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1 Physical Activity Sciences
Laboratory, ABSTRACT Pérusse, Louis, Gregory Collier, Jacques Gagnon,
Arthur S. Leon, D. C. Rao, James S. Skinner, Jack H. Wilmore,
André Nadeau, Paul Z. Zimmet, and Claude Bouchard. Acute and
chronic effects of exercise on leptin levels in humans.
J. Appl. Physiol. 83(1): 5-10, 1997.
exercise training; body fat; HERITAGE Family Study
INTRODUCTION OBESITY IS ASSOCIATED WITH several morbid conditions
such as non-insulin-dependent diabetes mellitus, dyslipidemias,
cardiovascular disease, and some forms of cancer and therefore
represents a major health problem. Although excess caloric intake
and/or reduced energy expenditure from physical activity may
be responsible for the increased prevalence of obesity (16, 24),
genetic factors appear to be important determinants of the
susceptibility to become obese (2). Despite the large number of studies
on the genetic and nongenetic determinants of obesity (2, 4),
relatively little is known about the genes likely involved in the
regulation of body weight over an extended period of time.
A major breakthrough came with the cloning of the mouse obese
(ob) gene (29) and its receptor
(27). The ob gene codes for a protein
of 146 amino acids, known as leptin, secreted by the white adipose
tissue. Soon after the discovery of the
ob gene, three studies have shown that
administration of leptin to the obese
(ob/ob)
mouse was associated with a reduction of adiposity, a decrease in serum
glucose and insulin levels, and an increase in metabolic rate and
locomotor activity (5, 10, 19). These studies suggest that leptin plays
a central role in the regulation of food intake and energy balance in
mice.
No mutations in the ob gene have been
identified in humans so far, but ob
gene expression and serum leptin levels were found to be highly
correlated with percentage of body fat and to decline after weight loss
(6, 17). Large variations in serum leptin concentrations have been
noted for a given level of body fat (6), suggesting that other factors
may be involved in the regulation of leptin levels.
Among these factors, insulin, corticosteroids, free fatty acids, and
food intake have been implicated (7, 9, 18, 21, 23), but little is
known about the role of exercise. Exercise represents the most variable
fraction of energy expenditure in humans. Considering the role of
leptin on energy expenditure in the obese mouse and the role of
exercise in maintenance of diet-induced weight loss, exercise could be
an important determinant of leptin levels in human. Very few studies
have investigated the effects of exercise and endurance training on
leptin levels. One study performed in animals has shown that acute
exercise in rats was associated with a 30% reduction of the expression
of the ob gene in the adipose tissue
(30). In humans, only two studies have been reported. In one study,
leptin concentrations were measured in 13 lean (average percent body
fat of 9.7%) long-distance male runners before and after completion of
a 20-mile treadmill run at 70% of maximal oxygen uptake
( MATERIAL AND METHODS
The acute (single bout of exercise) and chronic (exercise
training) effects of exercise on plasma leptin were investigated in 97 sedentary adult men (n = 51) and women
(n = 46) participating in the HERITAGE
Family Study. Exercise training consisted of a standardized 20-wk
endurance training program performed in the laboratory on a
computer-controlled cycle ergometer. Maximal oxygen uptake, body
composition assessed by hydrostatic weighing, and fasting insulin level
were also measured before and after training. Pre- and posttraining
blood samples were obtained before and after completion of a maximal
exercise test on the cycle ergometer. Exercise training resulted in
significant changes in maximal oxygen uptake (increase in both genders)
and body compostion (reduction of fat mass in men and increase in
fat-free mass in women). There were considerable interindividual
differences in the leptin response to acute and chronic effects of
exercise, some individuals showing either increase or reduction in
leptin, others showing almost no change. On average, leptin levels were
not acutely affected by exercise. After endurance training was
completed, leptin levels decreased significantly in men (from 4.6 to
3.9 ng/ml; P = 0.004) but not in
women. However, after the training-induced changes in body fat mass
were accounted for, the effects of exercise training were no longer
significant. Most of the variation observed in leptin levels after
acute exercise or endurance training appears to be within the
confidence intervals of the leptin assay. We conclude that there are no
meaningful acute or chronic effects of exercise, independent of the
amount of body fat, on leptin levels in humans.
O2 max) (12). Pre- and
postexercise leptin concentrations were 2.19 ± 0.32 and 2.14 ± 0.35 (SE) ng/ml, respectively. These results suggest
that, in trained individuals (average
O2 max of 62.9 ± 2.2 ml · min
1 · kg1),
acute exercise has no effects on circulating leptin levels (12). In
another study, of sedentary postmenopausal women aged 60-72 yr,
leptin levels were evaluated in response to exercise training
consisting of a 2-mo flexibility exercise program followed by a 9-mo
exercise program that included walking, jogging, and stair climbing
(13). Significant reductions in serum leptin levels were observed after
exercise training, but these were explained by changes in fat mass
(13). The present study was undertaken to assess both the acute effects
of exercise and chronic effects of endurance training on plasma leptin
levels in sedentary adult men and women.
O2 max for 30 min per
session at the beginning, increasing progressively toward an intensity
of 75% of O2 max for
50 min during the last 6 wk of the training protocol. Training
intensities were adjusted individually by a computer system that
recorded all training data and automatically adjusted the power output of the cycle ergometer to keep the heart rate response of the subject
within 5 beats of the programmed heart rate at all times during all
training sessions.
80°C until determination of leptin levels. Plasma
total proteins were also measured to account for the effects of
hemoconcentration during the test.
Plasma leptin determination.
Leptin levels were measured by radioimmunoassay (Linco, St. Charles,
MO). The assay detects human leptin with a sensitivity (lowest
detectable level) of 0.5 ng/ml in plasma. The intra-assay coefficient
of variation was 7%.
Statistical analyses.
The acute and chronic effects of exercise on leptin levels were
assessed separately in men and women by using a repeated-measures analysis of variance for one factor, the time effect. For acute effects, the time has three levels, i.e., Rest, 50W, and Max, whereas
for chronic effects the time has two levels, i.e., pre- and
posttraining. All the analyses were performed by using SAS software
(version 6.08) for personal computer.
RESULTS
The effects of the endurance training program on body composition,
fasting glucose and insulin, and
O2 max are presented in
Table 1 for men and women separately. The
endurance training resulted in significant
(P < 0.001) improvements of
O2 max, which increased
from 3.3 to 3.8 l/min in men (15.7%) and from 2.1 to 2.5 l/min in
women (18.8%). The endurance training resulted in significant
(P < 0.0001) decreases in fat mass
and percent body fat in men but not in women. Significant increases in
fat-free mass were also observed in both men and women. No significant changes in indicators of glucose and insulin metabolism were noted after exercise training.
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The average plasma leptin levels measured at Rest before endurance
training were 4.6 ± 4.4 ng/ml in men and 11.9 ± 8.5 ng/ml in
women. As a group, the subjects of the present study were not obese,
with average body mass index values of 25 and 23 in men and women,
respectively, and a mean percent body fat of 21% in men compared with
26% in women. Plasma leptin levels were strongly correlated with
percent body fat in both men (r = 0.83, P < 0.0001) and women
(r = 0.74, P < 0.0001), as illustrated in Fig.
1. Leptin levels were also significantly
correlated (results not shown) with fasting insulin
(r = 0.54, P < 0.0001 for men;
r = 0.43, P < 0.01 for women).
; Pearson's correlation coefficient
(r) = 0.83, P < 0.0001] and 46 women (
;
r = 0.74, P < 0.0001).
The acute and chronic effects of exercise on leptin levels are summarized in Table 2. On average, the pretraining leptin levels remained unchanged during the exercise test (P values adjusted for hemoconcentration), with values from 4.6 to 4.7 ng/ml in men (P = 0.78) and from 11.9 to 11.7 ng/ml in women (P = 0.45). The same trend was observed posttraining, with no significant effects in men (P = 0.61) and women (P = 0.77).
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The effects of exercise training on leptin levels are also summarized
in Table 2. After endurance training, men exhibited significant
reductions in leptin levels measured either at Rest (P = 0.004), 50W
(P = 0.009), or at Max
(P = 0.044), with average training-induced changes (
) in leptin levels of 0.67,
0.59, and 0.45 ng/ml, respectively. In women, the chronic
effects of exercise training on leptin levels were not significant,
except for an increase (11.7 vs. 13.0 ng/ml;
P = 0.03) noted at Max. To determine
whether the effects of exercise training were attributable to changes
in fat mass, the analyses were repeated by adding this covariable in
the model. As indicated by the P
values given in Table 2, the effects of training on leptin were no
longer significant after changes in fat mass are accounted for.
Figure 2 presents the individual pre- and posttraining plasma leptin values measured at Rest in men (Fig. 2A) and women (Fig. 2B) separately. There were considerable interindividual differences in the leptin response to exercise training, some individuals showing increases and others showing decreases or no changes after endurance training.
DISCUSSION
Administration of leptin to the ob/ob mouse reveals that leptin influences oxygen consumption, locomotor activity, and heat production (10, 19), suggesting that this hormone plays an important role in the regulation of energy expenditure besides its effect on the control of food intake. The present study was undertaken to study the leptin response to the acute (single bout of exercise) and chronic (20 wk of exercise training) effects of exercise in men and women.
Our results indicate that leptin levels are not altered during exercise
and that endurance training is associated with a reduction in
circulating levels of leptin in men but not in women. Men exhibited a
significant (P < 0.0001) reduction
of 6% in percent body fat in response to training compared with a
nonsignificant reduction of 2% in women. After changes in fat mass in
the analyses are accounted for, the effects of training were no longer
significant, suggesting that there are no chronic effects of exercise
on leptin levels, independent of fat mass changes. However, this
adjustment appears to have different effects in men and women. As
indicated in Table 2, adjustment for fat mass resulted in an increase
of the P values for chronic effects in
men, whereas in women the opposite effect was observed. This
observation suggests that the leptin response to exercise is gender
specific. To further investigate this issue, we computed correlations
between leptin levels measured at Rest before training and their
changes after endurance training with changes in body composition. No
association was observed between pretraining leptin levels and changes
in body composition, but changes in leptin levels were found to be
correlated with changes in body composition in women (0.34 
r 0.37;
P < 0.01) but not in men. Because
the leptin response to endurance training was negatively correlated
with the pretraining leptin levels (r = 0.33 and r = 0.32 in
men and women, respectively), we computed correlations between changes
in leptin and body composition after accounting for the effects of
pretraining leptin levels. The same trend was observed, with no
association in men, whereas the association observed in women became
more significant (0.39 r 0.49;
P < 0.005). These associations will
need to be investigated further with a larger sample size, but they are
in agreement with studies that have shown that there are gender
differences in leptin levels independent of body composition (11, 22).
One factor that could contribute to this gender difference in leptin levels and their response to training is the sex hormones. The leptin levels of pre- and postmenopausal women after adjustment for fat mass were compared in two different studies, one reporting no significant difference (11), whereas another reported significantly higher levels in premenopausal women (22). In postmenopausal women, fat mass-adjusted leptin levels were reported to be unaltered by hormone replacement therapy (11, 13). These studies suggest that after differences in body fat mass are accounted for, leptin levels in women are independent of reproductive status (pre- vs. postmenopausal women) and exogenous sex hormones (hormone replacement therapy).
The absence of significant fat loss in women after the endurance training program could be explained by modifications of their dietary intake. Although energy intake was not assessed in the present study, cholesterol and fat intake were monitored with the EPAT (Eating Pattern Assessment Tool) questionnaire (20). The Eating Pattern Assessment Tool questionnaire is a simple tool used to score the frequency of ingestion of high-fat high-cholesterol food groups. On the basis of this questionnaire, no significant changes were noted in the intake of fat and cholesterol over the 20-wk of endurance training among participants of the HERITAGE study (A. Walker et al., unpublished observations).
Studies in animals suggest that insulin could play a role in the modulation of ob gene expression (7, 23). Recent in vivo (clamp studies) and in vitro (adipocytes from adipose tissue biopsies) studies have shown that there are no acute effects of insulin on leptin secretion (8, 15, 28). A number of studies have shown that exercise training is associated with improvements in glucose tolerance and insulin sensitivity (1). Results of the present study based on fasting insulin or insulin-to-glucose ratio suggest that insulin sensitivity was not altered by endurance training, which could perhaps explain the absence of chronic effects of regular exercise on leptin levels.
Another important finding of this study is the presence of large interindividual differences in the leptin response to exercise. Despite moderate changes in average leptin values, some individuals exhibited a large increase or decrease in leptin levels, whereas others showed no change. A few factors have to be considered in the interpretation of these results. The first is that exercise training might produce alterations in the production and/or clearance of leptin that could not be reflected by a single plasma measurement of leptin levels at a given point in time. Furthermore, there is now evidence that leptin circulates in either a free form (presumably the bioactive form) or is bound to leptin-binding proteins and that the ratio of these two forms varies between lean and obese individuals (26). Furthermore, the same study has shown that in lean subjects with 21% or less body fat, which is a level similar to the men in the present study, the majority of leptin (60-98%) circulated in the bound form and that fasting had no effects on bound leptin (26). This observation could explain the absence of an exercise training effect on total leptin as measured in the present study.
Second, leptin levels used for this report were not measured in a fasting state. This could partly explain the variation observed in the leptin response. However, this is not likely to be a major factor, because results from other studies suggest that leptin levels do not rise postprandially (8, 25). Moreover, leptin levels also exhibit diurnal variation, with a rise during the overnight fast (25) and a fall in the morning if fasting is prolonged (14). In the present study, blood samples for leptin assays were taken at the same time of the day before and after training, and diurnal variation could not be responsible for the interindividual differences observed in the leptin response to exercise training.
In summary, results of this study suggest that there are no acute or chronic effects of exercise on leptin levels in humans, independent of changes in fat mass. As a matter of fact, most of the variation in leptin levels associated with acute exercise or with endurance training appeared to be within the confidence intervals of the leptin assay, although one cannot rule out a minor contribution from other sources.
ACKNOWLEDGEMENTS
We thank all the co-principal investigators, investigators, co-investigators, local project coordinators, research assistants, laboratory technicians, and secretaries who contributed to the study.
FOOTNOTES
Address for reprint requests: L. Pérusse, Physical Activity Sciences Laboratory, Laval Univ. Ste-Foy, Québec, Canada G1K 7P4 (E-mail: Louis.Perusse{at}edp.ulaval.ca).
Received 4 December 1996; accepted in final form 12 March 1997.
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H. Yamazaki, M. Arai, S. Matsumura, K. Inoue, and T. Fushiki Intracranial administration of transforming growth factor-beta 3 increases fat oxidation in rats Am J Physiol Endocrinol Metab, September 1, 2002; 283(3): E536 - E544. [Abstract] [Full Text] [PDF]
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R. Lau, W. D. Blinn, A. Bonen, and D. J. Dyck Stimulatory effects of leptin and muscle contraction on fatty acid metabolism are not additive Am J Physiol Endocrinol Metab, July 1, 2001; 281(1): E122 - E129. [Abstract] [Full Text] [PDF]
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Y. C. Chagnon, T. Rice, L. Perusse, I. B. Borecki, M.-A. Ho-Kim, M. Lacaille, C. Pare, L. Bouchard, J. Gagnon, A. S. Leon, et al. Genomic scan for genes affecting body composition before and after training in Caucasians from HERITAGE J Appl Physiol, May 1, 2001; 90(5): 1777 - 1787. [Abstract] [Full Text] [PDF]
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 J. E Reseland, S. A Anderssen, K. Solvoll, I. Hjermann, P. Urdal, I. Holme, and C. A Drevon Effect of long-term changes in diet and exercise on plasma leptin concentrations Am. J. Clinical Nutrition, February 1, 2001; 73(2): 240 - 245. [Abstract] [Full Text] [PDF]
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 T. T. Fung, F. B. Hu, J. Yu, N.-F. Chu, D. Spiegelman, G. H. Tofler, W. C. Willett, and E. B. Rimm Leisure-Time Physical Activity, Television Watching, and Plasma Biomarkers of Obesity and Cardiovascular Disease Risk Am. J. Epidemiol., December 15, 2000; 152(12): 1171 - 1178. [Abstract] [Full Text] [PDF]
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F. S. L. Thong, R. Hudson, R. Ross, I. Janssen, and T. E. Graham Plasma leptin in moderately obese men: independent effects of weight loss and aerobic exercise Am J Physiol Endocrinol Metab, August 1, 2000; 279(2): E307 - E313. [Abstract] [Full Text] [PDF]
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L. K. Hilton and A. B. Loucks Low energy availability, not exercise stress, suppresses the diurnal rhythm of leptin in healthy young women Am J Physiol Endocrinol Metab, January 1, 2000; 278(1): E43 - E49. [Abstract] [Full Text] [PDF]
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S. B. Bramlett, J. Zhou, R. B. S. Harris, S. L. Hendry, T. L. Witt, and J. J. Zachwieja Does beta 3-adrenoreceptor blockade attenuate acute exercise-induced reductions in leptin mRNA? J Appl Physiol, November 1, 1999; 87(5): 1678 - 1683. [Abstract] [Full Text] [PDF]
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M. Halle, A. Berg, U. Garwers, D. Grathwohl, W. Knisel, and J. Keul Concurrent reductions of serum leptin and lipids during weight loss in obese men with type II diabetes Am J Physiol Endocrinol Metab, August 1, 1999; 277(2): E277 - E282. [Abstract] [Full Text] [PDF]
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B. Gutin, L. Ramsey, P. Barbeau, W. Cannady, M. Ferguson, M. Litaker, and S. Owens Plasma leptin concentrations in obese children: changes during 4-mo periods with and without physical training Am. J. Clinical Nutrition, March 1, 1999; 69(3): 388 - 394. [Abstract] [Full Text] [PDF]
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W. J. Pasman, M. S. Westerterp-Plantenga, and W. H. M. Saris The effect of exercise training on leptin levels in obese males Am J Physiol Endocrinol Metab, February 1, 1998; 274(2): E280 - E286. [Abstract] [Full Text] [PDF]
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R. V. Considine Invited Editorial on "Acute and chronic effects of exercise on leptin levels in humans" J Appl Physiol, July 1, 1997; 83(1): 3 - 4. [Abstract] [Full Text] [PDF]
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ABSTRACT
