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Section on Gerontology and Geriatric Medicine, Wake Forest University School of Medicine (T.Y., B.J.N.), Winston-Salem, North Carolina 27157; Diabetes Research Institute, University of Miami School of Medicine (D.M.B.), Miami, Florida 33136; and Division of Gerontology, University of Maryland School of Medicine (A.S.R.), Baltimore, Maryland 21201
Address all correspondence and requests for reprints to: Dr. Tongjian You, Section on Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157. E-mail: tyou{at}wfubmc.edu.
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Abstract |
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, and their soluble receptors (sIL-6R, sTNFR1, and sTNFR2), and whether changes in these inflammatory markers are related to changes in regional lipolysis in obese (body mass index, 32.78 ± 4.73) postmenopausal women (diet alone, n = 17; diet plus exercise, n = 17). All inflammatory markers were measured by an ELISA method. In vitro lipolysis was evaluated by measuring glycerol release using a one-step enzymatic fluorometric technique. Six months of diet and diet plus exercise decreased total and abdominal fat to a similar degree. Diet plus exercise, but not diet alone, decreased plasma levels of C-reactive protein, IL-6, sIL-6R, and sTNFR1 and increased basal and postreceptor stimulated lipolysis in both abdominal and gluteal regions. Changes in abdominal stimulated lipolysis correlated significantly with changes in plasma IL-6 (r = –0.39) and TNFR1 (r = –047). Thus, diet plus exercise training, but not diet alone, is effective in reducing chronic inflammation in obese postmenopausal women. In addition, modification of chronic inflammation is associated with changes in local adipose tissue metabolism in response to diet and exercise. |
Introduction |
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) and the acute phase reactant C-reactive protein (CRP), is an independent predictor of several chronic diseases, including coronary heart disease (1, 2), stroke (3, 4), and diabetes (5). In addition, inflammation is likely to be a causative underlying mechanism of atherosclerosis and insulin resistance (6). Lifestyle changes, such as weight loss and increases in physical activity, are advocated for the treatment of these chronic diseases (7, 8), and data are emerging that suggest that these treatments may be beneficial in part due to their antiinflammatory effects.
Previous studies show that weight loss via a hypocaloric diet reduces concentrations of CRP, TNF, and IL-6 in obese women (9, 10, 11, 12). In addition, recent evidence indicates that long-term exercise training may reduce chronic inflammation. In observational studies, lower IL-6 and CRP levels as well as other markers of inflammation (fibrinogen and white blood cell count) are found in individuals who are the most physically active (13) and the most physically fit (14). Intervention studies show that chronic exercise training reduces circulating concentrations of cytokines or their soluble receptors (15, 16, 17, 18, 19, 20). However, mechanisms by which exercise training influence these inflammatory markers are not entirely known. As many cytokines are produced and secreted from adipose tissue, a local effect of exercise on adipose tissue itself may play an important role in this process.
Aerobic exercise training increases in vitro adipocyte lipolysis (21, 22, 23, 24). In addition, aerobic exercise training blunts decreases in abdominal and gluteal adipocyte lipolysis that occur with caloric restriction in postmenopausal women (25). The mechanism is related to an exercise-induced increase in postreceptor stimulation of hormone-sensitive lipase (HSL) via the cAMP pathway. As hypocaloric diet and exercise training alter both chronic inflammation and adipose tissue metabolism, it is of interest to determine whether decreases in inflammatory markers are related to increases in adipocyte lipolysis in response to diet and exercise.
In the present study we hypothesized that the combination of diet and exercise would be more effective in reducing chronic inflammation than diet alone in obese postmenopausal women. In addition, we hypothesized that changes in plasma inflammatory markers in response to diet and exercise would be related to changes in regional adipocyte lipolysis. Thus, the purpose of this study was to confirm our previous finding that exercise training blunts caloric restriction-induced decreases in adipocyte lipolysis and to determine whether 1) addition of exercise training to a dietary-induced weight loss program is more effective in reducing plasma concentrations of CRP, IL-6, and TNF as well as concentrations of their soluble receptors (sIL-6R, sTNFR1, and sTNFR2); and 2) changes in plasma concentrations of CRP, IL-6, TNF, and their soluble receptors are related to changes in abdominal and gluteal adipocyte lipolysis.
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Subjects and Methods |
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Healthy, nonsmoking, overweight and obese [body mass index (BMI), 25–40 kg/m2], postmenopausal (no menstruation for at least 1 yr) women, aged 50–70 yr, were recruited from the Baltimore metropolitan area for participation in this study. The women were sedentary (<20 min of exercise, twice weekly) and weight-stable (<2.0 kg weight change) for at least 1 yr before enrollment. All women provided informed consent to participate in the study according to the guidelines of the University of Maryland institutional review board for human research. Initial evaluations included a medical history review, physical examination, fasting blood profile, and 12-lead resting electrocardiogram. Subjects with evidence of untreated hypertension (blood pressure, >160/90 mm Hg), hypertriglyceridemia (triglyceride, >400 mg/dl), cancer, liver, renal or hematological disease, other medical disorders, or orthopedic limitations that would affect exercise were excluded. Women were given a 2-h oral glucose tolerance test to exclude those with diabetes (fasting blood glucose, >126 mg/dl; 2-h glucose, >200 mg/dl). On a second screening visit, the subjects underwent a graded exercise test to exclude those with an abnormal cardiovascular response to exercise. Fifty women were eligible for the study and were enrolled randomly in groups of 10–12 women to either a hypocaloric diet only (diet, n = 26) or diet plus exercise (n = 24) intervention for a period of 6 months.
Study design
Baseline measurements of body composition, body fat distribution, maximal aerobic capacity (VO2max), and adipocyte lipolysis were performed after at least 2 wk of weight stability before the interventions. Subjects reported to the facility on the first day for the measurement of body composition and VO2max. To eliminate the effects of physical activity on inflammation and adipocyte lipolysis, subjects were asked to remain sedentary, and the blood draw and fat biopsies were performed at least 48 h after the VO2max test. The blood draw and fat biopsies took place at the same time in the morning (0700–0900 h) after an overnight fast before and after the interventions. All women were free of active infection for at least 1 wk before testing.
During the 6-month interventions, all subjects met weekly in a group setting with a registered dietitian for instruction in the principles of a hypocaloric diet designed to elicit a 0.5- to 1.0-kg weight loss/wk (
250–350 kcal/d deficit). The dietary instruction focused on nutrition education, eating behavior, stress management, control of portion sizes, and modification of binge eating and other adverse habits. Women were asked to record their daily food intake in terms of dietary exchanges. These food records were reviewed weekly by the registered dietitian, and feedback was given to the participant to encourage compliance with the prescribed calorie deficit. In addition, the diet plus exercise group walked on a treadmill 3 d/wk at a target heart rate calculated from the Karvonen equation (HRR x (intensity) + resting heart rate, where heart rate reserve (HRR) is the maximal heart rate minus the resting heart rate obtained from each subject’s VO2max test. The duration and intensity of the exercise progressed from 20 min at 50–55% of HRR during the first week of exercise to 45–60 min at 65–70% HRR by the third month. The subjects warmed up and cooled down by walking or pedaling a stationary bike for 3–5 min at a slow pace. To ensure compliance with the training intensity, at least two heart rate readings were taken during the exercise and recorded in an exercise log book. Body weight was recorded once a week in both groups. The average compliance with the diet classes was 80% for the diet only group and 78% for the diet plus exercise group. The average compliance with the exercise sessions was 78%.
After the interventions, the women were weight-stabilized (<0.5 kg weight change) on a eucaloric diet for a period of 2 wk before retesting. The diet plus exercise group continued to exercise during this period, and the postintervention blood draw and fat biopsies occurred at least 36–48 h after the last exercise session.
Body composition
Waist (minimal circumference) and hip (maximal gluteal protuberance) circumferences were measured in duplicate. Percent body fat, fat-free (bone and lean tissue) mass, and fat mass were measured using dual energy x-ray absorptiometry (model DPX-L, Lunar Radiation Corp., Madison, WI). A single-slice computed tomography scan taken midway between L4 and L5 was performed using a GE Hi-Light computed tomography scanner to measure abdominal visceral and sc adipose tissue areas as previously described (26).
Maximal aerobic capacity
VO2max was measured on a motor-driven treadmill (Quinton Instruments, Seattle, WA) during a progressive exercise test to voluntary exhaustion as previously described (27). A valid VO2max was obtained when at least two of these three criteria were met: 1) maximal heart rate greater than 90% of age-predicted maximal heart rate (220 beats/min – age), 2) respiratory exchange ratio of at least 1.10, and 3) plateau in VO2 (<200 ml/min change) with increasing work rate.
Inflammatory markers
Plasma (EDTA) concentrations of IL-6, TNF, and their soluble receptors (sIL-6R, sTNFR1, and sTNFR2) were measured in duplicate, and the average of the two values was used for data analyses. Duplicate samples that did not provide a coefficient of variation less than 15% were reanalyzed, and all values were averaged for data analyses. All cytokines and cytokine-soluble receptors were measured using Quantikine ELISA kits (R&D Systems, Minneapolis, MN). CRP was measured using an automated immunoanalyzer (Immulite, Diagnostics Products Corp., Los Angeles, CA). The CRP assay has a sensitivity of 0.01 mg/dl, with a calibration range of up to 25 mg/dl. In our laboratory, the inter- and intraassay coefficients of variation for IL-6 were 5.4 and 3.5%, respectively; those for TNF were 11.8 and 6.2%, respectively; and those for the soluble receptor assays were under 5%. The inter- and intra-assay coefficients of variation for the CRP assay were 7.5 and 4.4%, respectively.
Adipocyte lipolysis
Subcutaneous adipose tissue from both the abdominal and gluteal regions was taken by aspiration with a 16-gauge needle under local anesthesia (2% xylocaine) after an overnight fast. Adipocytes were isolated in a Krebs-Ringer N-2-hydroxyethylpiperazine-N''-2-ethanesulfonic acid buffer (pH 7.4) containing 4% BSA, 5 mM glucose, 200 nM adenosine, and 1 mg/ml collagenase. Isolation took place in a shaking water bath at 100 rpm at 37 C for 45 min. Isolated cells were filtered through 250-µm nylon mesh, washed three times with enzyme-free Krebs-Ringer N-2-hydroxyethylpiperazine-N''-2-ethanesulfonic acid buffer, and resuspended to a final concentration of 20,000–30,000 cells/ml. The diameters of 100 cells/site were counted in an aliquot of the cell suspension to calculate the average cell weight. Total lipid weight per aliquot was measured by Dole’s extraction and then divided by individual cell weight to obtain the cell number (27).
Extracellular glycerol release was used as the indicator of adipocyte lipolysis. Aliquots (0.75 ml) of the cell suspension were placed in polyethylene tubes containing nothing (basal) or dibutyryl cAMP (dcAMP; 2 mM) and incubated in a water bath at 37 C for 2 h. The reaction was stopped by the addition of 76 µl 2.5 M perchloric acid. The glycerol concentration in each tube was measured by a one-step enzymatic fluorometric technique (28). The rate of adipocyte lipolysis is expressed as micromoles of glycerol per 106 cells per 2 h.
Statistics
Statistical analyses were performed using JMP version 4.0 for Windows (SAS Institute, Inc., Cary, NC). The CRP, IL-6, and TNF data were not normally distributed, so the logarithm of each was used for parametric statistical analyses. First, within-group differences in baseline characteristics of women who completed the study and those who dropped out were determined by t test. For women who completed the study, within-group differences between pre- and postintervention measures of all variables were determined using a paired t test. Differences between the treatment groups at baseline and most changes over time in response to the interventions were determined by t test. Where baseline differences appeared, covariance analysis was used to compare between-group changes using baseline values as a covariate. Spearman correlation coefficients were calculated for relationships between changes in variables. Correlation coefficients between changes in lipolysis and inflammation were calculated using total and abdominal sc fat changes as covariates. All data are presented as the mean ± SE, and the level of significance was set at P < 0.05 for all analyses.
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Results |
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Thirty-four (diet, n = 17; diet plus exercise, n = 17) of the initial 50 women completed all aspects of the study. Fourteen women dropped out of the program due to personal reasons, relocation, and/or time constraints. Two women completed the interventions, but did not complete postintervention testing and therefore did not have measures of body composition, inflammation, and lipolysis. Women with higher baseline abdominal fat, as indicated by waist to hip ratio (P < 0.01) and visceral fat area, were more likely to drop out with diet restriction. Women of older age (P < 0.05) and with lower baseline aerobic ability (P < 0.05) dropped out more with diet plus exercise. The results of the 34 women who completed the study are presented in this section.
At baseline, there were no differences in age, body composition, body fat distribution, or aerobic fitness between the two groups (Table 1
). After the 6-month interventions, both groups lost a similar amount of body weight, consisting mostly of adipose tissue (Table 1). Likewise, there were similar reductions in percent body fat and abdominal visceral and sc adipose tissue areas between the groups. Fat-free mass and waist to hip ratio did not change significantly in either group. Absolute VO2max decreased with diet only (P < 0.05), but increased with diet plus exercise (P < 0.05). Changes in absolute VO2max were significantly different between the groups (Table 1).
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Baseline concentrations of CRP, IL-6, TNF, sIL-6R, and TNF soluble receptors were not different between the groups (Table 2). None of the cytokines or cytokine soluble receptors changed with diet only, whereas CRP, IL-6, sIL-6R, and TNFR1 decreased with diet plus exercise (Table 2). Changes in IL-6, sIL-6R, and sTNFR1 were significantly different between the groups (Fig. 1).
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Effects of diet and diet plus exercise on regional adipocyte lipolysis
Due to insufficient adipose tissue obtained from the biopsies, abdominal lipolysis data were not available in seven women (diet only, 3; diet plus exercise, 4) and gluteal lipolysis data were not available in four women (diet only, 2; diet plus exercise, 2). There were no baseline differences in abdominal and gluteal adipocyte sizes between the two groups (Table 3). Both abdominal and gluteal adipocyte sizes did not change with diet alone, but significantly decreased in the diet plus exercise group (Table 3). At baseline, basal and dcAMP-stimulated lipolysis in abdominal adipocytes did not differ between the groups, but gluteal adipocyte lipolysis was higher in the diet only group (P < 0.05; Table 3). Basal and dcAMP-stimulated lipolysis significantly increased (Table 3) in both abdominal and gluteal adipocytes with diet plus exercise, but did not change with diet alone. Changes in abdominal dcAMP-stimulated lipolysis were significantly different between the groups (P < 0.05; Fig. 2).
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We also analyzed the relationships between changes in inflammatory markers and changes in adipocyte lipolysis (basal and dcAMP-stimulated) in the entire cohort combined. Changes in IL-6 (r = –0.39; P < 0.05) and sTNRF1 (r = –0.47; P = 0.01) correlated negatively with changes in abdominal dcAMP-stimulated lipolysis (Fig. 3). Total and abdominal sc fat changes did not influence these significant correlations in a multivariate model. There were no significant correlations between any of the inflammatory markers and gluteal lipolysis.
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Discussion |
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and sTNFR2, and had significantly different changes over time in IL-6, sIL-6R, and sTNFR1 concentrations than women who underwent diet intervention only. In addition, greater decreases in sIL-6R and sTNFR1 were seen in women whose VO2max increased the most, although the significant correlations may just appear by chance due to the low statistical power. These findings indicate that diet plus exercise, but not diet alone, is effective in reducing markers of inflammation in older, obese women.
It has been postulated that physical activity may lower the risk of coronary heart disease in part by prevention or reduction of excess inflammation (13). Our data are consistent with emerging epidemiological and clinical trial evidence that regular physical activity results in a reduced inflammatory state (13, 15, 16, 17, 18, 19, 20). Findings of previous intervention studies show that aerobic exercise decreases circulating concentrations of CRP in healthy subjects as well as patients at risk for heart disease (16, 18). We found that CRP decreased with diet plus exercise, but not with diet alone. Some (19, 29), but not all (20), previous studies also show that blood levels of TNF are reduced with exercise training. Similar to the results reported by Conraads et al. (20), we did not see a decrease in TNF, but did observe a decline in TNFR1 with diet and exercise. As circulating TNF1 has a longer half-life than TNF, it was hypothesized that it serves to prolong the biological effects of TNF at the tissue level (30). Thus, the lack of a decrease in TNF itself with exercise training may be a result of its transient production and short half-life, whereas decreases in TNFR1 may be more reflective of actual TNF function.
Presently, we can only speculate about the biological mechanisms by which regular aerobic exercise reduces inflammation, especially given that strenuous acute exercise often increases cytokine production due to muscle/connective tissue injury (31, 32). Because IL-6, TNF, and their receptors are highly expressed in adipose tissue and are elevated in obese individuals (33, 34, 35), the loss of body fat with exercise could be one method by which it lowers inflammation. However, in the current study women in the diet plus exercise group decreased proinflammatory cytokines more than those in the diet only group despite a similar losses of body weight and of total and abdominal adipose tissue. Although visceral fat amount has been linked to circulating levels of proinflammatory cytokines (36), in our study visceral fat loss was similar in the two treatment groups. In addition, the relationship between greater physical activity and physical fitness, and less inflammation observed in epidemiological studies is independent of overall and abdominal obesity (13, 14). Therefore, there must be some mechanism by which chronic exercise itself lowers inflammation.
At the present time, there are several potential mechanisms by which exercise training could alter the regulation of inflammation. Most likely, the ability of exercise to reduce expression and serum levels of leukocyte adhesion molecules (17), and thus to inhibit monocyte-endothelial cell interaction, is a possible mechanism. Alternatively, exercise training may reduce mononuclear cell production of proinflammatory cytokines by reducing chronic oxidative stress via enhancing antioxidant defenses (37), by decreasing expression of cytokines in muscle tissue (38), or by reducing daily bouts of hypoxia, a stimulator of proinflammatory cytokine expression (39), via training of the cardiorespiratory system. Finally, as IL-6 can exhibit immunological suppressive effects (40), its repeated release from contracting muscle during bouts of acute exercise may serve to down-regulate overall inflammation (31).
Although previous studies have shown that diet alone reduces concentrations of CRP (9, 10), IL-6 (11), and TNF (12), there were no overall changes in any of the inflammatory markers in women who underwent diet only in the current study. We believe that the lack of a statistically significant decrease in this group is probably due to the relatively small decrease in body weight compared with that in previous studies. Currently, obesity-associated inflammation has been linked with oxidative stress, because nutritional challenge stimulates the production of reactive oxygen species, which causes nuclear factor-
B induced inflammation (41, 42). Caloric restriction can reduce oxidative stress (43, 44) and thus may modify chronic inflammation through this mechanism. However, changes in oxidative stress and inflammatory markers may not be parallel in response to diet (44), which suggests that other unidentified mechanism(s) may also be involved.
Exercise training stimulates in vitro lipolysis due to the enhancement of ß-adrenergic pathway efficiency (24, 25, 26) and a decrease in -adrenergic efficiency (21, 22, 23, 24). Exercise training also blunts insulin-induced suppression of adipocyte lipolysis (24, 45). Our previous study shows that basal and dcAMP-stimulated lipolysis in both abdominal and gluteal regions decrease with hypocaloric diet, but exercise training blunts the declines with diet in obese postmenopausal women (25). Therefore, the cellular adaptation to exercise training may also include a stimulation of HSL activity, which is regulated by phosphorylation-dephosphorylation via cAMP-dependent protein kinase. In the current study we did not see diet-induced declines in lipolysis, possibly due to the relatively small weight loss. However, we observed a stimulatory effect of exercise training on basal and dcAMP-stimulated lipolysis in both regions. These results support our previous finding that exercise may up-regulate in vitro lipolysis through a postreceptor mechanism, possibly at the HSL step.
Interestingly, our results showed that changes in the inflammatory markers IL-6 and TNFR1 are associated with changes in abdominal dcAMP-stimulated lipolysis. This is the first study that links changes in inflammation and regional fat tissue metabolism in particular, not just fat mass. Considering the decreases in inflammatory markers and the increases in basal and stimulated lipolysis in the diet plus exercise group compared with the diet alone group, the correlations are probably due to the effect of exercise training. However, the correlations are not significant when only the exercise training group is included in the analysis. This may be due to the insufficient statistical power in that group. Regardless, there must be some pathway that links changes in inflammation and abdominal lipolysis with diet and exercise.
Under normal physiological conditions, proinflammatory cytokines induce lipolysis at rest (46, 47) and after acute aerobic exercise (48). However, changes in inflammatory markers with chronic exercise are different. As adipose tissue is a critical organ that produces and secrets proinflammatory cytokines and their soluble receptors, and lipolysis occurs in adipose tissue, it is reasonable to consider that a change in fat mass is an important factor that links changes in inflammation and lipolysis. In this study, however, the correlations between changes in inflammatory markers (IL-6 and TNFR1) and abdominal lipolysis remain significant even after total and abdominal fat changes were added to the model. This suggests that another physiological mechanism(s) links changes in inflammation and lipolysis with diet and exercise.
Obesity is associated with a number of metabolic complications, including changes in the plasma lipid profile, such as an increase in free fatty acids (FFA) (49). An increase in FFA can result in the activation of proinflammatory genes that are modulated by nuclear factor-B (42). As FFA is an end product of lipolysis, an increase in FFA may suppress lipolysis through a postreceptor pathway, possibly by suppressing HSL expression and function (50). Long-term diet plus exercise treatment can reduce plasma FFA, which is independently associated with inflammatory markers (51). Moreover, a reduced FFA may up-regulate lipolysis through the above pathway. Current evidence demonstrates regional differences in the expression of genes encoding certain functional proteins in adipocytes (52). It is quite possible that a change in HSL expression is greater in abdominal fat than in gluteal fat in response to the FFA reduction following diet and exercise treatment. In addition, proinflammatory gene expression in abdominal fat is higher than that in gluteal fat and therefore contributes more to the reduction in systemic inflammation in response to diet and exercise. However, as circulating FFA was not measured in our study, this is only a postulated mechanism. More studies are needed to investigate the possible mechanism(s) of the link between local (abdominal) lipolysis and inflammation in response to diet and exercise.
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Acknowledgments |
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Footnotes |
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Abbreviations: CRP, C-reactive protein; dcAMP, dibutyryl cAMP; FFA, free fatty acid; HRR, heart rate reserve; HSL, hormone-sensitive lipase; sIL-6R, IL-6 soluble receptor; sTNFR, TNF soluble receptor; VO2max, maximal aerobic capacity.
Received July 28, 2003.
Accepted January 13, 2004.
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| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
) and diet plus exercise (
) groups. Log-transformed values were used to perform the statistical analyses for CRP, IL-6, and TNF
, P < 0.05; 
) and diet plus exercise (•).