Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans

Formes, Kevin J.; Zhang, Peizhen; Tierney, Nancy; Schaller, F.; Shi, Xiangrong

doi:10.1152/ajpheart.00662.2009

Cited by 25 publications

(16 citation statements)

References 49 publications

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“…Nevertheless, increased vascular volume was not maintained after a 3‐month sedentary period. Other recent studies also underline the beneficial effects of exercise, generally chronic exercise, for cerebral vascularization in both aged (251–254) and non‐aged (255–257) individuals, invariably accompanied by measurable neuroprotective effects (258). In this regard, it is necessary to differentiate between the effects of mild‐to‐moderate exercise over longer periods that increase cerebral flow and those of heavy, strenuous and intensive exercise that reduce cerebral blood flow, as well as individual preferences and circumstances (259–263).…”

Section: Exercise and Angiogenesismentioning

confidence: 96%

Physical exercise alleviates debilities of normal aging and Alzheimer’s disease

Archer

2010

Acta Neurologica Scandinavica

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Both healthy aging and the pathologic incidence of disorders associated with aging involve an array of debilities. Physical exercise harnesses implicit and inherent biologic characteristics amenable to the putative interventional influences under clinical, institutional or laboratory conditions. The neurodegenerative and pathophysiologic progressions that constitute Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), normal aging, and different animal models of AD have shown the existence of several putative mechanisms. A large variety of moderating factors have demonstrated that the ever-proliferating plethora of neurotrophic factors, neurogenesis as observed through generality of expression and neuronal arborization. The insistent efficacy of brain vascular angiogenesis may delay also the comorbid incidence of depressive disorders with dementia pathology. The pathogenesis of aging may be contained by selective treatments: these diverse conditions, linked to the basis of the aging concept, have been shown, to greater or lesser extents, to respond to a variety of scheduled applications of physical exercise. The range of reports that provide accounts of the mechanisms mediating the positive progressive response to exercise intervention is far-ranging; these studies indicate that subtle changes at molecular, neuronal, vascular and epigenetic levels may exert notable consequence at functional expression and, perhaps most essentially, offer convincing expectancy of significant benefits.

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Section: Exercise and Angiogenesismentioning

confidence: 96%

Physical exercise alleviates debilities of normal aging and Alzheimer’s disease

Archer

2010

Acta Neurologica Scandinavica

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“…Baseline normoxic data were averaged over 1 min before the first and fifth hypoxic bouts. Five-minute steady-state RRI before day 1 and day 14 hypoxic exposures were analyzed using power spectral analysis (Welch option) after fast-Fourier transform with the data analysis and display program (DADiSP, Cambridge, MA) as previously described (11,17,54). Low-frequency power between 0.04 and 0.14 Hz and high-frequency power between 0.15 and 0.40 Hz of RRI variability were extracted and compared between day 1 and day 14.…”

Section: Participantsmentioning

confidence: 99%

Two-week normobaric intermittent hypoxia exposures enhance oxyhemoglobin equilibrium and cardiac responses during hypoxemia

Zhang

Downey

Chen

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Intermittent hypoxia (IH) is extensively applied to challenge cardiovascular and respiratory function, and to induce physiological acclimatization. The purpose of this study was to test the hypothesis that oxyhemoglobin equilibrium and tachycardiac responses during hypoxemia were enhanced after 14-day IH exposures. Normobaric-poikilocapnic hypoxia was induced with inhalation of 10% O2 for 5-6 min interspersed with 4 min recovery on eight nonsmokers. Heart rate (HR), arterial O2 saturation (SaO 2), and end-tidal O2 (PetO 2) were continuously monitored during cyclic normoxia and hypoxia. These variables were compared during the first and fifth hypoxic bouts between day 1 and day 14. There was a rightward shift in the oxyhemoglobin equilibrium response following 14-day IH exposures, as indicated by the greater PetO 2 (an index of arterial Po2) at 50% of SaO 2 on day 14 compared with day 1 [33.9 ± 1.5 vs. 28.2 ± 1.3 mmHg (P = 0.005) during the first hypoxic bout and 39.4 ± 2.4 vs. 31.4 ± 1.5 mmHg (P = 0.006) during the fifth hypoxic bout] and by the augmented gains of ΔSaO 2/ΔPetO 2 (i.e., deoxygenation) during PetO 2 from 65 to 40 mmHg in the first (1.12 ± 0.08 vs. 0.80 ± 0.02%/mmHg, P = 0.001) and the fifth (1.76 ± 0.31 vs. 1.05 ± 0.06%/mmHg, P = 0.024) hypoxic bouts. Repetitive IH exposures attenuated (P = 0.049) the tachycardiac response to hypoxia while significantly enhancing normoxic R-R interval variability in low-frequency and high-frequency spectra without changes in arterial blood pressure at rest or during hypoxia. We conclude that 14-day IH exposures enhance arterial O2 delivery and improve vagal control of HR during hypoxic hypoxemia.

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“…More recently, studies have shown that exercise also exerts positive changes on the cerebral vasculature [1, 7, 23–28], including preserved CBF in areas associated with aging and AD using ASL [29], higher middle cerebral artery blood flow velocity in young and older adults using transcranial doppler ultrasound [23, 24, 27, 29], and associations between physical fitness, vascular function and cognitive performance in older women [24]. Studies investigating differences in CBF between fit and sedentary individuals have revealed that CBF was 17% higher in highly fit men when compared to sedentary adults [23], and that the systemic circulation benefits of exercise seem to extend to the brain in fit postmenopausal women compared to their sedentary counterparts [24].…”

Section: Introductionmentioning

confidence: 99%

Increased Hippocampal Blood Flow in Sedentary Older Adults at Genetic Risk for Alzheimer's Disease

Zlatar

Wierenga

Bangen

et al. 2014

JAD

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Resting cerebral blood flow (CBF) decreases with age; however regulatory increases in hippocampal CBF have been associated with genetic risk (Apolipoprotein E [APOE] ε4 carriers) for Alzheimer’s disease (AD). Although physical activity (PA) exerts beneficial effects on CBF in healthy elders, the effects of sedentary behaviors on CBF remain unknown. We measured resting hippocampal CBF (via arterial spin labeling magnetic resonance imaging) and sedentary time/PA (via accelerometry) on 33 cognitively healthy adults (ages 52–81), 9 of which were APOE ε4 carriers. Results indicate that the relationship between sedentary time and CBF in the left hippocampus differs by APOE status, whereby APOE ε4 carriers show higher CBF as a function of longer sedentary time (B=10.8, SE=3.17, β= .74, t=3.41, p<.01) compared to noncarriers (B=1.4, SE = 2.7, β=.096, t=.51, p=.61), possibly suggesting a CBF regulatory response to compensate for metabolic alterations in dementia risk. These preliminary data suggest that the relationship between CBF and sedentary time is different in APOE ε4 carriers and noncarriers and that sedentary time may act as a behavioral risk factor for CBF dysregulation in those at genetic risk for developing AD. More research is needed to further understand the role of sedentary behaviors and physical activity on CBF, especially in individuals at genetic risk of developing AD.

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Chronic physical activity mitigates cerebral hypoperfusion during central hypovolemia in elderly humans

Cited by 25 publications

References 49 publications

Physical exercise alleviates debilities of normal aging and Alzheimer’s disease

Physical exercise alleviates debilities of normal aging and Alzheimer’s disease

Two-week normobaric intermittent hypoxia exposures enhance oxyhemoglobin equilibrium and cardiac responses during hypoxemia

Increased Hippocampal Blood Flow in Sedentary Older Adults at Genetic Risk for Alzheimer's Disease

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