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Dietary intervention remains a popular, albeit challenging, approach for combating obesity. In recent years, dietary interventions that increase consumption of medium-chain triglycerides (MCT) instead of long-chain triglycerides (LCT) have gained attention. Pre-clinical research has demonstrated that rats fed a high-fat diet (HFD) induce adiposity, but a dietary shift from LCT to MCT suppresses this effect. To date, the extent to which this effect operates via suppressed hyperphagia is not fully understood. In the present study, we sought to determine how consuming a HFD composed of different fat types affects energy intake, adiposity, and hippocampal brain-derived neurotropic factor (BDNF) levels. Rats were assigned to one of four diet groups – rat chow (CHOW), LCT-enriched HFD (LCT-HFD), MCT-enriched HFD (MCT-HFD), or coconut oil-enriched HFD (COCO-HFD), which composes a mixture of LCT and MCT. In Experiment 1, all animals were given <i>ad libitum</i> access to their assigned diet, whereas in Experiments 2 and 3, HFD-subjects were pair-fed to CHOW to prohibit hyperphagia. In Experiments 1 and 2, subjects were aged 20-24 weeks, whereas in Experiment 3, subjects were aged 10-11 weeks. Across experiments, we found that the effect of MCT consumption on suppressing HFD-induced adiposity is causally related to suppressed HFD-induced hyperphagia. Additionally, we failed to detect an effect of HFD consumption on hippocampal BDNF. Therefore, our findings did not support or oppose the hypothesis that MCT consumption attenuates HFD-induced BDNF deficiency. Future studies should focus on determining the causal relationship between MCT consumption, energy expenditure, and HFD-induced adiposity.

<p dir="ltr">Past research has extensively explored the benefits of acute aerobic exercise (AE) on memory and executive functions. Additionally, the cross-sectional relationship between muscle strength – a direct outcome of RE – and cognition is unknown, despite the simultaneous onset of muscle and cognitive decline in one’s thirties. However, the effects of acute resistance exercise (RE) on cognition remain understudied, despite the growing popularity of RE and evidence that RE may have distinct effects on cognition.. Therefore, the present study aimed to broaden our understanding of the connection between muscle strength and hippocampal-dependent memory and to investigate the influence of RE on memory and executive function.</p><p dir="ltr">A sample of 125 healthy young adults (18-50 years old) completed this study. On the first day of testing, subjects completed a cognitive battery testing aspects of hippocampal dependent memory, spatial abilities, and working memory, a maximal muscle strength testing session including handgrip strength and one-rep-max testing, and maximal aerobic capacity testing. Subjects completed a bioelectrical impedance assessment (BIA) body scan to measure body composition on Day 2. Day 3 consisted of a randomized controlled trial (RCT), where subjects completed either 42 minute moderate intensity RE (n = 62) or a seated rest (n = 61). Cognitive testing including a memory recognition task, an inhibitory control task, and a working memory task were performed both before and after the intervention. Subjects also completed lactate, blood pressure, and blood draw (only a subset of subjects (n = 59)) before and after intervention.</p><p dir="ltr">The results first revealed that after controlling for known covariates, those with greater handgrip strength performed better on mental rotation tasks (t = 2.14, p = 0.04, Δr2= 0.04), while those with higher upper-body relative strength did better on recognition (t = 2.78, p = 0.01, Δr2 = 0.06) and pattern separation (t = 2.03, p = 0.04, Δr2= 0.04) tasks. Further, while there was no acute effect of RE on memory performance, response times during measures of inhibitory control (t = 4.15, p < 0.01, d = 0.40) and working memory decreased after exercise (t = 7.01, p < 0.01, d = 0.46), along with decreases in P3 latency during the inhibitory control task (t =-5.99, p < 0.01, d = 0.58). Additionally, blood lactate (t =-17.18, p < 0.01, d = 2.06), serum brain derived neurotropic factor (BDNF) (t = -4.17, p < 0.01, d = 0.66), and systolic blood pressure (t = -10.58, p < 0.01, d = 0.99) all increased following RE, while diastolic blood pressure (t = 4.90, p < 0.01,d = 0.50) decreased. Notably, the change in systolic blood pressure (t = -2.83, p = 0.01, Δr2 = 0.06) was associated with improvements in behavioral measures of inhibitory control, changes in lactate (t = -2.26, p = 0.03, Δr2 = 0.04) and systolic blood pressure (t = -3.30, p < 0.01, Δr2 = 0.08) were also related to improved behavioral changes in working memory, and changes in lactate (t = -3.31, p < 0.01, Δr2= 0.08) and BDNF (t = -2.12, p = 0.04, Δr2= 0.08) related to faster P3 latency during inhibitory control. Importantly, these associations between physiological and cognitive changes were consistent across both exercise and rest groups, suggesting that physiological changes were linked to improved cognitive performance regardless of group assignment.</p><p dir="ltr">In conclusion, this study highlights the positive relationships between cross-sectional muscle strength and aspects of memory and spatial abilities, with distinct contributions from handgrip and upper body strength. Furthermore, acute RE was shown to enhance executive functions, particularly in terms of processing speed during inhibitory control (response time and P3 latency) and working memory (response time). This study suggests that RE can be a valid way to garner exercise-induced benefits on executive functions potentially through its influence on lactate, BDNF, and blood pressure, however, since these effects were evident regardless of intervention, more work is needed to determine if RE-induced changes have the same mechanisms. Overall, these findings underscore the potential benefits of muscle strength and RE on enhancing executive function in young and middle-aged adults.</p>