.Journal of Clinical Endocrmology and Metabolism Vol.15, No.

1
Copyright (* 199‘2 by The Endocrine Society Prrnted in U.S.A.

Effect of Low and High Intensity Exercise on Circulating

Growth Hormone in Men*
NANCY E. FELSING, JO ANNE BRASEL, AND DAN M. COOPER?
Divisions of Respiratory and Critical Care, and Endocrinology, Department of Pediatrics, Harbor- UCLA
Medical Center, UCLA School of Medicine, Torrance, California 90509

ABSTRACT 0.05; epinephrine was 1,113 & 519 pmol/L us. 496 + 273, P < 0.05; and
We hypothesized that circulating GH would increase only if a norepinephrine was 7.89 & 3.45 nmole/L us. 2.83 * 1.34, P < 0.05). GH
threshold of work intensity [corresponding to the anerobic or lactate did not increase significantly from preexercise baseline during low
threshold (LT)] was exceeded. Ten healthy male volunteers (18-35 yr) intensity exercise (e.g., GH after lo-min low intensity exercise changed
first performed ramp-type progressive cycle-ergometer exercise to de- from baseline values by 1.5 & 2.0 fig/L, NS). Although lactate was
termine the LT and the maximal oxygen uptake. On subsequent morn- elevated after 5-min of high intensity exercise, peak GH was signifi-
ings after an overnight fast, each subject performed bouts of 1, 5, and cantly elevated (mean increase above baseline of 7.7 + 2.4 pg/L, P <
10 min constant work rate exercise of either high intensity (above LT) 0.05) only after 10 min of high intensity exercise (increases in 9 of 10
or low intensity (below LT). A l-h interval separated exercise bouts. subjects). The GH increase occurred despite simultaneous increases in
Gas exchange (breath-by-breath), GH, immunoreactive insulin, glu- both IRI and glucose. A minimum duration of 10 min, high intensity
cose, lactate, pyruvate, and epinephrine and norepinephrine were meas- exercise consistently increased circulating GH in adult males. (J Clin
ured at regular intervals. After the lo-min bouts of high compared with Endocrinol Metab 75: 157-162, 1992)
low intensity exercise, lactate was 7.2 f 3.7 mmol/L us. 1.4 + 1.3, P <

E XERCISE AFFECTS GH secretory patterns, and this GH

effect likely plays a role in growth and in the training
phenomenon (l-4). The exercise duration or intensity that
used to determine exercise intensity. In most studies, the
work rate chosen is equivalent to 60-70% of the subject’s
maximal oxygen uptake (irO,max). By and large, these pro-
will elicit a reproducible and substantial GH pulse in humans tocols represent submaximal high intensity exercisesince the
is not precisely known. There are reasonsto believe that the lactate threshold (LT) occurs between 40-60% of vO,max in
GH response to increasing work intensity is nonlinear in healthy subjects (26). But some of the subjects may have
nature and may be characterized by a threshold: The purpose exercised above and others below their LT for the following
of this study was to test whether or not a work-intensity reasons.Investigators often used predicted rather than meas-
threshold could be identified for the GH response. ured vOzmax, and most did not measurethe LT in individual
Although the magnitude of the GH response is related to subjects. This, combined with the large intersubject variabil-
work intensity (5-8), there is great variability in the reported ity of ir02max and the LT, may have confounded the inves-
amplitude and duration of exercise-induced GH response in tigators’ ability to precisely determine work rate intensity.
humans. The variability might be explained by the fact that The duration of the exercise input in previous studies
in previous studies, some subjects exercised below, whereas tended to be long (the mean of Table 1 is 44 min). In contrast,
others worked above a threshold for GH release. The GH naturally occurring patterns of activity in adults and children
responsemay be correlated to the lactate responseto exercise are shorter. Thus, we specifically examined the effects of
(9-11) which increases in a nonlinear manner with work short bursts of exercise more likely to mimic physiologically
intensity (12). Finally, other stressresponses,e.g. circulating significant patterns of activity.
catecholamines, are disproportionately elevated during
heavy compared to light exercise (13, 14). We hypothesized
that exercise would elicit a significant GH pulse only when Subjects and Methods
the work rate exceeded the anaerobic or lactic acid threshold Subjects (Table 2)
(high intensity exercise). The latter refers to the work rate
Ten healthy adult male volunteers participated in the study. They
above which circulating lactic acid increases(15, 16).
ranged in age from 18-35 yr old (mean 27 + 5 yr). None of the subjects
Table 1 reviews 10 studies of the acute GH response to were smokers, suffered from chronic diseases, or took drugs or medica-
exercise (5, 17-25). It highlights the diversity of approaches tions, None of these individuals trained as competitive athletes, but
most participated in some form of regular exercise. The study was
Received September 23, 1991. approved by the institutional Human Subjects’ Committee, and each
Address requests for reprints to: Dan M. Cooper, M.D., N-4, 1000 participant granted informed consent.
West Carson Street, Torrance, California 90509.
* This work was supported by USPHS Grants HD-26939 and HL- Protocol
11907 and by General Clinical Research Grant RR-00425.
t Recipient of the Career Investigator Award of the American Lung The protocol consisted of three exercise sessions each performed on
Association. different days, separated by at least 1 week. On day one each volunteer

157
158 FELSING ET AL. JCE & M. 1992
Vol75.Nol

TABLE 1. Representative previous studies of the effect of exercise on circulating GH

Lactate thresh- Duration

Work intensity
old (min)
(17) 1990 Predicted Not measured 66% irO,max 6
(18) 1990 Predicted Not measured 70% VOzmax 15
(19) 1990 Measured Not measured 65% $‘O,max -90
(20) 1990 Predicted Not measured 60% vO,max 30
(21) 1989 Measured Measured Equal to LT -80
(22) 1988 Measured Not measured 70% V02max 60
(23) 1987 Not measured Not measured 1, 1.5, and 2 watt/kg for 15
5-min periods
(24) 1986 Measured Not measured 60% v02max 60
(5) 1985 Measured Not measured 63 (10 min), 86 (10 -26
min), 100 (5-7 min)
(25) 1981 Not measured Not measured 55 watt/m* 60

TABLE 2. Subject age, weight, height, and exercise gas exchange characteristics

LT iiO,~ClX LT Low WR High WR

Subject Age (rd Wt (Kg) Ht (cm)
(% VO,max) (ml/min kg) (ml/min kg) (% VOZm3X) (% VO*max)
1 35 80 178 47 38 18 18 68
2 24 75 180 59 37 22 24 14
3 28 86 185 48 49 23 25 75
4 27 89 185 64 41 26 23 58
5 32 81 178 70 49 35 26 78
6 21 81 190 50 43 21 20 69
7 29 93 196 80 38 30 32 82
8 18 14 187 54 40 22 24 74
9 27 58 173 45 46 21 17 68
10 29 58 170 43 48 21 23 73
Mean 27 78 182 56 43 24 23 72
SD 5 11 8 12 5 5 4 6

performed progressive ramp-type cycle ergometry to determine the combined dead space of 90 mL. O2 and CO* tensions were determined
VO>max and the LT (see below). The next two sessions consisted of l-, by mass spectrometry from a sample drawn continuously from the
5-, and lo-min of constant work rate exercise on the cycle ergometer. mouthpiece at 1 mL/s. The inspired and expired volumes and gas tension
An hour of rest separated each exercise burst. For one session, the work signals upderwent analog-to-digital conversion, from which oxygen
rate chosen corresponded to 50% of the difference between the subject’s uptake (V02) (standard temperature pressure dry), CO, production
LT and VOzmax (high intensity exercise), whereas for the other session (VCO*) (standard temperature pressure dry), and minute ventilation (v,)
all work rates corresponded to 50% of the subject’s lactate threshold (body temperature pressure saturated) were calculated on-line, breath-
(low intensity). by-breath as previously described (27). The breath-by-breath data were
For a given session, subjects always performed a fixed sequence of then interpolated to l-s time intervals.
exercise duration (l-, 5-, IO-min), but the order of the exercise intensity
(i.e. high intensity day, low intensity day) was randomized. We chose
this protocol because we anticipated that lo-min exercise bouts would Noninvasive determination of LT and vO,max
be the most likely to elicit GH responses and it was performed last to
minimize possible confounding effects of a prior GH pulse on subse- The LT and 7j02max were measured noninvasively from the gas
quent pulses. We chose a l-h interval between exercise bouts. This was exchange data obtained during the progressive exercise. The lactate
a balance between, on the one hand, allowing sufficient time for gas threshold was defined as the V02 at which the ventilatory equivalent
exchange parameters, lactate, and hormones levels to return to baseline, for O2 ($,/$O,) and the end tidal O2 (PetOz),in<reased without an
and, on the other hand, minimizing the possibility of spontaneous GH increase in the ventilatory qquivalent for CO* (VE/VC02) and the end
pulses and too prolonged a fasting period. tidal CO2 (PetCO>) (28). VOzmax was defined as the highest VOZ
The subjects arrived at approximately 0800 h on the morning of a achieved by the subject.
low or high intensity exercise study. We chose the morning to perform
the study because fewer naturally occurring GH pulses are seen during
the morning hours (after about 0800-0900 h). They were instructed to GH, glucose, insulin, lactate, and catecholamines
refrain from any exercise and to remain fasted for at least 12 h before
the study. An antecubital venous catheter was placed for intermittent An in-house RIA was used to measure GH using WHO standard no.
blood sampling. Baseline blood samples were taken at 10 and 5 min 66/217, antisera generated in-house, and hGH from NIDDK for iodi-
before the first (1 min) exercise burst. The subject performed the exercise, nation purposes. The GH intraassay variability is less than lo%, inter-
then samples were taken every 10 min during the rest period. This was assay variability is 12.6%, and the sensitivity is 0.5 pg/L. Insulin was
repeated after the 5- and lo-min bursts. An additional sample was also measured using an in-house RIA using standard from Wellcome
obtained during exercise (at 5 min) during the last (lo-min) exercise equated to first IRP 66/304, antiporcine antibody from ICN and porcine
period. Breath-by-breath gas exchange measurements were made 5 min insulin from Lilly for iodination. The insulin intraassay variability is less
before, during, and 10 min after each exercise period. than lo%, interassay variability is 11.5%, and the sensitivity 7 pmol/L.
Glucose was measured using the Abbott bichromatic analyzer using the
Abbott UV glucose kit. The glucose intraassay variability is 2.1% and
Gas exchange measurements the interassay variability is 2.4%. Lactate was measured spectrophoto-
The subjects breathed through a mouthpiece connected to a low metrically using the Behring Stat-pack rapid lactate test. The lactate
impedance turbine volume transducer and a breathing valve with a intraassay variability is 2.8%, the interassay variability is 3.5%, and the
 GH AFTER LOW- AND HIGH-INTENSITY EXERCISE

sensitivity is 0.55 mmol/L. Pyruvate was measured enzymatically using

the Perkin Elmer luminescence spectrophotometer. Pyruvate intraassay
variability is 4% and interassay variability is 12%. Catecholamines 7
[norepinephrine (NE), epinephrine (E)] were measured by the radioen- $6
zymatic method. For NE the intraassay variability is less than 10% and
the interassay
For E the intraassay
variability is 10.6%, and the sensitivity
variability is less than lo%, interassay
is 0.12 nmol/L.
is 14.6%,
E5
and the sensitivity is 109 pmol/L. -54
z 3
Statistical analysis ;2
Repeated measures analysis of variance was used to describe the 4 1
patterns of the multiple samples of GH, other hormones, and substrates.
Separate analyses were performed for the preexercise values, the peak 0
1 min 5 min 10 min
value, and the A (i.e. the difference between peak and preexercise
values). The preexercise values were taken as the level of hormone or FIG. 2. Mean peak serum lactate levels (minus baseline) and SE after
substrate immediately before the l-, 5-, or lo-min exercise bout. When 1, 5, and 10 min of low (hollow bars) and high (hatched bars) intensity
analysis of variance (ANOVA) was found to be significant, Duncan’s exercise. * indicates P < 0.05.
Multiple Range test was used to determine intergroup significance.
Unless otherwise stated, values are presented as mean +_ SD. A P value
less than 0.05 was considered significant.

Results
Gas exchange parameters
The individual subject age, weight, height, and exercise
gas exchange characteristics are shown in Table 2. As ex-
pected, the VOz reached a steady state during the 5- and lo-
min low intensity exercise bouts but not for high intensity
exercise (Fig. 1). V02, of course, increased significantly with Time (min)
exercise duration for both low and high intensity exercise.
With 10 min of exercise, the peak VO, was 4 and 9 times FIG. 3. Mean GH and SE (closed circles) and VO, (lines) after 1, 5,
and 10 min of low (left panel) and high (right panel) intensity exercise.
greater, on average, than baseline for low and high intensity * indicates P < 0.05. Clear vertical bars represent the exercise bouts.
exercise, respectively. GH significantly increased only after 10 min of high intensity exercise.

Lactate and pyruvate (Fig. 2) for peak lactate among the subjects was 57%. Qualitatively
similar results were found for the lactate-to-pyruvate ratios.
As expected, lactate concentrations were increased during
all durations of high intensity exercise. There were no sub-
GH (Fig. 3)
stantial differences between the two baseline lactate values;
however, the lactate levels immediately before the lo-min Spontaneous GH pulses (judged by inordinately elevated
high intensity exercise bout were slightly but significantly preexercise GH with patterns suggesting upward or down-
higher (P < 0.01) than the baseline levels and than those ward slopes) occurred in only one subject. There were no
before the 5-min exercise bouts. The coefficient of variation significant differences between the two baseline GH levels.
GH responsesto exercise were quite variable in magnitude
3.0 7
among the subjects; the ratio of peak pulse to baselineranged
from 0.7 to 14 after low intensity exercise and from 0.5 to
51 after high intensity exercise. After low intensity exercise,
exercise-associatedincreasesin GH for the group as a whole
were not statistically significant. Two of the 10 subjectshad
disproportionately greater GH pulses than the others and
their GH pulses account by and large for the increase in the
mean GH concentration after 5 and 10 min of exercise.After
the lo-min high intensity bout there was a significant GH
pulse in 9 of 10 subjects (mean peak of 7.7 & 2.4 pg/L ZIS.a
mean baselineof 1.7 f 2.4 pg/L, P < 0.05). The smallincrease
in GH after 5-min of high intensity exercise was not statis-
tically significant. The coefficient of variation for the peak
Time (min) GH pulse after 10 min in the high intensity range was 85%.
FIG. 1. VO, during low and high intensity exercise in a representative After the lo-min high intensity exercise bout, the peak GH
subject. Note that VO, did not achieve a steady state during high pulse occurred at a mean of 29 + 12 min after the onset of
intensity (above LT) exercise even though the work rate was constant. exerciseand occurred significantly (P < 0.05) later than those
160 FELSING ET AL. JCE & M. 1992
Voll5.Nol

of lactate (15 min), E (10 min), NE (11 min), and insulin (21 Discussion
min).
The gas exchange and lactate data demonstrate that we
achieved the goal of identifying low- and high-intensity
Glucose and insulin (Fig. 4) exercise in the subjects. The lo-min period of high-intensity
(above the lactate threshold) exerciseconsistently resulted in
After low intensity exercise, glucose increased by 0.39 + bursts of GH secretion in adult males. In contrast, low
0.11 mmol/L (P < 0.05) for 5-min exercise and by 0.28 + intensity exercise, including the lo-min protocols, did not
0.11 mmol/L for lo-min bouts. With high intensity exercise, elicit significant GH responses.Despite rigorous control over
significant increases (P < 0.05) were found after the I-min the work rate, our data, like most previous studies, revealed
(0.28 f 0.06 mmol/L), 5-min (0.39 + 0.11 mmol/L), and lo- great subject-to-subject variability in the peak GH response
min (0.61 + 0.11 mmol/L) protocols. Low intensity exercise achieved (nb., the coefficient of variation among the subjects
had no significant effect on insulin. During high intensity was higher for GH than for lactate and catecholamines).
exercise, insulin increased significantly (P < 0.05) after the Thus, whereas there does appear to be a minimum threshold
1-min (29 -C 7 pmol/L), 5-min (50 + 14 pmol/L), and lo- of exercise duration and intensity necessary for a GH pulse,
min (29 + 7 pmol/L) protocols. exerciseintensity alone cannot entirely predict the amplitude
and duration of the subsequent GH response.
The onset of the GH response to exercise was later and
Catecholamines (Fig. 5) less consistent than the gas exchange, lactate, and other
During low intensity protocols, significant increaseswere hormonal responses.The elevation in GH induced by exer-
found for E after the lo-min exercise bout and for NE after cise lasted far longer than both the lo-min exercise bout
the l- and IO-min bouts. Both E and NE increased with the itself and the other substrate and hormonal responsesstud-
ied. The time required to achieve a GH responsein our study,
high intensity protocols after the 5- and IO-min bouts. The
between 5 and 10 min, was similar to that observed by
magnitude of the increase in catecholamines after low inten-
Sutton and Lazarus (9) who used a 20-min protocol. The
sity was substantially less than that observed after the high
peak GH in their study also occurred at about 30 min after
intensity protocols. The coefficient of variation for peak NE the onset of exercise, i.e. after the exercise bout was com-
among the subjects was 45% and for epinephrine was 49%. pleted. It appears that 10 min of high intensity exercise are
necessary to reliably stimulate pituitary secretion of GH.
2 200- The disappearance of GH from the circulation follows a
2 s first-order exponential decay (29-32), and reported half-
E 150-

.3
.&
2
$6

100 - -5
E

z
cJi!...jii.1
Ji.,&L
* . l
times range from 8.9 min (30) to as high as 27 min (32). A
variety of techniques, including deconvolutional analysis (29,
33), has been used to quantify pituitary GH secretion during
spontaneous pulses. We constructed a simple single com-
c 8
50.5, partment model in which GH is transported from the pitui-
tary to the circulation with first-order kinetics, and follows a
0 40 60 120 160 200
first-order disappearance from the plasma. Iterative nonlin-
0 40 60 120 160 200
Time (min)
ear curve-fitting techniques (34) were used to calculate the
time constants and the amount of GH secreted from the
FIG. 4. Mean glucose and SE (open circles) and mean insulin and SE
(closed circles) after 1, 5, and 10 min of low (left panel) and high (right mean GH levels during and after the IO-min high intensity
panel) intensity exercise. * indicates P < 0.05 for peak over baseline protocol. The following equation was used:
values. Clear vertical bars represent the exercise bouts. Both insulin
and glucose increased consistently after high intensity exercise.
where A represents the GH released consequent to the
‘t 1000 c i
exercise stimulus, 71 corresponds to the disappearance
time constant (equivalent to the half-time divided by 0.69)
for GH from the plasma compartment, r2 corresponds to
the time constant of GH release from the pituitary com-
partment to the plasma, and t is the time in min. (A 5-
min delay was included in the model).
A reasonably good fit was seen when 27 min was used
as the value for the half-time of plasma GH disappearance
(Fig. 6). The analysis predicted a total GH pulse of 0.061
I-min 5-min IO-min I-min 5-min lo-min
mg when using the mean weight of our subjects (78 kg)
FIG. 5. Mean peak values (minus baseline) t SE for NE (left panel) and a GH volume of distribution of 4.4% (35). The model
and E (right panel) after 1, 5, and 10 min of low (hollow bars) and high
(hatched bars) intensity exercise. * indicates P < 0.05 compared to low suggests a t% of the GH release into the plasma of 11 f
intensity exercise. 3 min, and a mean GH secretory rate over four half-lives
 GH AFTER LOW- AND HIGH-INTENSITY EXERCISE

(44) demonstrated that exercising hamsters grew at faster

rates than did sedentary animals, and the exercising ani-
mals had greater frequency and amplitude of spontaneous
GH pulses. More recently, Grindeland et al. (1) studied
the effect of exercise and administration of exogenous
GH on muscle growth in hypophysectomized rats re-
covering from hindlimb suspension. Their preliminary
data show that the most marked increases in muscle mass
occurred with the combination of exercise and GH. In
contrast, the training effect in humans can occur with
I -_I
exercise protocols that are above or below the subject’s
0 10 20 JO 40 50 60 70 60 lactate threshold (45); and DeVol and co-workers (46)
Time (min) showed that training induced muscle hypertrophy with
FIG. 6. Mean + SE for GH (closed circles) during and after 10 min of increases in muscle tissue insulin-like growth factor-I
high intensity exercise. The dashed line is a cubic splines best-fit curve
for the GH data. The solid line is the best fit curve for the exponential
messenger RNA even in hypophysectomized animals.
model as described in the text. Apparently, the growth and hypertrophy observed in
response to exercise is modulated by both GH-dependent
of 0.41 pg/L. min, a value comparable in magnitude to and GH-independent processes.
those found from spontaneous pulses (36). Ten minutes of constant work rate, high intensity ex-
The data show that the GH response to exercise likely ercise is a minimum stimulus for consistent GH release in
has a different mechanism than other known physiolog- adult males. Whether or not such patterns of activity
ical stimuli. Hypoglycemia and/or rapid falls in glucose represent naturally occurring, physiologically important
concentration, for example, cause GH release (37), but, as GH stimuli remains unknown. It is intriguing that the
shown in Fig. 4, subjects remained euglycemic and glu- character of the exercise stimulus may be as important as
cose concentrations tended to increase. Classically, insulin the total work done in eliciting the GH response. Van-
can be used to stimulate GH by inducing hypoglycemia. helder et al. (7) demonstrated that a series of 1-min bursts
In our studies, insulin increased significantly following of very high intensity exercise resulted in a greater GH
short bursts of high intensity exercise with no evidence response than constant work rate exercise (20 min) in
of hypoglycemia. It has been reported that insulin de- which the work expenditure and duration of the two
creases during long term exercise (e.g. greater than 40 protocols were the same. The importance of the pattern
min) (38), but recent data in human subjects during and of exercise is highlighted by recent findings that the
after short term high intensity exercise demonstrate either pulsatile nature of GH release may optimize its overall
no change or, consistent with our results, increases in effect on growth (47). Finally, our data add to the body
plasma insulin (39-41). In addition, both insulin and GH of evidence that GH pulses in response to exercise, unlike
were increasing simultaneously following exercise (peak spontaneous GH pulses, are accompanied by increases in
insulin occurred at 21 min; peak GH at 29 min). It would other tissue growth mediators (insulin, catecholamines).
be difficult to conclude from these observations that in- Perhaps this hormonal “milieu” is as important to growth
sulin either directly or indirectly stimulated the exercise- and training as is the elevation in GH itself.
induced GH pulses.
Both E and NE were significantly elevated after both
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