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Review
Neuropsychobiology 2009;59:191–198
DOI: 10.1159/000223730
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
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
Introduction
Neurodegenerative diseases become more prevalent as
individuals age and, therefore, represent a serious issue
for the healthcare system. Since inactivity is the number
one risk factor for many diseases, physical activity has
become an emerging topic of interest for many investiga-
tors. Exercise might act as an efficient and low-cost ad-
junctive factor in the treatment and prevention of age-re-
lated neurodegenerative processes
[1, 2] . Recent studies
have focused on the correlation between physical activity
and mental health
[3–6] . Clinical evidence has demon-
strated that exercise has a positive relationship with the
outcome of different mental diseases, such as depression,
Alzheimer’s disease and Parkinson’s disease, improving
not only patients’ quality of life but the disease itself
[7–9] .
Some authors state that the influence of exercise on brain
functioning might be related to the human evolutionary
process, since physical activity is associated with surviv-
al. It has been suggested that individuals who exercise
might show a biological advantage over sedentary indi-
viduals
[4] . Indeed, exercise is related to enhanced cogni-
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.
Key Words
Physical activity ⴢ Major depression ⴢ Alzheimer’s disease ⴢ
Parkinson’s disease, elderly
Abstract
The relationship be tween physical activity and mental health
has been widely investigated, and several hypotheses have
been formulated about it. Specifically, during the aging pro-
cess, physical exercise might represent a potential adjunc-
tive treatment for neuropsychiatric disorders and cognitive
impairment, helping delay the onset of neurodegenerative
processes. Even though exercise itself might act as a stressor,
it has been demonstrated that it reduces the harmful effects
of other stressors when performed at moderate intensities.
Neurotransmitter release, neurotrophic factor and neuro-
genesis, and cerebral blood flow alteration are some of the
concepts involved. In this review, the potential effects of ex-
ercise on the aging process and on mental health are dis-
cussed, concerning some of the recent findings on animal
and human research. The overwhelming evidence present
in the literature today suggests that exercise ensures suc-
cessful brain functioning. Copyrig ht © 2009 S. Karger AG, Bas el
Receive d: October 6, 2008
Accepted af ter revision: Februar y 22, 2009
Publishe d online: June 10, 2009
André a Camaz Desla ndes
Center for A lzheimer Disease and Related Disorders , Institute of Psych iatry
Universidade Federal do R io de Janeiro, Rua Syl vio da Rocha Pollis 300, C asa 02
Recreio dos Bandeirantes 22793.395, R io de Janeiro, RJ (Bra zil)
Tel. +55 21 7896 9778, Fax +55 21 3328 5020, E-Mail ade slandes@uf rj.br
© 2009 S . Karger AG, Basel
0302–282X/09/0594–0191$26.00/0
Accessible online at:
www.karger.com/nps
Deslandes /Moraes /Ferreira /Veiga /
Silveira
/Mouta /Pompeu /Coutinho /Laks
Neuropsychobiolog y 2009;59:191–198
192
This revision, which focuses on the relationship be-
tween exercise and mental health, is divided into: (1) clin-
ical studies that investigated the effect of exercise as a
non-pharmacological treatment of mental illness, and (2)
studies that hypothesized a neurophysiological pathway
to explain the relationship between exercise and mental
health.
M e t h o d
A computer search of PubMed and IsiWeb was con-
ducted using a combination of the key words exercise ,
physical activity , and elderly with the specific mental dis-
order (major depression, Alzheimer’s disease, Parkinson’s
disease). Articles that did not specify methods of clinical
diagnosis and that did not measure effects of exercise
were excluded. Also, studies that measured other comor-
bid conditions were excluded. After all exclusions, the fi-
nal result comprised 32 articles. They are presented in
table 1 (8 articles), table 2 (8 articles) and table 3 (16 ar-
ticles). The other studies referenced in this review con-
tribute to the understanding of the mechanism of action
of exercise related to maintaining a healthy brain.
Mental Health and Exercise: Clinical Evidences in
Elderly Subjects
Physical Exercise and Major Depression
A recent study has shown the overall prevalence of de-
pression in the elderly to be 22%, and that a sedentary
Tab le 1. Summary of physical exercise interventions for elderly patients with major depressive disorder (MDD)
Reference Sample Age, years Diagnostic
criteria
Type of
exercise
Intervention
duration
Primary outcomes Exercise group
improvement
Singh
et al.** [24]
16 E
16 C
71.381.2 DSM-IV ST 20 weeks BDI, HDRS, SF36 BDI, HDRS, SF36
Blumenthal
et al.* [20]
41 M (sertraline)
39 E
44 M + E
5786.5 DSM-IV AT 16 weeks BDI, HDRS BDI, HDRS
Babyak
et al.* [21]
41 M (sertraline)
39 E
44 M + E
5786.5 DSM-IV AT 16-week
follow-up
10 months
BDI, HDRS Lower rates of
depression (clini-
cal diagnostic)
Singh
et al.** [25]
15 E
14 C
7182.0 DSM-IV ST 20-week
follow-up
26 months
BDI, PGMS BDI, PGMS
Herman
et al.* [22]
48 M (sertraline)
53 E
55 M + E
56.7286.45 DSM-IV AT 16 weeks Dropout
remission (HDRS)
Low dropout
(NS)
Mather
et al. [23]
42 E
43 C
63
65
ICD-10 AT 10 weeks HDRS, GDS HDRS, GDS
Singh
et al. [26]
18 E (high intensity)
17 E (low intensity)
19 control
6985
7087
6987
DSM-IV ST 8 weeks HDRS, GDS HDRS, GDS
Blumenthal
et al. [7]
53 E (home-based)
51 E (supervised)
49 M (sertraline)
49 placebo
5288DSM-IV AT 16 weeks HDRS HDRS
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 Statistica l Classification
of Diseases and Related Health Problems.
Exercise and Mental Health:
Many Reasons to Move
Neuropsychobiolog y 2009;59:191–198
193
lifestyle is significantly correlated to depression morbid-
ity
[12] . Dunn et al. [13] showed that only 37 studies have
studied exercise in major depressed (MDD) patients, out
of a thousand papers on the issue. Reviews have suggest-
ed that exercise is an effective treatment for depression
[14 –17] . Other studies have also examined the effect of
physical exercise on the prevention of depression
[18 , 19] .
Despite the fact that data on elderly patients are even
scarcer, investigations have shown an inverse relation-
ship between aerobic
[7, 20–23] and strength training
[24 –26] and depression in the elderly ( table 1 ). The effi-
cacy of the se intervent ions is i nf luenced by diagnosis, in-
tensity of exercise, and instruments used to evaluate re-
sponse
[13 , 27] . For example, aerobic exercise at an inten-
sity consistent with public health recommendations can
be regarded as an ef fective treatment of mild and moder-
ate MDD. On the other hand, the effects of low-intensity
exercise are comparable to placebo effects
[27] . In a recent
study, Blumenthal et al.
[7] evaluated MDD patients with
different treatments, namely sertraline, placebo, home-
based exercise, and supervised exercise. Although the au-
thors observed a higher remission rate with sertraline
(47%) and exercise (45%), placebo response was also high,
suggesting that a considerable portion of therapeutic re-
sp ons e i s a ls o de te rm in ed by the at te nt io n prov id ed to th e
patient and to his/her own expectations regarding the
treatment. Overall, there is little evidence for a possible
dose-response effect of exercise on major depression.
Physical Exercise and Alzheimer’s Disease
Although epidemiological studies have associated ex-
ercise with reduced risk to develop Alzheimer’s disease
(AD), the biological bases of such benefits remain incon-
clusive
[28] . AD, a neurodegenerative disease, is charac-
terized by the formation of  -amyloid plaques, neuronal
loss in the hippocampus, reduced cholinergic function
Tab le 2. Summary of physical exercise interventions for elderly patients with Alzheimer’s disease
Reference Sample Age Type of exercise Intervention
duration
Primary outcomes Exercise group
improvement
Palleschi
et al. [39]
15 E 7481.5 aerobic 3 months MMSE, attentional
and verbal tests
MMSE, attentional
and verbal tests
Arkin
[36]
24 E 78.888.0 aerobic, flexibility,
strength and balance
at least
1 year
strength and aerobic
capacity, GDS
strength and
aerobic capacity
Teri
et al. [39]
76 E
77 C
7886
7888
aerobic, flexibility,
strength and balance
3 months SF36, SIP,
HDRS, CSDD
SF36, CSDD
HDRS
Mahendra
and Arkin [40]
24 E 78.888.0 aerobic, flexibility,
strength and balance
at least
1 year
strength and aerobic
capacity, GDS,
caregiver evaluation
strength, aerobic capacity,
caregiver evaluation
Rolland
et al. [8]
67 E
67 C
82.887.8
83.187
aerobic, flexibility,
strength and balance
12 months Katz ADLs Restrain ADL decline
Williams and
Tappen [34]
30 E (sw)
31 E (ce)
29 C
8886.32 aerobic, flexibility,
strength and balance
16 weeks DMAS, CSDD
AMS, OAS
DMAS, CSDD
AMS, OAS
Arkin [37] 24 E 78.888.0 aerobic, flexibility,
strength and balance
at least
1 year
MMSE, CDR, CERAD,
ABCD, WAIS-R
MMSE, ABCD
WAIS-R comprehension
Williams and
Tappen [35]
16 E (sw)
17 E (ce)
12 C
87.985.95 aerobic, flexibility,
strength and balance
16 weeks DMAS, CSDD
AMS, OAS
DMAS, CSDD
AMS, OAS
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.
Deslandes /Moraes /Ferreira /Veiga /
Silveira
/Mouta /Pompeu /Coutinho /Laks
Neuropsychobiolog y 2009;59:191–198
194
Tab le 3. Summary of physical exercise interventions for elderly patients with Parkinson’s disease
Reference Sample Age Type of exercise Interven-
tion dura-
tion, weeks
Primary outcomes Exercise group
improvement
Comella
et al. [51]
18 E
18C
66.8 general exercise
and PT
4 UPDRS UPDRS
Schenkman
et al. [50]
23 E
23 C
55–84 individual flexibility 10 spinal flexibility and
physical performance
functional reach and
spinal flexibility
Reuter
et al. [49]
16 E 65.485.9 combined: aerobic gait,
flexibility, strength
14 UPDRS, MMSE, BTM
CURS, AMQZ, SIP
UPDRS, BTM and
CURS
Baatile
et al. [48]
6 E 72.783.7 pole striding 8 UPDRS; PDQ-39 ADLs
Niewboer
et al. [47]
33 E 66.2 functional training 6 UPDRS, activity scale score activity scale score
Bergen
et al. [46]
4 E
4 C
56.886.5
63.589.2
aerobic 16 movement initiation,
VO2 peak
movement initiation
VO2 peak
Hirsch
et al. [9]
9 E (B)
6 E (S + B)
75.181.8
70.882.8
balance and strength 10 SOT, strength strength, gait
Lun
et al. [52]
8 E (Home)
11 E (PT)
6588balance, flexibility
and strength
8 UPDRS total and motor
TUG, BBS, ABC scale
UPDRS motor
Protas
et al. [54]
9 E
9 C
71.387.4
73.788.5
gait and step training 8 reduce in falls, increase
in steps and gait
reduce in falls, increase
in steps and gait
Miyai
et al. [45]
11 E (BWSTT)
9 E (PT)
69.581.9
69.881.5
BWSTT and PT 4 UPDRS, ambulation speed ambulation speed and
number of steps
Burini
et al. [44]
22 E 65.286.5 aerobic and qigong 14 UPDRS, PDQ39, 6-min
walk, BDI, BD’S
6 min walk, VO2max,
double product peak
Dibble
et al. [56]
10 E
9 C
64.389.6
67.0810.2
eccentric resistance 12 mobility, muscle force,
quadriceps muscle volume
mobility, muscle force,
quadriceps muscle
volume
De Paula
et al. [55]
20 E 61.589.8 aerobic, strength and
flexibility
12 NHP NHP
Ashburn
et al. [53]
65 E
65 C
72.789.6
71.688.8
strength, balance and
aerobic
6 BBT, SAS, QoL
functional reach
functional reach, QoL
Herman
et al. [43]
9 E 7086.8 aerobic 6 UPDRS, PDQ39, SPPB,
gait speed
PDQ39, UPDRS SPPB,
gait speed
Cakit
et al. [42]
21 E
10 C
71.886.4 speed-dependent
treadmill
8 BBT, DGI, FES walking
distance
BBT, DGI, FES walking
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 Questionnai re of Zeersen; A BC Scale = Activities-Specific Ba lance Confidence S cale; 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.
Exercise and Mental Health:
Many Reasons to Move
Neuropsychobiolog y 2009;59:191–198
195
and cognitive deter ioration. Environmental sti muli a long
with genetic factors are thought to influence the onset of
the disease. Among the lifestyle changes associated with
AD prevent ion, exercise is seen as one of the most i mpor-
tant ones
[29] . Several studies have reported the relation-
ship between physical activity and reduced incidence of
dementia or cognitive deterioration
[29–32] . A recent
analysis of 10 studies investigating the effects of motor
intervention treatments for subjects with dementia sug-
gested positive effects of this non-pharmacological ap-
proach
[33] . The efficacy of motor intervention was con-
firmed in affective status, psychosocial function, physical
health and function, and caregiver distress. In another
study, Teri et al.
[31] observed that daily 30 min of physi-
cal training (aerobic, f lexibility and strengt h) reduced the
numb er of hospitalizat ions in 153 A D patients. It als o de-
creased depressive symptoms and improved quality of
life. Rolland et al.
[8] evaluated 134 patients and demon-
strated that, after a year of exercise intervention, the ex-
ercise group improved quality of life, as compared to the
sedentary group. Other studies showed significant mood
improvement in older adults with AD
[34 , 35] . In a recent
st udy, Wi lliams a nd Tappen
[34] observed an antidepres-
sant effect of exercise in severe AD. However, such inves-
tigations are still scarce and very little is known about the
efficiency of exercise as a protective factor in AD
[31, 34–
40] ( table 2 ).
Physical Exercise and Parkinson’s Disease
Parkinson’s disease (PD) is associated with genetic,
environmental, and behavioral factors. Motor alterations
are expressed as tremor, rigidity and hypokinesia, as well
as posture and balance changes
[41] . Such alterations are
directly associated with falls and fatigue experienced by
the patients. Exercise might help by protecting against
the disease as well as an adjunctive treatment
[42–57] .
Epidemiological studies have suggested that exercise is
related to a reduced risk of developing PD. Also, clinical
studies have investigated the effectiveness of exercise,
mainly focusing on motor performance, gait, and activi-
ties o f da ily livi ng (A DLs)
[58 , 59] . Thacker et al. [57] have
demonstrated that the intensity of exercise might inf lu-
ence the neuroprotective response. Higher intensities of
exercise would be positively related to a protective factor,
when compared to lower intensities. Goede et al.
[59] ob-
served that physical activity is significantly beneficial to
PD patients, improving their quality of life, walking
skills, and reducing neurological symptoms. In fact, im-
proving functional capabilities as a consequence of
strength and balance training might positively inf luence
their independence and quality of life, not necessarily be-
cause of neurochemical alterations. Therefore, strength
improvement also has an essential role in daily activities.
Parkinsonians (idiopathic) who accomplished a 10-week
strength and balance program developed strength and
reduced the number of falls
[9] . Although somewhat lim-
ited, evidence suggests that exercise training is beneficial
to patients w ith PD, especially in functional capacit y and
ADLs improvement ( table 3 ).
Neurophysiological Hypothesis
The protective effect of exercise could be explained by
the hormesis theory, in which low doses of toxins and/or
radiation can exert beneficial effects in organisms
[60] .
Radak et al.
[61, 62] extended the hormesis theory to in-
clude reactive oxygen species (ROS), suggesting that the
beneficial effects of regular exercise are partly based on
its ability to generate ROS. Exercise-induced ROS pro-
duction plays a role in the induction of antioxidants,
DNA repair and protein-degrading enzymes, resulting in
decreases in the incidence of oxidative stress-related dis-
eases. Exercise would, therefore, increase the circulation
of the same proinflammatory cytokines that are normal-
ly upregulated during a stress response. However, exer-
cise may also upregulate anti-inf lammatory cytokines,
and with time, increase the immune system threshold for
stress
[63] .
Exercise increases the release and synthesis of several
neurotrophic factors related to better cognitive function-
ing, neurogenesis, angiogenesis and plasticity. The brain-
derived neurotrophic factor (BDNF) and the insulin-like
growth factor (IGF-1) are the factors that have been in-
vestigated the most. Animal research supports the idea
that BDNF is essential for hippocampal functioning, syn-
aptic plasticity, learning, and modulation of depression
[5, 64, 65] . Studies have shown that exercise elevates the
level of BDNF in the rat hippocampus, acting just like a
regular antidepressive drug
[66] . Winter et al. [67] ob-
served an increase in BDNF in humans running at a high
intensity (blood lactate level 1 10 mmol/l). Moreover, the
authors showed that exercise accelerates learning. The
IGF-1 is another neurotrophic factor correlated with cog-
nitive improvement. IGF-1 is also correlated with neuro-
genesis, since its release starts several processes related to
the proliferation of progenitor cells in the subgranular
zone. Exercise increases IGF-1 levels, which are dimin-
ished in elderly adults with poor cognitive performance
[68] . Since strength training increases testosterone and
Deslandes /Moraes /Ferreira /Veiga /
Silveira
/Mouta /Pompeu /Coutinho /Laks
Neuropsychobiolog y 2009;59:191–198
196
IGF-1 levels, some authors argue that strength training
might have an advantage over cardiovascular training.
For example, Cassilhas et al.
[69] observed improved cog-
nitive functioning and higher IGF-1 levels in a group of
elderly individuals after 6 months of strength training.
Nottebohm [70] hypothesized that testosterone is the key
to higher BDNF levels. In the brain, testosterone is aro-
matized in estradiol, and several studies have showed the
correlation between estradiol and cognitive and mood
aspects. Another important aspect is the regulation of the
amyloid levels by IGF-1, since IGF-1 is inversely corre-
lated with the  -amyloid peptide.
I n addition to BD NF a nd IGF-1, exe rcise a ls o reg ul ate s
the expression of vascular endothelial growth factor
(VEGF). VEGF regulates endothelial cell proliferation
and angiogenesis, but also has neurotrophic, neuropro-
tective, and neurogenic effects. While IGF-1 and BDNF
mediate behavioral improvements as a consequence of
exercise, the interactive effects of IGF-1 and VEGF seem
to coordinate exercise-induced neurogenesis and angio-
genesis. Exercise-induced angiogenesis is associated with
an increase in brain VEGF
[65] . Pereira et al. [71] ob-
served an in vivo correlation of exercise-induced neuro-
genesis and angiogenesis in the adult dentate gyrus,
which was based on an increase of cerebral blood volume
in this specific area.
Stress, depression and aging would decrease neuro-
trophic expression and neurogenesis in the brain, and
both antidepressants and exercise would reverse these ef-
fects
[5, 65] . Kempermann [72] proposed that major de-
pression might result from a disturbance in neuronal
plasticity and adult hippocampal neurogenesis. Neuro-
genesis in the adult hippocampus might improve cogni-
tive processes (e.g., memory functioning) and treatment
of several psychiatric diseases (e.g., depression). Volun-
ta ry exercise enha nced neurogenesis in the dentate gyrus
of the adult mouse
[73] . Stemming from these findings,
the focus on the relationship between exercise and mental
health has taken a new direction: neurogenesis in the
adult human brain.
Exercise increases several neurotransmitters, such as
serotonin (5-HT), dopamine (D), acetylcholine (ACh)
and norepinephrine (NE). Moreover, exercise increases
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]
observed a strong increase in peripheral catecholamine
plasma levels (NE, 5-HT and D) after intense physical
exercise in humans, and associated it to learning and
memory improvements. However, peripheral catechol-
amines do not cross the blood-brain barrier. A possible
mechanism, then, is the calcium-calmodulin system,
since exercise leads to increased serum calcium levels,
and calcium is transported to the brain. This, in turn,
enhances brain dopamine synthesis through a calmodu-
lin-dependent system, and increases dopamine levels. In
addition, exercise releases anandamide, which in turn,
increases the dopamine release. Sparling et al.
[75] re-
ported the first evidence that exercise at a moderate in-
tensity activates the endocannabinoid system. They
showed elevated plasma anandamide levels in runners
and cyclists when compared to sedentary controls. The
analgesia, sedation, anxiolysis, and a sense of well-being
wit h physic al ac tivity would b e relat ed to this neurophy s-
iological pathway
[76] . This mechanism seems to better
explain the analgesic effects of exercise rather than the
endorphin hypothesis. Plasmatic endorphin levels do not
necessarily represent levels in the brain, due to the block-
ade of the blood-brain barrier. Hence, studies have shown
that the endorphin release only occurs at high exercise
intensities. A recent study showed in vivo evidence that
release of endogenous opioids occurs in frontolimbic
brain regions after exercise, which has been related to the
level of euphoria after running
[77] .
Cerebral activity is positively correlated with an in-
crease in oxygen and glucose uptake and with an increase
in regional cerebral blood flow (CBF). Exercise is related
to an increase in CBF in several cortical and subcortical
areas
[78] . Adenine nucleotides play a major role in the lo-
cal control of CBF. In 1979, Forrester
[79] proposed that
circulating nucleotides and derivatives released from ac-
t ive sk el et al mus cle ac hi ev e le vel s i n t he ar ter ia l blood t ha t
would affect cerebral metabolism, by a system of ‘meta-
bolic communication’ in the body mediated by circulating
purine compounds. The levels of adenosine triphosphate
(ATP), a potent vasodilator, increase during exercise and
could be a mechanism involved in CBF regulation. Cere-
bral perfusion is also dependent on nitric oxide (NO), and
physical activity upregulates endothelial NO synthesis
and improves angiogenesis and CBF
[80] . Moreover, exer-
cise increases the production of VEGF which is believed
to be the primary growth factor associated with capillary
formation in the developing brain
[5, 65] .
Conclusion
Although exercise improves quality of life, prevents
falls, increases balance, strength, and improves ADLs,
the efficacy of an exercise intervention after the onset of
Exercise and Mental Health:
Many Reasons to Move
Neuropsychobiolog y 2009;59:191–198
197
the disease is not commonly assessed and, therefore,
needs to be investigated with randomized clinical trials.
Neuropsychological aspects, invasive measurements
(e.g., neurotrophic factors, neurotransmitters, hor-
mones), neuroimaging studies, or some physiological
markers associated with clinical parameters could help
elucidate the potential role of exercise as a non-pharma-
cological treatment of mental disorders. Our review pres-
ents recent findings in clinical and animal investigations
concerning the effects of exercise on general brain func-
tioning. Although this is a promising research topic, the
study of the real effects of exercise as an adjunctive treat-
ment of mental illness still has a long way to go.
Role of Funding Source
Funding for this study came from FAPERJ. The funding
sources had no further role in study design, the collection, analy-
sis and interpretation of the data, in the writing of the report, and
in the decision to submit the paper for publication.
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