Bibliografisk note

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The literature search was conducted on four independent databases: PubMed, Embase, PsycINFO, and Cochrane (Fig. 1). The search string consisted of terms supporting the eligibility criteria by incorporating a definition of intervention type along with terms searching for exercise-induced effects on brain metabolites as measured by 1H-MRS. The string incorporated keywords and MeSH terms from other reviews assessing acute exercise on a variety of brain variables [15]. No filters were applied. The final search was done on the September 8, 2022 in all four databases using the following string:Brain connectivity is altered both in aging and in neurodegeneration [29]. In the face of ageing, remaining physically active can help maintain brain connectivity [30,31]. Accordingly, measuring GABA in relation to other markers of brain aging and neurodegeneration may help us to understand individual differences in connectivity effects – particularly since some studies show positive effects of exercise on connectivity [30,32], while others do not [33]. Exercise-induced GABA increases measured by MRS have been proposed to reflect intracellular increases utilized to support the energetic demands of the mitochondria [24]. Mechanisms of energy metabolism, including mitochondrial function, adaptively modify and protect neuronal networks. Therefore, interventions maintaining these functions have been suggested as a preventative strategy for Alzheimer's disease (AD) [34]. In male rats with AD, GABA-containing compounds have been shown to prevent mitochondrial dysfunction [35]. While three studies reported an increase in GABA after exercise, one study found no significant changes. Future PA-studies should investigate GABA changes in older individuals who experience a cognitive decline to better understand how these changes are potentially associated with benefits in cognition induced by exercise.As NAA exists in high concentrations within neurons, it is often interpreted as a “a neuronal marker” [5]. For instance, findings of increased or decreased NAA levels are, respectively, interpreted as being indicative of neurogenesis and neurodegeneration - conditions at opposite ends of the neuronal integrity spectrum [41,42]. One prominent hypothesis in the exercise-brain literature is that exercise enhances hippocampal neurogenesis, which is in turn conducive to improved cognitive function [43]. If NAA is interpreted as a neuronal marker, then findings of increased NAA levels following exercise could be interpreted in support of the hypothesis that exercise promotes neuronal integrity.ND is supported by funding from the Lundbeck Foundation (Grant Nr. R380-2021-1269).

Funding Information:
ND is supported by funding from the Lundbeck Foundation (Grant Nr. R380-2021-1269 ).

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