Closed-Loop Reflex Responses of the Lateral Ankle Musculature From Various Thresholds During a Lateral Ankle Sprain Perturbation.

CONTEXT: Latency is a reliable temporal metric used to evaluate sensorimotor integration of the fibularis longus (FL) and fibularis brevis (FB) during lateral ankle sprain perturbations. Currently, no clinical recommendations exist to select appropriate thresholds to evaluate the closed-loop reflex response of the lateral ankle musculature. The purpose of this study was to assess threshold value on latency of the FL and FB during an unanticipated inversion perturbation that simulates the mechanism of a lateral ankle sprain. DESIGN: Descriptive laboratory study. METHODS: Twenty healthy adults with no history of lateral ankle sprain injury completed an unanticipated single-leg drop landing onto a 25° laterally inclined force platform from a height of 30 cm. Surface electromyography recorded muscle activity data from the FL and FB during the inversion perturbation. Latency was identified at points where muscle activity exceeded 2, 5, and 10 SD above the average muscle activity 200 milliseconds prior to foot contact, and compared across threshold value using a 1-way analysis of variance (P < .05). RESULTS: The 2 SD threshold was significantly shorter than both 5 SD and 10 SD thresholds for the FL (P < .01) and FB (P < .01). Likewise, the 5 SD threshold was significantly shorter than the 10 SD thresholds for FL (P = .004) and FB (P = .003). CONCLUSIONS: More sensitive thresholds results in a shorter closed-loop reflexive response compared to the more rigorous thresholds. We recommend that selection of the appropriate threshold to identify latency of the lateral ankle musculature should be based on the device used to simulate a lateral ankle sprain and the ankle inversion velocity produced during the ankle inversion perturbation.

Psychological and financial impact of the COVID-19 pandemic during the first stages of the pandemic: Brazilian orthodontists´ perspective.

INTRODUCTION: Brazil faced a catastrophic situation in the coronavirus pandemic. Due to the high risk of contamination and spread of COVID-19, dentist have been attending only urgency and emergency services in Brazil at the beginning of the pandemic. OBJECTIVE: This research aimed to evaluate the psychological and financial impacts caused by the coronavirus pandemic in Brazilian orthodontists. METHODS: This population-based cross-sectional study collected demographic data and mental health measurements from 404 orthodontists. Depression, anxiety, insomnia, and distress were evaluated through Brazilian versions of the 9-item Patient Health Questionnaire (9-PHQ), the 7-item Generalized Anxiety Disorder scale and Mini-Tracking (GAD), the 7-item Insomnia Severity Index (ISI), and the 22-item Impact of Event Scale-Revised (IES-R), respectively. The demographic data of the sample was described using descriptive statistics. The data was analyzed according to sex, professional status, and economic income. Comparisons were performed using Chi-square tests, Mann-Whitney U tests, and Kruskal-Wallis followed by post-hoc tests. RESULTS: Females, graduate students, and lower incomes subgroups showed higher levels of depression, anxiety, insomnia, and distress. Most orthodontists showed moderate to extreme financial and professional concerns during the pandemic. CONCLUSION: The coronavirus pandemic negatively affected the psychological health and increased the financial concerns of the Brazilian orthodontists, mainly female, graduate students, and with income below 10k participants.

Exercise-Induced Antisenescence and Autophagy Restoration Mitigate Metabolic Disorder-Induced Cardiac Disruption in Mice.

INTRODUCTION: Metabolic disorder promotes premature senescence and poses more severe cardiac dysfunction in females than males. Although endurance exercise (EXE) has been known to confer cardioprotection against metabolic diseases, whether EXE-induced cardioprotection is associated with mitigating senescence in females remains unknown. Thus, the aim of the present study was to examine metabolic disorder-induced cardiac anomalies (cellular senescence, metabolic signaling, and autophagy) using a mouse model of obese/type 2 diabetes induced by a high-fat/high-fructose (HFD/HF) diet. METHODS: Female C57BL/6 mice (10 wk old) were assigned to three groups ( n = 11/group): normal diet group (CON), HFD/HF group, and HFD/HF diet + endurance exercise (HFD/HF + EXE) group. Upon confirmation of hyperglycemia and overweight after 12 wk of HFD/HF diet, mice assigned to HFD/HF + EXE group started treadmill running exercise (60 min·d -1 , 5 d·wk -1 for 12 wk), with HFD/HF diet continued. RESULTS: EXE ameliorated HFD/HF-induced body weight gain and hyperglycemia, improved insulin signaling and glucose transporter 4 (GLUT4) levels, and counteracted cardiac disruption. EXE reversed HFD/HF-induced myocyte premature senescence (e.g., prevention of p53, p21, p16, and lipofuscin accumulation), resulting in suppression of a senescence-associated secretory phenotype such as inflammation (tumor necrosis factor α and interleukin-1ß) and oxidative stress (protein carbonylation). Moreover, EXE restored HFD/HF-induced autophagy flux deficiency, evidenced by increased LC3-II concomitant with p62 reduction and restoration of lysosome function-related proteins (LAMP2, CATHEPSIN L, TFEB, and SIRT1). More importantly, EXE retrieved HFD/HF-induced apoptosis arrest (e.g., increased cleaved CASPASE3, PARP, and TUNEL-positive cells). CONCLUSIONS: Our study demonstrated that EXE-induced antisenescence phenotypes, autophagy restoration, and promotion of propitiatory cell removal by apoptosis play a crucial role in cardiac protection against metabolic distress-induced cardiac disruption.

Vitamin D (VD3) Intensifies the Effects of Exercise and Prevents Alterations of Behavior, Brain Oxidative Stress, and Neuroinflammation, in Hemiparkinsonian Rats.

In the present study, we investigated the effects of physical exercise in the presence of Vitamin D3 (VD3), on 6-hydroxydopamine (6-OHDA)-lesioned hemiparkinsonian rats. The animals were divided into sham-operated (SO), 6-OHDA-lesioned, and 6-OHDA-lesioned plus VD3 (1 µg/kg, 21 days), in the absence (no exercise, NE) and presence (with exercise, WE) of physical exercise on a treadmill (30 min, speed of 20 cm/s, once a day/21 days). This procedure started, 24 h after the stereotaxic surgery (injections of 6-OHDA into the right striatum). The animals were then subjected to behavioral (rotarod, open field, and apomorphine tests) and their brain areas were dissected for neurochemical, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) determinations, and immunohistochemical studies for tyrosine hydroxylase (TH), dopamine transporter (DAT), and vitamin D receptor (VD3R). The effects on the brain oxidative stress: nitrite/nitrate, glutathione (GSH), and malondialdehyde (MDA) measurements were also evaluated. Behavioral changes of the 6-OHDA lesioned group were improved by exercise plus VD3. Similar results were observed in dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations increased by exercise and VD3, compared with SO groups. Additionally, tyrosine hydroxylase (TH) and dopamine transporter (DAT) immunoexpressions were decreased in the 6-OHDA-lesioned groups, with values normalized after exercise and VD3. The VD3 receptor immunoexpression decreased in the 6-OHDA (NE) group, and this was attenuated by exercise, especially after VD3. While 6-OHDA lesions increased, VD3 supplementation decreased the oxidative stress, which was intensified by exercise. VD3 showed neuroprotective properties that were intensified by physical exercise. These VD3 actions on hemiparkinsonian rats are possibly related to its antioxidant and anti-inflammatory effects.

Endurance exercise-mediated metabolic reshuffle attenuates high-caloric diet-induced non-alcoholic fatty liver disease.

INTRODUCTION AND AIM: Non-alcoholic fatty liver disease (NAFLD) is one of the most common diseases in the United States. Metabolic distress (obese diabetes) is the main causative element of NAFLD. While there is no cure for NAFLD, endurance exercise (EEx) has emerged as a therapeutic strategy against NAFLD. However, mechanisms of EXE-induced hepatic protection especially in female subjects remain unidentified. Thus, the aim of the study is to examine molecular mechanisms of EXE-induced hepatic protection against diet-induced NAFLD in female mice. MATERIAL AND METHODS: Nine-week-old female C57BL/6J mice were randomly divided into three groups: normal-diet control group (CON, n=11); high-fat diet/high-fructose group (HFD/HF, n=11); and HFD/HF+EEx group (HFD/HF+EEx, n=11). The mice assigned to HFD/HF and HFD/HF+EEx groups were fed with HFD/HF for 12 weeks, after which the mice assigned to the EEx group began treadmill exercise for 12 weeks, with HFD/HF continued. RESULTS: EEx attenuated hepatic steatosis, reduced de novo lipogenesis (reduction in ATP-Citrate- Lyase and diacylglycerol-O-acyltransferase 1), and enhanced mitochondrial biogenesis and fatty-acid activation (oxidative phosphorylation enzymes and Acyl-CoA synthetase1). Also, EEx prevented upregulation of gluconeogenic proteins (glyceraldehyde-3-phosphate dehydrogenase, glucose-6-phosphatase, and phosphoenolpyruvate-carboxykinase1), premature senescence (suppression of p53, p22, and p16, tumor-necrosis-factor-α, and interleukin-1ß, and oxidative stress), and autophagy deficiency. Furthermore, EXE reversed apoptosis arrest (cleaved cysteine-dependent-aspartate-directed protease3 and Poly-(ADP-ribose)-polymerase1). CONCLUSION: EEx-mediated reparations of metabolic and redox imbalance (utilization of pentose phosphate pathway), and autophagy deficiency caused by metabolic distress critically contribute to preventing/delaying severe progression of NAFLD. Also, EEx-induced anti-senescence and cell turnover are crucial protective mechanisms against NAFLD.

Effects of vitamin D (VD3) supplementation on the brain mitochondrial function of male rats, in the 6-OHDA-induced model of Parkinson's disease.

Mitochondria dysfunction is an important factor involved in PD pathogenesis. We reported neuroprotective actions of vitamin D (VD3) on a PD model, and now we investigated the VD3 effects on the brain mitochondrial function. We focused on oxygen consumption, respiratory control ratio (RCR), ADP/O ratio, mitochondria swelling, H2O2 production, and SOD activity. Additionally, immunohistochemistry assays for the dopamine system markers (TH and DAT) and mitochondrial markers (VDAC1 and Hsp60) were also carried out in the striata. Young adult male Wistar rats (250 g, 2.5 months age) were anesthetized and subjected to stereotaxic surgery and injection of saline (SO group) or 6-OHDA, into the right striatum. Brain mitochondria were isolated from the groups: sham-operated (SO), 6-OHDA, 6-OHDA pretreated with VD3 for 7, days before the 6-OHDA lesion (6-OHDA+VD3, pre-) or treated with VD3 for 14 days, after the 6-OHDA lesion (6-OHDA+VD3, post-). VD3 prevented decreases in oxygen consumption, RCR, and ADP/O ratio observed after 6-OHDA injury. Noteworthy, a very low (oxygen consumption and RCR) or no improvement (ADP/O) were observed in the 6-OHDA+VD3 post- group. VD3 also prevented the increased mitochondria swelling and H2O2 production and a decrease in SOD activity, respectively, in the 6-OHDA injured mitochondria. Also, VD3 supplementation protected the hemiparkinsonian brain from decreases in TH and DAT expressions and decreased the upregulation of mitochondrial markers, as VDAC 1 and Hsp60. In conclusion, VD3 showed neuroprotective actions on brain mitochondria injured by 6-OHDA and should stimulate translational studies focusing on its use as a therapeutic strategy for the treatment of neurodegenerative diseases as PD.

Nutrition in Cycling.

Cycling is predominantly an endurance sport in which fuel utilization for energy production relies on the availability and delivery of oxygen to exercising muscle. Nutrition and training interventions to improve endurance performance are continually evolving, but ultimately, prescription should aim to generate improvements in cycling power and velocity while prioritizing athlete health and well-being. The wide range of cycling events and the different environments in which events take place pose a variety of nutrition-related challenges for cyclists. This review addresses some of these challenges and highlights recent advancements in nutrition for cycling performance.

Psychological and financial impact of the COVID-19 pandemic during the first stages of the pandemic: Brazilian orthodontists´ perspective

ABSTRACT Introduction: Brazil faced a catastrophic situation in the coronavirus pandemic. Due to the high risk of contamination and spread of COVID-19, dentist have been attending only urgency and emergency services in Brazil at the beginning of the pandemic. Objective: This research aimed to evaluate the psychological and financial impacts caused by the coronavirus pandemic in Brazilian orthodontists. Methods: This population-based cross-sectional study collected demographic data and mental health measurements from 404 orthodontists. Depression, anxiety, insomnia, and distress were evaluated through Brazilian versions of the 9-item Patient Health Questionnaire (9-PHQ), the 7-item Generalized Anxiety Disorder scale and Mini-Tracking (GAD), the 7-item Insomnia Severity Index (ISI), and the 22-item Impact of Event Scale-Revised (IES-R), respectively. The demographic data of the sample was described using descriptive statistics. The data was analyzed according to sex, professional status, and economic income. Comparisons were performed using Chi-square tests, Mann-Whitney U tests, and Kruskal-Wallis followed by post-hoc tests. Results: Females, graduate students, and lower incomes subgroups showed higher levels of depression, anxiety, insomnia, and distress. Most orthodontists showed moderate to extreme financial and professional concerns during the pandemic. Conclusion: The coronavirus pandemic negatively affected the psychological health and increased the financial concerns of the Brazilian orthodontists, mainly female, graduate students, and with income below 10k participants.

RESUMO Introdução: O Brasil enfrentou uma situação catastrófica durante a pandemia do coronavírus. Devido ao alto risco de contaminação e disseminação do vírus da COVID-19, os cirurgiões-dentistas passaram a realizar apenas atendimentos de urgência ou emergência no início da pandemia. Objetivo: O presente estudo teve como objetivo avaliar o impacto financeiro e psicológico causado pela pandemia do coronavírus nos ortodontistas brasileiros. Métodos: Este estudo transversal de base populacional coletou os dados demográficos e o impacto da pandemia em 404 ortodontistas. Depressão, ansiedade, insônia e angústia foram avaliadas, respectivamente, por meio da versão em português do Questionário de Saúde do Paciente (PHQ-9), do módulo de transtorno de ansiedade generalizada (GAD) do Mini-Tracking (GAD/Mini-Tracking), do Índice de Severidade de Insônia (ISI) e o do Impact of Events Scale-Revised (IES-R). As características demográficas da amostra foram apresentadas por meio de estatística descritiva. Os dados foram analisados de acordo com o sexo, situação profissional e renda econômica. As comparações foram realizadas utilizando os testes de Qui-quadrado, Mann-Whitney U e Kruskal-Wallis, seguidos de testes post-hoc (p<0,05). Resultados: Mulheres, estudantes de pós-graduação e profissionais com menores rendas apresentaram níveis mais altos de depressão, ansiedade, insônia e angústia. A maioria dos ortodontistas mostrou preocupação financeira e profissional moderada a extrema durante a pandemia. Conclusão: A pandemia do coronavírus afetou negativamente a saúde psicológica dos ortodontistas brasileiros e aumentou as preocupações financeiras desses profissionais. As mulheres, os estudantes de pós-graduação e os participantes com renda mensal menor que R$10 mil foram os grupos mais afetados.

Three-dimensional pharyngeal airway space changes after bimaxillary advancement.

INTRODUCTION: The probability of improvement in the upper airway space (UAS) with orthognathic surgery should be considered during the surgical-orthodontic treatment decision, providing not only an esthetic, but also a functional benefit for the patient. OBJECTIVE: The purpose of this study was to evaluate the 3D changes in the upper airway space after maxillomandibular advancement surgery (MMA). METHODS: A retrospective analysis of 56 patients, 21 male and 35 female, with a mean age of 35.8 ± 10.7 years, who underwent MMA was performed. Pre- and postoperative cone-beam computed tomography scans (CBCT) were obtained for each patient, and the changes in the UAS were compared using Dolphin Imaging 11.7 software. Two parameters of the pharyngeal airway space (PAS) were measured: airway volume (AV) and minimum axial area (MAA). Paired t-test was used to compare the data between T0 and T1, at 5% significance level. RESULTS: There was a statistically significant increase in the UAS. Bimaxillary advancement surgery increased the AV and the MAA, on average, by 73.6 ± 74.75% and 113.5 ± 123.87%, respectively. CONCLUSION: MMA surgery tends to cause significant increase in the UAS; however, this increase is largely variable.

Three-dimensional pharyngeal airway space changes after bimaxillary advancement

ABSTRACT Introduction: The probability of improvement in the upper airway space (UAS) with orthognathic surgery should be considered during the surgical-orthodontic treatment decision, providing not only an esthetic, but also a functional benefit for the patient. Objective: The purpose of this study was to evaluate the 3D changes in the upper airway space after maxillomandibular advancement surgery (MMA). Methods: A retrospective analysis of 56 patients, 21 male and 35 female, with a mean age of 35.8 ± 10.7 years, who underwent MMA was performed. Pre- and postoperative cone-beam computed tomography scans (CBCT) were obtained for each patient, and the changes in the UAS were compared using Dolphin Imaging 11.7 software. Two parameters of the pharyngeal airway space (PAS) were measured: airway volume (AV) and minimum axial area (MAA). Paired t-test was used to compare the data between T0 and T1, at 5% significance level. Results: There was a statistically significant increase in the UAS. Bimaxillary advancement surgery increased the AV and the MAA, on average, by 73.6 ± 74.75% and 113.5 ± 123.87%, respectively. Conclusion: MMA surgery tends to cause significant increase in the UAS; however, this increase is largely variable.

RESUMO Introdução: A probabilidade de melhoria do espaço aéreo superior (EAS) com cirurgia ortognática deve ser considerada durante a decisão do tratamento ortodôntico-cirúrgico, proporcionando não somente um benefício estético, mas também funcional, para o paciente. Objetivo: O objetivo do presente estudo foi avaliar as alterações 3D no espaço das vias aéreas superiores após a cirurgia de avanço maxilomandibular (AMM). Métodos: Foi realizada uma análise retrospectiva de 56 pacientes, 21 homens e 35 mulheres, com média de idade de 35,8 ± 10,7 anos, submetidos a AMM. Foram obtidas tomografias computadorizadas de feixe cônico (TCFC) pré- e pós-operatórias para cada paciente, e as alterações no EAS foram comparadas usando o software Dolphin Imaging v. 11.7. Foram medidos dois parâmetros do espaço aéreo faríngeo (EAF): volume das vias aéreas (VVA) e área axial mínima (AAM). Foi utilizado o teste t pareado para comparar os dados entre T0 e T1, com nível de significância de 5%. Resultados: Houve um aumento estatisticamente significativo no EAS. A cirurgia de avanço bimaxilar aumentou o volume das vias aéreas (VVA) e a área axial mínima (AAM) em média 73,6 ± 74,75% e 113,5 ± 123,87%, respectivamente. Conclusão: A cirurgia de AMM tende a causar o aumento significativo do EAS; no entanto, esse aumento é altamente variável.

Vitamin D (VD3) antioxidative and anti-inflammatory activities: Peripheral and central effects.

Vitamin D (VD3, cholecalciferol), besides its role on bone calcium homeostasis, has also been shown to present anti-inflammatory actions. The objectives of the present work were to further extend these findings, focusing onVD3action mechanisms at the molecular level and onits central and peripheral effects. For that, VD3 antinociceptive and mainly anti-inflammatory activities were evaluated by acute models of nociception (formalin test) and inflammation (carrageenan-induced paw edema), in mice pretreated orally for 7 days with VD3 (0.5 and 1.0 mg/kg). Afterwards, the edematous paws were evaluated by immunohistochemical assays for TNF-alpha. In addition, brains from mice pretreated with VD3, at the same conditions, were harvested for iNOS andCOX-2 immunohistochemical (IHC) assays. The anti-inflammatory effect of VD3 on human neutrophil degranulation was evaluated by the release of myeloperoxidase (MPO) activity, as well as by the reactive oxygen species production. VD3 significantly reduced the licking time in the formalin test, at the second phase (inflammatory pain). VD3 also reduced the edema volume and the number of polymorphonuclear (PMN) cells, as well as the TNF-alpha expression in the edematous paws, compared with the control group. Furthermore, VD3 significantly decreased iNOS and COX-2 expressions in brain areas, such as hippocampus and prefrontal cortex, and inhibited the degranulation of activated neutrophils by the reduction of ROS production and MPO release. Based in these results, VD3 presents anti-inflammatory and antioxidative effects, manifested at peripheral and central sites as showed in the present work for the first time.

Endurance Exercise Attenuates Doxorubicin-induced Cardiotoxicity.

PURPOSE: Endurance exercise (EXE) preconditioning before DOX treatment confers cardioprotection; however, whether EXE postconditioning (i.e., EXE intervention after the completion of DOX treatment) is cardioprotective remains unknown. Thus, the aim of the present study was to investigate if EXE postconditioning provides cardioprotection by testing the hypothesis that EXE-autophagy upregulation and NADPH oxidase 2 (NOX2) downregulation would be linked to cardioprotection against DOX-induced cardiotoxicity. METHODS: C57BL/6 male mice were assigned into three groups: control (CON, n = 10), doxorubicin (DOX, n = 10), and doxorubicin + endurance exercise (DOX + EXE, n = 10). Animals assigned to DOX and DOX + EXE groups were intraperitoneally injected with DOX (5 mg·kg each week for 4 wk). Forty-eight hours after the last DOX treatment, the mice assigned to DOX + EXE performed EXE on a motorized treadmill at a speed of 13-15 m·min for 60 min·d for 4 wk. RESULTS: EXE prevented DOX-induced apoptosis and mitigated tissue damages. Although DOX did not modulate auto/mitophagy, EXE significantly enhanced its flux (increased LC3-II levels, reduced p62 levels, and increased autophagosomes with mitochondria) along with increased mitochondrial fission (DRP1) and reduced fusion markers (OPA1 and MFN2). Interestingly, EXE-induced autophagy against DOX occurred in the absence of alterations of autophagy inducer AMPK or autophagy inhibitor mTOR signaling. EXE prohibited DOX-induced oxidative damages by suppressing NOX2 levels but without modulating other key antioxidant enzymes including MnSOD, CuZnSOD, catalase, and GPX1/2. CONCLUSION: Our data provide novel findings that EXE-induced auto/mitophagy promotion and NOX2 downregulation are linked to cardioprotection against DOX-induced cardiotoxicity. Importantly, our study shows that EXE postconditioning intervention is effective and efficacious to prevent DOX-induced cardiac injuries.

Effects of Weighted Vest Loading During Daily Living Activities on Countermovement Jump and Sprint Performance.

PURPOSE: Wearing a weighted vest (WV) during daily living and training can enhance jump and sprint performance; however, studies examining the efficacy of this method in female populations is limited. This study examined the effect of wearing a WV during daily living and training on countermovement jump (CMJ), change-of-direction, and sprint performance. METHODS: Trained females were separated into intervention (n = 9) and control (n = 10) groups. The intervention group wore WVs of ∼8% body mass 4 days per week for 8 hours per day (32 h/wk total), and 3 training sessions per week for the first 3 weeks. Subsequently, 3 weeks of regular training without WV stimulus was completed. The control group received no intervention and continued normal training for 6 weeks. Average and best performance was assessed on the single CMJ, four continuous CMJ, t-test change-of-direction drill, and a 25-m sprint at baseline, week 3, and week 6. RESULTS: No significant interactions or group effects were found. However, significant time main effects revealed increases in average rate of force development during the CMJ from baseline to week 3 (P = .048) and week 6 (P = .013), whereas peak vertical ground reaction force increased during the four continuous CMJ from baseline to week 3 (P = .048) and week 6 (P = .025) for both groups. CONCLUSIONS: The lower relative WV load used in this study failed to elicit significant improvements in jump and sprint performance in comparison with routine training, or that which have been found in past investigations with elite male athletes completing high-intensity performance tasks with greater WV loads.

Endurance Exercise Prevents Metabolic Distress-induced Senescence in the Hippocampus.

PURPOSE: Metabolic disorder such as obesity and type 2 diabetes caused by excess caloric intake is associated with an increased risk of neurodegenerative diseases. Endurance exercise (EXE) has been suggested to exert neuroprotective effects against the metabolic distress. However, the exact underlying molecular mechanisms responsible for the exercise-induced neuroprotection have not been fully elucidated. In this study, we investigated whether EXE-induced neuroprotection is associated with cellular senescence, neuroinflammation, and oxidative stress using a mouse model of obesity induced by a high-fat/high-fructose diet. METHODS: C57BL/6 female mice (10 wk old) were randomly divided to three groups: normal chow diet group (CON, n = 11), high-fat diet/high-fructose (HFD/HF) group (n = 11), and high-fat diet/high-fructose + endurance exercise (HFD/HF + EXE) group (n = 11). HFD/HF + EXE mice performed treadmill running exercise for 60 min·d, 5 d·wk for 12 wk. RESULTS: Our data showed that EXE ameliorated HFD/HF-induced weight gain, fasting blood glucose levels, and visceral fat gain. More importantly, HFD/HF diet promoted cellular senescence, whereas EXE reversed it, evidenced by a reduction in the levels of p53, p21, p16, beta-galactosidase (SA-ß-gal), and lipofuscin. Furthermore, EXE prevented HFD/HF-induced neuroinflammation (e.g., tumor necrosis factor-α and interleukin-1ß) by inhibiting toll-like receptor 2 downstream signaling cascades (e.g., tumor necrosis factor receptor-associated factor 6, c-Jun N-terminal kinase, and c-Jun) in parallel with reduced reactive glial cells. This anti-inflammatory effect of EXE was associated with the reversion of HFD/HF-induced cellular oxidative stress. CONCLUSION: Our study provides novel evidence that EXE-induced antisenescence against metabolic distress in the hippocampus may be a key neuroprotective mechanism, preventing neuroinflammation and oxidative stress.

Association of health empowerment and handgrip strength with intention to participate in physical activity among community-dwelling older adults.

INTRODUCTION: Health empowerment is an individual's perceived control and competence related to health and health care. The projected increased growth of the older adult population calls for a health-related empowerment movement in health education that targets older adults. Using the theory of planned behavior, the purpose of this study was to investigate the association of health empowerment and handgrip strength with intention to participate in physical activity among older adults. METHODS: The Korean Health Empowerment Scale (K-HES) was used as a measure of health empowerment. Handgrip strength was used as a measure of muscle strength. Intention to participate in physical activity was measured using five items. Participants of this study included 103 community-dwelling older adults (Mage = 76.45 ±â€¯9.395; Male = 42, Female = 61). RESULTS: Statistical analyses revealed all participants were knowledgeable about the health benefits of exercise and most participated in regular physical activity (n = 84.5%). The majority had normal handgrip strength (n = 60.7%) and most indicated strong intentions to participate in regular physical activity (n = 85%). A stepwise multiple regression revealed health empowerment significantly and positively (F(1,101) = 30.511, p < .001, R2 = 0.232, R2Adjusted = 0.224) associated intention to participate in physical activity. Health empowerment explained 23.2% of the variance in intentions. There was no significant contribution of muscle strength on intention. DISCUSSION: Findings suggest overall health empowerment may be affected by a variety of subscales such as problem-solving, obtaining support, motivation, psychosocial coping, and decision making. CONCLUSION: Future research should explore potential associations between health empowerment and intention to participate in physical activity.

Anticipating ankle inversion perturbations during a single-leg drop landing alters ankle joint and impact kinetics.

Anticipatory responses to inversion perturbations can prevent an accurate assessment of lateral ankle sprain mechanics when using injury simulations. Despite recent evidence of the anticipatory motor control strategies utilized during inversion perturbations, kinetic compensations during anticipated inversion perturbations are currently unknown. The purpose of this investigation was to examine the influence of anticipation to an inversion perturbation during a single-leg drop landing on ankle joint and impact kinetics. Fifteen young adults with no lateral ankle sprain history completed unanticipated and anticipated single-leg drop landings onto a 25° laterally inclined platform from a height of 30 cm. One-dimensional statistical parametric mapping (SPM) was used to analyze net ankle moments and ground reaction forces (GRF) during the first 150 ms post-landing, while peak GRFs, time to peak GRF, peak and average loading rates were compared using a dependent samples t-test (p ≤ 0.05). Results from the SPM analysis revealed significantly greater plantar flexion moment from 58 to 83 ms post-landing (p = 0.004; d = 0.64-0.77), inversion moment from 89 to 91 ms post-landing (p = 0.050; d = 0.58-0.60), and medial GRF from 62 to 97 ms post-landing (p < 0.001; d = 1.00-2.39) during the unanticipated landing condition. Moreover, significantly greater peak plantarflexion (p < 0.001; d = 1.10) and peak inversion moment (p = 0.007; d = 0.94), as well as greater peak (p = 0.002; d = 1.03) and average (p = 0.042; d = 0.66) medial loading rates, were found during the unanticipated landing condition. Our findings suggest alterations to ankle joint and impact kinetics occur during a single-leg drop landing when inversion perturbations are anticipated. Researchers and practitioners using drop-landings onto a tilted surface to assess lateral ankle sprain injury risk should consider implementing protocols that mitigate anticipatory responses.

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats.

BACKGROUND: The deficiency in 1α, 25-dihydroxyvitamin D3 (VD3) seems to increase the risk for neurodegenerative pathologies, including Parkinson's disease (PD). The majority of its actions are mediated by the transcription factor, VD3 receptor (VD3R). METHODS: The neuroprotective effects of VD3 were investigated on a PD model. Male Wistar rats were divided into the following groups: sham-operated (SO), 6-OHDA-lesioned (non-treated), and 6-OHDA-lesioned and treated with VD3 (7 days before the lesion, pre-treatment or for 14 days after the 6-OHDA striatal lesion, post-treatment). Afterwards, the animals were subjected to behavioral tests and euthanized for striatal neurochemical and immunohistochemical assays. The data were analyzed by ANOVA and the Tukey test and considered significant for p < 0.05. RESULTS: We showed that pre- or post-treatments with VD3 reversed behavioral changes and improved the decreased DA contents of the 6-OHDA group. In addition, VD3 reduced the oxidative stress, increased (TH and DAT), and reduced (TNF-alpha) immunostainings in the lesioned striata. While significant decreases in VD3R immunoreactivity were observed after the 6-OHDA lesion, these changes were blocked after VD3 pre- or post-treatments. We showed that VD3 offers neuroprotection, decreasing behavioral changes, DA depletion, and oxidative stress. In addition, it reverses partially or completely TH, DAT, TNF-alpha, and VD3R decreases of immunoreactivities in the non-treated 6-OHDA group. CONCLUSIONS: Taken together, VD3 effects could result from its anti-inflammatory and antioxidant actions and from its actions on VD3R. These findings should stimulate translational research towards the VD3 potential for prevention or treatment of neurodegenerative diseases, as PD.

Modulation of mitochondrial phenotypes by endurance exercise contributes to neuroprotection against a MPTP-induced animal model of PD.

AIM: Endurance exercise (EE) has been reported to confer neuroprotection against Parkinson's disease (PD); however, underlying molecular mechanisms of the protection remain still unclear. Since mitochondrial impairment is commonly observed in the brain of PD patients and animals, this study investigated whether EE-induced neuroprotection is associated with mitochondrial phenotypes, using a mouse model of PD induced by intraperitoneal administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MAIN METHODS: SH-SY5Y cells were cultured with a neurotoxin MPP+ known to cause PD-like symptoms to examine if modifications of mitochondrial morphology are linked to etiology of PD. For in vivo experiments, C57BL/6 male mice were randomly assigned to four groups: control (CON, n = 12), endurance exercise (EXE, n = 12), MPTP (MPTP, n = 12) and MPTP plus endurance exercise (MPTP + EXE, n = 12). Mice assigned to endurance exercise performed treadmill running at 12 m/min for 60 min/day, 5 days/week for 6 weeks. KEY FINDINGS: SH-SY5Y cells exposed to a neurotoxin MPP+ exhibited mitochondrial fragmentation and diminished mitochondrial proteins, and cell death. Similarly, animals administered with MPTP displayed comparable impairments in the substantia nigra pars compacta (SNpc). In contrast, EE intervention restored motor function to control levels and reduced apoptosis. These propitious effects of EE were associated with mitochondrial phenotypic changes such as upregulated anti-apoptotic proteins (e.g., MCL-1 and BLC-2), reduced a pro-apoptotic protein (e.g., AIF), and improved mitochondrial biogenesis and fusion. SIGNIFICANCE: Our finding that EE-induced mitochondrial phenotypic changes that resist mitochondrial impairment and cell death against PD introduce potential insight into mitochondria as a new therapeutic target for PD.

Endurance Exercise Mediates Neuroprotection Against MPTP-mediated Parkinson's Disease via Enhanced Neurogenesis, Antioxidant Capacity, and Autophagy.

Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction. Growing evidence has demonstrated that endurance exercise (EE) confers neuroprotection against PD. However, the exact molecular mechanisms responsible for exercise-induced protection of dopaminergic neurons in PD remain unclear. Since oxidative stress plays a key role in the degenerative process of PD. We investigated whether EE-induced neuroprotection is associated with enhanced antioxidative capacity and autophagy, using a mouse model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration. C57BL/6 male mice were randomly assigned to four groups: control (CON, n = 12), exercise (EXE, n = 12), MPTP (MPTP, n = 12) and MPTP + exercise (MPTP + EXE, n = 12). Our data demonstrated that while MPTP treatment impaired motor function, EE restored MPTP-induced motor deficits. Our biochemical data showed that EE-induced neuroprotection occurs in combination with multiple synergic neuroprotective pathways: (1) increased neurogenesis shown by an increase in BrdU-positive neurons; (2) diminished loss of dopaminergic neurons evidenced by upregulated tyrosine hydroxylase (TH) and dopamine transporter (DAT) levels; (3) increased antioxidant capacity (e.g., CuZnSOD, CATALASE, GPX1/2, HO-1, DJ1 and PRXIII); and (4) enhanced autophagy (LC3 II, p62, BECLIN1, BNIP3, LAMP2, CATHEPSIN L and TFEB). Our study suggests that EE-induced multiple synergic protective pathways including enhanced neurogenesis, antioxidative capacity, and concordant autophagy promotion contribute to restoration of impaired dopaminergic neuronal function caused by PD. Thus, PD patients should be encouraged to actively participate in regular EE as a potent nonpharmacological therapeutic strategy against PD.

Correction to: Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection.

The article Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection, written by Youngil Lee.