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      Effects of Aerobic Exercise on Cortisol Stress Reactivity in Response to the Trier Social Stress Test in Inpatients with Major Depressive Disorders: A Randomized Controlled Trial

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          Abstract

          Physical activity is associated with a favourable (blunted) cortisol stress reactivity in healthy people. However, evidence from experimental study and with psychiatric patients is missing. This study examines whether exercise training impacts on cortisol stress reactivity in inpatients with major depressive disorder (MDD). These new insights are important because the stress reactivity of healthy people and patients with severe symptoms of depression might differ. Methods: The study was designed as a randomized controlled trial (trial registration number: NCT02679053). In total, 25 patients (13 women, 12 men, mean age: 38.1 ± 12.0 years) completed a laboratory stressor task before and after a six-week intervention period. Nine samples of salivary free cortisol were taken before and after the Trier social stress test (TSST). Fourteen participants took part in six weeks of aerobic exercise training, while 11 patients were allocated to the control condition. While the primary outcome of the study was depressive symptom severity, the focus of this paper is on one of the secondary outcomes (cortisol reactivity during the TSST). The impact of aerobic exercise training was examined with a repeated-measures analysis of variance. We also examined the association between change in depression and cortisol response via correlational analysis. Cortisol reactivity did not change from baseline to post-intervention, either in the intervention or the control group. Participation in six weeks of aerobic exercise training was not associated with participants’ cortisol reactivity. Moreover, depressive symptom change was not associated with change in cortisol response. Aerobic exercise training was not associated with patients’ stress reactivity in this study. Because many patients initially showed a relatively flat/blunted cortisol response curve, efforts might be needed to find out which treatments are most efficient to promote a normalization of HPA axis reactivity.

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          An Inventory for Measuring Depression

          A. Beck (1961)
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            Stress and the individual. Mechanisms leading to disease.

            This article presents a new formulation of the relationship between stress and the processes leading to disease. It emphasizes the hidden cost of chronic stress to the body over long time periods, which act as a predisposing factor for the effects of acute, stressful life events. It also presents a model showing how individual differences in the susceptibility to stress are tied to individual behavioral responses to environmental challenges that are coupled to physiologic and pathophysiologic responses. Published original articles from human and animal studies and selected reviews. Literature was surveyed using MEDLINE. Independent extraction and cross-referencing by us. Stress is frequently seen as a significant contributor to disease, and clinical evidence is mounting for specific effects of stress on immune and cardiovascular systems. Yet, until recently, aspects of stress that precipitate disease have been obscure. The concept of homeostasis has failed to help us understand the hidden toll of chronic stress on the body. Rather than maintaining constancy, the physiologic systems within the body fluctuate to meet demands from external forces, a state termed allostasis. In this article, we extend the concept of allostasis over the dimension of time and we define allostatic load as the cost of chronic exposure to fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful. This new formulation emphasizes the cascading relationships, beginning early in life, between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease. There are now empirical studies based on this formulation, as well as new insights into mechanisms involving specific changes in neural, neuroendocrine, and immune systems. The practical implications of this formulation for clinical practice and further research are discussed.
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              The increasing burden of depression

              Recent epidemiological surveys conducted in general populations have found that the lifetime prevalence of depression is in the range of 10% to 15%. Mood disorders, as defined by the World Mental Health and the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, have a 12-month prevalence which varies from 3% in Japan to over 9% in the US. A recent American survey found the prevalence of current depression to be 9% and the rate of current major depression to be 3.4%. All studies of depressive disorders have stressed the importance of the mortality and morbidity associated with depression. The mortality risk for suicide in depressed patients is more than 20-fold greater than in the general population. Recent studies have also shown the importance of depression as a risk factor for cardiovascular death. The risk of cardiac mortality after an initial myocardial infarction is greater in patients with depression and related to the severity of the depressive episode. Greater severity of depressive symptoms has been found to be associated with significantly higher risk of all-cause mortality including cardiovascular death and stroke. In addition to mortality, functional impairment and disability associated with depression have been consistently reported. Depression increases the risk of decreased workplace productivity and absenteeism resulting in lowered income or unemployment. Absenteeism and presenteeism (being physically present at work but functioning suboptimally) have been estimated to result in a loss of $36.6 billion per year in the US. Worldwide projections by the World Health Organization for the year 2030 identify unipolar major depression as the leading cause of disease burden. This article is a brief overview of how depression affects the quality of life of the subject and is also a huge burden for both the family of the depressed patient and for society at large.
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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                11 May 2020
                May 2020
                : 9
                : 5
                : 1419
                Affiliations
                [1 ]Sport Science Section, Department of Sport, Exercise and Health, University of Basel, CH-4052 Basel, Switzerland; Serge.brand@ 123456unibas.ch (S.B.); flora.colledge@ 123456unibas.ch (F.C.); Uwe.puehse@ 123456unibas.ch (U.P.)
                [2 ]Psychiatric Services Solothurn, 4503 Solothurn, Switzerland; Christian.Imboden@ 123456pkwyss.ch (C.I.); Martin.Hatzinger@ 123456spital.so.ch (M.H.)
                [3 ]Private Clinic Wyss, 3053 Muenchenbuchsee, Switzerland
                [4 ]Clinic Sonnenhalde, 4125 Riehen, Switzerland; Johannes.Beck@ 123456sonnenhalde.ch
                [5 ]University Psychiatric Clinics (UPK), Center for Affective, Stress and Sleep Disorders, University of Basel, 4002 Basel, Switzerland; edith.holsboer@ 123456gmail.com
                [6 ]Substance Abuse Prevention Research Center and Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah 6715847141, Iran
                [7 ]University Psychiatric Clinics (UPK), Neurobiology Laboratory for Brain Aging and Mental Health, University of Basel, 4002 Basel, Switzerland; anne.eckert@ 123456upkbs.ch
                Author notes
                [* ]Correspondence: markus.gerber@ 123456unibas.ch ; Tel.: +41-61-207-4783; Fax: +41-61-207-4789
                [†]

                These authors have contributed equally to this study.

                Author information
                https://orcid.org/0000-0001-6140-8948
                https://orcid.org/0000-0001-9912-0413
                https://orcid.org/0000-0003-1228-316X
                Article
                jcm-09-01419
                10.3390/jcm9051419
                7291068
                32403243
                052f733d-ee61-46bf-98a9-6cd613c80411
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 02 April 2020
                : 05 May 2020
                Categories
                Article

                cortisol,depression,exercise training,physical activity,stress reactivity

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