Aerobic exercise improves cognition and cerebrovascular regulation in older adults

Guadagni, Veronica; Drogos, Lauren L.; Tyndall, Amanda V.; Davenport, Margie H.; Anderson, Todd J.; Eskes, Gail A.; Longman, R. Stewart; Hill, Michael D.; Hogan, David B.; Poulin, Marc J.

doi:10.1212/wnl.0000000000009478

Cited by 101 publications

(111 citation statements)

References 49 publications

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“…The lack of observed exercise effects on amyloid, cognitive, or brain structure outcomes despite clear exercise related effects on physiologic outcomes (cardiorespiratory fitness) leads us to hypothesize that the brain benefits of aerobic exercise observed widely in the literature are not driven by effects on AD pathology but instead are likely driven by the mitigation of aging related vascular or other non-amyloid pathologies. Indeed, recent work has identified cerebrovascular outcomes and important mediators of cognitive change following exercise [ 5 , 14 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of aerobic exercise on amyloid accumulation in preclinical Alzheimer’s: A 1-year randomized controlled trial

et al. 2021

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Background Our goal was to investigate the role of physical exercise to protect brain health as we age, including the potential to mitigate Alzheimer’s-related pathology. We assessed the effect of 52 weeks of a supervised aerobic exercise program on amyloid accumulation, cognitive performance, and brain volume in cognitively normal older adults with elevated and sub-threshold levels of cerebral amyloid as measured by amyloid PET imaging. Methods and findings This 52-week randomized controlled trial compared the effects of 150 minutes per week of aerobic exercise vs. education control intervention. A total of 117 underactive older adults (mean age 72.9 [7.7]) without evidence of cognitive impairment, with elevated (n = 79) or subthreshold (n = 38) levels of cerebral amyloid were randomized, and 110 participants completed the study. Exercise was conducted with supervision and monitoring by trained exercise specialists. We conducted 18F-AV45 PET imaging of cerebral amyloid and anatomical MRI for whole brain and hippocampal volume at baseline and Week 52 follow-up to index brain health. Neuropsychological tests were conducted at baseline, Week 26, and Week 52 to assess executive function, verbal memory, and visuospatial cognitive domains. Cardiorespiratory fitness testing was performed at baseline and Week 52 to assess response to exercise. The aerobic exercise group significantly improved cardiorespiratory fitness (11% vs. 1% in the control group) but there were no differences in change measures of amyloid, brain volume, or cognitive performance compared to control. Conclusions Aerobic exercise was not associated with reduced amyloid accumulation in cognitively normal older adults with cerebral amyloid. In spite of strong systemic cardiorespiratory effects of the intervention, the observed lack of cognitive or brain structure benefits suggests brain benefits of exercise reported in other studies are likely to be related to non-amyloid effects. Trial registration NCT02000583; ClinicalTrials.gov.

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Section: Discussionmentioning

confidence: 99%

Effect of aerobic exercise on amyloid accumulation in preclinical Alzheimer’s: A 1-year randomized controlled trial

et al. 2021

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“…The quantitative aspect is what acts in the first play. It is in fact well established that acute exercise increases the cardiac output for adaptation to the increased needs mentioned above, thus leading to a prompt increase in the cerebral vascular flow [123][124][125][126]. Regular PA, on the other hand, can induce increased regional cerebral blood flow by promoting qualitative modifications, angiogenesis and collateral vessels recruitment; the mechanism of recruitment of already existing collateral vessels has a protective effect towards the circle of Willis against high-grade extra or intracranial stenosis or occlusion to reduce risk of watershed infarctions, thus making exercise a modulator factor of cerebral autoregulation [127].…”

Section: Anti-ischemic Effects Of Physical Activitymentioning

confidence: 99%

“…During PA, the increased need for oxygen and energetic substrates leads to the activation of many mechanisms whose ultimate effect is to determine an increased cerebral blood flow and to maintain neurovascular integrity. This aim is exerted both by asserting a boosting of cardiac contractility (quantitative effect) [123][124][125][126] and by a local cerebral modulation of neurovascular dynamic (qualitative effect) through the recruitment of collateral vessels [127] and the stimulation of angiogenic processes [130]. VEGF, vascular endothelial growth factor; VEGFR-2, vascular endothelial growth factor receptor 2; ANG-2, Angiopoietin-2.…”

Section: Anti-ischemic Effects Of Physical Activitymentioning

confidence: 99%

Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

Raimondo

Rizzo

Musiari

et al. 2020

IJMS

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One of the major obstacles that prevents an effective therapeutic intervention against ischemic stroke is the lack of neuroprotective agents able to reduce neuronal damage; this results in frequent evolution towards a long-term disability with limited alternatives available to aid in recovery. Nevertheless, various treatment options have shown clinical efficacy. Neurotrophins such as brain-derived neurotrophic factor (BDNF), widely produced throughout the brain, but also in distant tissues such as the muscle, have demonstrated regenerative properties with the potential to restore damaged neural tissue. Neurotrophins play a significant role in both protection and recovery of function following neurological diseases such as ischemic stroke or traumatic brain injury. Unfortunately, the efficacy of exogenous administration of these neurotrophins is limited by rapid degradation with subsequent poor half-life and a lack of blood–brain-barrier permeability. Regular exercise seems to be a therapeutic approach able to induce the activation of several pathways related to the neurotrophins release. Exercise, furthermore, reduces the infarct volume in the ischemic brain and ameliorates motor function in animal models increasing astrocyte proliferation, inducing angiogenesis and reducing neuronal apoptosis and oxidative stress. One of the most critical issues is to identify the relationship between neurotrophins and myokines, newly discovered skeletal muscle-derived factors released during and after exercise able to exert several biological functions. Various myokines (e.g., Insulin-Like Growth Factor 1, Irisin) have recently shown their ability to protects against neuronal injury in cerebral ischemia models, suggesting that these substances may influence the degree of neuronal damage in part via inhibiting inflammatory signaling pathways. The aim of this narrative review is to examine the main experimental data available to date on the neuroprotective and anti-ischemic role of regular exercise, analyzing also the possible role played by neurotrophins and myokines.

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“…In addition to these broad health outcomes, recent work has examined the potential effects of movement-related behaviors (e.g., aerobic vs. resistance) on cognitive function [6][7][8][9][10][11][12][13][14][15][16][17][18][19], including memory function. We do recognize, however, that additional research is needed that makes a side-to-side comparison between aerobic and resistance exercise on memory.…”

Section: Introductionmentioning

confidence: 99%

Does Aerobic and Resistance Exercise Influence Episodic Memory through Unique Mechanisms?

2020

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Aerobic and resistance exercise (acute and chronic) independently and collectively induce beneficial responses in the brain that may influence memory function, including an increase in cerebral blood flow, neurogenesis, neuroelectrical alterations, and protein production. However, whether aerobic and resistance exercise improve memory via similar or distinct mechanisms has yet to be fully explained. Here, we review the unique influence of aerobic and resistance exercise on neural modulation, proteins, receptors, and ultimately, episodic memory. Resistance training may optimize neural communication, information processing and memory encoding by affecting the allocation of attentional resources. Moreover, resistance exercise can reduce inflammatory markers associated with neural communication while increasing peripheral and central BDNF (brain-derived neurotrophic factor) production. Aerobic training increases hippocampal levels of BDNF and TrkB (Tropomyosin receptor kinase B), protein kinases and glutamatergic proteins. Likewise, both aerobic and anaerobic exercise can increase CREB (cAMP response element-binding protein) phosphorylation. Thus, we suggest that aerobic and resistance exercise may influence episodic memory via similar and, potentially, distinct mechanisms.

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Aerobic exercise improves cognition and cerebrovascular regulation in older adults

Cited by 101 publications

References 49 publications

Effect of aerobic exercise on amyloid accumulation in preclinical Alzheimer’s: A 1-year randomized controlled trial

Effect of aerobic exercise on amyloid accumulation in preclinical Alzheimer’s: A 1-year randomized controlled trial

Role of Regular Physical Activity in Neuroprotection against Acute Ischemia

Does Aerobic and Resistance Exercise Influence Episodic Memory through Unique Mechanisms?

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