Examining the Mechanisms behind Exercise's Multifaceted Impacts on Body Composition, Cognition, and the Gut Microbiome in Cancer Survivors: Exploring the Links to Oxidative Stress and Inflammation

Abstract

This review focuses on the effects of exercise on various health-related outcomes in cancer survivors, encompassing body composition, cognitive function (including sleep), and gut microbiome health. By analyzing multiple studies, we aimed to summarize the existing evidence and shed light on underlying mechanisms. The findings strongly suggest that exercise serves as a multifaceted non-pharmacological strategy, playing a significant role in improving the overall health of cancer survivors by effectively reducing inflammation and oxidative stress. Exercise plays a crucial role in preventing muscle wasting, diminishing the presence of reactive oxygen species and pro-inflammatory cytokines, and enhancing antioxidant systems. Furthermore, exercise displays notable benefits in terms of executive cognitive functioning and fatigue alleviation, largely attributed to its anti-inflammatory impact on the central nervous system and its ability to induce neurogenesis via growth factors. Additionally, exercise positively influences microbial diversity, reduces gut inflammation, and enhances neurogenesis through the gut-brain axis. Our key findings underscore the reduction of oxidative stress and inflammation as primary mechanisms by which exercise effectively enhances health outcomes in cancer survivors. By delving deeper into these candidate mechanisms, we aim to provide valuable guidance for future research and interventions targeting the symptoms experienced by cancer survivors.

Keywords: cachexia; cancer survivor; cognitive impairment; exercise; fatigue; gut microbiome; inflammation; oxidative stress; quality of life; sarcopenia.

Figure 1

A comprehensive summary illustrating the impact of exercise on cognitive function, behavior, body composition, and the gut microbiome in cancer survivors, demonstrating potential underlying mechanisms. Created with BioRender.com. Abbreviations: Mammalian target of rapamycin (mTOR); phosphoinositide-3 kinase (PI3K); mammalian target of rapamycin complex 1 (mTORC1); mammalian target of rapamycin complex 2 (mTORC2); ubiquitin–proteasome system (UPS); forkhead box protein O1 (FOXO1); hypothalamic–pituitary–adrenal glucocorticoid (HPAG); tumor necrosis factor α (TNF-α); C-reactive protein (CRP); lipopolysaccharide (LPS); brain-derived neurotrophic factor (BDNF); vascular endothelial growth factor (VEGF); insulin-like growth factor (IGF); short-chain fatty acid (SFCA); body mass index (BMI).