Effects of Exercise and Physical Activity on Anxiety

Abstract

The beneficial effects of regular physical activity on health are indisputable in the field of modern medicine. Exercise is often the first step in lifestyle modifications for the prevention and management of chronic diseases. According to a US Department of Health and Human Services report on physical activity, regular exercise significantly reduced causes of mortality by up to 30% for men and women (DHHS, 2002). These health benefits are seen consistently across all age groups and racial/ethnic categories. The Centers for Disease Control and Prevention currently recommends 30 min of moderate- to high-intensity exercise for at least 5 days a week for all healthy individuals (DHHS, 2002).

In addition to significantly lowering causes of mortality, regular exercise and physical activity lowers prevalence of chronic disease(s). There is a strong evidence to support that 2–2.5 h of moderate- to high-intensity exercise per week is sufficient to reduce one’s risk for the occurrence of a chronic disease(s). Numerous epidemiological studies have shown that exercise improves one’s self-esteem, and a sense of wellbeing. Individuals who exercise regularly exhibit slower rates of age-related memory and cognitive decline in comparison to those who are more sedentary. Such observations have provided the basis for using exercise to improve memory and cognition in cognitive disorders such as Alzheimer’s Dementia. Adults who engage in regular physical activity experience fewer depressive and anxiety symptoms, thus supporting the notion that exercise offers a protective effect against the development of mental disorders (van Minnen et al., 2010).

Anxiety disorders are common psychiatric conditions with a lifetime prevalence of nearly 29% in the United States (Kessler et al., 2005). These disorders are chronic, debilitating, and impact multiple aspects of one’s life. The economic burden of anxiety disorders in the US was estimated to be $42.3 billion in the 1990s (Greenberg et al., 1999). The prominent anxiety disorders defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) are General Anxiety Disorder (GAD), Panic Disorder (PD), Posttraumatic Stress Disorder (PTSD), Obsessive Compulsive Disorder (OCD), Social Anxiety Disorder, and Specific Phobia (APA, 2000). The exact etiology and pathophysiology of these conditions is not fully understood. Comprehending the effects of exercise and physical activity on the mechanisms of anxiety disorders might further our knowledge of these psychiatric disorders. The purpose of this article is to highlight the known and emerging mechanisms that may result in the anxiolytic effects of exercise.

Full text

www.frontiersin.org April 2013 | Volume 4 | Article 27 | 1
OpiniOn Article
publishe d: 23 A pril 2013
doi: 10.3389 /fpsyt.2013.00027
PSYCHIATRY
IntroductIon
The beneficial effects of regular physical
activity on health are indisputable in the
field of modern medicine. Exercise is often
the first step in lifestyle modifications for
the prevention and management of chronic
diseases. According to a US Department
of Health and Human Services report on
physical activity, regular exercise signifi-
cantly reduced causes of mortality by up
to 30% for men and women (DHHS, 2002).
These health benefits are seen consistently
across all age groups and racial/ethnic cate-
gories. The Centers for Disease Control and
Prevention currently recommends 30 min
of moderate- to high-intensity exercise for
at least 5 days a week for all healthy indi-
viduals (DHHS, 2002).
In addition to significantly lower-
ing causes of mortality, regular exercise
and physical activity lowers prevalence of
chronic disease(s). There is a strong evi-
dence to support that 2–2.5 h of moder-
ate- to high-intensity exercise per week is
sufficient to reduce one’s risk for the occur-
rence of a chronic disease(s). Numerous
epidemiological studies have shown that
exercise improves one’s self-esteem, and a
sense of wellbeing. Individuals who exercise
regularly exhibit slower rates of age-related
memory and cognitive decline in compari-
son to those who are more sedentary. Such
observations have provided the basis for
using exercise to improve memory and
cognition in cognitive disorders such as
Alzheimer’s Dementia. Adults who engage
in regular physical activity experience fewer
depressive and anxiety symptoms, thus
supporting the notion that exercise offers a
protective effect against the development of
mental disorders (van Minnen et al., 2010).
Anxiety disorders are common psychi-
atric conditions with a lifetime prevalence
of nearly 29% in the United States (Kessler
et al., 2005). These disorders are chronic,
debilitating, and impact multiple aspects of
one’s life. The economic burden of anxi-
ety disorders in the US was estimated to be
$42.3 billion in the 1990s (Greenberg et al.,
1999). The prominent anxiety disorders
defined in the Diagnostic and Statistical
Manual of Mental Disorders (DSM-IV)
are General Anxiety Disorder (GAD),
Panic Disorder (PD), Posttraumatic Stress
Disorder (PTSD), Obsessive Compulsive
Disorder (OCD), Social Anxiety Disorder,
and Specific Phobia (APA, 2000). The
exact etiology and pathophysiology of
these conditions is not fully understood.
Comprehending the effects of exercise and
physical activity on the mechanisms of anxi-
ety disorders might further our knowledge
of these psychiatric disorders. The purpose
of this article is to highlight the known and
emerging mechanisms that may result in the
anxiolytic effects of exercise.
PhysIologIcal MechanIsMs
Broadly, regular exercise results in physi-
ological changes and adaptations in the
human body. Studies have shown that regu-
lar aerobic exercise is associated with lower
sympathetic nervous system and hypotha-
lamic-pituitary-adrenal (HPA) axis reactiv-
ity (Crews and Landers, 1987; Åstrand, 2003;
Jackson and Dishman, 2006; Rimmele et al.,
2007).
hyPothalaMIc-PItuItary-adrenal
axIs
The HPA axis plays a critical role in develop-
ing adaptive responses to physical and psy-
chological stressors (De Kloet et al., 2005).
Dysregulations in the HPA axis have long
been implicated in the manifestations of
depressive and anxiety symptoms (Landgraf
et al., 1999; Steckler et al., 1999). Acute stress
leads to alterations in adrenocorticotropic
hormone (ACTH) and excess levels of
glucocorticoids. Chronic stress, as seen
in PTSD, has been associated with lower
concentrations of peripheral cortisol and
upregulation of the glucocorticoid recep-
tors resulting in increased central feedback
sensitivity. Depending on the experimen-
tal paradigm used for chronic stress, some
studies have shown decreased plasma ACTH
and corticosterone levels while other studies
have shown increased corticosterone secre-
tion (Irwin et al., 1986; Kant et al., 1987). In
preclinical studies, voluntary exercise alters
the releases of corticotrophin-releasing
factor (CRF) from the hypothalamus and
ACTH from the anterior pituitary (Salmon,
2001; Droste et al., 2003). These findings
suggest that exercise induced changes in
the HPA axis modulates stress reactivity
and anxiety in humans.
MonoaMIne systeM
Abnormalities in monoamine function in
the brain have been implicated in the patho-
physiology of anxiety spectrum disorders. In
animal studies, learned helplessness resulting
from chronic electric shock was associated
with a reduced release of serotonin in the
frontal cortex (Miller et al., 1975; Petty et al.,
1992). Learned helplessness is also associated
with a depletion of norepinephrine (Petty
et al., 1993). It is postulated that the reduc-
tions in serotonergic and noradrenergic lev-
els reflects synthesis not being able to keep up
with demand (Charney et al., 2004). Animal
models also provide evidence that regular
aerobic exercise increases serotonergic and
noradrenergic levels in the brain, similar to
the effects of antidepressants (Praag, 1982;
Veale, 1987; Chaouloff, 1989; Meeusen
and De Meirleir, 1995). Researchers have
observed increased extraneuronal uptake
of norepinephrine and increased levels of
norepinephrine in the hippocampus and
frontal cortex of rodents after treadmill
training and wheel running (Dunn et al.,
1996; Dishman, 1997). Increases in serotonin
Effects of exercise and physical activity on anxiety
Elizabeth Anderson 1 and Geetha Shivakumar1,2*
1 VA North Texas Health Care System, Dallas, TX, USA
2 Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA
*Correspondence: geetha.shivakumar@va.gov
Edited by:
Eduardo Lusa Cadore, Federal University of Rio Grande do Sul, Brazil
Reviewed by:
Eduardo Lusa Cadore, Federal University of Rio Grande do Sul, Brazil

Frontiers in Psychiatry | Affective Disorders and Psychosomatic Research April 2013 | Volume 4 | Article 27 | 2
Anderson and Shivakumar Effects of exercise on anxiety
synthesis, metabolism, and release have
been noted following exercise (Dunn and
Dishman, 1991; Meeusen and De Meirleir,
1995; Wilson and Marsden, 1996; Chaouloff,
1997). Animal models utilizing chronic vol-
untary wheel running have also shown small
increases in serotonergic neural activity in
the dorsal raphe nucleus, an area of brain
that is abundant in serotonergic neurons,
during uncontrollable stress (Greenwood
et al., 2003). Treadmill exercise training also
increases levels of prepro-galanin mRNA,
suggesting that gene expression for galanin
is sensitive to the stress from exercise train-
ing and may have a “neuromodulating role”
in the noradrenergic response in the locus
ceruleus, an area of brain rich in noradren-
ergic neurons (O’Neal et al., 2001).
oPIoId systeM
Another possible mechanism for the anxio-
lytic effects of exercise is via mediation by
the endogenous opioid system. Endogenous
opioids have a role in the regulation of mood
and emotional responses (Bodnar and Klein,
2005). For example, abnormal levels of both
central and peripheral β-endorphins have
been discovered in individuals diagnosed
with depression (Scarone et al., 1990; Darko
et al., 1992). The endorphin hypothesis posits
that the mood elevations and reduced anxiety
following acute exercise is due to the release
and binding of β-endorphins (endogenous
opioids) to their receptor sites in the brain.
Studies demonstrate that exercise increases
endogenous opioid activity in the central and
peripheral nervous system and may induce a
euphoric state and reduce pain (Harber and
Sutton, 1984; Morgan, 1985; North et al.,
1990; Thorén et al., 1990). When opioid
antagonists were administered following
regular exercise, the endorphin produced
analgesic effects were attenuated, but there
were no changes in the mental health benefits
suggesting that the exercise-related surge in
endorphins may not completely account for
mental health benefits in these studies (Carr
et al., 1981; Moore, 1982; Howlett et al., 1984;
Thorén et al., 1990; Yeung, 1996).
neurotroPIc Factors
Brain-derived neurotrophic factor (BDNF),
the most abundant neurotrophin in the
brain has been linked to both anxiety and
depression. Stress-induced depressive and
anxious behaviors are correlated with
decreased BDNF levels especially in the hip-
pocampus (Duman and Monteggia, 2006).
Furthermore, infusions of BDNF into the
dorsal raphe nucleus have been shown to
have an a antidepressant effect (Altar, 1999).
Evidence also suggests that BDNF may be
a mediator of the anxiety reducing effects
of antidepressant medications (Chen et al.,
2006). Increases in BDNF following physical
activity have also been observed. Following
20 days of voluntary wheel running com-
pared to non-wheel running rats, BDNF
mRNA levels increased in the hippocam-
pus and caudal neocortex (Meeusen and De
Meirleir, 1995; Russo-Neustadt et al., 1999).
These changes in BDNF increases function-
ing in the serotonergic system and may pro-
mote neuronal growth (Altar, 1999).
evIdence For neurogenesIs
New neuronal growth in the adult brain,
particularly in the hippocampus, has been
implicated in the treatment of psychiatric
conditions including depression and anxi-
ety (Eisch, 2002). Detection and evaluation
of hippocampal neurogenesis is an active
area of investigation in recent years (Eisch,
2002). In primate models of chronic stress,
the hippocampus has been shown to be
highly sensitive to the toxic effects of exces-
sive glucocorticoids, thus impairing the
process of neurogenesis (Uno et al., 1989).
Neuroplasticity is further supported by the
stress-related changes found in studies of
hippocampus function. Animal studies have
shown exercise up regulates hippocampal
neurogenesis (Duman et al., 2001). Exercise
is also believed to positively influence sur-
rogate measures of adult hippocampal
neurogenesis such as β-endorphins, vas-
cular endothelial growth factor, BDNF,
and serotonin, all of which are thought be
common pathophysiologic mechanisms for
anxiety disorders.
PsychologIcal MechanIsMs
anxIety sensItIvIty and exPosure
Anxiety sensitivity is a term for the tendency
to misinterpret and catastrophize anxiety-
related sensations based on the belief that
they will result in disastrous physical, psy-
chological, and/or social outcomes (Broman-
Fulks and Storey, 2008; Smits et al., 2008).
McWilliams and Asmundson (2001) found
an inverse relationship between anxiety sen-
sitivity and exercise frequency and suggested
that this relationship was due to avoidance
of the physiological sensations of exercise
that may be interpreted as anxiety and
panic. A number of research studies have
pointed to the effectiveness of short-term
aerobic exercise to reduce anxiety sensitiv-
ity (Broman-Fulks and Storey, 2008; Smits
et al., 2008; Ströhle et al., 2009). Exposing
someone with high anxiety sensitivity to the
physiological symptoms they fear, such as
rapid heartbeat, in the context of physical
exercise increases their tolerance for such
symptoms (McWilliams and Asmundson,
2001). This exposure reveals that the feared
physiological sensations may be uncom-
fortable, but do not pose a serious threat
(Ströhle et al., 2009). Repeated exposures
through regular aerobic exercise may also
facilitate habituation to the feared sensations
(Beck and Shipherd, 1997).
selF-eFFIcacy
According to social cognitive theory, one’s
sense of self-efficacy regarding their ability
to exert control over potential threats has an
important relationship to anxiety arousal.
Individuals who trust their ability to man-
age potential threats (high self-efficacy) are
not plagued by thoughts of worry and expe-
rience lower levels of anxiety arousal. Based
on the theory of self-efficacy, Bandura pos-
ited that a treatment will be successful if
it is able to rebuild a sense of self-efficacy
by supplying experiences of self-mastery. It
has been debated that exercise can increase
self-efficacy by supplying experiences of
successfully coping with the stress of exer-
cising (Petruzzello et al., 1991). As fitness
improves, the individual receives feedback
of greater endurance, less pain, greater
duration capabilities, etc. As a result, self-
efficacy should increase (Petruzzello et al.,
1991). In fact, one study suggeste d that exer-
cise with an emphasis on increasing self-
efficacy, in this case, martial arts, was more
effective in reducing state anxiety than exer-
cise such as riding a stationary bike (Bodin
and Martinsen, 2004). In a study examining
the relationship between exercise intensity
and self-efficacy effects on anxiety reduc-
tion in a non-clinical population, research-
ers found that the influence of self-efficacy
on decreased anxiety was exhibited in the
moderate intensity exercise group, but not
in the light- and high-intensity exercise
groups (Katula et al., 1999). These two
studies suggest that exercise providing an
optimal level of challenge best utilizes the
power of self-efficacy.

www.frontiersin.org April 2013 | Volume 4 | Article 27 | 3
Anderson and Shivakumar Effects of exercise on anxiety
economic burden of anxiety disorders in the 1990s.
J. Clin. Psychiatry 60, 427–435.
Greenwood, B. N., Foley, T. E., Day, H. E., Campisi, J.,
Hammack, S. H., Campeau, S., et al. (2003). Freewheel
running prevents learned helplessness/behavioral
depression: role of dorsal raphe serotonergic neurons.
J. Neurosci. 23, 2889–2898.
Harber, V., and Sutton, J. (1984). Endorphins and exercise.
Sports Med. 1, 154.
Howlett, T. A., Tomlin, S., Ngahfoong, L., Rees, L. H., Bullen,
B. A., Skrinar, G. S., et al. (1984). Release of beta endor-
phin and met-enkephalin during exercise in normal
women: response to training. Br. Med. J. 288, 1950.
Irwin, J., Ahluwalia, P., Zacharko, R. M., and Anisman, H.
(1986). Central norepinephrine and plasma corticos-
terone following acute and chronic stressors: influence
of social isolation and handling. Pharmacol. Biochem.
Behav. 24, 1151–1154.
Jackson, E. M., and Dishman, R. K. (2006).
Cardiorespiratory fitness and laboratory stress: a
meta-egression analysis. Psychophysiology 43, 57–72.
Kant, G. J., Leu, J. R., Anderson, S. M., and Mougey, E. H.
(1987). Effects of chronic stress on plasma corticoster-
one, ACTH and prola ctin. Physiol. Behav. 40, 775–779.
Katula, J. A., Blissmer, B. J., and McAuley, E. (1999). Exercise
intensity and self-efficacy effects on anxiety reduction
in healthy, older adults. J. Behav. Med. 22, 233–247.
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas,
K. R., and Walters, E. E. (2005). Lifetime prevalence
and age-of-onset distributions of DSM-IV disorders
in the National Comorbidity Survey Replication. Arch.
Gen. Psychiatry 62, 593–602. [See comment; Erratum
appears in Arch. Gen. Psychiatry (2005) 62(7), 768].
Landgraf, R., Wigger, A., Holsboer, F., and Neumann,
I. (1999). Hyper-reactive hypothalamo-pituitary-
adrenocortical axis in rats bred for high anxiety-
related behaviour. J. Neuroendocrinol. 11, 405–407.
McWilliams, L. A., and Asmundson, G. J. G. (2001). Is
there a negative association between anxiety sensitiv-
ity and arousal-increasing substances and activities?
J. Anxiety Disord. 15, 161–170.
Meeusen, R., and De Meirleir, K. (1995). Exercise and
brain neurotransmission. Sports Med. 20, 160–188.
Miller, W., Seligman, M., and Kurlander, H. (1975).
Learned helplessness, depression, and anxiety. J . Ner v.
Ment. Dis. 161, 347–357.
Moore, M. (1982). Endorphins and exercise: a puzzling
relationship. Phys. Sportsmed. 10, 111–114.
Morgan, W. P. (1985). Affective beneficence of vigorous
physical activity. Med. Sci. Sports Exerc. 17, 94–100.
North, T. C., McCullagh, P., and Tran, Z. V. (1990). Effect
of exercise on depression. Exerc. Sport Sci. Rev. 18, 379.
O’Neal, H. A., Van Hoomissen, J. D., Holmes, P. V., and
Dishman, R. K. (2001). Prepro-galanin messenger
RNA levels are increased in rat locus coeruleus after
treadmill exercise training. Neurosci. Lett. 299, 69–72.
Petruzzello, S. J., Landers, D., Hatfield, B., Kubitz, K., and
Salazar, W. A. (1991). A meta-analysis on the anx-
iety-reducing effects of acute and chronic exercise.
Outcomes and mechanisms. Sports Med. 11, 143–182.
Petty, F., Kramer, G., and Wilson, L. (1992). Prevention of
learned helplessness: in vivo correlation with cortical
serotonin. Pharmacol. Biochem. Behav. 43, 361–367.
Petty, F., Kramer, G., Wilson, L., and Chae, Y.-L. (1993).
Learned helplessness and in vivo hippocampal
norepinephrine release. Pharmacol. Biochem. Behav.
46, 231–235.
Praag, H. V. (1982). Neurotransmitters and CNS disease.
Lancet 12, 1259–1264.
dIstractIon
Distraction or “time out” has been proposed
as another reason why exercise is effective at
reducing anxiety. Based on their study that
found that distraction techniques such as
meditation, and quiet rest were as effective
as a single session of exercise in reducing
state anxiety, Bahrke and Morgan (1978)
suggested that the anxiolytic benefits of
exercise may result from it being a distrac-
tion from stressors and a “time out” from
daily activities. The results of meta-analy-
ses supporting this hypothesis are mixed.
Exercise and cognitively based distraction
techniques were shown to have equal effec-
tiveness at reducing state anxiety, however
exercise was more effective in reducing
trait anxiety (Petruzzello et al., 1991). In
addition, the anxiolytic effects of exercise
have been shown to last for a longer period
of time than those produced by therapies
based on distraction techniques (Raglin and
Morgan, 1985).
conclusIon
There is strong evidence from animal
studies that exercise and regular activity
positively impacts the pathophysiological
processes of anxiety. Numerous studies
and meta-analyses show that exercise is also
associated with reduced anxiety in clinical
settings. Similar to the heterogenic nature
of the anxiety, no single mechanism suffi-
ciently accounts for the anxiolytic nature of
exercise. Physical activity positively impacts
a number of biological, as well as psycholog-
ical, mechanisms. The role of exercise in the
enhancement of neurogenesis in humans
has drawn significant attention in recent
years and its implications for anxiety dis-
orders are an exciting area of investigation.
Future studies are needed to further this
type of work, as well as studies specifically
exploring clinical applications of exercise in
anxiety disorders.
acknowledgMents
This work was supported by VISN 17 New
Investigator Award (PI Shivakumar).
reFerences
Altar, C. A. (1999). Neurotrophins and depression. Trends
Pharmacol. Sci. 20, 59–62.
APA. (2000). Diagnostic and Statistical Manual of Mental
Disorders, Text Revision, 4th Edn. Washington, D.C.:
American Psychiatric Association.
Åstrand, P.-O. (2003). Textbook of Work Physiology:
Physiological Bases of Exercise. Champaign: Human
Kinetics Publishers.
Bahrke, M. S., and Morgan, W. P. (1978). Anxiety reduc-
tion following exercise and meditation. Cognit. Ther.
Res. 2, 323–333.
Beck, J. G., and Shipherd, J. C. (1997). Repeated exposure
to interoceptive cues: does habituation of fear occur in
panic disorder patients? A preliminary report. Behav.
Res. Ther. 35, 551–557.
Bodin, T., and Martinsen, E. W. (2004). Mood and self-
efficacy during acute exercise in clinical depression. A
randomized, controlled study. J. Sport Exerc. Psychol.
26, 623–633.
Bodnar, R. J., and Klein, G. E. (2005). Endogenous opiates
and behavior: 2004. Peptides 26, 2629–2711.
Broman-Fulks, J. J., and Storey, K. M. (2008). Evaluation
of a brief aerobic exercise intervention for high anxiety
sensitivity. Anxiety Stress Coping 21, 117–128.
Carr, D. B., Bullen, B. A., Skrinar, G. S., Arnold, M. A.,
Rosenblatt, M., Beitins, I. Z., et al. (1981). Physical
conditioning facilitates the exercise-induced secretion
of beta-endorphin and beta-lipotropin in women. N.
Engl. J. Med. 305, 560–563.
Chaouloff, F. (1989). Physical exercise and brain mono-
amines: a review. Acta Physiol. Scand. 137, 1–13.
Chaouloff, F. (1997). Effects of acute physical exercise on cen-
tral serotonergic systems. Med. Sci. Sports Exerc. 29, 58–62.
Charney, D. S., Nestler, E. J., and Bunney, B. S. (2004).
Neurobiology of Mental Illness. Oxford: Oxford
University Press.
Chen, Z.-Y., Jing, D., Bath, K. G., Ieraci, A., Khan, T., Siao,
C.-J., et al. (2006). Genetic var iant BDNF (Val66Met)
polymorphism alters anxiety-related behavior. Sci.
Signal. 314, 140.
Crews, D. J., and Landers, D. M. (1987). A meta-analytic
review of aerobic fitness and reactivity to psycho-
social stressors. Med. Sci. Sports Exerc. 19(Suppl. 5),
S114–S120.
Darko, D., Risch, S., Gillin, J., and Golshan, S. (1992).
Association of beta-endorphin with specific clinical
symptoms of depression. Am. J. Psychiatry 149, 1162.
De Kloet, E. R., Joëls, M., and Holsboer, F. (2005). Stress
and the brain: from adaptation to disease. Nat. Rev.
Neurosci. 6, 463–475.
DHHS. (2002). Physical Activity Fundamental to
Preventing Disease. Washington: U.S. Department of
Health and Human Services, Office of the Assistant
Secretary for Planning and Evaluation.
Dishman, R. K. (1997). Brain monoamines, exercise, and
behavioral stress: animal models. Med. Sci. Sports
Exerc. 29, 63–74.
Droste, S. K., Gesing , A., Ulbricht, S., Müller, M. B., Linthorst,
A. C., and Reul, J. M. (2003). Effects of long-term vol-
untary exercise on the mouse hypothalamic-pituitary-
adrenocortical axis. Endocrinology 144, 3012–3023.
Duman, R. S., and Monteggia, L. M. A. (2006).
Neurotrophic model for stress-related mood disor-
ders. Biol. Psychiatry 59, 1116–1127.
Duman, R. S., Nakagawa, S., and Malberg, J. (2001).
Regulation of adult neurogenesis by antidepressant
treatment. Neuropsychopharmacology 25, 836–844.
Dunn, A. L., and Dishman, R. K. (1991). Exercise and the neu-
robiology of depression. Exerc. Sport Sci. Rev. 19, 41–98.
Dunn, A. L., Reigle, T. G., Youngstedt, S. D., and
Armstrong, R. B. (1996). Brain norepinephrine
and metabolites after treadmill training and wheel
running in rats. Med. Sci. Sports Exerc. 28, 204–209.
Eisch, A. J. (2002). Adult neurogenesis: implications for
psychiatry. Prog. Brain Res. 138, 315–342.
Greenberg, P. E., Sisitsky, T., Kessler, R. C., Finkelstein,
S. N., Berndt, E. R., Davidson, J. R., et al. (1999). The

Frontiers in Psychiatry | Affective Disorders and Psychosomatic Research April 2013 | Volume 4 | Article 27 | 4
Anderson and Shivakumar Effects of exercise on anxiety
Raglin, J. S., and Morgan, W. P. (1985). Influence of vigor-
ous exercise on mood state. Behav. Ther. 8, 179–183.
Rimmele, U., Zellweger, B. C., Marti, B., Seiler, R.,
Mohiyeddini, C., Ehlert, U., et al. (2007). Trained
men show lower cortisol, heart rate and psycho-
logical responses to psychosocial stress compared
with untrained men. Psychoneuroendocrinology 32,
627–635.
Russo-Neustadt, A., Beard, R. C., and Cotman, C. W.
(1999). Exercise, antidepressant medications, and
enhanced brain derived neurotrophic factor expres-
sion. Neuropsychopharmacology 21, 679–682.
Salmon, P. (2001). Effects of physical exercise on anxiety,
depression, and sensitivity to stress: a unifying theory.
Clin. Psychol. Rev. 21, 33–61.
Scarone, S., Gambini, O., Calabrese, G., Sacerdote, P.,
Bruni, M., Carucci, M., et al. (1990). Asymmetrical
distribution of beta-endorphin in cerebral hemi-
spheres of suicides: preliminary data. Psychiatry Res.
32, 159–166.
Smits, J. A., Berry, A. C., Rosenfield, D., Powers, M. B.,
Behar, E., and Otto, M. W. (2008). Reducing anxi-
ety sensitivity with exercise. Depress. Anxiety 25,
689–699.
Steckler, T., Holsboer, F., and Reul, J. M. (1999).
Glucocorticoids and depression. B est Pract. Res. Clin.
Endocrinol. Metab. 13, 597–614.
Ströhle, A., Graetz, B., Scheel, M., Wittmann, A., Feller, C.,
Heinz, A., et al. (2009). The acute antipanic and anxio-
lytic activity of aerobic exercise in patients with panic
disorder and healthy control subjects. J. Psychiatr. Res.
43, 1013–1017.
Thorén, P., Floras, J. S., Hoffmann, P., and Seals, D. R.
(1990). Endorphins and exercise: physiological
mechanisms and clinical implications. Med. Sci. Sports
Exerc. 22, 417–428.
Uno, H., Tarara, R., Else, J. G., Suleman, M. A., and
Sapolsky, R. M. (1989). Hippocampal damage asso-
ciated with prolonged and fatal stress in primates. J.
Neurosci. 9, 1705–1711.
van Minnen, A., Hendriks, L., and Olff, M. (2010). When
do trauma experts choose exposure therapy for PTSD
patients? A controlled study of therapist and patient
factors. Behav. Res. Ther. 48, 312–320.
Veale, D. M. W. D. C. (1987). Exercise and mental health.
Acta Psychiatr. Scand. 76, 113–120.
Wilson, W., and Marsden, C. (1996). In vivo meas-
urement of extracellular serotonin in the ventral
hippocampus during treadmill running. Be hav.
Pharmacol. 7, 101.
Yeung, R. R. (1996). The acute effects of exercise on mood
state. J. Psychosom. Res. 40, 123–141.
Conflict of Interest Statement: The authors declare
that research was conducted in the absence of any
commercial or financial relationships that could be
construed as a potential conflict of interest.
Received: 11 April 2013; accepted: 11 April 2013; published
online: 23 April 2013.
Citation: Anderson E and Shivakumar G (2013) Effects of
exercise and physical activity on anxiety. Front. Psychiatry
4:27. doi: 10.3389/fpsyt.2013.00027
This article was submitted to Frontiers in Affective Disorders
and Psychosomatic Research, a specialty of Frontiers in
Psychiatry.
Copyright © 2013 Anderson and Shivakumar. This is
an open-access article distributed under the terms of the
Creative Commons Attribution License, which permits use,
distribution and reproduction in other forums, provided the
original authors and source are credited and subject to any
copyright notices concerning any third-party graphics etc.