354 research outputs found

    The physiological and clinical importance of cardiorespiratory fitness in people with abdominal aortic aneurysm

    Get PDF
    NEW FINDINGS: What is the topic of this review? This review focuses on the physiological impact of abdominal aortic aneurysm (AAA) on cardiorespiratory fitness and the negative consequences of low fitness on clinical outcomes in AAA. We also discuss the efficacy of exercise training for improving cardiorespiratory fitness in AAA. What advances does it highlight? We demonstrate the negative impact of low fitness on disease progression and clinical outcomes in AAA. We highlight potential mechanistic determinants of low fitness in AAA and present evidence that exercise training can be an effective treatment strategy for improving cardiorespiratory fitness, postoperative mortality and disease progression. ABSTRACT: An abdominal aortic aneurysm (AAA) is an abnormal enlargement of the aorta, below the level of the renal arteries, where the aorta diameter increases by >50%. As an aneurysm increases in size, there is a progressive increase in the risk of rupture, which ranges from 25 to 40% for aneurysms >5.5 cm in diameter. People with AAA are also at a heightened risk of cardiovascular events and associated mortality. Cardiorespiratory fitness is impaired in people with AAA and is associated with poor (postoperative) clinical outcomes, including increased length of hospital stay and postoperative mortality after open surgical or endovascular AAA repair. Although cardiorespiratory fitness is a well‐recognized prognostic marker of cardiovascular health and mortality, it is not assessed routinely, nor is it included in current clinical practice guidelines for the management of people with AAA. In this review, we discuss the physiological impact of AAA on cardiorespiratory fitness, in addition to the consequences of low cardiorespiratory fitness on clinical outcomes in people with AAA. Finally, we summarize current evidence for the effect of exercise training interventions on cardiorespiratory fitness in people with AAA, including the associated improvements in postoperative mortality, AAA growth and cardiovascular risk. Based on this review, we propose that cardiorespiratory fitness should be considered as part of the routine risk assessment and monitoring of people with AAA and that targeting improvements in cardiorespiratory fitness with exercise training might represent a viable adjunct treatment strategy for reducing postoperative mortality and disease progression

    Does respiratory drive modify the cerebral vascular response to changes in end‐tidal carbon dioxide?

    Get PDF
    What is the central question of this study? An interaction exists between the regulatory systems of respiration and cerebral blood flow (CBF), because of the same mediator (carbon dioxide, CO ) for both physiological systems. The present study examined whether the traditional method for determining cerebrovascular reactivity to CO (cerebrovascular reactivity; CVR) is modified by changes in respiration. What is the main finding and its importance? CVR was modified by voluntary changes in respiration during hypercapnia. This finding suggests that an alteration in the respiratory system may under- or over-estimate CVR determined by traditional methods in healthy adults.The cerebral vasculature is sensitive to changes in the arterial partial pressure of carbon dioxide (CO ). This physiological mechanism has been well established as a cerebrovascular reactivity to CO (CVR). However, arterial CO may not be an independent variable in the traditional method to assess CVR since the cerebral blood flow (CBF) response is partly affected by the activation of respiratory drive or higher centers in the brain. We hypothesized that CVR is modified by changes in respiration. To test our hypothesis, in the present study, ten young healthy subjects performed hyper- or hypo-ventilation to change end-tidal CO (P CO ) under different concentrations of CO gas inhalation (0, 2.0, 3.5%). We measured middle cerebral artery mean blood flow velocity (MCAVm) by transcranial Doppler to identify the CBF response to change in P CO during each condition. At each F CO condition, P CO was significantly altered by changes in ventilation, and MCA Vm changed accordingly. However, the relationship between changes in MCV Vm and P CO as a response curve of CVR was reset upwards and downwards by hypo- and hyper-ventilation, respectively, compared with CVR during normal-ventilation. The findings of the present study may provide the possibility that an alteration in respiration under- or over-estimates CVR determined by the traditional methods

    Disparities in registration and use of an online patient portal among older adults: findings from the LitCog cohort

    Get PDF
    (C) The Author 2015. Published by Oxford University Press on behalf of the American Medical Informatics Association. All rights reserved.Financial disclosure: This project was supported by the National Institute on Aging (R01 AG030611), the National Center for Research Resources (5UL1RR025741), and the National Center for Advancing Translational Sciences (Grant 8UL1TR000150). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Smith is currently supported by a Cancer Research UK Fellowship

    Exercise training reduces the acute physiological severity of post-menopausal hot flushes.

    Get PDF
    A hot-flush is characterised by feelings of intense heat, profuse elevations in cutaneous vasodilation and sweating, and reduced brain blood flow. Exercise training reduces self-reported hot-flush severity, but underpinning physiological data are lacking. We hypothesised that exercise training attenuates the changes in cutaneous vasodilation, sweat rate and cerebral blood flow during a hot flush. In a preference trial, 18 symptomatic post-menopausal women underwent a passive heat stress to induce hot-flushes at baseline and follow-up. Fourteen participants opted for a 16-week moderate intensity supervised exercise intervention, while 7 participants opted for control. Sweat rate, cutaneous vasodilation, blood pressure, heart rate and middle cerebral artery velocity (MCAv) were measured during the hot-flushes. Data were binned into eight equal segments, each representing 12.5% of hot flush duration. Weekly self-reported frequency and severity of hot flushes were also recorded at baseline and follow-up. Following training, mean hot-flush sweat rate decreased by 0.04 mg·cm2 ·min-1 at the chest (95% CI: 0.02-0.06, P = 0.01) and by 0.03 mg·cm2 ·min-1 (0.02-0.05, P = 0.03) at the forearm, compared with negligible changes in control. Training also mediated reductions in cutaneous vasodilation by 9% (6-12) at the chest and by 7% (4-9) at forearm (P≤0.05). Training attenuated hot flush MCAv by 3.4 cm/s (0.7-5.1, P = 0.04) compared with negligible changes in control. Exercise training reduced the self-reported severity of hot-flush by 109 arbitrary units (80-121, P<0.001). These data indicate that exercise training leads to parallel reductions in hot-flush severity and within-flush changes in cutaneous vasodilation, sweating and cerebral blood flo
    corecore