Regular exercise and dietary supplements with antioxidants each have the potential to improve cognitive function and attenuate cognitive decline, and, in some cases, they enhance each other. Our current results reveal that low-intensity exercise (mild exercise, ME) and the natural antioxidant carotenoid astaxanthin (AX) each have equivalent beneficial effects on hippocampal neurogenesis and memory function. We found that the enhancement by ME combined with AX in potentiating hippocampus-based plasticity and cognition is mediated by leptin (LEP) made and acting in the hippocampus. In assessing the combined effects upon wild-type (WT) mice undergoing ME with or without an AX diet for four weeks, we found that, when administrated alone, ME and AX separately enhanced neurogenesis and spatial memory, and when combined they were at least additive in their effects. DNA microarray and bioinformatics analyses revealed not only the up-regulation of an antioxidant gene, ABHD3, but also that the up-regulation of LEP gene expression in the hippocampus of WT mice with ME alone is further enhanced by AX. Together, they also increased hippocampal LEP (h-LEP) protein levels and enhanced spatial memory mediated through AKT/STAT3 signaling. AX treatment also has direct action on human neuroblastoma cell lines to increase cell viability associated with increased LEP expression. In LEP-deficient mice (ob/ob), chronic infusion of LEP into the lateral ventricles restored the synergy. Collectively, our findings suggest that not only h-LEP but also exogenous LEP mediates effects of ME on neural functions underlying memory, which is further enhanced by the antioxidant AX.hippocampal leptin | mild exercise | astaxanthin | antioxidant | spatial memory P ositive lifestyle changes including physical activity and diet are believed to be beneficial for promoting brain health and slowing cognitive decline of Alzheimer's disease (AD). Exercise is an important factor in improving hippocampus-related cognition by enhancing adult hippocampal neurogenesis (AHN) in rodents (1). Although dietary supplements such as docosahexaenoic acid (DHA) and epicatechin (EGCG) have been shown to potentiate the effects of voluntary exercise on memory function (2-4), voluntary exercise alone, not in combination with EGCG, improves AHN and memory functions (5, 6). However, previous animal studies were limited in their applicability to clinical trials because of the uncertainty concerning exercise intensity. To translate our mild exercise (ME) animal model to humans, we developed a quantitative evaluation system based on lactate threshold (LT) and showed that ME has beneficial effects on AHN and spatial memory in animals (7, 8) and on hippocampal memory function in young humans (9). This raises the question of whether, for translation to humans, a combined intervention of dietary supplements and ME could enhance memory function and neuronal plasticity.While mechanisms of exercise-enhanced hippocampal function are not fully understood, several molecular factors includin...

A pre-diabetic population has an increased risk of cognitive decline as well as type 2 diabetes mellitus (T2DM). The present study investigated whether the progression of memory dysfunction and dysregulated brain glycogen metabolism is prevented with four months of exercise intervention from the pre-symptomatic stage in T2DM rat model. Memory function and biochemical and molecular profiles were assessed in the pre-symptomatic stage of OLETF rats, a T2DM model, with LETO rats as genetic control. These rats were subjected to light- or moderate-intensity treadmill running for four months with repetition of the same experiments. Significant hippocampal-dependent memory dysfunction was observed in the pre-symptomatic stage of OLETF rats, accompanied by downregulated levels of hippocampal monocarboxylate transporter 2 (MCT2), a neuronal lactate-transporter, without alteration in hippocampal glycogen levels. Four months of light or moderate exercise from the pre-symptomatic stage of T2DM normalized glycemic parameters and also hippocampal molecular normalization through MCT2, glycogen, and brain-derived neurotrophic factor (BDNF) levels with the improvement of memory dysfunction in OLETF rats. A four-month exercise regimen from the pre-symptomatic stage of T2DM at light and moderate intensities contributed to the prevention of the development of T2DM and the progression of cognitive decline with hippocampal lactate-transport and BDNF improvement.

Introduction: Exercise becomes a stress when performed at an intensity above the lactate threshold (LT) because at that point the plasma adrenocorticotropic hormone (ACTH), a marker of stress response, increases. It is possible that the exercise-induced ACTH response is regulated at least by arginine vasopressin (AVP) and possibly by corticotropin-releasing hormone (CRH), but this remains unclear. To clarify the involvement of these factors, it is useful to intervene pharmacologically in the regulatory mechanisms, with a physiologically acceptable exercise model. Methods: We used a special stress model of treadmill running (aerobic exercise) for male Wistar rats, which mimic the human physiological response, where plasma ACTH levels increase at just above the LT for 30 min. Animals were administered the AVP V1b receptor antagonist SSR149415 (SSR) and/or the CRH type 1 receptor antagonist CP154526 (CP) intraperitoneally before the exercise, which allowed the monitoring of exercise-induced ACTH response. Immunocytochemical evaluation of activated AVP and CRH neurons with exercise was performed for the animals’ hypothalami. Results: A single injection of either antagonist, SSR or CP, resulted in inhibited ACTH levels after exercise stress. Moreover, the combined injection of SSR and CP strongly suppressed ACTH secretion during treadmill running to a greater extent than each alone. The running-exercise-induced activation of both AVP and CRH neurons in the hypothalamus was also confirmed. Conclusion: These results lead us to hypothesize that AVP and CRH are cooperatively involved in exercise-induced ACTH response just above the LT. This may also reflect the stress response with moderate-intensity exercise in humans.

This study seeks to clarify the current situation and associated factors regarding Work Engagement (WE) among midwives working in advanced care facilities, which bear the brunt of care for high-risk pregnancies, as well as the contribution of WE to quality of care. A self-administered questionnaire survey was conducted in 2016 with the participation of 503 midwives working in 36 general perinatal maternal and child medical centers and with 125 nurses working at a university hospital selected for analysis as a comparison group. The survey used the Utrecht Work Engagement Scale and the Brief Job Stress Questionnaire, subjecting all results to multiple regression analysis to adjust the sample size. Results revealed that WE among midwives was not found to be significantly different from that among nurses. WE among midwives was found to be positively associated with the "presence of a role model" and "doctor support". In addition, WE as well as "career opportunities" and the "presence of a role model" were associated with quality of care (adjusted R 2 =0.137, P < 0.05). From the study, WE among midwives working at advanced perinatal care facilities was not found to be different from that among nurses working at university hospitals. Among factors contributing to higher WE, the presence of a role model and relationships of trust with physicians were found to be those that represented the occupational characteristics of midwifery.

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