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.

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.

Physical Fitness of Police Academy Cadets: Baseline Characteristics and Changes During a 16-Week Academy.

Police academies traditionally emphasize the importance of being physically fit. The purpose of this research was to determine cadet baseline physical fitness characteristics and assess effectiveness of a 16-week training program. Sixty-eight cadets (61 men, 7 women) volunteered to have baseline physical fitness characteristics assessed, and 55 cadets (49 men, 6 women) completed further testing at weeks 8 and 16. The testing comprised hand grip (strength), arm crank (upper-body power), 30 seconds Wingate (lower body power), sum of skinfolds and percentage body fat (body composition), 40-yard dash (sprint speed), 1 repetition maximum bench press (strength), T-test (agility), and sit-and-reach (flexibility). In addition, cadets completed standardized state testing (push-ups, sit-ups, vertical jump, and half-mile shuttle run). The training program consisted of 1 hour sessions, 3 d·wk, including aerobic, plyometrics, body weight, and resistance exercise. Significant changes were found in agility (p < 0.01), upper-body and lower-body peak power (p ≤ 0.05), sit-ups (p < 0.01), push-ups (p ≤ 0.05) across the first 8 weeks, and in agility (p ≤ 0.05), lower-body peak power (p ≤ 0.05), sit-ups (p < 0.01), push-ups (p ≤ 0.05), half-mile shuttle run (p < 0.01) across the full 16 weeks. However, none of the variables showed significant change across the second half of the program (weeks 8-16). A number of individual parameters of physical fitness showed evidence of improvement in the first 8 weeks, whereas none of the variables showed significant improvement in the second 8 weeks. This suggests modifications could be made to increase overall effectiveness of cadet physical training specifically after the 8-week mark.

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.

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.

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.

A comparison of injuries, limited-duty days, and injury risk factors in infantry, artillery, construction engineers, and special forces soldiers.

OBJECTIVES: We compared injuries/risk factors in infantry soldiers (I), construction engineers (CE), combat artillery (CA), and Special Forces (SF) during their operational and fitness activities. METHODS: Anthropometrics, ethnicity, and fitness data were collected before review of medical records. RESULTS: Injury rates for I, CE, and CA were 4.0, 7.2, and 5.5 injuries/100 soldier-months, respectively; over 70% of them resulted from overuse. SF soldiers had an injury rate of 3.5 injuries/100 soldier-months, 50% of them reported as traumatic. Average limited-duty days (LDDs) were threefold higher in SF. Smoking, BMI > or =25, and APFT run time for 3.2 km >14 minutes were risk factors in I. Caucasian ethnicity, height <170.2 cm, weight > or =90 kg, and BMI > or =25 were risk factors in CE and CA. Age >27 years old was a risk factor in SF. CONCLUSIONS: Greater emphasis should be placed on risk factor identification and testing strategies to reduce injuries among SF and other troops.

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.

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.

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.

Intertester reliability of brachial artery flow-mediated vasodilation using upper and lower arm occlusion in healthy subjects.

The assessment of endothelial function as brachial artery flow-mediated vasodilatation is a widely used technique that determines the effect of risk factor intervention and may have the potential to predict the clinical benefit of antiatherogenic therapy. Previous studies suggest that flow-mediated dilation is greater using the upper-arm occlusion technique, but no data are available to compare intertester reliability between technicians. This study was undertaken to compare the amount of hyperemia between upper and lower occlusion techniques and to determine reproducibility between testers. Nineteen healthy adults, ages 25 to 50, were included in the study. Brachial artery vasodilatation was measured 1 and 3 minutes post cuff deflation and was compared with the baseline and expressed as a percent change. There was a tester effect in the percent change in diameter across all measurements. The results of this study reveal inconsistencies between testers when using a blood pressure cuff to induce hyperemia for the assessment of endothelial function through brachial artery flow-mediated vasodilation. However, upper arm as compared to lower arm blood pressure cuff occlusion results in significantly greater hyperemia and vasodilatation, even though there was a difference in measurements between testers.

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.

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.

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.

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

Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury. However, although the body of evidence supporting EICA and EICM is growing, the molecular mechanisms of EICA and EICM and their possible roles in cardioprotection against an I/R injury are poorly understood. Here, we introduce the general mechanisms of autophagy in an attempt to integrate potential molecular pathways of EICA and EICM and also highlight a potential insight into EICA and EICM in cardioprotection against an I/R insult.

The acute effect of aerobic exercise on brachial artery endothelial function in renal transplant recipients.

This study compared the effect of a 30-minute walk on brachial artery endothelial vasodilatation in kidney transplant (KT) recipients and healthy controls (HCs). Endothelial-dependent vasodilatation was measured by ultrasound before and after exercise. The HCs experienced a significant increase in vasodilatation after exercise 1 minute postocclusion when compared with the KT recipients (22%+/-13% vs 3%+/-4%; P<.05). Also, the HCs had a significantly higher vasodilatation from pre-treadmill walk to post-treadmill walk (1 minute postocclusion) when compared with KT recipients (from 3%+/-6% to 22%+/-13% vs 1%+/-3% to 3%+/-4%; P<.05). This acute vasodilatory response observed in the HCs may be related to the immediate release of nitric oxide and the combined response to shear stress and exercise. The KT recipients had several coronary artery disease risk factors that may have adversely affected endothelial function.

Cardiac Kinetophagy Coincides with Activation of Anabolic Signaling.

PURPOSE: Growing evidence has shown that endurance exercise is a strong inducer of autophagy in various tissues. Thus, we define here endurance exercise-induced autophagy as "kinetophagy" derived from the Greek terms "kineto" (movement), "auto" (self), and "phagy" (eating). Currently, the exact cellular mechanisms responsible for kinetophagy remain unclear; hence, we examined kinetophagy signaling transduction pathways occurring during acute endurance exercise (AEE). METHODS: C57BL/6 mice were randomly assigned to either AEE (n = 7) or control sedentary group (CON, n = 7). After 5 d of treadmill running acclimation, mice performed 60 min of a single bout of treadmill running at 12 m · min(-1) on a 0% grade. Hearts were excised immediately 1 h after exercise and homogenized for Western blot analyses. RESULTS: Our data showed that AEE promoted kinetophagy flux (an increase in LC3-II to LC3-I ratio and LC3-II levels and a reduction in p62 levels) with Beclin-1 levels suppressed but Atg7 levels elevated compared with those in the sedentary group. We also observed that AEE increased lysosome-associated membrane protein and cathepsin L, linked to the termination process of autophagy, and that AEE augmented potent autophagy inducers (i.e., adenosine monophosphate kinase phosphorylation, BNIP3, and HSP70). Moreover, we found that exercise-mediated BNIP3 upregulation is associated with hypoxia-inducing factor 1α rather than FoxO3a. Intriguingly, we found for the first time that kinetophagy parallels with anabolic signaling activation (Akt and mammalian target of rapamycin). CONCLUSIONS: Our findings provide evidence that AEE results in kinetophagy without a time-associated elevation in Beclin-1 but with the presence of Akt-mTOR activation and that AEE-induced activation of anabolic signaling is not associated with kinetophagy promotion.

Associations Between Functional Movement Screening, the Y Balance Test, and Injuries in Coast Guard Training.

Tests that have the ability to predict injuries in various military and athletic populations are important because of the role they could play in primary prevention. Functional Movement Screen (FMS) and Y Balance Tests (YBT) may provide this prognostic ability. This study examined the association between injuries and age, physical characteristics, FMS, and upper and lower body YBTs among Coast Guard Maritime Security Response Team (MSRT) candidates. Thirty-one male Coast Guard Maritime Security Response Team candidates were administered the 7 FMS tests and lower- and upper-body YBTs before their intense 2-month training course. Age, height, weight, and body mass index were also obtained. Physical training-related injuries were recorded during the course. Injury incidence was 41%. Older age and lower scores on either FMS or the upper-body YBT were associated with higher injury risk. Performance of the lower-body YBT was not associated with injury risk. This is the first investigation showing that lower scores on the upper-body YBT were associated with higher injury risk and is in consonance with previous investigations demonstrating associations between lower FMS scores and higher injury risk. Certain limitations need to be addressed. Future studies should determine if FMS and the YBTs have prognostic ability in other populations.

Effects of long-term resistance exercise training on autophagy in rat skeletal muscle of chloroquine-induced sporadic inclusion body myositis.

PURPOSE: We examined whether resistance exercise training restores impaired autophagy functions caused by Chloroquine (CQ)-induced Sporadic Inclusion Body Myositis (sIBM) in rat skeletal muscle. METHODS: Male wistar rats were randomly assigned into three groups: Sham (n = 6), CQ (n = 6), and CQ + Exercise (CE, n = 6). To create a rat model of sIBM, rats in the CQ and CE group were intraperitoneally injected with CQ 5 days a week for 16 weeks. Rats in the CE group performed resistance exercise training 3 times a week for 8 weeks in conjunction with CQ starting from week 9 to week 16. During the training period, maximal carrying load, body weight, muscle weight, and relative muscle weight were measured. Autophagy responses were examined by measuring specific markers. RESULTS: While maximal carrying capacity for resistance exercise training was dramatically increased in the CE group, no significant changes occurred in the skeletal muscle weight as well as in the relative muscle weight of CE compared to the other groups. CQ treatment caused significant increases in the levels of Beclin-1 and p62, and decreases in the levels of LAMP-2 proteins. Interestingly, no significant differences in the LC3-II/I ratio or the LC3-II protein levels were observed. Although CQ-treatment groups suppressed the levels of the potent autophagy inducer, BNIP3, p62 levels were decreased in only the CE group. CONCLUSION: Our findings demonstrate that sIBM induced by CQ treatment results in muscle degeneration via impaired autophagy and that resistance exercise training improves movable loading activity. Finally, regular exercise training may provide protection against sIBM by enhancing the autophagy flux through p62 protein.