISES)
      Liverpool, England, United Kingdom