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Exercise and circulating cortisol levels: The intensity threshold effect
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ABSTRACT. This study examined the influence of exercise intensity upon the cortisol response of the hypothalamic-pituitary-
adrenal (HPA) axis. Specifically, we examined exercise at intensities of 40, 60, and 80% maximal oxygen uptake (VO2max) in an
attempt to determine the intensity necessary to provoke an increase in circulating cortisol. Twelve active moderately trained
men performed 30 min of exercise at intensities of 40, 60, and 80% of their VO2max, as well as a 30-min resting-control session
involving no exercise on separate days. Confounding factors such as time of day – circadian rhythms, prior diet – activity pat-
terns, psychological stress, and levels of exercise training were controlled. Cortisol and ACTH were assessed in blood collect-
ed immediately before (pre-) and after (post-) each experimental session. Statistical analysis involved repeated measures anal-
ysis of variance and Tukey post-hoc testing. The percent change in cortisol from pre- to post-sampling at each session was: rest-
ing-control, 40, 60, and 80% sessions (mean±SD) =–6.6±3.5%, +5.7±11.0%, +39.9±11.8%, and +83.1±18.5%, respectively. The 60%
and 80% intensity magnitude of change was significantly greater than in the other sessions, as well as from one to another. The
ACTH responses mirrored those of cortisol, but only the 80% exercise provoked a significant (p<0.05) increase pre- to post-ex-
ercise. The calculated changes in plasma volume for the resting-control, 40%, 60%, and 80% sessions were: +2.2±3.0%, –9.9±5.0%,
–15.6±3.5%, and –17.2±3.3%, respectively. Collectively, the cortisol findings support the view that moderate to high intensity ex-
ercise provokes increases in circulating cortisol levels. These increases seem due to a combination of hemoconcentration and
HPA axis stimulus (ACTH). In contrast, low intensity exercise (40%) does not result in significant increases in cortisol levels, but,
once corrections for plasma volume reduction occurred and circadian factors were examined, low intensity exercise actually re-
sulted in a reduction in circulating cortisol levels.
(J. Endocrinol. Invest. 31: ??-??, 2008)
©2008, Editrice Kurtis
INTRODUCTION
Cortisol is a glucocorticoid hormone secreted by the adrenal
cortex in response to physical, psychological, or physiological
stressors (1, 2). One specific stressor known to drastically
modify the circulating levels of cortisol in the human body is
physical exercise (3, 4).
In response to exercise, the hypothalamus secretes CRH. In
turn, CRH activates the anterior pituitary, stimulating the re-
lease of ACTH, and this stimulates the adrenal cortex to re-
lease cortisol (5). Once released, cortisol is taken up by a vari-
ety of tissues throughout the body, such as skeletal muscle, adi-
pose tissue, and the liver. At these different tissues, the pres-
ence of cortisol mediates critical physiological processes which
aid in exercise capacity and recovery, e.g., promoting proteins in
the skeletal muscle to be broken down into amino-acids, and
triglycerides in adipose tissue to be hydrolyzed into free fatty
acids and glycerol (1, 4, 5). In addition, the presence of very high
circulating levels of cortisol may stimulate gluconeogenesis in
the liver, providing additional carbohydrate for energy produc-
tion (5). The secretion of cortisol is regulated by negative feed-
back, in which high circulating levels signal the anterior pituitary
to decrease ACTH secretion. Conversely, increased levels of
ACTH and, or cortisol can signal the hypothalamus to decrease
CRH secretion. This interconnected feedback loop is referred
to as the hypothalamic-pituitary-adrenocortical (HPA) axis (6).
As previously noted, exercise can act as a stimulus to the HPA
axis, resulting in significant increases in circulating cortisol lev-
els. Cortisol levels increase at a rate relatively proportional to
the exercise intensity, but reach a final level dependent upon
the total duration (time) of an exercise session (3, 4). This
acute exercise response can be influenced by exercise training
status, but appears to be vastly different only when comparing
sedentary individuals to highly trained individuals (1, 7).
Interestingly, there is some ambiguity in the literature regarding
the minimum intensity of exercise (i.e., threshold), necessary to
provoke a cortisol response from the HPA axis (1, 8). Most ex-
ercise physiology reference sources suggest that exercise at or
above 60% of an individual’s maximal oxygen consumption
(VO2max) generally produces a significant increase in circulating
cortisol. However, several studies have shown exercise at or
above this intensity have failed to provoke a cortisol response
(9-11). It is unclear why these studies failed to see significant cor-
tisol increases. One reason may relate to the research study de-
sign employed. Cortisol is a highly circadian hormone and in some
cases researchers have not conducted an appropriate resting-
control evaluation of cortisol profiles prior to exercise manipu-
lations. Thuma et al. have stressed the need for such a resting-
control evaluation to account for the circadian nature of the hor-
mone (8). This lack of agreement between studies, where some
show certain intensities of exercise increase cortisol and others
do not, suggests additional research is warranted to help identi-
fying the intensity of exercise – threshold necessary to provoke
a cortisol response. Obviously, the identification of such a thresh-
old could be a critical methodological consideration when at-
tempting to design certain endocrine research studies.
As noted, the exercise stimulus to increase cortisol levels is
due not just to the intensity but also to the duration of ex-
Key-words: Endocrine, physical activity, stress hormones.
Correspondence: A.C. Hackney, PhD, Professor Exercise Physiology - Nutrition, Fetzer
Building - CB # 8700 UNC-CH, Chapel Hill, NC 27599-8700, USA.
E-mail: ach@email.unc.edu
Accepted April 21, 2008.
J. Endocrinol. Invest. 31: ??-??, 2008
E.E. Hill1, E. Zack1, C. Battaglini1, M. Viru2, A. Viru2, and A.C. Hackney1
1Endocrine Section, Applied Physiology Laboratory, Department of Exercise & Sport Science, University of North Carolina, Chapel Hill, North Carolina, USA;
2Institute of Exercise Biology and Physiotherapy, Tartu University, Tartu, Estonia
RAPID COMMUNICATION
E.E. Hill, E. Zack, C. Battaglini, et al.
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ercise (or a combination of both factors interacting) (4). For
this reason, it is necessary, if examining the cortisol response,
to keep either the duration or intensity of exercise constant
and manipulate the other in order to identify the individual ef-
fect of each contributing factor more clearly. With all of the
above factors in mind, this study was designed with the in-
tent of examining the influence of exercise intensity upon the
cortisol response from the HPA axis. Specifically, we exam-
ined 30 min of exercise at intensities of 40, 60, and 80%
VO2max in an attempt to determine the intensity necessary
to provoke an increase in circulating cortisol. Additionally,
plasma volume shifts were examined as ACTH responses
were in order to elucidate potential mechanistic aspects of
any cortisol changes detected (i.e., hemoconcentration vs se-
cretory stimuli to adrenal cortex).
MATERIALS AND METHODS
Subjects
Subjects reported to our laboratory approximately 4 h post-
prandial on 5 separate occasions (7). Session I included com-
pletion of an informed consent, a medical screening, skin-fold
measurements for body fat estimation [skinfolds (12)] and a
VO2max exercise test. Approximately 1 week later, the sub-
jects underwent experimental testing sessions consisting of
30-min cycling bouts at 40, 60, or 80% of VO2max and a 30-min
resting period, which served as a control session for com-
paring the exercise sessions. These sessions were completed
in random order, occurred on different days, and were sepa-
rated by at least 48 h. Subjects were instructed to maintain
and control their diet (i.e., eucaloric diet with a minimum of
50% of daily calories coming from carbohydrate sources) and
reduce activity level (i.e., rest) preceding the first visit and to
replicate these behaviors before each ensuing experimental
session visit.
Experimental procedures
Exercise duration (30 min) was fixed in order to ensure that
any changes in cortisol levels were due to intensity and not to
some combination of intensity and duration, and was based
upon duration recommendations appearing in the literature
(4). In addition, the highest intensity of exercise (80%) was se-
lected because it was felt few people would be able to maintain
a greater intensity for durations of 30 min (13).
The subjects in this study were healthy, trained males, aged
18-30 yr who were recruited from the University of North
Carolina at Chapel Hill and surrounding areas. In order to be
included in the study, subjects were required to pass a medi-
cal physical examination, to demonstrate normal scores on the
RESTQ anxiety inventory (14), and to sign an informed consent
statement prior to beginning participation in the study. During
the 12 months leading up to the study, subjects trained a min-
imum of 3 days per week (~60 min per day), with at least 1
day including cycling exercise. Exclusion criteria included, but
were not limited to, a prior history of hormonal disorders,
mental illness, consistent body weight loss pattern, or a diet
deficient in carbohydrate intake (assessed via medical history
and questionnaire and nutritional survey).
Maximal oxygen consumption testing
Prior to beginning the VO2max test, each subject was allowed
to warm up and stretch. The warm-up was limited to 5 min
of cycling at a workload below that of the first testing stage
workload. Warm-up procedures were recorded and repeated
for each subsequent exercise session. Following the warm-up
period, the subject completed the VO2max test on a Monark
cycle ergometer (Monark model 818E, Sweden). The initial
workload for each subject was determined based on their
training history, and was increased at 3-min intervals until vo-
litional fatigue. Heart rate (HR) was monitored each minute
using a Polar HR monitor (Polar model F1, Finland) and respi-
ratory gases were recorded every 15 sec using the TrueMax
2400 Metabolic Measurement System (Parvo Medics, UT,
USA). The test was considered valid if at least two of the fol-
lowing criteria were met: respiratory exchange ratio >1.15,
HR±10 beats of age-predicted maximum, and/or a plateau in
VO2with an increase in workload (15).
Exercise sessions
Subjects reported to the laboratory and completed the RESTQ
questionnaire. If a normal score was achieved on the RESTQ
[i.e., a low level of emotional stress (14)], subjects were al-
lowed to begin a 30-min supine rest. A 3-ml blood sample was
taken at the end of the rest period (pre-sample). Subjects then
completed a 5-min warm-up at approximately 10-20% of
VO2max on a cycle ergometer. After the warm-up, subjects
began 30-min of cycling exercise at the pre-determined work-
load, intensity (40, 60, or 80% VO2max). Once at the prescribed
intensity, respiratory measures were taken every 10 min (3
min of measurement) to ensure that the subject remained at
the prescribed workload, intensity and HR was recorded at 5-
min intervals. Immediately at the end of the 30-min exercise
bout, a 3-ml post-exercise blood sample was taken. After
blood sampling, the subject was directed to cool down by per-
forming easy cycling for 5-10 min, and was permitted to leave
the laboratory once HR dropped below 100 bpm. The time of
day for all exercise testing was standardized and controlled in
order to minimize circadian hormonal fluctuations. These con-
ditions and procedures were replicated exactly for all 3 exer-
cise experimental sessions.
Resting-control session
A randomly selected sub-sample of the subjects in this study
completed a 30-min resting-control session. This session was
arranged to mimic all aspects (prior diet, physical activity, time
of day, etc.) of the experimental (exercise) sessions, except
that subjects rested quietly for 30-min rather than exercising
on a cycling ergometer. Blood samples were collected as not-
ed above pre- and post- the 30-min resting-control period.
Blood procedures-analysis
Blood samples were collected via the venipuncture procedures
using a 3-cc Vanishpoint®syringe with a 25 gauge, 1.5 cm nee-
dle (Retractable Technologies, Inc., TX, USA). All subjects
were familiar with the venipuncture procedure from previous
research study participation. The collected whole blood spec-
imens were transferred into 3-ml Vacutainer®tubes treated
with EDTA (Becton Dickinson Systems, NJ, USA) and placed
on ice immediately.
Whole blood was used to measure hematocrit (Hct) and
hemoglobin (Hb) in order to quantify any plasma volume shift
using the Dill and Costill equation (16). Hct was measured
in triplicate using microcapillary tubes (Fisher Scientific, PA,
USA) and read using a micro-Hct reader (International
Cortisol and exercise intensity
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Equipment Company, MA, USA). Hb was measured in tripli-
cate using the cyanmethemoglobin reaction procedure (17)
and quantified on a Milton-Roy 1201 spectrophotometer. The
remaining blood specimens were spun using a Centra 8 re-
frigerated centrifuge at 4 C and 3000 rpm for 10 min
(International Equipment Company, MA). The separated plas-
ma was transferred into cryo-freeze tubes and stored at –80
C in an ultra-freezer (Revco Scientific Inc., NC, USA) until
all samples were ready to be analyzed. Finally, cortisol was
measured in duplicate using a single-antibody, solid-phase
methodology radioimmunoassay technique (DPC Inc., CA,
USA). ACTH was measured in duplicate using a sandwich-
style enzyme-linked immunosorbent assay technique (MD
Biosciences Inc, MN, USA). All assay between and within co-
efficients of variation was less than 10%.
Statistical analysis
All statistical analyses were performed using SPSS [(v 15.0),
LEAD Technologies, Inc., IL, USA]. Descriptive statistics
(mean±SD) were computed for height, weight, age, and VO2max.
A repeated measures analysis of variance was used to analyze
percentage of VO2, changes in cortisol – ACTH levels and plas-
ma volume change. A Tukey post-hoc test was used to deter-
mine pair wise differences (α=0.05) where appropriate.
RESULTS
Twelve male subjects participated in this study, their charac-
teristics (X±SD) were as follows: age =26±3 yr, height
=1.78±0.06 m, weight = 72.8±7.5 kg. The estimated body fat
percentage and body mass index (BMI) for the subjects were
7.8±3.2% and 22.9±2.0 kg/m2, respectively. Subjects had a mean
VO2max of 65.5± .1 ml/kg/min (4.80±0.63 l/min), which placed
them above the 90th percentile in aerobic capacity for men be-
tween the ages of 20 and 29 yr according to the American
College of Sports Medicine (15). This aerobic classification is
supported by the subjects’ training history, as they had been
exercise training for a mean of 8.3±4.9 yr.
The actual intensities for the 3 submaximal exercise sessions
the subjects completed were: 38.0±2.09%, 57.5±3.3%, and
77.4±4.0% of VO2max. All exercise intensities were found to
be significantly different from each other (p<0.05). These in-
tensities were very close to the desired prescribed intensities
of 40, 60, and 80% of VO2max. Even though the actual exercise
intensities varied slightly from the prescribed exercise intensi-
ties, the exercise trials will be referred to as 40, 60, and 80%
throughout this paper. HR and rating of perceived exertion
are summarized in Table 1 and further suggest that the sub-
jects’ 3 exercise bouts were of a physiological difference and
caused varying amounts of stress as was desired.
Figure 1 depicts the mean cortisol levels (±confidence inter-
val) for the pre- and post- blood samples [exercise (no.=12)
and resting-control (no.=6) sessions]. The pre- cortisol lev-
els were not found to be significantly different from one an-
other for each of the 4 experimental sessions (p>0.05). The
post-sample cortisol level in the 30-min resting-control ses-
sion was significantly reduced (p<0.05) from its respective
pre-sample. In the 40% exercise session there was no change
in the post-sample cortisol compared to the pre-sample.
However, exercise caused a significant increase (p<0.01) in
cortisol levels (post-) compared to pre-exercise samples in
both the 60 and 80% sessions. Furthermore, the post-sample
cortisol levels in the 60 and 80% sessions were significantly
different from one another as well as being greater than both
the 40% and resting-control sessions post-samples. Finally, the
latter 2 post-samples (40% and resting-control) did not differ
from one another. The percent change in cortisol from pre- to
post-sample at the resting-control, 40, 60, and 80% sessions
was –6.6±3.5%, +5.7±11.0%, +39.9±11.8%, and +83.1±18.5%,
respectively.
The ACTH hormonal responses are depicted in Table 2. These
responses mirrored closely those of cortisol. In the resting-
control session ACTH decreased (non-significantly, p>0.05),
was unchanged pre- to post-exercise in the 40% session
(p>0.05), and was significant or approaching significant changes
in the 60% (p<0.08) and 80% sessions (p<0.05). There was,
however, a greater degree of variability in these data [most
likely due to the small sample size (no.=4)] which mostly like-
ly compounded the chance to find further statistical signifi-
cance. Regrettably, methodological problems prevented fur-
ther blood specimen analysis for this hormone.
The calculated changes in plasma volume for the resting-con-
trol, 40, 60, and 80% sessions were: +2.2±3.0%, –9.9±5.0%,
–15.6±3.5%, and –17.2±3.3%, respectively. The plasma volume
changes in response to all exercise sessions were significantly
greater than those observed during the resting-control ses-
sion. Also, the 60 and 80% reductions were significantly greater
than in the 40% exercise session (p<0.05), but did not signifi-
cantly differ from one another.
Table 1 - The heart rate (HR) and rating of perceived exertion (RPE) re-
sponses that correspond to the 3 30-min exercise sessions (mean±SD).
Exercise intensity
40% 60% 80%
Time HR RPE HR RPE HR RPE
(min) (bpm) (bpm) (bpm)
10 114±9 9±2 144±12 13±2 166±9 15±3
20 116±9 10±2 148±11 13±2 172±7 16±2
30 119±8 9±3 153±12 14±2 173±10 16±2
Fig. 1 - The mean cortisol (±confidence intervals) response for each of the
experimental sessions used in this research study. The increases at post-ex-
ercise sampling at 60% and 80% intensity are significantly greater than at
pre-exercise sampling. The * denotes statistical significance (p<0.05) in re-
spective pre- to post- comparisons.
Cortisol (μg/dl)
28
26
24
22
20
18
16
14
12
10
8
6
4
Pre- Post-
Time (30 min)
*
*
Resting- control
40% intensity
60% intensity
80% intensity
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E.E. Hill, E. Zack, C. Battaglini, et al.
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DISCUSSION
The intent of this study was to examine the influence of exer-
cise intensity on the cortisol response of the HPA axis to 30
min of exercise at intensities of 40, 60, and 80% of VO2max in
order to determine which intensity elicited an increase in cir-
culating hormonal levels. The findings support the concept that
moderate to high intensity (60%, 80%) exercise will provoke
significant increases in circulating cortisol. These increases
seem to be brought about by a combination of hemoconcen-
tration and well as enhanced secretion stimuli (i.e., ACTH)
within the HPA axis. In contrast, low intensity (40%) exercise
does not result in significant increases in circulating cortisol
levels. In fact, if one considers the resting-control cortisol re-
sponse, and the plasma volume reduction within this exercise
session, then the 40% intensity actually results in a reduction
in circulating hormonal levels.
The current findings are in agreement with several similarly
designed studies. Specifically, those conducted by Davies and
Few (3), Bloom (18), Luger et al. (19), and Rudolph and
McAuley (20). Many aspects of the present study were con-
structed to model after the classic work of Davies and Few
just mentioned. For this reason, we feel that the conclusions
reached by those investigators are appropriate here too.
Specifically that: (a) a “threshold intensity” of ~60% or greater
VO2max will elicit elevations in circulating cortisol; (b) the ele-
vations observed most likely represent increases in the rate
of glandular secretion and are not due to decreases in the
metabolic clearance rate (MCR); and (c) the lack of elevation
at the low intensity exercise may reflect increased MCR, in
particular target tissue uptake of the hormone (3).
Divergent findings from the present study, however, have been
reported by some investigators. Jacks et al. (10) found 60 min
of exercise at 45, 60, and 75% of VO2max resulted in significant
cortisol increases at only the highest exercise intensity. Duclos
et al. (9) also found no change in cortisol levels with 20 min of
exercise at either 50 or 80% of VO2max. Interestingly, in this
same study, when the 50% intensity exercise was extended to
120 min there was still no significant increase in cortisol levels.
The lack of agreement between the present study and those
seeing either no increase with exercise, or an increase at on-
ly very high exercise intensities could be due to several fac-
tors. One such factor is exercise training background (2, 18,
21). More highly trained individuals typically have a higher in-
tensity threshold necessary to provoke an increase in cortisol
(5, 21). The level of training in the subjects, as assessed by
VO2max levels reported, seems to differ broadly across these
various studies just mentioned. Another critical factor affect-
ing hormonal outcomes is the timing used in the blood sam-
pling protocol. Specific to cortisol, Daly et al. (22) reported
that the time-point at which blood samples are collected with
respect to exercise (immediately at the end, 10 min, 20 min
into recovery, etc.) can greatly affect the interpretation of da-
ta outcomes due to the hormonal half-life. The collection time
of blood samples was also vastly different across the present
and the comparative studies noted above. In a similar fashion,
the highly circadian aspects of cortisol make it necessary to
conduct an appropriate resting-control evaluation of cortisol
profiles prior to exercise manipulations (8), which not all of
these studies with divergent results incorporated into their
research designs.
As mentioned earlier, some researchers question the validity
of certain studies concerning the influence of various exercise
intensities upon circulating cortisol (1, 8). Some of this criticism
is based upon the lack of control of confounding factors which
interact with exercise to affect cortisol responses. The pre-
sent study attempted to negate these confounding factors; that
is, we controlled for time of day – circadian rhythms, prior di-
et – activity patterns, levels of exercise training, psychological
stress, and utilized resting-control session to determine “nor-
mal” cortisol responses when exercise is not conducted.
Because of the care we took in conducting our research, we
strongly feel that our data are highly valid.
In conclusion, the present work supports the view that mod-
erate to high intensity exercise will provoke increases in cir-
culating cortisol levels. In contrast, low intensity exercise does
not result in increases in cortisol levels. Once corrections for
plasma volume reduction are conducted and circadian factors
examined, low intensity exercise of 40% VO2max results in a
reduction in circulating cortisol levels.
Table 2 - The ACTH responses at the control-resting and the three 30-min exercise sessions (mean±SD). The * denotes statistical significance (p<0.05) and
the
γ
denotes approaching significance (p<0.08) in respective pre- to post- comparisons.
Experimental sessions
Hormone Resting-control 40% intensity 60% intensity 80% intensity
Time
Pre- Post- Pre- Post- Pre- Post- Pre- Post-
ACTH (pg/ml) 13.5±4.4 9.1±4.9 12.2±4.3 10.8±5.4 12.3±4.1 20.1±6.0γ12.9±6.3 43.2±11.3*
Cortisol and exercise intensity
5
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