Exercise intensity matters: A review on evaluating the effects of aerobic exercise intensity on muscle-derived neuroprotective myokines

IF 4.9 Q1 CLINICAL NEUROLOGY

Alzheimer''s and Dementia: Translational Research and Clinical Interventions Pub Date : 2025-02-19 DOI:10.1002/trc2.70056

Navabeh Zare, David J. Bishop, Itamar Levinger, Mark A. Febbraio, James R. Broatch

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Abstract

Exercise as a medical intervention is effective to help prevent and manage many chronic and complex diseases, including dementia. There is evidence to suggest that regular aerobic exercise protects against age-related brain atrophy and reduces the risk of cognitive decline. The mechanisms by which exercise infers a neuroprotective effect remain to be established but may be related to a maintenance of brain volume and neuronal survival, improved cerebrovascular density and function, and/or increased synaptic plasticity. In addition, there is growing evidence to suggest the beneficial effects of exercise on brain health and cognitive function are, at least in part, mediated by factors released by skeletal muscle during contraction. The fact that the brain responds to exercise suggests that muscle-derived peripheral factors, or “myokines,” may play a key role in muscle–brain crosstalk and exercise neuroprotection. However, the most effective “dose” of aerobic exercise to promote beneficial changes in these myokine pathways is currently unknown. Specifically, most of the evidence to date is from studies that have used moderate-intensity exercise, and research investigating the merit of high-intensity exercise is scarce. Considering the well-established role of high-intensity interval training in protecting against numerous medical conditions, more research is needed to identify the most effective “dose” of exercise to improve the beneficial effects of these myokines.

Highlights

Neuroprotection through exercise: Regular aerobic exercise mitigates age-related brain atrophy and cognitive decline via multiple mechanisms, including brain volume maintenance, improved cerebrovascular function, and synaptic plasticity.
Myokines as mediators: Muscle-derived factors (myokines) play a crucial role in muscle–brain crosstalk, significantly contributing to the neuroprotective effects of exercise.
Intensity matters: The review underscores the necessity to define and study exercise intensity, revealing high-intensity exercise may be as effective, if not more, in promoting neuroprotective myokine levels compared to moderate-intensity exercise.
Future research directions: This review emphasizes the need for well-controlled studies to explore the optimal exercise dose for enhancing myokine pathways and their implications for neurodegenerative disease prevention.

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运动强度的影响：评价有氧运动强度对肌肉源性神经保护肌因子的影响的综述

运动作为一种医疗干预手段，可以有效地帮助预防和控制包括痴呆在内的许多慢性和复杂疾病。有证据表明，有规律的有氧运动可以防止与年龄相关的脑萎缩，降低认知能力下降的风险。运动推断神经保护作用的机制仍有待建立，但可能与维持脑容量和神经元存活，改善脑血管密度和功能，和/或增加突触可塑性有关。此外，越来越多的证据表明，运动对大脑健康和认知功能的有益影响，至少在一定程度上是由骨骼肌收缩时释放的因子介导的。大脑对运动有反应的事实表明，肌肉衍生的外周因子，或“肌肉因子”，可能在肌肉-大脑相互作用和运动神经保护中发挥关键作用。然而，有氧运动促进这些肌因子通路有益变化的最有效“剂量”目前尚不清楚。具体来说，到目前为止，大多数证据都来自使用中等强度运动的研究，而调查高强度运动优点的研究很少。考虑到高强度间歇训练在预防多种疾病方面的作用，需要更多的研究来确定最有效的运动“剂量”，以提高这些肌因子的有益作用。通过运动保护神经：定期有氧运动通过多种机制减轻与年龄相关的脑萎缩和认知能力下降，包括维持脑容量、改善脑血管功能和突触可塑性。肌因子作为介质：肌源性因子（Myokines）在肌脑串扰中起着至关重要的作用，对运动的神经保护作用有重要贡献。强度问题：该综述强调了定义和研究运动强度的必要性，揭示了与中等强度运动相比，高强度运动在促进神经保护性肌因子水平方面可能同样有效，甚至更有效。未来的研究方向：本综述强调需要进行良好的对照研究，以探索增强肌因子通路的最佳运动剂量及其对神经退行性疾病预防的意义。

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来源期刊

Alzheimer''s and Dementia: Translational Research and Clinical Interventions Medicine-Psychiatry and Mental Health

CiteScore

10.10

自引率

2.10%

发文量

134

审稿时长

10 weeks

期刊介绍： Alzheimer''s & Dementia: Translational Research & Clinical Interventions (TRCI) is a peer-reviewed, open access,journal from the Alzheimer''s Association®. The journal seeks to bridge the full scope of explorations between basic research on drug discovery and clinical studies, validating putative therapies for aging-related chronic brain conditions that affect cognition, motor functions, and other behavioral or clinical symptoms associated with all forms dementia and Alzheimer''s disease. The journal will publish findings from diverse domains of research and disciplines to accelerate the conversion of abstract facts into practical knowledge: specifically, to translate what is learned at the bench into bedside applications. The journal seeks to publish articles that go beyond a singular emphasis on either basic drug discovery research or clinical research. Rather, an important theme of articles will be the linkages between and among the various discrete steps in the complex continuum of therapy development. For rapid communication among a multidisciplinary research audience involving the range of therapeutic interventions, TRCI will consider only original contributions that include feature length research articles, systematic reviews, meta-analyses, brief reports, narrative reviews, commentaries, letters, perspectives, and research news that would advance wide range of interventions to ameliorate symptoms or alter the progression of chronic neurocognitive disorders such as dementia and Alzheimer''s disease. The journal will publish on topics related to medicine, geriatrics, neuroscience, neurophysiology, neurology, psychiatry, clinical psychology, bioinformatics, pharmaco-genetics, regulatory issues, health economics, pharmacoeconomics, and public health policy as these apply to preclinical and clinical research on therapeutics.