Exercise Influences in Depressive Disorders: Symptoms, Biomarkers and Telomeres

Abstract

The 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. 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

Full text

Volume 1 • Issue 1 • 1000e101
Clin Depress, an open access journal
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Research Article Open Access
Archer, Clin Depress 2015, 1:1
Editorial Open Access
Clinical Depression
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ISSN: 2572-0791
Exercise Influences in Depressive Disorders: Symptoms, Biomarkers and
Telomeres
Trevor Archer*
Department of Psychology, University of Gothenburg, Box 500, S-405 30 Gothenburg, Sweden
Editorial
e exact mechanisms concerning how exercise aects the brain,
under conditions of health or disorder, are not fully understood and
the literature lacks a suciency of well-designed studies concerning
the eects 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]. e benecial eects
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. e ameliorative eects of physical exercise upon
several biomarkers associated with depressive states: hypothalamic-
pituitary-adrenal (HPA) axis homeostasis, anti-neurodegenerative
eects, monoamine metabolism regulation and neuro-immune
functioning have been outlined [2]. e notion that physical exercise
may function as “scaolding” that buttresses available network
circuits, anti-inammatory 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 signicantly lower levels of depressive symptom severity [3].
An activity program based on “nordic walking”, i.e. using staves, was
shown to induce a positive eect on depressive symptoms and sleeping
disorders in elderly patients, suggesting that Nordic walking based
exercise programs should be developed for the elderly who suer from
depression or a sleeping disorder [4-5].
e notion of physical exercise as a “scaolding” 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. Scaolding 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 scaolding
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 inuence 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-droplet-
programming leading to mitochondrial remodeling. PGC-1α regulates
also mitochondrial biogenesis and function. In this regard, translational
studies that compared individuals who exercised physically with
sedentary individuals have identied a dramatically strong association
between the expression of intramuscular lipid droplet genes and
enhanced insulin action in the exercising individuals [8]. In the context
of depressive disorders, the notion of scaolding suggests that exercise/
*Corresponding author: Archer T, Department of Psychology, University of
Gothenburg, Box 500, S-405 30 Gothenburg, Sweden; Tel: +46 31 7864694;
E-mail: trevor.archer@psy.gu.se
Received: September 22, 2015; Accepted: September 25, 2015; Published:
October 28, 2015
Citation: Archer T (2015) Exercise Inuences in Depressive Disorders: Symptoms,
Biomarkers and Telomeres. Clin Depress 1: e101.
Copyright: © 2015 Archer T. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
activity mobilizes available and alternative neural and neuroimmune
circuits that may initiate and/or consolidate neuroreparative and anti-
inammatory processes, such as BDNF.
Despite proper understanding of how exercise aects brain
integrity and a paucity of well-designed, standardized studies on the
exercise intervention on depressive disorders, the consensus of much
of the existing remains in favour of the exercise antidepressant actions
suggest it to be a major alternative to traditional medication [1], albeit
in mild-to-moderate levels of disorder and with patient willingness [9].
e understanding of the mechanisms underlying the eects of exercise
on depression constitutes an essential step in the direction of the broad
use of exercise as an alternative treatment of depression in the eld.
In the present review paper, we have based our discussion in a model
that highlights the eects of exercise on key depressive symptoms, and
on key biomarkers of depression, rather than on depression as a global
outcome. In this regard, stress, intense or chronic, and likely both, is a
major agent [10] have proposed an hypothesis outlining a mechanism
through which physical exercise, as opposed to sedentary living,
promotes stress robustness in the face of intense uncontrollable stress.
According to this notion, individuals with a sedentary existence respond
to an intense acute uncontrollable stressor with excessive 5-HT and NA
activity and/or prolonged down-regulation of the CX3CL1-CX3CR1
axis resulting in activation and proliferation of hippocampal microglia
with consequent hippocampal-dependent memory decits and reduced
neurogenesis. Contrastingly, physically active individuals respond to
the same stressor with constrained 5-HT and NA activity and a rapidly
recovering CX3CL1-CX3CR1 axis responses resulting in the quieting of
microglia, and protection from negative cognitive and neurobiological
eects of stress. e CX3CL1-CX3CR1 expressing microglia lls an
important role in limiting neuroinammatory and neurodegenerative
damage in brain cells. e merit of this more detailed approach,
focusing on the various and specic eects of exercise on the dierent
facets of symptom-proles and biomarkers that buttress depressive
conditions, concerns the provision for increased understanding of the
general process and the perception of existing overall patterns through
a more meticulous examination of the far-reaching processes involved.
Telomeres, regions of repetitive nucleotide sequences (TTAGGG)-
DNA, protein-nucleotide complexes, at each end of a chromatid
maintained and lengthened by telomerase, shorten with cell division
leading eventually to cellular senescence and mortality [11].

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Volume 1 • Issue 1 • 1000e101
Citation: Archer T (2015) Exercise Inuences in Depressive Disorders: Symptoms, Biomarkers and Telomeres. Clin Depress 1: e101.
Clin Depress, an open access journal
ISSN: 2572-0791
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Volume 1 • Issue 1 • 1000e101
Citation: Archer T (2015) Exercise Inuences in Depressive Disorders: Symptoms, Biomarkers and Telomeres. Clin Depress 1: e101.
Clin Depress, an open access journal
ISSN: 2572-0791
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Citation: Archer T (2015) Exercise Inuences in Depressive Disorders:
Symptoms, Biomarkers and Telomeres. Clin Depress 1: e101.
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