TY - JOUR A1 - Scharhag, Jürgen A1 - Knebel, F. A1 - Mayer, Frank A1 - Kindermann, Wilfried T1 - Does marathon running damage the heart? - an update JF - Deutsche Zeitschrift für Sportmedizin : offizielles Organ der Deutschen Gesellschaft für Sportmedizin und Prävention (Deutscher Sportärztebund) e.V. (DGSP) und Weiterbildungsorgan der Österreichischen Gesellschaft für Sportmedizin und Prävention N2 - Since the legend of the ancient Marathon run, the risk of endurance exercise-induced cardiovascular damage or sudden cardiac death is discussed. In recent studies, the exercise-induced increases in cardiac biomarkers in endurance athletes as well as acute alterations in cardiac function and cardiovascular abnormalities have been reported. As elevations of the cardiac biomarkers troponin and BM) have been observed frequently for the vast majority of athletes after Marathon runs or strenuous exercise bouts followed by a decrease within a short period, a physiological reaction rather than a pathologicial cause is presumed. Also a transient decrease of cardiac function demonstrated by newer echocardiographic techniques (tissue Doppler or speckle tracking imaging, 3D echocardiography) after strenuous exercise often termed "cardiac fatigue" should not be considered necessarily as pathologic, as cardiac function also depends on hemodynamic load and heart rate. Furthermore, exercise-induced changes in cardiac function did not correlate with exercise-induced increases in cardiac biomarkers in most studies. The functional cardiac alterations can also be detected by magnetic resonance imaging (MRI) after Marathon runs. However, no signs of acute or chronic myocardial damage have been demonstrated in MRI studies in cardiovascular healthy athletes after running a Marathon, although especially in older athletes undetected cardiovascular diseases such as coronary artery disease or myocardial necrosis or fibrosis can be present. hi conclusion, according to recent studies. there seems to be a lack of evidence to support endurance exercise-induced cardiac damage in the healthy heart which is adapted tostrenous exercise by regular endurance training. Nevertheless, as running a Marathon results in a high cardiac load, a sufficient endurance training period as well as a preparticipation or regular medical screening to exclude relevant congenital or aquired cardiovascular diseases is recommended from a sports cardiology perspective to exclude relevant congenital or acquired cardiovascular diseases KW - Marathon KW - cardiac biomarkers KW - endurance exercise KW - athlete's heart KW - cardiac fatigue Y1 - 2011 SN - 0344-5925 VL - 62 IS - 9 SP - 293 EP - 298 PB - WWF-Verl.-Ges. CY - Greven ER - TY - JOUR A1 - Heinzel, Stephan A1 - Rapp, Michael Armin A1 - Fydrich, Thomas A1 - Ströhle, Andreas A1 - Teran, Christina A1 - Kallies, Gunnar A1 - Schwefel, Melanie A1 - Heissel, Andreas T1 - Neurobiological mechanisms of exercise and psychotherapy in depression BT - the SPeED studyRationale, design, and methodological issues JF - Clinical Trials N2 - Background/Aims: Even though cognitive behavioral therapy has become a relatively effective treatment for major depressive disorder and cognitive behavioral therapy-related changes of dysfunctional neural activations were shown in recent studies, remission rates still remain at an insufficient level. Therefore, the implementation of effective augmentation strategies is needed. In recent meta-analyses, exercise therapy (especially endurance exercise) was reported to be an effective intervention in major depressive disorder. Despite these findings, underlying mechanisms of the antidepressant effect of exercise especially in combination with cognitive behavioral therapy have rarely been studied to date and an investigation of its neural underpinnings is lacking. A better understanding of the psychological and neural mechanisms of exercise and cognitive behavioral therapy would be important for developing optimal treatment strategies in depression. The SPeED study (Sport/Exercise Therapy and Psychotherapyevaluating treatment Effects in Depressive patients) is a randomized controlled trial to investigate underlying physiological, neurobiological, and psychological mechanisms of the augmentation of cognitive behavioral therapy with endurance exercise. It is investigated if a preceding endurance exercise program will enhance the effect of a subsequent cognitive behavioral therapy. Methods: This study will include 105 patients diagnosed with a mild or moderate depressive episode according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed.). The participants are randomized into one of three groups: a high-intensive or a low-intensive endurance exercise group or a waiting list control group. After the exercise program/waiting period, all patients receive an outpatient cognitive behavioral therapy treatment according to a standardized therapy manual. At four measurement points, major depressive disorder symptoms (Beck Depression Inventory, Hamilton Rating Scale for Depression), (neuro)biological measures (neural activations during working memory, monetary incentive delay task, and emotion regulation, as well as cortisol levels and brain-derived neurotrophic factor), neuropsychological test performance, and questionnaires (psychological needs, self-efficacy, and quality of life) are assessed. Results: In this article, we report the design of the SPeED study and refer to important methodological issues such as including both high- and low-intensity endurance exercise groups to allow the investigation of dose-response effects and physiological components of the therapy effects. Conclusion: The main aims of this research project are to study effects of endurance exercise and cognitive behavioral therapy on depressive symptoms and to investigate underlying physiological and neurobiological mechanisms of these effects. Results may provide important implications for the development of effective treatment strategies in major depressive disorder, specifically concerning the augmentation of cognitive behavioral therapy by endurance exercise. KW - Major depressive disorder KW - depression KW - psychotherapy KW - cognitive behavioral therapy KW - endurance exercise KW - training KW - functional magnetic resonance imaging KW - brain-derived neurotrophic factor KW - basic psychological needs KW - cortisol Y1 - 2017 U6 - https://doi.org/10.1177/1740774517729161 SN - 1740-7745 SN - 1740-7753 VL - 15 IS - 1 SP - 53 EP - 64 PB - Sage Publ. CY - London ER - TY - GEN A1 - Henkel, Janin A1 - Buchheim-Dieckow, Katja A1 - Castro, José Pedro A1 - Laeger, Thomas A1 - Wardelmann, Kristina A1 - Kleinridders, André A1 - Jöhrens, Korinna A1 - Püschel, Gerhard Paul T1 - Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 807 KW - NAFLD KW - NASH KW - endurance exercise KW - FGF21 KW - glucose intolerance KW - cholesterol KW - oxidative stress Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-442384 SN - 1866-8372 IS - 807 ER - TY - JOUR A1 - Henkel, Janin A1 - Buchheim-Dieckow, Katja A1 - Castro, José Pedro A1 - Laeger, Thomas A1 - Wardelmann, Kristina A1 - Kleinridders, André A1 - Jöhrens, Korinna A1 - Püschel, Gerhard Paul T1 - Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH JF - Nutrients N2 - Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production. KW - NAFLD KW - NASH KW - endurance exercise KW - FGF21 KW - glucose intolerance KW - cholesterol KW - oxidative stress Y1 - 2019 U6 - https://doi.org/10.3390/nu11112709 SN - 2072-6643 VL - 11 IS - 11 PB - MDPI CY - Basel ER -