Review

Neuropsychobiology 2009;59:191–198 Received: October 6, 2008

Accepted after revision: February 22, 2009
DOI: 10.1159/000223730
Published online: June 10, 2009

Exercise and Mental Health:

Many Reasons to Move
Andréa Deslandes a Helena Moraes b Camila Ferreira c Heloisa Veiga c
Heitor Silveira b Raphael Mouta b Fernando A.M.S. Pompeu d
Evandro Silva Freire Coutinho a Jerson Laks b

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a
National School of Public Health, b Center for Alzheimer Disease and Related Disorders, and c Brain Mapping
and Sensorimotor Integration Laboratory, Institute of Psychiatry, Universidade Federal do Rio de Janeiro, and
d
Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

Key Words Introduction

Physical activity ⴢ Major depression ⴢ Alzheimer’s disease ⴢ
Parkinson’s disease, elderly Neurodegenerative diseases become more prevalent as
individuals age and, therefore, represent a serious issue
for the healthcare system. Since inactivity is the number
Abstract one risk factor for many diseases, physical activity has
The relationship between physical activity and mental health become an emerging topic of interest for many investiga-
has been widely investigated, and several hypotheses have tors. Exercise might act as an efficient and low-cost ad-
been formulated about it. Specifically, during the aging pro- junctive factor in the treatment and prevention of age-re-
cess, physical exercise might represent a potential adjunc- lated neurodegenerative processes [1, 2]. Recent studies
tive treatment for neuropsychiatric disorders and cognitive have focused on the correlation between physical activity
impairment, helping delay the onset of neurodegenerative and mental health [3–6]. Clinical evidence has demon-
processes. Even though exercise itself might act as a stressor, strated that exercise has a positive relationship with the
it has been demonstrated that it reduces the harmful effects outcome of different mental diseases, such as depression,
of other stressors when performed at moderate intensities. Alzheimer’s disease and Parkinson’s disease, improving
Neurotransmitter release, neurotrophic factor and neuro- not only patients’ quality of life but the disease itself [7–9].
genesis, and cerebral blood flow alteration are some of the Some authors state that the influence of exercise on brain
concepts involved. In this review, the potential effects of ex- functioning might be related to the human evolutionary
ercise on the aging process and on mental health are dis- process, since physical activity is associated with surviv-
cussed, concerning some of the recent findings on animal al. It has been suggested that individuals who exercise
and human research. The overwhelming evidence present might show a biological advantage over sedentary indi-
in the literature today suggests that exercise ensures suc- viduals [4]. Indeed, exercise is related to enhanced cogni-
cessful brain functioning. Copyright © 2009 S. Karger AG, Basel tive functioning and brain plasticity [10, 11]. Although
there is an increasing interest in the mechanisms sup-
porting the positive effects of exercise on mental health,
clinical evidence is still very limited.

© 2009 S. Karger AG, Basel Andréa Camaz Deslandes

0302–282X/09/0594–0191$26.00/0 Center for Alzheimer Disease and Related Disorders, Institute of Psychiatry
Fax +41 61 306 12 34 Universidade Federal do Rio de Janeiro, Rua Sylvio da Rocha Pollis 300, Casa 02
E-Mail [email protected] Accessible online at: Recreio dos Bandeirantes 22793.395, Rio de Janeiro, RJ (Brazil)
www.karger.com www.karger.com/nps Tel. +55 21 7896 9778, Fax +55 21 3328 5020, E-Mail [email protected]
Table 1. Summary of physical exercise interventions for elderly patients with major depressive disorder (MDD)

Reference Sample Age, years Diagnostic Type of Intervention Primary outcomes Exercise group
criteria exercise duration improvement

Singh 16 E 71.381.2 DSM-IV ST 20 weeks BDI, HDRS, SF36 BDI, HDRS, SF36
et al.** [24] 16 C
Blumenthal 41 M (sertraline) 5786.5 DSM-IV AT 16 weeks BDI, HDRS BDI, HDRS
et al.* [20] 39 E
44 M + E
Babyak 41 M (sertraline) 5786.5 DSM-IV AT 16-week BDI, HDRS Lower rates of
et al.* [21] 39 E follow-up depression (clini-
44 M + E 10 months cal diagnostic)
Singh 15 E 7182.0 DSM-IV ST 20-week BDI, PGMS BDI, PGMS
et al.** [25] 14 C follow-up
26 months

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Herman 48 M (sertraline) 56.7286.45 DSM-IV AT 16 weeks Dropout Low dropout
et al.* [22] 53 E remission (HDRS) (NS)
55 M + E
Mather 42 E 63 ICD-10 AT 10 weeks HDRS, GDS HDRS, GDS
et al. [23] 43 C 65
Singh 18 E (high intensity) 6985 DSM-IV ST 8 weeks HDRS, GDS HDRS, GDS
et al. [26] 17 E (low intensity) 7087
19 control 6987
Blumenthal 53 E (home-based) 5288 DSM-IV AT 16 weeks HDRS HDRS
et al. [7] 51 E (supervised)
49 M (sertraline)
49 placebo

ST = Strength training; AT = aerobic training; Group: E = exercise; C = control; M = medication. Depression rating scales:
HDRS = Hamilton Depression Rating Scale; BDI = Beck Depressive Inventory; GDS = Geriatric Depressive Scale; DSM-IV = Diag-
nostic and Statistical Manual for Mental Disorders. * and ** = Same initial sample; NS = not significant between groups; SF36 = 36-
Item Short Form Health Survey; PGMS = Philadelphia Geriatric Center Morale Scale; ICD-10 = International Statistical Classification
of Diseases and Related Health Problems.

This revision, which focuses on the relationship be- were excluded. Also, studies that measured other comor-
tween exercise and mental health, is divided into: (1) clin- bid conditions were excluded. After all exclusions, the fi-
ical studies that investigated the effect of exercise as a nal result comprised 32 articles. They are presented in
non-pharmacological treatment of mental illness, and (2) table 1 (8 articles), table 2 (8 articles) and table 3 (16 ar-
studies that hypothesized a neurophysiological pathway ticles). The other studies referenced in this review con-
to explain the relationship between exercise and mental tribute to the understanding of the mechanism of action
health. of exercise related to maintaining a healthy brain.

Method
A computer search of PubMed and IsiWeb was con- Mental Health and Exercise: Clinical Evidences in
ducted using a combination of the key words exercise, Elderly Subjects
physical activity, and elderly with the specific mental dis-
order (major depression, Alzheimer’s disease, Parkinson’s Physical Exercise and Major Depression
disease). Articles that did not specify methods of clinical A recent study has shown the overall prevalence of de-
diagnosis and that did not measure effects of exercise pression in the elderly to be 22%, and that a sedentary

192 Neuropsychobiology 2009;59:191–198 Deslandes /Moraes /Ferreira /Veiga /

Silveira /Mouta /Pompeu /Coutinho /Laks
Table 2. Summary of physical exercise interventions for elderly patients with Alzheimer’s disease

Reference Sample Age Type of exercise Intervention Primary outcomes Exercise group
duration improvement

Palleschi 15 E 7481.5 aerobic 3 months MMSE, attentional MMSE, attentional

et al. [39] and verbal tests and verbal tests
Arkin 24 E 78.888.0 aerobic, flexibility, at least strength and aerobic strength and
[36] strength and balance 1 year capacity, GDS aerobic capacity
Teri 76 E 7886 aerobic, flexibility, 3 months SF36, SIP, SF36, CSDD
et al. [39] 77 C 7888 strength and balance HDRS, CSDD HDRS
Mahendra 24 E 78.888.0 aerobic, flexibility, at least strength and aerobic strength, aerobic capacity,
and Arkin [40] strength and balance 1 year capacity, GDS, caregiver evaluation
caregiver evaluation
Rolland 67 E 82.887.8 aerobic, flexibility, 12 months Katz ADLs Restrain ADL decline
et al. [8] 67 C 83.187 strength and balance

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Williams and 30 E (sw) 8886.32 aerobic, flexibility, 16 weeks DMAS, CSDD DMAS, CSDD
Tappen [34] 31 E (ce) strength and balance AMS, OAS AMS, OAS
29 C
Arkin [37] 24 E 78.888.0 aerobic, flexibility, at least MMSE, CDR, CERAD, MMSE, ABCD
strength and balance 1 year ABCD, WAIS-R WAIS-R comprehension
Williams and 16 E (sw) 87.985.95 aerobic, flexibility, 16 weeks DMAS, CSDD DMAS, CSDD
Tappen [35] 17 E (ce) strength and balance AMS, OAS AMS, OAS
12 C

ADLs = Activities of daily living; SF36 = 36-Item Short-Form Health Surveys; ABCD = Arizona Battery for Communication Dis-
orders of Dementia; SIP = Sickness Impact Profile Mobility Subscale; DMAS = Dementia Mood Assessment Scale; CSDD = Cornell
Scale for Depression in Dementia; AMS = Alzheimer Mood Scale; OAS = Observed Affect Scale; HDRS = Hamilton Depression Rat-
ing Scale; E = exercise; C = control; sw = supervised walking; ce = comprehensive exercise; MMSE = Mini-Mental State Examination;
CDR = Clinical Dementia Rating; WAIS-R = Wechsler Adult Intelligence Test-Revised.

lifestyle is significantly correlated to depression morbid- study, Blumenthal et al. [7] evaluated MDD patients with
ity [12]. Dunn et al. [13] showed that only 37 studies have different treatments, namely sertraline, placebo, home-
studied exercise in major depressed (MDD) patients, out based exercise, and supervised exercise. Although the au-
of a thousand papers on the issue. Reviews have suggest- thors observed a higher remission rate with sertraline
ed that exercise is an effective treatment for depression (47%) and exercise (45%), placebo response was also high,
[14–17]. Other studies have also examined the effect of suggesting that a considerable portion of therapeutic re-
physical exercise on the prevention of depression [18, 19]. sponse is also determined by the attention provided to the
Despite the fact that data on elderly patients are even patient and to his/her own expectations regarding the
scarcer, investigations have shown an inverse relation- treatment. Overall, there is little evidence for a possible
ship between aerobic [7, 20–23] and strength training dose-response effect of exercise on major depression.
[24–26] and depression in the elderly (table 1). The effi-
cacy of these interventions is influenced by diagnosis, in- Physical Exercise and Alzheimer’s Disease
tensity of exercise, and instruments used to evaluate re- Although epidemiological studies have associated ex-
sponse [13, 27]. For example, aerobic exercise at an inten- ercise with reduced risk to develop Alzheimer’s disease
sity consistent with public health recommendations can (AD), the biological bases of such benefits remain incon-
be regarded as an effective treatment of mild and moder- clusive [28]. AD, a neurodegenerative disease, is charac-
ate MDD. On the other hand, the effects of low-intensity terized by the formation of ␤-amyloid plaques, neuronal
exercise are comparable to placebo effects [27]. In a recent loss in the hippocampus, reduced cholinergic function

Exercise and Mental Health: Neuropsychobiology 2009;59:191–198 193

Many Reasons to Move
Table 3. Summary of physical exercise interventions for elderly patients with Parkinson’s disease

Reference Sample Age Type of exercise Interven- Primary outcomes Exercise group
tion dura- improvement
tion, weeks

Comella 18 E 66.8 general exercise 4 UPDRS UPDRS

et al. [51] 18C and PT
Schenkman 23 E 55–84 individual flexibility 10 spinal flexibility and functional reach and
et al. [50] 23 C physical performance spinal flexibility
Reuter 16 E 65.485.9 combined: aerobic gait, 14 UPDRS, MMSE, BTM UPDRS, BTM and
et al. [49] flexibility, strength CURS, AMQZ, SIP CURS
Baatile 6E 72.783.7 pole striding 8 UPDRS; PDQ-39 ADLs
et al. [48]
Niewboer 33 E 66.2 functional training 6 UPDRS, activity scale score activity scale score
et al. [47]

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Bergen 4E 56.886.5 aerobic 16 movement initiation, movement initiation
et al. [46] 4C 63.589.2 VO2 peak VO2 peak
Hirsch 9 E (B) 75.181.8 balance and strength 10 SOT, strength strength, gait
et al. [9] 6 E (S + B) 70.882.8
Lun 8 E (Home) 6588 balance, flexibility 8 UPDRS total and motor UPDRS motor
et al. [52] 11 E (PT) and strength TUG, BBS, ABC scale
Protas 9E 71.387.4 gait and step training 8 reduce in falls, increase reduce in falls, increase
et al. [54] 9C 73.788.5 in steps and gait in steps and gait
Miyai 11 E (BWSTT) 69.581.9 BWSTT and PT 4 UPDRS, ambulation speed ambulation speed and
et al. [45] 9 E (PT) 69.881.5 number of steps
Burini 22 E 65.286.5 aerobic and qigong 14 UPDRS, PDQ39, 6-min 6 min walk, VO2max,
et al. [44] walk, BDI, BD’S double product peak
Dibble 10 E 64.389.6 eccentric resistance 12 mobility, muscle force, mobility, muscle force,
et al. [56] 9C 67.0810.2 quadriceps muscle volume quadriceps muscle
volume
De Paula 20 E 61.589.8 aerobic, strength and 12 NHP NHP
et al. [55] flexibility
Ashburn 65 E 72.789.6 strength, balance and 6 BBT, SAS, QoL functional reach, QoL
et al. [53] 65 C 71.688.8 aerobic functional reach
Herman 9E 7086.8 aerobic 6 UPDRS, PDQ39, SPPB, PDQ39, UPDRS SPPB,
et al. [43] gait speed gait speed
Cakit 21 E 71.886.4 speed-dependent 8 BBT, DGI, FES walking BBT, DGI, FES walking
et al. [42] 10 C treadmill distance distance

BWSTT = Body weight-supported treadmill training; DGI = Dynamic Gait Index; FES = Falls Efficacy Scale; BBT = Berg Balance
Test; Qigong = Chinese physiotherapy approach; MMSE = Mini-Mental State Examination; TUG = time to up and go; BD’S = Brown’s
Disability Scale; E = exercise; C = control; PT = physiotherapy; B = balance; S = strength; QoL = quality of life thermometer; BBS =
Berg Balance Scale; UPDRS = Unified Parkinson’s Disease Rating Scale; PDQ39 = 39-Item Parkinson’s Disease Questionnaire;
AMQZ = Adjective Mood Questionnaire of Zeersen; ABC Scale = Activities-Specific Balance Confidence Scale; SAS = Self-Assessment
Parkinson’s Disease Disability Scale; NHP = Nottingham Health Profile; BDI = Beck Depression Inventory; SPPB = Short Physical
Performance Battery; SIP= Sickness Impact Profile; SOT = Sensory Orientation Test; BMT = Basic Motor Test; CURS = Columbia
University Rating Scale.

194 Neuropsychobiology 2009;59:191–198 Deslandes /Moraes /Ferreira /Veiga /

Silveira /Mouta /Pompeu /Coutinho /Laks
and cognitive deterioration. Environmental stimuli along their independence and quality of life, not necessarily be-
with genetic factors are thought to influence the onset of cause of neurochemical alterations. Therefore, strength
the disease. Among the lifestyle changes associated with improvement also has an essential role in daily activities.
AD prevention, exercise is seen as one of the most impor- Parkinsonians (idiopathic) who accomplished a 10-week
tant ones [29]. Several studies have reported the relation- strength and balance program developed strength and
ship between physical activity and reduced incidence of reduced the number of falls [9]. Although somewhat lim-
dementia or cognitive deterioration [29–32]. A recent ited, evidence suggests that exercise training is beneficial
analysis of 10 studies investigating the effects of motor to patients with PD, especially in functional capacity and
intervention treatments for subjects with dementia sug- ADLs improvement (table 3).
gested positive effects of this non-pharmacological ap-
proach [33]. The efficacy of motor intervention was con-
firmed in affective status, psychosocial function, physical Neurophysiological Hypothesis
health and function, and caregiver distress. In another
study, Teri et al. [31] observed that daily 30 min of physi- The protective effect of exercise could be explained by
cal training (aerobic, flexibility and strength) reduced the the hormesis theory, in which low doses of toxins and/or

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number of hospitalizations in 153 AD patients. It also de- radiation can exert beneficial effects in organisms [60].
creased depressive symptoms and improved quality of Radak et al. [61, 62] extended the hormesis theory to in-
life. Rolland et al. [8] evaluated 134 patients and demon- clude reactive oxygen species (ROS), suggesting that the
strated that, after a year of exercise intervention, the ex- beneficial effects of regular exercise are partly based on
ercise group improved quality of life, as compared to the its ability to generate ROS. Exercise-induced ROS pro-
sedentary group. Other studies showed significant mood duction plays a role in the induction of antioxidants,
improvement in older adults with AD [34, 35]. In a recent DNA repair and protein-degrading enzymes, resulting in
study, Williams and Tappen [34] observed an antidepres- decreases in the incidence of oxidative stress-related dis-
sant effect of exercise in severe AD. However, such inves- eases. Exercise would, therefore, increase the circulation
tigations are still scarce and very little is known about the of the same proinflammatory cytokines that are normal-
efficiency of exercise as a protective factor in AD [31, 34– ly upregulated during a stress response. However, exer-
40] (table 2). cise may also upregulate anti-inflammatory cytokines,
and with time, increase the immune system threshold for
Physical Exercise and Parkinson’s Disease stress [63].
Parkinson’s disease (PD) is associated with genetic, Exercise increases the release and synthesis of several
environmental, and behavioral factors. Motor alterations neurotrophic factors related to better cognitive function-
are expressed as tremor, rigidity and hypokinesia, as well ing, neurogenesis, angiogenesis and plasticity. The brain-
as posture and balance changes [41]. Such alterations are derived neurotrophic factor (BDNF) and the insulin-like
directly associated with falls and fatigue experienced by growth factor (IGF-1) are the factors that have been in-
the patients. Exercise might help by protecting against vestigated the most. Animal research supports the idea
the disease as well as an adjunctive treatment [42–57]. that BDNF is essential for hippocampal functioning, syn-
Epidemiological studies have suggested that exercise is aptic plasticity, learning, and modulation of depression
related to a reduced risk of developing PD. Also, clinical [5, 64, 65]. Studies have shown that exercise elevates the
studies have investigated the effectiveness of exercise, level of BDNF in the rat hippocampus, acting just like a
mainly focusing on motor performance, gait, and activi- regular antidepressive drug [66]. Winter et al. [67] ob-
ties of daily living (ADLs) [58, 59]. Thacker et al. [57] have served an increase in BDNF in humans running at a high
demonstrated that the intensity of exercise might influ- intensity (blood lactate level 110 mmol/l). Moreover, the
ence the neuroprotective response. Higher intensities of authors showed that exercise accelerates learning. The
exercise would be positively related to a protective factor, IGF-1 is another neurotrophic factor correlated with cog-
when compared to lower intensities. Goede et al. [59] ob- nitive improvement. IGF-1 is also correlated with neuro-
served that physical activity is significantly beneficial to genesis, since its release starts several processes related to
PD patients, improving their quality of life, walking the proliferation of progenitor cells in the subgranular
skills, and reducing neurological symptoms. In fact, im- zone. Exercise increases IGF-1 levels, which are dimin-
proving functional capabilities as a consequence of ished in elderly adults with poor cognitive performance
strength and balance training might positively influence [68]. Since strength training increases testosterone and

Exercise and Mental Health: Neuropsychobiology 2009;59:191–198 195

Many Reasons to Move
IGF-1 levels, some authors argue that strength training amines do not cross the blood-brain barrier. A possible
might have an advantage over cardiovascular training. mechanism, then, is the calcium-calmodulin system,
For example, Cassilhas et al. [69] observed improved cog- since exercise leads to increased serum calcium levels,
nitive functioning and higher IGF-1 levels in a group of and calcium is transported to the brain. This, in turn,
elderly individuals after 6 months of strength training. enhances brain dopamine synthesis through a calmodu-
Nottebohm [70] hypothesized that testosterone is the key lin-dependent system, and increases dopamine levels. In
to higher BDNF levels. In the brain, testosterone is aro- addition, exercise releases anandamide, which in turn,
matized in estradiol, and several studies have showed the increases the dopamine release. Sparling et al. [75] re-
correlation between estradiol and cognitive and mood ported the first evidence that exercise at a moderate in-
aspects. Another important aspect is the regulation of the tensity activates the endocannabinoid system. They
amyloid levels by IGF-1, since IGF-1 is inversely corre- showed elevated plasma anandamide levels in runners
lated with the ␤-amyloid peptide. and cyclists when compared to sedentary controls. The
In addition to BDNF and IGF-1, exercise also regulates analgesia, sedation, anxiolysis, and a sense of well-being
the expression of vascular endothelial growth factor with physical activity would be related to this neurophys-
(VEGF). VEGF regulates endothelial cell proliferation iological pathway [76]. This mechanism seems to better

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and angiogenesis, but also has neurotrophic, neuropro- explain the analgesic effects of exercise rather than the
tective, and neurogenic effects. While IGF-1 and BDNF endorphin hypothesis. Plasmatic endorphin levels do not
mediate behavioral improvements as a consequence of necessarily represent levels in the brain, due to the block-
exercise, the interactive effects of IGF-1 and VEGF seem ade of the blood-brain barrier. Hence, studies have shown
to coordinate exercise-induced neurogenesis and angio- that the endorphin release only occurs at high exercise
genesis. Exercise-induced angiogenesis is associated with intensities. A recent study showed in vivo evidence that
an increase in brain VEGF [65]. Pereira et al. [71] ob- release of endogenous opioids occurs in frontolimbic
served an in vivo correlation of exercise-induced neuro- brain regions after exercise, which has been related to the
genesis and angiogenesis in the adult dentate gyrus, level of euphoria after running [77].
which was based on an increase of cerebral blood volume Cerebral activity is positively correlated with an in-
in this specific area. crease in oxygen and glucose uptake and with an increase
Stress, depression and aging would decrease neuro- in regional cerebral blood flow (CBF). Exercise is related
trophic expression and neurogenesis in the brain, and to an increase in CBF in several cortical and subcortical
both antidepressants and exercise would reverse these ef- areas [78]. Adenine nucleotides play a major role in the lo-
fects [5, 65]. Kempermann [72] proposed that major de- cal control of CBF. In 1979, Forrester [79] proposed that
pression might result from a disturbance in neuronal circulating nucleotides and derivatives released from ac-
plasticity and adult hippocampal neurogenesis. Neuro- tive skeletal muscle achieve levels in the arterial blood that
genesis in the adult hippocampus might improve cogni- would affect cerebral metabolism, by a system of ‘meta-
tive processes (e.g., memory functioning) and treatment bolic communication’ in the body mediated by circulating
of several psychiatric diseases (e.g., depression). Volun- purine compounds. The levels of adenosine triphosphate
tary exercise enhanced neurogenesis in the dentate gyrus (ATP), a potent vasodilator, increase during exercise and
of the adult mouse [73]. Stemming from these findings, could be a mechanism involved in CBF regulation. Cere-
the focus on the relationship between exercise and mental bral perfusion is also dependent on nitric oxide (NO), and
health has taken a new direction: neurogenesis in the physical activity upregulates endothelial NO synthesis
adult human brain. and improves angiogenesis and CBF [80]. Moreover, exer-
Exercise increases several neurotransmitters, such as cise increases the production of VEGF which is believed
serotonin (5-HT), dopamine (D), acetylcholine (ACh) to be the primary growth factor associated with capillary
and norepinephrine (NE). Moreover, exercise increases formation in the developing brain [5, 65].
the activity of some subtypes of receptors for neurotrans-
mitters changing the cortical/subcortical activity (for a
review, see Sarbadhikari and Saha [74]). Winter et al. [67] Conclusion
observed a strong increase in peripheral catecholamine
plasma levels (NE, 5-HT and D) after intense physical Although exercise improves quality of life, prevents
exercise in humans, and associated it to learning and falls, increases balance, strength, and improves ADLs,
memory improvements. However, peripheral catechol- the efficacy of an exercise intervention after the onset of

196 Neuropsychobiology 2009;59:191–198 Deslandes /Moraes /Ferreira /Veiga /

Silveira /Mouta /Pompeu /Coutinho /Laks
the disease is not commonly assessed and, therefore, tioning. Although this is a promising research topic, the
needs to be investigated with randomized clinical trials. study of the real effects of exercise as an adjunctive treat-
Neuropsychological aspects, invasive measurements ment of mental illness still has a long way to go.
(e.g., neurotrophic factors, neurotransmitters, hor-
mones), neuroimaging studies, or some physiological
markers associated with clinical parameters could help Role of Funding Source
elucidate the potential role of exercise as a non-pharma-
Funding for this study came from FAPERJ. The funding
cological treatment of mental disorders. Our review pres- sources had no further role in study design, the collection, analy-
ents recent findings in clinical and animal investigations sis and interpretation of the data, in the writing of the report, and
concerning the effects of exercise on general brain func- in the decision to submit the paper for publication.

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198 Neuropsychobiology 2009;59:191–198 Deslandes /Moraes /Ferreira /Veiga /

Silveira /Mouta /Pompeu /Coutinho /Laks