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American Journal

of Lifestyle Medicine
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Occupational Stress: The Influence of Obesity and Physical Activity/Fitness on Immune Function
Chun-Jung Huang and Edmund O. Acevedo
AMERICAN JOURNAL OF LIFESTYLE MEDICINE 2011 5: 486 originally published online 2 September 2011
DOI: 10.1177/1559827611418168
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American Journal of Lifestyle Medicine

Nov Dec 2011

Chun-Jung Huang, PhD,


and Edmund O. Acevedo, PhD

Occupational Stress:
The Inuence of Obesity
and Physical Activity/Fitness
on Immune Function
Abstract: Occupational stress can
affect physiological and psychological
homeostasis. In addition, the
occupational challenges associated
with firefighting and law enforcement
have been linked to increased
mortality ratios for ischemic heart
disease when compared with other
population cohorts. Laboratory studies
have shown that the exacerbation of
stress hormones (eg, catecholamines)
following dual challenge (physical
and psychological stress) may affect
immune system responses, which
may partially explain the link
between cardiovascular disease and
inflammation. Physical fitness has been
shown to attenuate both cardiovascular
and inflammatory cytokine responses
following physical and/or psychological
stress; however, criteria for safe and
effective occupation-specific fitness
levels have not been established.
In addition, firefighters and police
officers have high overweight and
obesity rates, which also contribute
significantly to the development
of cardiovascular disease. Future
investigation on the possible interaction
(additive or synergistic) of obesity and
psychological stress on the development
of cardiovascular diseases in these

professions is warranted, and a


criterion for fitness level should be
established for safe and effective
participation in occupation-related
activities.
Keywords: firefighters; police; military;
exercise; psychological stress; immunity;
cytokines; inflammation; obesity

unique combination of physical and


psychological stress. This combined
challenge may be associated with
elevated mortality risks.1 For example,
law enforcement officers and firefighters
have high mortality rates for ischemic
heart disease.1-4 Furthermore, Kales and
colleagues5 have demonstrated that
fire suppression activities result in an

A critical area of current interest is


the link between the CVD
[cardiovascular disease] and the
immune system that may explain, at
least in part, the relationship
between stress and CVD.
Overview of Occupational
Stress and the
Immune System
Numerous occupations, especially
emergency responders (ie, firefighters,
ambulance personnel, and police
officers), are often subject to a

increased risk of death to firefighters


(12-136 times higher) when compared
with nonemergency duties. These
professionals are exposed to a broad
range of stressful stimuli that may affect
the development of cardiovascular
disease (CVD). A critical area of current
interest is the link between the CVD and

DOI: 10.1177/1559827611418168. From the Department of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, Florida (CJH) and the
Department of Health and Human Performance, Virginia Commonwealth University, Richmond, Virginia (EOA). Address correspondence to Chun-Jung Huang, PhD, 777
Glades Road, FH-11A, Rm 126A, Boca Raton, FL 33431; e-mail: chuang5@fau.edu.
For reprints and permissions queries, please visit SAGEs Web site at http://www.sagepub.com/journalsPermissions.nav.
Copyright 2011 The Author(s)
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vol. 5 no. 6

the immune system that may explain, at


least in part, the relationship between
stress and CVD.
Stress hormones (ie, cortisol and
catecholamines) are thought to have
detrimental effects on the immune
system, leading to an imbalance between
innate (immediate antigen-nonspecific
defense) and adaptive immunity (specific
response to a particular foreign antigen
creating immunological memory) via
cytokine release from immune cells.6
In response to acute stress, the innate
immune promptly prepares to provide
immune protection followed by adaptive
immunity when exposed to repeated
or prolonged stress, whereas chronic
stress can suppress these immune
defenses. This stressimmune interaction
is an important antiviral defense and
fosters the elimination of invading
microorganisms.7,8 This review will focus
on the stress-induced changes in immune
cell distribution,9-12 which ensures that
the bodies immune response is efficient
or elicits an effective immunoprotection.
More directly related to the
cardiovascular system, this review will
also focus on the stress-induced proinflammatory response. Finally, recent
studies have reported approximately
77% overweight and obesity rates in
professionals such as young emergency
responders (firefighters and ambulance
recruits), police officers, and military
personnel.13-16 Thus, this review will also
discuss the synergistic effects of physical
activity, obesity, and psychological stress
on inflammation, which may enhance
our understanding of the link between
obesity, stress, and CVD.
CatecholamineInduced Immune
Cell Redistribution to
Concurrent Stress
Many studies in
psychoneuroimmunology have
investigated the effects of physical and
psychological stress on immune system
responses. An appropriate distribution of
peripheral immune cells provides for the
performance of surveillance and effector
functions of the immune system.17
The release of both catecholamines

American Journal of Lifestyle Medicine

and cortisol in response to either


psychological stress or physical stress
can mediate changes in the immune
cell distribution.18,19 However, Isowa
and colleagues11 have concluded that,
under acute psychological stress, the
influence of cortisol on immune function
is minimal and that the acute immune
response is primarily regulated by
catecholamines.
A number of experimental protocols
using laboratory-induced acute
psychological stressors have observed
transient immune cell redistribution via
b-adrenergic activation.10,18,20,21 Specifically,
following acute psychological stress,
elevation in monocytes, natural killer
(NK) cells, and cytotoxic T cells have been
observed,9,10,22 whereas helper T cells and
B cells have been shown to decrease.9-12
Furthermore, in response to acute physical
stress (physical activity), the magnitude of
these immune cell responses is dependent
on exercise intensity and duration.23
High-intensity exercise has been shown
to induce the release of catecholamines
with corresponding alterations in various
immune cells.24 Typically, following
exercise monocytes and NK cells exhibit
the greatest fluctuation followed by T
cells and B cells.25,26 Previous research
has demonstrated that the percentage
of CD3+ T cells and CD19+ B cells
(adaptive immunity) decrease with an
elevation in the percentage of NK cells
(innate immunity) following incremental
exercise.27 These findings indicate that
acute stress enhances innate immunity
and possibly suppresses adaptive
immunity and that these alterations can
be likely enhanced at higher intensities
of psychological and physical stress. The
appropriate redistribution of immune
cells in response to psychological and/
or physical stress is imperative to an
effective and efficient immune response
in preparation for potential invaders and
injury.17,28 This direction of enhancement
and suppression on immune function
is dependent on the duration and
magnitude of stress response. However,
when exposed to chronic stress,
immunoprotection can be suppressed
by decreasing immune cell number and
function, thereby promoting susceptibility
to diseases.

Previous studies have demonstrated


greater epinephrine (EPI) and
norepinephrine (NE) responses
to combined mental and physical
stress (dual stress condition) relative
to physical challenge/stress alone
in apparently healthy individuals29
and professional firefighters.30 This
finding suggests that the greater
catecholamine response to dual stress
may further alter the components of
innate immunity, specifically the proinflammatory components. Furthermore,
this response may be associated with
the combined mental and physical
stress of conducting fire suppression
activities and help explain the high
mortality rates in firefighters.5,31
Recently, Huang et al32 examined the
associations among catecholamines
and immune cell distribution in
professional firefighters exposed to a
computerized firefighting strategies and
tactics drill (FSTD; mental challenge)
while participating in moderate intensity
exercise. Firefighters participated in 2
counterbalanced exercise conditions on
a cycle ergometer: 37 minutes of cycle
ergometry at 60% Vo2max (exercise alone
condition; EAC) and 37 minutes of cycle
ergometry at 60% Vo2max along with 20
minutes of FSTD (firefighting strategies
condition; FSC). As expected, FSC elicited
significantly greater HR, NE, and EPI
when compared with EAC. Furthermore,
both EAC and FSC elicited increases in
NK cells. The percentages of CD3+ T
cells, CD3+CD4+ helper T cells, CD4/
CD8 ratio, CD19+ B cells, and total
lymphocytes were lower immediately
following both conditions. Although no
group differences were found in this
study, these results provide the basis for
further examination of the lymphocyte
subset redistribution following prolonged
or repeated bouts of physical and/or
psychological stress.
In addition, Huang et al32 found that
following the dual challenge, NE area
under the curve was negatively correlated
with percentage of CD19+ B cells
immediately after challenge, and HR was
negatively associated with the percentage
change in the CD4/CD8 ratio from before
to after challenge. These elevations in
NE and heart rate simultaneously in
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American Journal of Lifestyle Medicine

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response to the dual challenge suggest


greater sympathetic activation that, in
turn, could possibly explain the alteration
in the distribution of lymphocyte subsets,
resulting in ineffective cell-mediated
immune responses.33,34 It is important
to note that firefighters are engaged in
fire suppression activities with standard
work-to-rest ratios; approximately 15 to
20 minutes of work and then resting for
approximately 10 minutes.35 The repeated
workrest regimen of firefighting may
potentially exacerbate catecholamine
and heart rate responses,36,37 further
contributing to the perturbation of
lymphocyte subsets. Early studies have
reported reduced NK and cytotoxic cell
number/cytotoxicity and suppression
of lymphocyte proliferation in humans
after exposure to chronic stress.38,39 The
examination of the lymphocyte subset
redistribution following prolonged
or repeated bouts of physical and/or
psychological stress is warranted.
Synopsis

Elevated stress hormones alter immune


cell responses, and this important immune
system response coordinates a number
of the bodys adaptations to the stressor.
However, a combined physical and
psychological stress often experienced
chronically by emergency responders
exacerbates these stress hormone
responses, which may be a contributing
factor to the elevated risk of CVD and
increased proportionate mortality risks.
A greater understanding of stress
immune system interaction can assist in
finding strategies (eg, exercise training) to
overcome the inherent psychobiological
challenges associated with mentally and
physically demanding professions.
The Synergistic Effects
of Concurrent Stress
on Inflammation
Singhai40 has stated that one of
the earliest subclinical stages in the
atherosclerotic process is an impairment
of endothelium-dependent vasodilation,
also known as endothelial dysfunction,
and acute psychological stress induces
transient endothelial dysfunction.41 One
potential mechanism that links acute

psychological stress to endothelial


dysfunction is the level of circulating
pro-inflammatory cytokines, such as
tumor necrosis factor-a (TNF-a) and
interleukin-6 (IL-6), which have been
shown to play important roles in the
initiation and propagation of vascular
inflammation and may provide insight
into the mechanisms that explain the
inflammatory processes in health and
stress-related diseases.7,8,42-44
Many studies have used laboratoryinduced acute psychological stressors
to examine the inflammatory response.
Previous research has suggested
that individuals who have a greater
laboratory-induced stress response
are more likely to experience higher
stress in daily life,45 and this response
is associated with increased risk
for atherosclerosis.46 An increase in
circulating TNF-a and IL-6 was observed
following acute psychological stress47 via
activation of nuclear factor-kappa B.48,49
In addition, previous research has shown
that acute psychological stress exposure
is also associated with increased proinflammatory cytokine, IL-2 levels.50
Using a more prolonged stress model,
Uchakin et al51 have examined several
inflammatory cytokines following 24
hours of an examination in medical
students and found that IL-2 levels were
lower than the control group, but no
changes were observed in interferon-g
(IFN-g) and IL-10. Furthermore, Kang and
Fox52 also examined chronic academic
stress during examinations and found
that decreased IL-2 (in both peripheral
blood mononuclear cell [PBMC] and
whole blood measures) and IFN-g (only
PBMC) levels were observed whereas an
elevation was seen in IL-6 (in both PBMC
and whole blood measures).
The magnitude and direction of
inflammatory cytokine response (eg,
IL-2 and IL-6) to exercise vary and are
dependent on the acute or chronic nature
of the stimuli (intensity and duration).
For example, Akimoto et al53 examined
the effects of brief anaerobic maximal
exercise and found that plasma IL-12
increased significantly after exercise.
IL-12 has been demonstrated to generate
the IL-2 response, further enhancing
the activity of cytotoxic T cells and NK

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cells.54-56 In addition, Steensberg et al57


found that IL-6 increased following
2.5-h of treadmill exercise at 75% of
maximal oxygen uptake. It is important
to note that although IL-6 acts as a proinflammatory cytokine, it has also been
identified as an anti-inflammatory agent.
More specifically, Steensberg et al58
infused IL-6 to attain intense exerciseinduced concentrations in human
subjects and observed elevated antiinflammatory cytokines (eg, IL-10) 1
hour after IL-6 infusion. These findings
indicate that an elevation in circulating
IL-6 following exercise may initiate a
reciprocal anti-inflammatory response
that can promote recovery.
In a recent study, Ramey et al2
examined the inflammatory cytokine
response in law enforcement officers
and found that the job demand
(physical and psychological) assessed
by the Job Content Questionnaire was
positively associated with resting IL-b
and IL-6. Furthermore, Huang and
colleagues30 examined stress hormone
and immunological responses to a dual
challenge in professional firefighters.
This study used an FSTD as the mental
challenge and cycling at 60% of Vo2max
(physical stress) as described above.
This combination of physical and
psychological challenge activated the
sympatheticadrenalmedullary axis,
eliciting the release of catecholamines
(NE and EPI) and elevating HR.
Furthermore, firefighters demonstrated
greater IL-2 levels following the dual
challenge with a significant increase in
CD56+ lymphocytes (mostly NK cells)
in both conditions, but no change
was observed in cytotoxic T cells and
IL-6. These findings suggest that the
addition of a mental challenge to
physical stress can alter the hormonal
and immunological responses during
firefighting activities and, if exacerbated
or prolonged, may play a role in the
development of stress-related diseases.
Other investigators have found changes
in IL-6 following exercise using a
different protocol.59 More specifically,
Brenner et al59 used a protocol of 2
hours of cycle ergometry at 60% Vo2max,
whereas the duration in the Huang
et al study was 37 minutes. Furthermore,

vol. 5 no. 6

although the study by Huang et al30


did not demonstrate elevations in IL-6,
it is possible that changes occurred
following the last measure that was
taken at 1 hour of recovery. Previously,
an increase in IL-6 has been reported
to occur between 45 and 120 minutes
after acute psychological stress (eg,
Stroop Color Word and Mirror Tracing
Tasks).60-63 Interestingly, Groer et al64
examined blood and salivary IL-6 levels
in police officers following simulated
incident scenarios: motorcycle scenario
(2 minutes of a chase and traffic stop of a
person on a motorcycle) and workplace
scenario (6 minutes of tracking a gunman
through a building). This study did not
find elevated blood IL-6 levels in either
scenario, but a significant increase
in salivary IL-6 was observed in the
workplace scenario group after 10 and
30 minutes of stimulation. To foster a
better understanding of the cytokine
responses to occupational stress, further
studies with extended recovery periods
are needed.
A limited number of studies have
used a combination of acute laboratory
stressors as a paradigm to examine
the neuroendocrine and immuneinflammatory adaptations to physical
and mental challenge. To alleviate
the potential for the negative health
outcomes in these occupations (ie,
firefighting and law enforcement),
investigators should examine possible
mechanisms that may help explain
the inflammatory processes in health
and stress-related diseases. In turn, a
greater understanding of inflammatory
responses will facilitate efforts to address
the potential negative impact of the
immune system responses associated
with professions exposed to the dual
challenge.
Psychoneuroimmunological
Responses and Physical
Activity/Fitness
The benefits of physical activity
and fitness on physiological and
psychological health have been widely
investigated. One of the purported
benefits associated with aerobic fitness

American Journal of Lifestyle Medicine

is the attenuation of the cardiovascular


response during psychological stress
and recovery.65-67 Dienstbier65 has
proposed that this physiologically
toughened response is demonstrated by
an attenuation of central nervous system
activation, including the sympathoadrenal
axis, in response to a perceived threat.
More specifically, aerobically trained
individuals exhibit lower reactivity of the
sympathetic nervous system
(eg, heart rate) following acute
psychological stress.67-69 Furthermore,
physically active individuals have
exhibited lower state anxiety
responses.69,70 Although criteria for
safe and effective fitness level has not
been established in many occupations,
the International Association of Fire
Fighters71 and the National Fire Protection
Association72 have recommended
that firefighters achieve a maximal
oxygen uptake of at least 42 ml/kg/
min. Previous studies have documented
firefighter fitness levels (Vo2max) and
found an average Vo2max of 35 ml/kg/
min.32,73 However, Roberts et al73 has also
demonstrated an improvement in fitness
level (Vo2max) of 28% (35-45 ml/kg/min)
following 16 weeks of exercise training.
Most important, Yoo et al74 showed that
approximately 23% of law enforcement
officers who reported metabolic
syndrome were physically inactive. In a
cross-sectional study of 527 firefighters,
Durand et al75 demonstrated the CVD
risk factors such as triglyceride and lowdensity lipoprotein cholesterol levels
are negatively associated with time
and frequency of physical activity per
week. Furthermore, epidemiological
evidence consistently shows that regular
physical activity and exercise are
effective prevention and treatment for
CVD, type II diabetes, and stress-related
diseases.76-80 More specifically, previous
research has examined the effects of
physical fitness on the inflammatory
response. For example, a reduction in
pro-inflammatory levels (TNF-a and IL-6)
was found in patients with coronary
heart disease following aerobic exercise
training,81 and lower IL-6 concentrations
have been observed in individuals who
had self-reported higher physical activity

levels.82 In a cross-sectional study of


1004 participants, those who participated
in moderate to high physical activity
exhibited lower resting IL-6 levels
compared with sedentary individuals.83
Additionally, participation in exercise
training may result in beneficial
adaptations of physiological systems
(eg, low inflammatory response) that
are activated during acute psychological
stress. Interestingly, in response to
acute psychological stress, physical
fitness is associated with a diminished
pro-inflammatory cytokine response.84
Poole et al85 have also shown that mood
change is associated with IL-6 levels
following exercise withdrawal and
training. These findings indicate that
increased physical activity and higher
levels of physical fitness may result in
a more resilient immune defense and
greater stress protection. Thus, exercise
training program is likely a beneficial
intervention to reduce the risks of CVD
and stress-related diseases in occupations
such as firefighting and law enforcement,
and consideration should be given to
annual physical performance evaluations.
Future Research
Directions: Obesity and
Psychological Stress
Obesity-attributable illnesses are
associated with chronic inflammatory
responses such as elevated proinflammatory cytokine production and
activation of inflammatory signaling
pathways.86 A recent study reported
77% of young emergency responders
(firefighters and ambulance recruits)
were overweight and obese.13 Further
studies also reported similar overweight
and obese rates in other professions
such as law enforcement14 and the
military profession.14-16 Along with
physical illnesses, obesity is associated
with psychosocial disorders such as
depression and chronic anxiety.87,88
Interestingly, Yoo and Franke89 have
reported that obesity is the most
significant contributor of CVD in female
law enforcement officers, who elicit a
higher job-related stress level than male
law enforcement officers. Furthermore,
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chronic stress has been shown to be


associated with disturbances of the
hypothalamicpituitaryadrenal and
sympatheticadrenalmedullary axes
and is linked to abdominal adiposity.90
For example, elevated cortisol responses
to mental stress are associated with
high central adiposity,91-93 and with
corresponding elevations in pulse
pressure and heart rate.94,95 Interestingly,
Wirtz et al45 have demonstrated that
individuals with higher body mass index
demonstrated lower glucocorticoid
sensitivity, resulting in a diminished
ability to inhibit production of TNF-a
following acute psychological stress.
This finding suggests that in response
to acute psychological stress individuals
with higher body mass index exhibit
elevations in pro-inflammatory
cytokine production (eg, TNF-a) due to
diminished glucocorticoid suppression.
Recent studies have shown that obese
subjects exhibit higher circulating and
in vitro IL-6 levels compared with
normal-weight subjects in response to
acute psychological stress.92,96 Because
b-adrenergic receptors have been
shown to have an inhibitory effect
on the release of pro-inflammatory
cytokines (ie, TNF-a and IL-6),97,98
these results suggest the possibility that
obesity could diminish the inhibitory
effect of b-adrenergic receptors on the
release of pro-inflammatory cytokines
in response to psychological stress. In
addition, leptin, an adipocyte-derived
hormone, is positively associated with
elevated percentage body fat and
plays an important role in metabolism,
adiposity, and vascular inflammation,
and it has recently been implicated
in the development of coronary heart
disease.99 Furthermore, recent research
has shown that people who undergo
acute psychological stress demonstrate
increases in leptin levels, and these
increases are positively correlated with
waist circumference.100,101 Brydon and
colleagues101 also showed that a positive
correlation between basal circulating
leptin and IL-6 responses in response to
mental stress.
It is important to note that a recent
investigation has demonstrated that

peripheral blood mononuclear cells were


involved in the elevated concentrations
of pro-inflammatory cytokines (eg,
TNF-a and IL-6) in obese individuals,102
but no differences in the number
of immune cell subsets including
peripheral blood mononuclear cells
(eg, monocytes and lymphocytes)
have been observed between normalweight and obese subjects following
acute psychological stress.92 This
suggests that the association of obesity
with pro-inflammatory cytokines in
response to acute psychological stress
is not likely due to differences in
immune cell subsets, and thus, the
possible mechanisms contributing to
the relationship of the stress response,
obesity, and pro-inflammatory
cytokines still remains unknown. Future
investigation on the possible interaction
(additive or synergistic) of obesity and
psychological stress on the development
of cardiovascular diseases in these
professions is warranted and may help in
finding practical and innovative strategies
(eg, weight loss, exercise training, and
pharmacological interventions) for the
prevention and treatment of stressrelated diseases.
Conclusion
Occupational stress, in particular
combined physical and psychological
stress, often experienced by firefighter,
military personnel, and law enforcement
officers may be a contributing factor
to the elevated risk of CVD and stressrelated diseases and relative increased
mortality. Many studies have supported
the benefits of physical activity on
physiological and psychological health
including greater immune defense and
stress protection. Furthermore, high
rates of obesity have been reported in
many occupations, and studies have
demonstrated that obesity exacerbates
the inflammatory responses (eg, elevated
pro-inflammatory cytokine production)
following psychological stress. Thus, it
seems apparent that a criterion for fitness
level should be established for safe and
effective participation in occupationrelated activities. Fitness training

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programs should also be implemented


to improve physical fitness levels for
workers in these occupations, and
annual physical fitness and performance
evaluations should be conducted. Finally,
while the mechanisms contributing to
the relationship of the stress response,
obesity, and pro-inflammatory cytokines
still remains unknown, programs to
encourage and support emergency
responders in achieving and/or
maintaining healthy body weight may
produce health benefits. AJLM
References
1.

Hessl SM. Police and corrections. Occup


Med. 2001;16:39-49.
2. Ramey SL, Downing NR, Franke WD,
Perkhounkova Y, Alasagheirin MH.
Relationships among stress measures,
risk factors and inflammatory biomarkers
in law enforcement officers [published
online ahead of print May 17, 2011]. Biol
Res Nurs. doi:10.1177/1099800410396356
3. Baris D, Garrity TJ, Telles JL, Heineman EF,
Olshan A, Zahm SH. Cohort mortality
study of Philadelphia firefighters. Am J Ind
Med. 2001;39:463-476.
4. Calvert GM, Merling JW, Burnett CA.
Ischemic heart disease mortality and
occupation among 16- to 60-yearold males. J Occup Environ Med.
1999;41:960-966.
5. Kales SN, Soteriades ES, Christophi
CA, Christiani DC. Emergency duties
and deaths from heart disease among
firefighters in the United States. N Engl J
Med. 2007;356:1207-1215.
6. Elenkov IJ, Chrousos GP. Stress hormones,
proinflammatory and anti-inflammatory
cytokines, and autoimmunity. Ann N Y
Acad Sci. 2002;966:290-303.
7. Paulose M, Bennett BL, Manning AM,
Essani K. Selective inhibition of TNFalpha induced cell adhesion molecule.
Microb Pathog. 1998;25:33-41.
8. Black PH. The inflammatory
consequences of psychologic stress:
relationship to insulin resistance, obesity,
atherosclerosis and diabetes mellitus,
type II. Med Hypotheses. 2006;67:
879-891.
9. Mills PJ, Dimsdale JE, Nelesen RA, Dillon E.
Psychologic characteristics associated
with acute stressor-induced leukocyte
subset redistribution. J Psychosom Res.
1996;40:417-423.
10. Willemsen G, Carrol D, Ring C, Drayson M.
Cellular and mucosal immune reactions
to mental and cold stress: associations

vol. 5 no. 6

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

with gender and cardiovascular reactivity.


Psychophysiology. 2002;39:222-228.
Isowa T, Ohira H, Murashima S. Reactivity
of immune, endocrine and cardiovascular
parameters to active and passive acute
stress. Biol Psychol. 2004;65:101-120.
Burleson MH, Malarkey WB, Casioppo JT,
et al. Postmenopausal hormone replacement:
effects on autonomic, neuroendocrine, and
immune reactivity to brief psychological
stressors. Psychosom Med. 1998;60:17-25.
Tsismenakis AJ, Christophi CA, Burress JW,
Kinney AM, Kim M, Kales SN. The
obesity epidemic and future emergency
responders. Obesity (Silver Spring).
2009;17:1648-1650.
Franke WD, Ramey SL, Shelley MC 2nd.
Relationship between cardiovascular
disease morbidity, risk factors, and stress
in a law enforcement cohort. J Occup
Environ Med. 2002;44:1182-1189.
Ramey SL, Downing NR, Franke WD.
Milwaukee police department retirees:
cardiovascular disease risk and morbidity
among aging law enforcement officers.
AAOHN J. 2009;57:448-453.
Hsu LL, Nevin RL, Tobler SK, Rubertone MV.
Trends in overweight and obesity among
18 year-old applicants to the United States
military, 1993-2006. J Adolesc Health.
2007;41:610-612.
Dhabhar FS, Miller AH, McEwen BS,
Spencer RL. Effects of stress on immune
cells distribution. Dynamics and
hormonal mechanisms. J Immunol.
1995;154:5511-5527.
Benschop RJ, Schedlowski M, Wienecke H,
Jacobs R, Schmidt RE. Adrenergic
control of natural killer cell circulation
and adhesion. Brain Behav Immun.
1997;11:321-332.
Rhind SG, Shek PN, Shephard RJ. The
impact of exercise on cytokines and
receptor expression. Exerc Immunol Rev.
1995;1:97-148.
Benschop RJ, Nijkamp FP, Ballieux RE,
Heijnen CJ. The effects of betaadrenoceptor stimulation on adhesion
of human natural killer cells to
cultured endothelium. Br J Pharmacol.
1994;113:1311-1316.
Benschop RJ, Rodriguez-Feuerhahn M,
Schedlowski M. Catecholamine-induced
leukocytosis: early observations, current
research, and future directions. Brain
Behav Immun. 1996;10:77-91.
Bosch JA, Berntson GG, Cacioppo JT,
Dhabhar FS, Marucha PT. Acute stress
evokes selective mobilization of T cells that
differ in chemokine receptor expression:
a potential pathway linking immunologic
reactivity to cardiovascular disease. Brain
Behav Immun. 2003;17:251-259.

American Journal of Lifestyle Medicine

23. Gleeson M. Nieman DC, Pedersen BK.


Exercise, nutrition, and immune function. J
Sports Sci. 2004;22:115-125.
24. Natale VM, Brenner IK, Moldoveanu AI,
Vasiliou P, Shek P, Shephard RJ. Effects of
three different types of exercise on blood
leukocyte count during and following
exercise. So Paulo Med J. 2003;121:9-14.
25. Hong S, Mills PJ. Effects of an exercise
challenge on mobilization and surface
marker expression of monocyte subsets
in individuals with normal vs. elevated
blood pressure. Brain Behav Immun.
2008;22:590-599.
26. Rhind SG, Shek PN, Shinkai S, Shepard RJ.
Effects of moderate endurance exercise
and training on in vitro lymphocyte
proliferation, interleukin-2 (IL-2)
production, and IL-2 receptor expression.
Eur J Appl Physiol. 1996;74:348-360.
27. Moyna NM, Acker GR, Fulton JR, et al.
Lymphocyte function and cytokine
production during incremental exercise in
active and sedentary males and females.
Int J Sports Med. 1996;17:585-591.
28. Dhabhar FS, McEwen BS. Acute stress
enhances while chronic stress suppresses
cell-mediated immunity in vivo: a potential
role for leukocyte trafficking. Brain Behav
Immun. 1997;11:286-306.
29. Webb HE, Weldy ML, Fabianke-Kadue EC,
Orndorff GR, Kamimori GH, Acevedo EO.
Psychological stress during exercise:
cardiorespiratory and hormonal response.
Eur J Appl Physiol. 2008;104:973-981.
30. Huang CJ, Webb HE, Garten RS,
Kamimori GH, Evans RK, Acevedo EO.
Stress hormones and immunological
responses to a dual challenge in
professional firefighters. Int J Psychophysiol.
2010;75:312-318.
31. Beaton R, Murphy S, Johnson C, Pike K,
Corneil W. Exposure to duty-related
incident stressors in urban firefighters
and paramedics. J Trauma Stress.
1998;11:821-828.
32. Huang CJ, Webb HE, Garten RS,
Kamimori GH, Acevedo EO. Psychological
stress during exercise: lymphocyte subset
redistribution in firefighters. Physiol Behav.
2010;101:320-326.
33. Kimura K, Isowa T, Ohira H, Murashima S.
Temporal variation of acute stress response
in sympathetic nervous and immune
systems. Biol Psychol. 2005;70:131-139.
34. Kimura K, Isowa T, Matsunaga M,
Murashima S, Ohira H. The temporal
redistribution pattern of NK cells under
acute stress based on CD62L adhesion
molecule expression. Int J Psychophysiol.
2008;70:63-69.
35. US Fire Administration. Health and
Wellness Guide. Emmitsburg, MD: Federal

36.

37.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.

48.

Emergency Management Agency, US Fire


Administration; 2004. (Publication No.
FA-267)
Ray MR, Basu C, Roychoudhury S,
Banik S, Lahiri T. Plasma catecholamine
levels and neurobehavioral problems
in Indian firefighters. J Occup Health.
2006;48:210-215.
Ronsen O, Haug E, Pedersen BK, Bahr R.
Increased neuroendocrine response to a
repeated bout of endurance exercise. Med
Sci Sports Exerc. 2001;33:568-575.
Kiecolt-Glaser JK, Glaser R, Gravenstein S,
Malarkey WB, Sheridan J. Chronic stress
alters the immune response to influenza
virus vaccine in older adults. Proc Natl
Acad Sci U S A. 1996;93:3043-3047.
Maisel AS, Michel MC. Beta-adrenorecetor
control of immune function in congestive
heart failure. Br J Clin Pharmacol.
1990;30:49S-53S.
Singhai A. Endothelial dysfunction: role
in obesity-related disorders and the
early original of CVD. Proc Nutr Soc.
2005;64:15-22.
Ghiadoni L, Donald AE, Cropley M, et al.
Mental stress induces transient endothelial
dysfunction in humans. Circulation.
2000;102:2473-2478.
Ridker PM, Rifai N, Pfeffer M, Sacks F,
Lepage S, Braunwald E. Elevation of
tumor necrosis factor-alpha and increased
risk of recurrent coronary events after
myocardial infarction. Circulation.
2000;101:2149-2153.
Niskanen L, Laaksonen DE, Nyyssonen K,
et al. Inflammation, abdominal obesity,
and smoking as predictors of hypertension.
Hypertension. 2004;44:859-865.
Tosi MF. Innate immune responses
to infection. J Allergy Clin Immunol.
2005;116:241-249.
Wirtz PH, Ehlert U, Emini L, Suter T.
Higher body mass index (BMI) is
associated with reduced glucocorticoid
inhibition of inflammatory cytokine
production following acute psychological
stress in men. Psychoneuroendocrinology.
2008;33:1102-1110.
Kamarck TW, Everson SA, Kaplan GA, et al.
Exaggerated blood pressure responses
during mental stress are associated with
enhanced carotid atherosclerosis in
middle-aged Finnish men: findings from
the Kuopio Ischemic Heart Disease Study.
Circulation. 1997;96:3842-3848.
Steptoe A, Willemsen G, Owen N, Flower L,
Mohamed-Ali V. Acute mental stress
elicits delayed increases in circulating
inflammatory cytokine levels. Clin Sci
(Lond). 2001;101:185-192.
Barnes PJ, Karin M. Nuclear factor-kappaB:
a pivotal transcription factor in chronic

491

Downloaded from ajl.sagepub.com at WALDEN UNIVERSITY on August 27, 2014

American Journal of Lifestyle Medicine

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

Nov Dec 2011

inflammatory diseases. N Engl J Med.


1997;226:1066-1071.
Bierhaus A, Wolf J, Andrassy M, et al. A
mechanism converting psychosocial stress
into mononuclear cell activation. Proc
Natl Acad Sci U S A. 2003;100:1920-1925.
Heinz A, Hermann D, Smolka MN, et al.
Effects of acute psychological stress on
adhesion molecules, interleukins and
sex hormones: implications for coronary
heart disease. Psychopharmacology (Berl).
2003;165:111-117.
Uchakin PN, Tobin B, Cubbage
M, Marshall G Jr, Sams C. Immune
responsiveness following academic stress
in first-year medical stress. J Interferon
Cytokine Res. 2001;21:687-694.
Kang DH, Fox C. Th1 and Th2 cytokine
responses to academic stress. Res Nurs
Health. 2001;24:245-257.
Akimoto T, Akama T, Tatsuno M, Saito M,
Kono I. Effect of brief maximal exercise on
circulating levels of interleukin-12. Eur J
Appl Physiol. 2000;81:510-512.
Kobayashi M, Fitz L, Ryan M, et al.
Identification and purification of natural
killer cell stimulatory factor (NKSF), a
cytokine with multiple biologic effects
on human lymphocyte. J Exp Med.
1989;170:827-845.
Morel PA, Oriss TB. Crossregulation
between Th1 and Th2 cells. Crit Rev
Immunol. 1998;18:275-303.
Stern AS, Podlaski FJ, Hulmes JD,
et al. Purification to homogeneity
and partial characterization of cytoxic
lymphocyte maturation factor from human
B-lymphoblastoid cells. Proc Natl Acad Sci
U S A. 1990;87:6808-6812.
Steensberg A, Toft AD, Bruunsgaard H,
Sandmand M, Halkjaer-Kristensen J,
Pedersen BK. Strenuous exercise
decreases the percentage of type 1 T
cells in the circulation. J Appl Physiol.
2001;9:1708-1712.
Steensberg A, Fischer CP, Keller C,
Mller K, Pedersen BK. IL-6 enhances
plasma IL-1ra, IL-10, and cortisol in
humans. Am J Physiol Endocrinol Metab.
2003;285:E433-E437.
Brenner IK, Natale VM, Vasiliou P,
Moldoveanu AI, Shek PN, Shephard RJ.
Impact of three different types of exercise
on components of the inflammatory
response. Eur J Appl Physiol Occup
Physiol. 1999;80:452-460.
Brydon L, Edwards S, Mohamed-Ali V,
Steptoe A. Socioeconomic status and stressinduced increases in interleukin-6. Brain
Behav Immun. 2004;18:281-290.
Kunz-Ebrecht SR, Mohamed-Ali V, Feldman
PJ, Kirschbaum C, Steptoe A. Cortisol
responses to mild psychological stress are

62.

63.

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

inversely associated with proinflammatory


cytokines. Brain Behav Immun.
2003;17:373-383.
Owen N, Steptoe A. Natural killer cell and
proinflammatory cytokine responses to
mental stress: associations with heart rate
and heart rate variability. Biol Psychol.
2003;63:101-115.
Steptoe A, Owen N, Kunz-Ebrecht S,
Mohamed-Ali V. Inflammatory cytokines,
socioeconomic status, and acute stress
responsivity. Brain Behav Immun.
2002;16:774-784.
Groer M, Murphy R, Bunnell W, et al.
Salivary measures of stress and immunity
in police officers engaged in simulated
critical incident scenarios. J Occup Environ
Med. 2010;52:595-602.
Dienstbier RA. Arousal and physiological
toughness: Implications for mental
and physical health. Psychol Rev.
1989;96:84-100.
Sothmann MS, Buckworth J, Claytor RP,
Cox RH, White-Welkley JE, Dishman RK.
Exercise training and the cross-stressor
adaptation hypothesis. Exerc Sport Sci Rev.
1996;24:267-287.
Spalding TW, Lyon LA, Steel DH, Hatfield BD.
Aerobic exercise training and
cardiovascular reactivity to psychological
stress in sedentary young normotensive
men and women. Psychophysiology.
2004;41:552-562.
Acevedo EO, Webb HE, Weldy ML,
Fabianke EC, Orndorff GR, Starks MA.
Cardiorespiratory response of high fit
and low fit subjects to mental challenge
during exercise. Int J Sports Med.
2006;27:1013-1022.
Rimmele U, Seiler R, Marti B, Wirtz PH,
Ehlert U, Heinrichs M. The level of
physical activity affects adrenal and
cardiovascular reactivity to psychosocial
stress. Psychoneuroendocrinology.
2009;34:190-198.
Rimmele U, Zellweger BC, Marti B,
et al. Trained men show lower cortisol,
heart rate and psychological responses
to psychosocial stress compared with
untrained men. Psychoneuroendocrinology.
2007;32:627-635.
International Association of Fire Fighters.
The Fire Service Joint Labor Management
Wellness-Fitness Initiative. 2nd ed.
Washington, DC: International Association
of Fire Fighters; 2000.
National Fire Protection Association.
NFPA Association 1582: Standard on
Comprehensive Occupational Medical
Program for Fire Departments. Quincy, MA:
National Fire Protection Association; 2007.
Roberts MA, ODea J, Boyce A, Mannix ET.
Fitness levels of firefighter recruits

492

Downloaded from ajl.sagepub.com at WALDEN UNIVERSITY on August 27, 2014

before and after a supervised exercise


training program. J Strength Cond Res.
2002;16:271-277.
74. Yoo H, Eisenmann J, Franke W.
Independent and combined influence
of physical activity and perceived stress
on the metabolic syndrome in male law
enforcement officers. J Occup Environ Med.
2009;51:46-53.
75. Durand G, Tsismenakis AJ, Jahnke SA,
Baur DM, Christophi CA, Kales SN.
Firefighters physical activity: relation to
fitness and cardiovascular disease risk
[published online ahead of print February
28, 2011]. Med Sci Sports Exerc.
76. Booth FW, Chakravarthy MV, Gordon SE,
Spangenburg EE. Waging war on physical
inactivity: using modern molecular
ammunition against an ancient enemy. J
Appl Physiol. 2002;93:3-30.
77. Barlow CE, LaMonte MJ, Fitzgerald SJ,
Kampert JB, Perrin JL, Blair SN.
Cardiorespiratory fitness is an
independent predictor of hypertension
incidence among initially normotensive
healthy women. Am J Epidemiol.
2006;163:142-150.
78. Nabkasorn C, Miyai N, Sootmongkol A,
et al. Effects of physical exercise on
depression, neuroendocrine stress
hormones and physiological fitness
in adolescent females with depressive
symptoms. Eur J Public Health.
2006;16:179-184.
79. Ketelhut RG, Franz IW, Scholze J. Regular
exercise as an effective approach in
antihypertensive therapy. Med Sci Sports
Exerc. 2004;36:4-8.
80. Warburton DE, Nicol CW, Bredin SS.
Health benefits of physical activity: the
evidence. CMAJ. 2006;174:801-809.
81. Goldhammer E, Tanchilevitch A, Maor I,
Beniamini Y, Rosenschein U, Sagiv M.
Exercise training modulates cytokines
activity in coronary heart disease patients.
Int J Cardiol. 2005;100:93-99.
82. Pischon T, Hankinson SE, Hotamisligil GS,
Rifai N, Rimm EB. Leisure-time physical
activity and reduced plasma levels of
obesity-related inflammatory markers. Obes
Res. 2003;11:1055-1064.
83. Elosua R, Bartali B, Ordovas JM, Corsi AM,
Lauretani F, Ferrucci L; InCHIANTI
Investigators. Association between
physical activity, physical performance,
and inflammatory biomarkers in an
elderly population: the InCHIANTI
study. J Gerontol Ser A Biol Sci Med Sci.
2005;60:760-767.
84. Hamer M, Steptoe A. Association between
physical fitness, parasympathetic control,
and proinflammatory responses to mental
stress. Psychosom Med. 2007;69:660-666.

vol. 5 no. 6

85. Poole L, Hamer M, Wawrzyniak AJ,


Steptoe A. The effects of exercise
withdrawal on mood and inflammation
cytokine responses in humans. Stress.
2011;14:439-447.
86. Festa A, DAgostino R Jr, Howard G,
Mykknen L, Tracy RP, Haffner SM.
Chronic subclinical inflammation as
part of the insulin resistance syndrome:
the Insulin Resistance Atherosclerosis
Study (IRAS). Circulation.
2000;102:42-47.
87. Petry NM, Barry D, Pietrzak RH, Wagner JA.
Overweight and obesity are associated
with psychiatric disorders: results from the
National Epidemiologic Survey on alcohol
and related conditions. Psychosom Med.
2008;70:288-297.
88. Stunkard AJ, Faith MS, Allison KC.
Depression and obesity. Biol Psychiatry.
2003;54:330-337.
89. Yoo H, Franke WD. Stress and
cardiovascular disease risk in female law
enforcement officers. Int Arch Occup
Environ Health. 2011;84:279-286.
90. Bjorntorp P. Do stress reactions cause
abdominal obesity and comorbidities?
Obes Rev. 2001;2:73-86.
91. Epel ES, McEwen B, Seeman T, et al. Stress
and body shape: stress-induced cortisol
secretion is consistently greater among

American Journal of Lifestyle Medicine

women with central fat. Psychosom Med.


2000;62:623-632.
92. Benson S, Arck PC, Tan S, et al. Effects of
obesity on neuroendocrine, cardiovascular
and immune cell responses to acute
psychological stress in premenopausal
women. Psychoneuroendocrinology.
2009;34:181-189.
93. Rosmond R, Dallman M, Bjorntorp P.
Stress-related cortisol secretion in men:
relationships with abdominal obesity and
endocrine, metabolic, and hemodynamic
abnormalities. J Clin Endocrinol Metab.
1998;83:1853-1859.
94. Ljung T, Holm G, Friberg P, et al. The
activity of the hypothalamic-pituitary-adrenal
axis and the sympathetic nervous system in
relation to waist/hip circumference ratio in
men. Obes Res. 2000;8:487-495.
95. Waldstein SR, Burns HO, Toth MJ,
Poehlman ET. Cardiovascular reactivity
and central adiposity in older
African Americans. Health Psychol.
1999;18:221-228.
96. Huang CJ, Stewart JK, Franco RL, et al.
LPS-stimulated tumor necrosis factor-alpha
and interleukin-6 mRNA and cytokine
responses following acute psychological
stress [published online ahead of print May
19, 2011]. Psychoneuroendocrinology.
doi:10.1016/j.psyneuen.2011.04.009

97. Hasko G, Szabo C. Regulation of cytokine


and chemokine production by transmitters
and co-transmitters of the autonomic
nervous system. Biochem Pharmacol.
1998;56:1079-1087.
98. Nance DM, Sanders VM. Autonomic
innervations and regulation of the
immune system (1987-2007). Brain Behav
Immun. 2007;21:736-745.
99. Wannamethee SG, Tchernova J,
Whincup P, et al. Plasma leptin:
associations with metabolic,
inflammatory and haemostatic risk
factors for cardiovascular disease.
Atherosclerosis. 2007;191:418-426.
100. Otsuka R, Yatsuya H, Tamakoshil K,
Matsushita K, Wada K, Toyoshima H.
Perceived psychological stress and
serum leptin concentrations in
Japanese men. Obesity (Silver Spring).
2006;14:1832-1838.
101. Brydon L, Wright CE, ODonnell K, Zachary
I, Wardle J, Steptoe A. Stress-induced
cytokine responses and central adiposity
in young women. Int J Obes (Lond).
2008;32:443-450.
102. Ghanim H, Aljada A, Hofmeyer D, Syed
T, Mohanty P, Dandona P. Circulating
mononuclear cells in the obese are in
a proinflammatory state. Circulation.
2004;110:1564-1571.

493

Downloaded from ajl.sagepub.com at WALDEN UNIVERSITY on August 27, 2014

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