Why the study?
The mechanisms mediating the protective effects of high intrinsic cardiorespiratory fitness against metabolic, cardiac, and brain impairments in non-obese versus obese conditions remain incompletely understood.
Does high intrinsic cardiorespiratory fitness protect against metabolic, cardiac, and brain impairments in non-obese versus obese untrained rats?
Does high intrinsic cardiorespiratory fitness protect against metabolic, cardiac, and brain impairments in non-obese versus obese untrained rats?
High intrinsic cardiorespiratory fitness protects against obesity-induced premature aging and associated metabolic, cardiac, and brain impairments in a rat model.
High CRF may mitigate obesity-related impairments in rat models; hypothesis-generating and leaves open human translation.
BACKGRUOUND: High cardiorespiratory fitness (CRF) protects against age-related diseases. However, the mechanisms mediating the protective effect of high intrinsic CRF against metabolic, cardiac, and brain impairments in non-obese versus obese conditions remain incompletely understood. We aimed to identify the mechanisms through which high intrinsic CRF protects against metabolic, cardiac, and brain impairments in non-obese versus obese untrained rats. METHODS: Seven-week-old male Wistar rats were divided into two groups (n=8 per group) to receive either a normal diet or a highfat diet (HFD). At weeks 12 and 28, CRF, carbohydrate and fatty acid oxidation, cardiac function, and metabolic parameters were evaluated. At week 28, behavior tests were performed. At the end of week 28, rats were euthanized to collect heart and brain samples for molecular studies. RESULTS: The obese rats exhibited higher values for aging-related parameters than the non-obese rats, indicating that they experienced obesity-induced premature aging. High baseline CRF levels were positively correlated with several favorable metabolic, cardiac, and brain parameters at follow-up. Specifically, the protective effects of high CRF against metabolic, cardiac, and brain impairments were mediated by the modulation of body weight and composition, the lipid profile, substrate oxidation, mitochondrial function, insulin signaling, autophagy, apoptosis, inflammation, oxidative stress, cardiac function, neurogenesis, blood-brain barrier, synaptic function, accumulation of Alzheimer's disease-related proteins, and cognition. Interestingly, this effect was more obvious in HFD-fed rats. CONCLUSION: The protective effect of high CRF is mediated by the modulation of several mechanisms. These effects exhibit greater efficacy under conditions of obesity-induced premature aging.
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Pantiya et al. (2022) studied this question.
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