Abstract
Regular physical activity (PA) improves cognitive functions, prevents brain atrophy, and delays the onset of cognitive decline, dementia, and Alzheimer’s disease. Presently, there are no specific recommendations for PA producing positive effects on brain health and little is known on its mediators. PA affects production and release of several peptides secreted from peripheral and central tissues, targeting receptors located in the central nervous system (CNS). This review will provide a summary of the current knowledge on the association between PA and cognition with a focus on the role of (neuro)peptides. For the review we define peptides as molecules with less than 100 amino acids and exclude myokines. Tachykinins, somatostatin, and opioid peptides were excluded from this review since they were not affected by PA. There is evidence suggesting that PA increases peripheral insulin growth factor 1 (IGF-1) levels and elevated serum IGF-1 levels are associated with improved cognitive performance. It is therefore likely that IGF-1 plays a role in PA induced improvement of cognition. Other neuropeptides such as neuropeptide Y (NPY), ghrelin, galanin, and vasoactive intestinal peptide (VIP) could mediate the beneficial effects of PA on cognition, but the current literature regarding these (neuro)peptides is limited.
Highlights
Cognition is a complex system encompassing processes such as episodic memory, working memory, executive function/inhibition, spatial learning, language/vocabulary comprehension, processing speed, and language/reading decoding [1]
These findings suggest that orexin-A might mediate beneficial effects of physical activity (PA) on cognition
This review attempted to summarize the current knowledge of the effects of PA induced peptide release on cognition
Summary
Cognition is a complex system encompassing processes such as episodic memory, working memory, executive function/inhibition, spatial learning, language/vocabulary comprehension, processing speed, and language/reading decoding [1]. This is thought to be generated by association connections between different cerebral cortex regions [2,3]. Inhibitory and stimulatory inputs strengthen (long term potentiation) or weaken (long term depression) the synaptic activities, rendering the connectivity a very dynamic process. C20h2a0n, 9g,e2s59r2epresent the molecular basis for learning and memory [4] This synaptic plas2toicfi2t5y can be influenced by several factors e.g., aging, diseases (obesity, diabetes, hypertension, dyslipidemia), toxins (smoking and alcohol), and exercise. At mean age 36, physical activity and fitness were assessed
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