Exercise Influences in Depressive Disorders: Symptoms, Biomarkers and Telomeres

Abstract

EditorialThe exact mechanisms concerning how exercise affects the brain, under conditions of health or disorder, are not fully understood and the literature lacks a sufficiency of well-designed studies concerning the effects of exercise training on depressive disorders. Nevertheless, the observed antidepressant actions of exercise are strong enough to warrant its application as a viable alternative to current medications in the treatment of depressive disorders [1]. The beneficial effects of exercise upon cognitive, executive function and working memory, emotional, self-esteem and depressed mood, motivational, anhedonia and psychomotor retardation, and somatic/physical, sleep disturbances and chronic aches and pains, categories of depression are discussed. The ameliorative effects of physical exercise upon several biomarkers associated with depressive states: hypothalamicpituitary-adrenal (HPA) axis homeostasis, anti-neurodegenerative effects, monoamine metabolism regulation and neuro-immune functioning have been outlined [2]. The notion that physical exercise may function as "scaffolding" that buttresses available network circuits, anti-inflammatory defences and neuroreparative processes, e.g. brain-derived neurotrophic factor (BDNF), holds a certain appeal. In older adults, it has been observed that exercise was associated with significantly lower levels of depressive symptom severity [3]. An activity program based on "nordic walking", i.e. using staves, was shown to induce a positive effect on depressive symptoms and sleeping disorders in elderly patients, suggesting that Nordic walking based exercise programs should be developed for the elderly who suffer from depression or a sleeping disorder [4][5].The notion of physical exercise as a "scaffolding" to buttress damage experienced under such conditions as traumatic brain damage and aging provokes the metaphor of transient measures, external to the buildings, that provides for construction, reconstruction and maintenance but not the buildings themselves. Scaffolding provides a normal process that continues across the lifespan involving that application and development of complementary, alternative neural circuits to achieve a particular cognitive goal (252); it is protective of cognition in the aging (or disabled) brain and is reinforced by physical exercise and cognitive engagement (which is harnessed during exercise. Under conditions of traumatic brain injury the notion of scaffolding suggests that exercise buttresses, more or less dependent on extent of injury, the surviving adaptive and neuroreparative processes [6][7]. Studies in transgenic mice and primary human skeletal myocyte studies have shown the critical influence of exercise-responsive transcriptional co-activator PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha, which regulates the genes controlling energy metabolism), in coordinating intramuscular lipid-dropletprogramming leading to mitochondrial remodeling. PGC-1α regulates also mitochondrial biogenesis and function...