Contactless exercise intervention in prenatal and postnatal period during COVID-19 lowers the risk of postpartum depression.

The COVID-19 pandemic has had a substantial adverse impact on the physical and mental health of pregnant and postpartum women, thereby increasing the risk of postpartum depression (PPD). This study aimed to evaluate the effectiveness of a continuous contactless exercise intervention in reducing the risk of depression during the prenatal and postnatal periods. The study utilized an interactive contactless exercise program consisting of Pilates movement over a 16-week period, with 8 weeks during pregnancy and 8 weeks after childbirth. Metabolic and psychological factors related to postpartum depression, including pain, stress, and stress-response markers, were analyzed. The results showed that the exercise intervention significantly alleviated postpartum depression by improving pain (Oswestry Disability Index: Non-exercise, 11.4 ± 14.8 versus Exercise, - 63.1 ± 18.4, p < .001) and stress factors (Edinburgh Postnatal Depression Scale: Non-exercise, 8.8 ± 8.72 versus Exercise, - 37.6 ± 9.13, p < .001; Perceived Stress Scale: Non-exercise, 9.21 ± 9.35 versus Exercise, - 20.7 ± 14.4, p < .001) caused by physical/structural imbalances in postpartum women. Additionally, the intervention improved the metabolic imbalances commonly observed after childbirth, including reductions in triglyceride (Interaction effect, p = .017), insulin (Interaction effect, p = .032), and cortisol levels (Interaction effect, p < .001), which are recognized risk factors for postpartum depression. Taken together, these findings suggest that contactless online exercise interventions can mitigate postpartum depression by addressing metabolic dysregulation that frequently occurs after delivery, especially in situations of social isolation caused by the pandemic.

Effects of Low-Load, High-Repetition Resistance Training on Maximum Muscle Strength and Muscle Damage in Elite Weightlifters: A Preliminary Study.

This study aimed to assess the impact of different resistance training (RT) loads and repetition on muscle damage, intramuscular anabolic signaling, and maximal muscle strength (MMS) in weightlifters. Eighteen male weightlifters were randomly assigned to 8 weeks of supervised RT regimes: high-load, low-repetition (HL), low-load, high-repetition (LH), and combination of HL and LH (COMBI). All groups exhibited a significant increase in skeletal muscle mass (SMM) and growth hormone levels, which ultimately contributed to improvement in MMS as indicated by 1-repetition maximum in the back squat and back muscle strength. Notably, while there were no significant changes in the mTOR protein, the phosphorylation of phosphorylation of p70 ribosomal protein S6 kinase 1 (p70S6K1), eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), and eukaryotic elongation factor 2 (eEF2), which are involved in muscle cell growth, was significantly affected by the different training regimens. More importantly, LH-RT led to a significant reduction in muscle damage markers, creatine kinase (CK) and lactate dehydrogenase (LDH), suggesting reduced recovery time and fatigue. Our results demonstrated that the LH-RT paradigm could be a viable alternative for weightlifters to enhance MMS and muscle hypertrophy similar to HL-RT, while reducing RT-induced muscle damage, ultimately contributing to the enhancement of exercise performance.

Exercise as an antidepressant: exploring its therapeutic potential.

The COVID-19 pandemic has increased the prevalence of depressive disorders worldwide, requiring alternative treatments beyond medication and psychotherapy. Exercise has positive effects on the brain; therefore, it has emerged as a promising therapeutic option for individuals with depression. Considerable research involving humans and animals offers compelling evidence to support the mental health benefits of physical activity or exercise mediated by the regulation of complex theoretical paradigms. However, challenges such as conducting long-term follow-up assessments and considering individual characteristics remain in human studies despite extensive efforts. While animal studies provide valuable insights into the potential benefits of exercise and its impact on outcomes related to depression and anxiety in rodents exposed to different stress paradigms, translating the findings to humans requires careful evaluation. More research is needed to establish precise exercise prescription guidelines and to better understand the complex relationship between exercise and depressive disorders. Therefore, this concise review explores the evidence supporting exercise intervention as an antidepressant treatment and its underlying mechanisms.

Exercise Reverses Amyloid ß-Peptide-Mediated Cognitive Deficits in Alzheimer's Disease Mice Expressing Mutant Presenilin-2.

PURPOSE: The molecular mechanisms by which physical exercise produces beneficial effects on pathologic features and behavioral symptoms of Alzheimer's disease (AD) are not well understood. Herein, we examined whether regular moderate exercise could improve cognitive function and produce transcriptomic responses in the brain. METHODS: Four groups of mice were studied: nontransgenic control, mice expressing the human presenilin-2 wild type, mice expressing the human presenilin-2 with the N141I mutation (Tg-PS2m), and Tg-PS2m that were subjected to treadmill exercise (TE) at a speed of 10 m·min-1 for 50 min·d-1, 5 d·wk-1, for 6 wk (Tg-PS2m/Ex). RESULTS: Tg-PS2m/Ex mice exhibited increased preference in exploring a novel object than Tg-PS2m in the novel object recognition test, whereas differences observed in the water maze test and passive avoidance test were not significant. Western blot and histological analyses using amyloid oligomer (A11) and ß-amyloid (6E10) antibody indicated that amyloid oligomer-reactive bands and plaque deposition in the hippocampus were reduced, although not significantly, after TE. Transcriptomic (RNA-sequencing) analysis and subsequent protein analysis revealed that the cell cycle regulatory gene, Cdc28 protein kinase regulatory subunit 2 (Cks2), was decreased, and the cell cycle- and apoptotic cell death-related factors, including cyclin D1, proliferating cell nuclear antigen, and cleaved caspase-3, were increased in the hippocampus of Tg-PS2m, whereas TE reversed their altered expression. CONCLUSIONS: The results support the hypothesis that the pathologic features and behavioral symptoms of AD caused by accumulation of amyloid ß-peptide in hippocampus, causing aberrant cell cycle reentry and apoptosis, can be reversed by regular exercise.

Comparison of intrinsic exercise capacity and response to acute exercise in ICR (Institute of Cancer Research) mice derived from three different lineages.

BACKGROUND: As a laboratory animal resource, the ICR mouse is commonly used in a variety of research fields. However, information on differences in exercise-related characteristics in ICR mice derived from different lineages and the underlying mechanisms remains to be elucidated. In this study, we investigated the intrinsic exercise capacity and a magnitude of response to acute exercise, and sought to identify mechanisms contributing to difference in Korl:ICR (a novel ICR lineage recently established by the National Institute of Food and Drug Safety Evaluation, Korea) and two commercialized ICR lineages derived from different origins (viz., A:ICR mouse from Orient Bio Com, the United States, and B:ICR mouse from Japan SLC Inc., Japan). RESULTS: Results showed that despite no significant difference in body weight and weight-proportioned tissue mass of heart and skeletal muscles among groups, the relatively low intrinsic exercise capacity and exaggerated response to acute exercise were identified in B:ICR comparted with Korl:ICR and A:ICR, as reflected by total work and lactate threshold (LT). Also, the mitochondrial efficiency expressed as the complex 1 and complex 1 + 2 respiratory control ratio (RCR) values for cardiac mitochondrial O2 consumption in B:ICR was significantly lower than that in Korl:ICR with higher level of state 2 respiration by glutamate/malate and UCP3 expression in cardiac muscle. CONCLUSIONS: Taken together, these results indicate that the intrinsic exercise capacity of ICR mouse varies according to lineages, suggesting the role of cardiac mitochondrial coupling efficiency as a possible mechanism that might contribute to differences in the intrinsic exercise capacity and magnitude of response to exercise.

Benefits of Exercise and Astaxanthin Supplementation: Are There Additive or Synergistic Effects?

A healthy lifestyle is essential for maintaining physical and mental health. Health promotion, with a particular emphasis on regular exercise and a healthy diet, is one of the emerging trends in healthcare. However, the way in which exercise training and nutrients from dietary intake interact with each other to promote additive, synergistic, or antagonistic effects on physiological functions leading to health promotion, and the possible underlying biomolecular mechanisms of such interactions, remain poorly understood. A healthy diet is characterized by a high intake of various bioactive compounds usually found in natural, organic, and fresh foodstuffs. Among these bioactive compounds, astaxanthin (ASX), a red carotenoid pigment especially found in seafood, has been recognized in the scientific literature as a potential nutraceutical due to its antioxidant, anti-inflammatory, and neurotrophic properties. Therefore, scientists are currently exploring whether this promising nutrient can increase the well-known benefits of exercise on health and disease prevention. Hence, the present review aimed to compile and summarize the current scientific evidence for ASX supplementation in association with exercise regimes, and evaluate the additive or synergistic effects on physiological functions and health when both interventions are combined. The new insights into the combination paradigm of exercise and nutritional supplementation raise awareness of the importance of integrative studies, particularly for future research directions in the field of health and sports nutrition science.

Treadmill Exercise Alleviates Brain Iron Dyshomeostasis Accelerating Neuronal Amyloid-ß Production, Neuronal Cell Death, and Cognitive Impairment in Transgenic Mice Model of Alzheimer's Disease.

Brain iron increases with age and abnormal brain iron metabolism is proving increasingly likely to be involved in the pathology of Alzheimer's disease (AD). The iron-regulatory effect of furin, a ubiquitously expressed proconvertase, might play an important role in AD. Therefore, there is an urgent need to study the effect of furin on iron regulation in AD. For that purpose, we aimed to determine the role of physical exercise in AD associated with brain iron dyshomeostasis. Treadmill exercise attenuated the AD-related abnormal brain iron regulation by furin in vivo, as demonstrated via experiments in aged APP-C105 mice. Next, we examined whether treadmill exercise decreases excessive iron, directly affecting amyloid-ß (Aß) production through the regulation of α-secretase-dependent processing of amyloid protein precursor (APP) involved in the modulation of furin activity. We first observed that cognitive decline and Aß-induced neuronal cell death were induced by disruption of APP processing via excess iron-induced disruption of furin activity in aged APP-C105 mice. The induced cognitive decline and cell death were attenuated by treadmill exercise. This result suggests that treadmill exercise alleviated cognitive decline and Aß-induced neuronal cell death by promoting α-secretase-dependent processing of APP through low iron-induced enhancement of furin activity. This is concomitant with decreasing levels of lipid peroxidation products and promoting antioxidant defense enzyme capacities. Therefore, iron-targeted therapeutic strategies involving treadmill exercise might be useful for patients with AD.

Comparative analysis of restraint stress-induced depressive-like phenotypes in C57BL/6N mice derived from three different sources.

C57BL/6NKorl mice are a novel mouse stock recently developed by the National Institute of Food and Drug Safety Evaluation in Korea. Extensive research into the nature of C57BL/6NKorl mice is being conducted. However, there is no scientific evidence for the phenotypic response to restraint stress (RST), a stress paradigm for modeling depressive disorders, in rodents. In this study, we investigated the repeated RST-induced depressive-like phenotypes in C57BL/6 N mouse substrains (viz., C57BL/6NKorl mice from Korea, C57BL/6NA mice from the United States, and C57BL/6NB mice from Japan) obtained from different sources. The results showed that C57BL/6 N mice derived from various sources exposed to repeated RST resulted in depressive-like phenotypes reflected by a similar degree of behavioral modification and susceptibility to oxidative stress in a duration-dependent manner, except for the distinctive features (increased body weight (BW) and tolerance to the suppression of BW gain by exposure to repeated RST) in C57BL/6NKorl mice. Taken together, the duration-dependent alteration in depressive-like phenotypes by repeated exposure to RST observed in this study may provide valuable insights into the nature of C57BL/6NKorl mice as an alternative animal resource for better understanding of the etiology of depressive disorders and the mechanisms of antidepressant actions.

Comparative analysis of dose-dependent neurotoxic response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in C57BL/6 N mice derived from three different sources.

MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is commonly used to induce nigrostriatal defects to induce parkinsonism and/or parkinsonian syndrome, to replicate the lesions seen in Parkinson's disease (PD), with use in numerous PD models in mice. It has been suggested that various biological characteristics including strain could result in differing mortality rates, sensitivity to MPTP administration, and reproducibility of lesions in mice, but there is no evidence on the sensitivity of C57BL/6 mice from different origins to MPTP and its associated pathological lesions. In this study, we investigated the magnitude of the dose-dependent response to acute MPTP administration in C57BL/6NKorl mice and two commercialized C57BL/6 stocks derived from the United States and Japan. We measured biological features (body weight, temperature, and composition), nigrostriatal neurotoxic responses (dopamine levels, tyrosine hydroxylase enzymes, and protein carbonylation) and motor function. In results, the three different C57BL/6 stocks exhibited similar overall neurotoxic response and locomotor impairment which increased in a dose-dependent manner with acute MPTP administration (10 mg/kg, 20 mg/kg, and 30 mg/kg, all with external heat support), although some of these differences were not significant. In conclusion, this study provides scientific evidence that C57BL/6NKorl mice can be used as an alternative animal model for practical and targeted PD research.

Association of exercise-induced autophagy upregulation and apoptosis suppression with neuroprotection against pharmacologically induced Parkinson's disease.

PURPOSE: We investigated whether treadmill exercise (TE)-induced neuroprotection was associated with enhanced autophagy and reduced apoptosis in a mouse model of pharmacologically induced Parkinson's disease (PD). METHODS: PD was induced via the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 male mice were randomly assigned to the following three groups: control (C57BL, n=10), MPTP with probenecid (MPTP/C, n=10), and MPTP/ C plus exercise (MPTP-TE, n=10). The MPTP-TE mice performed TE training (10 m/min, 60 min/day, 5 days/week) for 8 weeks. The rotarod test was used to assess motor function. RESULTS: TE restored MPTP/P-induced motor dysfunctionand increased tyrosine hydroxylase levels. Furthermore, TE diminished the levels of α-synuclein (α-syn), a neurotoxin; modulated the levels of autophagy-associated proteins, including microtubule-associated protein 1 light chain 3-II, p62, BECLIN1, BNIP3, and lysosomal-associated membrane protein-2, which enhanced autophagy; inhibited the activation of proapoptotic proteins (caspase-3 and BAX);and upregulated BCL-2, an antiapoptosis protein. CONCLUSION: Taken together, these results suggested that the TE-induced neuroprotection against MPTP-induced cell death was associated with enhanced autophagy and neuronal regeneration based on the findings of inhibited proapoptotic events in the brains of the TE-trained animals.

Neuroprotective effect of treadmill exercise possibly via regulation of lysosomal degradation molecules in mice with pharmacologically induced Parkinson's disease.

Dysfunction of mitophagy, which is a selective degradation of defective mitochondria for quality control, is known to be implicated in the pathogenesis of Parkinson's disease (PD). However, how treadmill exercise (TE) regulates mitophagy-related molecules in PD remains to be elucidated. Therefore, we aimed to investigate how TE regulates α-synuclein (α-syn)-induced neurotoxicity and mitophagy-related molecules in the nigro-striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mice. Our data showed that TE exhibited a significant restoration of tyrosine hydroxylase and motor coordination with suppression of α-syn expression, hallmarks of PD, possibly via up-regulation of lysosomal degradation molecules, LAMP-2 and cathepsin L, with down-regulation of p62, LC3-II/LC3-I ratio, PINK1 and parkin in the substantia nigra of MPTP mice. Therefore, these results suggest that treadmill exercise can be used as a non-invasive intervention to improve the pathological features and maintain a healthier mitochondrial network through appropriate elimination of defective mitochondria in PD.

Comparative analysis of basal locomotor activity-related metabolic phenotypes between C57BL/6 mice and ICR mice substrains derived from three different sources.

Animal model, as an indispensable tool for scientific purposes of biomedical researches and clinical application, is a commonly used in various researches. Regarding to this, it is necessary to establish the metabolic phenotype of animal model to minimize spurious interpretations and ensure a level of accuracy and reliability adequate for experimental research. However, the metabolic phenotype-related analysis within rodent strains derived from different source is nonexistent, especially in C57BL/6Korl mice and Korl:ICR mice (a domestic mouse strain). To compare the physiological and metabolic phenotypes over a period of time, we utilized the C57BL/6 mice (C57BL/6Korl, A:C57BL/6, and B:C57BL/6) and ICR mice (Korl:ICR, A:ICR, and B:ICR) derived from three different sources. Our data showed that average body weight, body temperature, food intake, and water consumption have a similar tendency among the C57BL/6 and ICR groups, except for the higher body weight of C57BL/6Korl mice over a period of time. Moreover, some significant differences was observed in adipose tissue mass and adipocyte size among the groups, with a higher tendency of C57BL/6Korl mice and Korl:ICR mice. Most importantly, resting metabolic rate (RMR) serves as an approximation of the metabolic phenotype showed no significant difference among the groups of C57BL/6 mice and ICR mice, except for the lower oxygen uptake of C57BL/6Korl mice compare to the A:C57BL/6 mice. Taken together, our data suggest that C57BL/6 mice and ICR mice derived from three different sources have an overall similar feature of physiological and metabolic phenotypes.