Abstract
Objective:
To examine exercise modality during weight loss on change in inflammation among older adults who are overweight or obese and have cardiometabolic disease.
Methods:
222 older adults with a mean ±SD age of 66.9 ±4.7 years and a mean ±SD BMI of 33.5 ±3.5 kg/m2 were randomized to weight loss (WL; n = 68), WL plus aerobic training (WL+AT; n = 79), or WL plus resistance training (WL+RT; n = 75) for 18 months. C-reactive protein (CRP) and interleukin-6 (IL-6) were measured at baseline, 6 months, and 18 months.
Results:
All groups lost significant weight from baseline to 18-months with average adjusted changes of −5.5% for WL, −9.0% for WL+AT, and −10.1% for WL+RT. WL+RT and WL+AT lost significantly more weight the WL (P<.05). At 18-months, CRP values in WL+RT were significantly lower than WL [2.25 pg/ml vs. 3.38 pg/ml; P=0.004]. The only difference in IL-6 was that, at 18-months, WL+RT was lower than WL+AT [2.32 pg/ml vs. 2.75 pg/ml; P=.03].
Conclusions:
The addition of RT during WL was more effective at reducing levels of CRP than WL. Although results were in the expected direction, there was no difference in CRP between WL and WL+AT.
Keywords: Aging, C-Reactive Protein, Clinical Trials, Exercise, Weight Loss
Introduction
Chronic low-grade inflammation is a consequence of aging1 and is associated with the risk of developing several age-associated chronic health conditions such as ischemic heart disease,2,3 diabetes,4 kidney disease,5 and Alzheimer’s disease.6 Low grade inflammation also predicts limitations in mobility7 and decline in reaction time among healthy older adults.8 Welty and colleagues9 posit chronic inflammation as a central mechanism underlying the pathophysiology of the metabolic syndrome (MetS), underscoring the importance of clinical interventions that target inflammation in this patient population. The intent of the current study is to evaluate the 18-month effects of weight loss (WL) and WL coupled with either resistance (WL+RT) or aerobic exercise training (WL+AT) on inflammatory biomarkers (C-reactive protein, CRP, and interleukin-6, IL-6) among older adults who are overweight or obese and have either MetS and/or cardiovascular disease (CVD).
Body fat is an active endocrine organ and obesity is associated with increased levels of inflammation, a relationship that is supported by recent reviews on the efficacy of weight loss in lowering biomarkers of inflammation.10,11 Although state-of-the-art weight loss interventions include physical activity,12 many commercial programs rely on diet alone. Additionally, most dietary weight loss studies that do promote increased physical activity focus on AT rather than RT. This is particularly important when studying inflammation in that AT may not confer an additive benefit beyond weight loss alone for reducing inflammation.13,14 Of note, Woods15 has argued that the effects of AT on inflammation are due to reductions in fat mass with training. Of particular significance to the current study is a recent meta-analysis of RT on inflammation in older adults that reported a moderate effect size for RT on reducing CRP and a marginal effect on IL-6.16
Given the importance of weight loss for older individuals who are overweight or obese and have MetS and/or CVD, these secondary analyses of a randomized trial data examined 18-month changes in CRP and IL-6 in response to WL, WL+AT, and WL+RT conducted within the community setting of three YMCAs.17 CRP and IL-6 are the most common biomarkers of chronic inflammation. While IL-6 is the primary cytokine leading to hepatic CRP production, both of these molecules have distinct biological roles and they have differential predictive capacity for several chronic diseases.18 In addition, they respond differently to diet and exercise interventions.19 A review of prior research on older adults illustrates that there is greater consistency for the effects of exercise on CRP than IL-6.15 In addition, much of the exercise-induced changes in CRP are a function of weight loss resulting from an exercise intervention. Based on the existing weight loss literature12,13 and reviews of exercise and inflammation,16,20 we hypothesized that combining physical activity with weight loss would lead to greater 18-month reduction in weight and inflammation than the WL group and expected larger effects for CRP than IL-6. Due to the existing meta-analysis of RT and inflammation, the fact that the effects of exercise on inflammation in older adults are more consistent for CRP than IL-6,15 and an earlier paper of ours in which we reported that WL+RT buffered the loss of lean mass compared to WL+AT,21 we also hypothesized that, after controlling for weight loss, WL+RT would exhibit greater reductions in CRP than either WL or WL+AT.
Methods
Participants.
The Cooperative Lifestyle Intervention Program-II (CLIP-II) study recruited older adults who were overweight or obese and had MetS and/or CVD into an 18-month RCT with three treatment groups: WL via caloric restriction only, WL+AT, or WL+RT. The primary outcomes were change in 400 m walking speed and strength. The methods have been described in detail.22 In brief, delivery of this single-blinded RCT occurred in three community YMCAs in Forsyth County, NC, with the interventions being delivered by YMCA staff members. Eligible participants were community-dwelling men and women aged 60–79 yrs who were low active (i.e., engaging in <60 min/week of moderate to vigorous physical activity) with a body mass index ≥ 28 and < 42 kg/m2, self-reported limitations in mobility, and documented evidence of CVD or an ATP II diagnosis of MetS.23 Self-reported disability was one of the inclusion criteria since the primary aim of this study concerned the combination of weight loss and different modes of physical activity on improvement in mobility among older adults with compromised physical function who were either overweight or obese. We recruited individuals with CVD or MetS as these obesity-related conditions are highly prevalent in older adults.24 Exclusion criteria included severe heart disease, severe systematic disease, having had a myocardial infarction or cardiovascular procedure in the previous three months, a blood glucose reading of ≥ 140 mg/dL, diagnoses of Type 1 or Type 2 diabetes, or a severe psychiatric condition. The institutional review board at Wake Forest School of Medicine approved the study protocol. The trial was monitored by an independent data and safety monitoring board and was registered at ClinicalsTrials.gov ().
Randomization.
Recruitment occurred in eight waves with randomization of participants within each wave to one of the three interventions. Randomization occurred following baseline testing using a block randomization scheme that was stratified by wave.
Intervention.
The three study arms received the same WL intervention in three 6-month phases: intensive (months 1–6), transition (months 7–12), and maintenance (months 13–18). During the initial intensive phase, participants met with trained staff members at a local YMCA for three group sessions and one individual session each month. The group sessions, which lasted 60 minutes, were tapered to two monthly sessions, and then one monthly session during the transition and maintenance phases, respectively. During the intensive phase, the content focused on key elements of self-regulation such as setting “smart” goals, promoting self-monitoring of caloric intake along with success in meeting caloric goals, and tools for relapse prevention. The transition phase continued to reinforce the use of effective self-regulation and also introduced topics related to healthy eating. The approach to weight loss involved state-of-the-art methods12,25 with the details having been published.22 The goal was to elicit a 0.3 kg/week weight loss in the intensive phase with a total weight loss of 7–10% of body mass. The caloric goal for individuals with a weight <250 pounds was 1200–1500 kcal/day and for those >250 pounds it was 1500–1800 kcal/day. The nutritional composition of the diet was 20–25% proteins, 25–30% fats, and 45–55% carbohydrates. Self-regulatory skills were developed through weekly homework assignments, and support among members was encouraged through weekly discussions of successes, failures, and methods for overcoming barriers to individual and group progress. The maintenance phase transitioned participants away from staff- and group-supported self-regulation toward personal responsibility for self-regulation. Intermittent group discussions continued to provide opportunities for group member support.
With regard to the exercise component of CLIP-II, individuals assigned to the WL+AT or WL+RT conditions engaged in four sessions of exercise training each week. The AT prescription consisted primarily of walking on an indoor track four days each week, and participants were guided toward achieving 45 minutes of uninterrupted exercise at a rating of perceived exertion (RPE) of 12–14 on the Borg RPE scale26 during each session. Those who received RT worked toward exercising for 45 minutes at an RPE of 15–18 on four days each week, completing exercises on eight Cybex resistance machines. During the first week, participants engaged in one set of 10–12 repetitions at 40% of their one-repetition max; a value determined during an orientation appointment. By weeks 3–12, the goal for participants was to complete three sets of 10–12 repetitions at 70% of their one-repetition max; a goal that was increased to 75% from week 13 onward. Additionally, during this final phase, participants completed the third set to volitional fatigue. If they were able to achieve at least 12 repetitions, the resistance was increased in an effort to maintain a consistent RPE.
Inflammatory Biomarkers
Blood samples were collected in the early morning after a 12-hour fast. All follow-up samples were collected at least 24 hours after an exercise session and blood sampling was postponed (1–2 weeks after recovery of all symptoms) in the event of an acute respiratory, urinary tract, or other infection. Plasma IL-6 assays were run using Quantikine enzyme-linked immunosorbent kits from R&D systems (Minneapolis, MN) and high-sensitivity CRP was assessed using an automated immunoanalyzer (IMMULITE; Diagnostics Products Corporation, Los Angeles, CA).
Analyses
The comparisons of interest in this paper were between WL vs. WL+RT, WL vs. WL+AT, and WL+RT vs. WL+AT on CRP and IL-6 at 18 months. We also report on the 6-month intermediate effects. We used two-sided tests at α = .05 following the intention-to-treat principle with no adjustment for multiplicity. To test the treatment effects, we employed mixed model analyses of covariance (ANCOVA) with an unstructured covariance matrix. Covariates included the baseline value of the outcome tested and sex, which were entered as fixed effects, as well as YMCA site and wave within site, which were entered as random effects. Overall significance tests for each of the models were conducted using likelihood ratio tests that compared the model presented to a model with only the intercept. Adjusted means and estimated treatment differences were calculated.
Results
Participant Characteristics.
A CONSORT diagram and detailed recruitment and retention information have been published previously.17 Of the 249 older adults randomized to treatment, 222 had blood collected at baseline and at either the 6- or 18-month follow-up. Loss to follow-up did not differ by condition at either time point. Table 1 provides the baseline characteristics for the 222 participants. There were no group differences on these variables and these data did not differ from the complete randomized sample.17 The mean (SD) age of participants was 66.9 (4.7) years, and the baseline BMI was 33.5 (3.5) kg/m2. The sample was largely female (71.2%), 67.6% were white, and the educational background was diverse. Specifically, 42.3% had a high school diploma as their final degree, and 55.9% had an associate’s degree or higher.
Table 1.
Descriptive Characteristics of Participants (n=222)*
| Mean (SD) or Frequency (%) | |
|---|---|
| Age in Years | 66.9 (4.7) |
| Female | 158 (71.2%) |
| Race | |
| African American | 66 (29.7%) |
| Hispanic | 2 (0.9%) |
| White | 150 (67.6%) |
| Other/Mixed/Missing | 4 (1.8%) |
| Highest Level of Education | |
| Less than high school diploma | 4 (1.8%) |
| High school/some college | 94 (42.3%) |
| Associate’s degree or higher | 124 (55.9%) |
| 400 M walk time (seconds) | 332.7 (58.4%) |
| Knee extensor muscle strength (Newton meters) | 94.6 (36.7%) |
| BMI | 33.5 (3.5) |
| CVD History | 58 (26.1%) |
| Diabetes | 42 (19.1%) |
| Arthritis | 133 (61.9%) |
| Hypertension | 163 (73.4%) |
| Cancer | 38 (17.2%) |
| Metabolic Syndrome | 186 (83.8%) |
Note. Medical conditions are based on self-report. A listing a these data by treatment group can be found in the main outcomes paper.17
Retention, Adherence and Weight Loss.
Median (25th, 75th percentiles) attendance to scheduled treatment sessions was 71.1% (40.5, 83.3) for WL, 83.1% (47.6, 92.9) for WL+AT, and 85.7% (70.7, 92.7) for WL+RT. All three groups lost significant weight from baseline (Figure 1) to 18-months with average adjusted changes of −5.5% [95%CI: −7.3 to −3.6%] for WL only, −9.0% [95%CI: −10.9 to −7.2%] for WL+AT, and −10.1% [95%CI: −11.9 to −8.2%] for WL+RT. The WL only group lost less weight than either WL+AT (mean difference 3.5%, P=0.0017) or WL+RT, (mean difference 4.6%, P<0.0001).
Figure 1.
Percent Change in Body Mass across the study by Treatment Group controlling for Sex, Site, Wave within Site, and baseline weight
Effects on CRP and IL-6 Unadjusted for Weight Loss.
At the time of baseline testing, all three treatment groups had equivalent levels of CRP and IL-6 (all Ps>.05): baseline means (SD) for CRP in pg/ml = 4.70 (1.11) for WL, 4.79 (1.12) for AT+WL, and 4.91 (1.12) for WL+RT; for IL-6 in pg/ml = 2.89 (1.06) for WL, 3.10 (1.06) for WL+AT, and 3.03 (1.06) for WL+RT.
Figures 2 & 3 and the top panels of Tables 2 & 3 show CRP and IL-6 values for the mixed model ANCOVAs by treatment group unadjusted for weight loss but adjusted for the baseline value of the outcome tested, sex, as well as YMCA site, and wave within site. In support of our first hypothesis, 18-month CRP values in WL+RT were significantly lower than WL only (P=0.004); although the WL+AT versus WL comparison was in the expected direction, it was not statistically meaningful (P>.05). Although not an explicit hypothesis for this study, the other significant comparison of interest at 18-months revealed that WL+RT had lower IL-6 than WL+AT (P=0.03). Inspection of the 6-month data, reveals that the 3 groups were essentially equivalent in changes from baseline for both CRP and IL-6.
Figure 2.
The 6- and 18-month Effects of the Interventions on CRP Controlling for Sex, Site, Wave within Site and Baseline CRP (The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale for this plot. For the mixed model, the n at baseline was 219, it was 210 at 6 months, and 178 at 18 months.)
Figure 3.
The 6- and 18-month Effects of the Interventions on IL-6 Controlling for Sex, Site, Wave within Site, and Baseline IL-6 (The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale for this plot. For the mixed model, the n at baseline was 219, it was 210 at 6 months, and 178 at 18 months.)
Table 2.
CRP Values (pg/ml) by Time of Assessment by Treatment Group and Unadjusted/Adjust for Δ Weight
| Group Means (SD for Baseline & 95% CIs for Follow-up)* Unadjusted for Δ Weight |
Treatment Group Differences (P values)* Unadjusted for Δ Weight |
|||||
|---|---|---|---|---|---|---|
| Time | WL | WL+ AT | WL+RT | WL vs. WL+AT | WL vs. WL+RT | WL+AT vs. WL+RT |
| 6-months | 3.64 (3.01, 4.40) |
3.26 (2.74, 3.88) |
3.07 (2.57, 3.66) |
−0.38 (0.40) |
−0.57 (0.20) |
−0.19 (0.63) |
| 18-Months | 3.38 (2.76, 4.15) |
2.60 (2.14, 3.16) |
2.25 (1.86, 2.72) |
−0.78 (0.07) |
−1.13 (0.004) |
0.35 (0.29) |
| Follow-up Group Means (95% CIs)* Adjusted for Δ Weight |
Treatment Differences (P values)* Adjusted for Δ Weight |
|||||
| Time | WL | WL+ AT | WL+RT | WL vs. WL+AT | WL vs. WL+RT | WL+AT vs. WL+RT |
| 6-months | 3.44 (2.85, 4.15) |
3.25 (2.74, 3.85) |
3.23 (2.71, 3.85) |
−0.19 (0.65) |
−0.21 (0.62) |
0.02 (0.96) |
| 18-Months | 3.09 (2.53, 3.78) |
2.65 (2.19, 3.21) |
2.38 (1.97, 2.87) |
−0.44 (0.27 |
−0.71 (0.06) |
−0.28 0.41) |
WL = weight loss; WL+AT = weight loss + aerobic training; WL+RT = weight loss + resistance training. The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale; these were what we plotted. Bolded P values were statistically significant. A sensitivity analysis conducted on complete data did not change interpretation of the results from the mixed model analysis. In the analysis on complete data only, the n for WL was 50, for WL+AT it was 58, and for WL+RT it was 61. Using the mixed model, we had 219 at baseline, 210 at 6-months, and 178 at 18-months.
Table 3.
IL-6 Values (pg/ml) by Time of Assessment by Treatment Group and Unadjusted/Adjust for Δ Weight
| Group Means (SD for Baseline & 95% CIs for Follow-up)* Unadjusted for Δ Weight |
Treatment Group Differences (P values)* Unadjusted for Δ Weight |
|||||
|---|---|---|---|---|---|---|
| Time | WL | WL+ AT | WL+RT | WL vs. WL+AT | WL vs. WL+RT | WL+AT vs. WL+RT |
| 6-months | 2.80 (2.48, 3.15) |
2.57 (2.30, 2.86) |
2.61 (2.34, 2.92) |
−0.23 (0.24) |
−0.19 (0.35) |
0.04 (0.81) |
| 18-Months | 2.64 (2.34, 2.99) |
2.75 (2.44, 3.10) |
2.32 (2.07, 2.61) |
0.11 (0.61 |
−0.32 (0.10) |
−0.43 (0.03) |
| Follow-up Group Means (95% CIs)* Adjusted for Δ Weight |
Treatment Differences (P values)* Adjusted for Δ Weight |
|||||
| Time | WL | WL+AT | WL+RT | WL vs. WL+AT | WL vs. WL+RT | WL+AT vs. WL+RT |
| 6-months | 2.76 (2.45, 3.12) |
2.56 (2.29, 2.86) |
2.64 (2.36, 2.96) |
−0.20 (0.30) |
−0.12 (0.54) |
0.08 (0.66) |
| 18-Months | 2.59 (2.28, 2.94) |
2.77 (2.45, 3.12) |
2.35 (2.10, 2.65) |
0.18 (0.41) |
−0.24 (0.23 |
−0.41 (0.04) |
WL = weight loss only; WL+AT = weight loss + aerobic training; WL+RT = weight loss + resistance training. The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale; these were what we plotted. Bolded P values were statistically significant. A sensitivity analysis conducted on complete data did not change interpretation of the results based on the mixed model analysis. In the analysis on complete data only, the n for WL was 49, for WL+AT it was 59, and for WL+RT it was 62. Using the mixed model, we had 222 at baseline, 211 at 6-months, and 181 at 18-months.
Weight Loss-Adjusted Models for CRP and IL-6.
Figures 4 and 5 and the lower panels of Tables 2 and 3 provide CRP and IL-6 values from the mixed models that also adjusted for time-dependent weight loss; that is, baseline to 6 months and 6 to 18 months. Our second hypothesis was that after controlling for time-dependent weight loss, WL+RT would exhibit larger reductions in CRP than either WL or WL+AT. However, this hypothesis was not supported (P>0.05). Because we had DXA data available on these participants we ran two other models, adding in change in time-dependent FFM both with and without time-dependent weight loss. The results of these analyses confirmed that it was change in body mass and adiposity that led to the differences in CRP between WL+RT and WL. Again, it is interesting to note that, at 18-months, the IL-6 values adjusted for weight loss in WL+RT remained lower than WL+AT (P=0.04).
Figure 4.
The 6- and 18-month Effects of the Interventions on CRP Controlling for Sex, Site, Wave within Site, Baseline CRP, and Weight Loss from Baseline to 6- and 18-months (The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale for this plot. For the mixed model, the n at baseline was 222, it was 211 at 6 months, and 181 at 18 months.)
Figure 5.
The 6- and 18-month Effects of the Interventions on IL-6 Controlling for Sex, Site, Wave within Site, Baseline IL-6, and Weight Loss from Baseline to 6- and 18-months (The analysis was performed on the log-transformed scale. We then exponentiated the estimated means and confidence interval limits to return to the original scale for this plot. For the mixed model, the n at baseline was 222, it was 211 at 6 months, and 181 at 18 months.)
Discussion
In support of our first hypothesis, at 18-months we found that WL+RT led to a greater reduction in CRP than WL. Although the comparison between WL+AT and WL for CRP was in the expected direction, it was not statistically significant. There were no statistically significant between-group effects for IL-6 other than WL+RT had lower mean values than WL+AT at the 18th month assessment.
Data from large observational studies27–30 show with considerable consistency that self-reported volume of physical activity is inversely related to biomarkers of inflammation, including CRP and IL-6. However, an important caveat in interpreting these data is that there may well be individual differences other than levels of physical activity driving these effects and, due to the large number of participants, effect sizes are often quite small yet statistically significant. Additionally, data from these studies do not allow one to delineate the causal pathway in the relationship between physical activity and inflammation.
Although there is not an extensive literature from RCTs examining the effects of an exercise intervention on inflammation in older adults, Nicklas and colleagues31 reported on secondary analyses from a large multi-center study involving pre-frail, older adults randomized to either a physical activity intervention with moderate-intensity walking as the primary mode of exercise or a health education control group. After 12 months of treatment, participants in the physical activity intervention had reductions in IL-6 as compared to the health education control group, an effect that was shown to be due to participants with higher baseline values of IL-6. Data from several smaller RCTs have provided mixed results,32–35 with Woods15 noting that the beneficial effects of AT on inflammation appear dependent on loss in fat mass. In fact, when older adults engaged in AT during weight loss, but lost no more weight than dietary weight loss, AT did not confer an added benefit for either CRP or IL-6.36 In contrast, a recent meta-analysis of RT training studies in older adults reported a moderate reduction in CRP with a marginal effect for IL-6, results that parallel our current findings when RT is combined with WL.
In an effort to evaluate whether the difference between WL+RT and WL on CRP was due to differences in lost weight, a second hypothesis involved adding a time-dependent weight loss covariate to the model. While the addition of this covariate did not totally explain away the CRP difference between WL+RT and WL, the effect was no longer statistically significant. Because we had available and have published DXA data on these participants,21 we conducted two other models, adding in change in time-dependent FFM both with and without time-dependent weight loss. The results of these analyses confirmed that it was change in body mass and adiposity that led to the differences in CRP between WL+RT and WL. Further support for this interpretation can be gleaned by comparing weight loss of the three groups across the 18-months of the study with change in CRP—Figures 1 and 2. Notice from the weight loss graph that all groups lost the most weight during the intensive phase of treatment which paralleled the change in CRP from baseline to 6 months. Between-group differences in body mass became more distinct from 6- to 18-months with differences of 3.5% between AT+WL and WL and 4.6% between WL+RT and WL. Because these data mirror the changes in CRP (Figure 2), an effect that was neutralized when we controlled for time-dependent weight loss, we conclude, as others have, that CRP is a biomarker of adiposity.15,36
Sardeli and colleagues16 have made the point that increased muscle mass through RT leads to higher levels of energy expenditure and improvement in insulin sensitivity thereby decreasing CRP. Of interest is a prior publication of ours from CLIP-II showing that the WL+RT group loss less lean mass than either WL+AT or WL.21 Also, an RT study with older women with MetS found that the reduction in CRP with training was related to increases in muscle mass,37 results that parallel a 12-month RT intervention among older adults with type 2 diabetes.38 It is also known that increases in IL-6 released by muscle during contraction have an anti-inflammatory effect in opposition to the IL-6 released by visceral adiposity which is pro-inflammatory.16,39 Specifically, IL-6 from muscle increases IL-10 and IL-1ra, both of which are anti-inflammatory, and does so in the absence of increasing the pro-inflammatory cytokines TNFα and IL-1β. Interestingly IL-15, which increases with muscle hypertrophy, is known to play a role in the lipolysis of liver fat and greater muscle mass is protective against the accumulation of visceral fat.40 This latter point is particularly important given the role that increasing visceral fat41,42 and decreasing muscle mass16,40 play in chronic elevated inflammation with aging.
We are unaware of any studies that have directly compared AT and whole body RT within the context of weight loss in relation to their effects on various pathways that may reduce systemic inflammation. Parenthetically, we would encourage investigators to examine the role that chronic low-grade inflammation, and interventions targeted to reduce such inflammation, has on the desire of older adults’ to be physically active. As noted by Petersen40 chronic inflammation in aging leads to anemia, fatigue, and muscle wasting, all of which encourage physical inactivity contributing to a vicious cycle that feeds functional decline and chronic disease. As Calle and Fernandez39 stated: “…the importance of maintaining adherence to an exercise program, specifically for obese individuals or those at risk for low grade inflammatory disease cannot be emphasized enough,” p. 262.
Limitations
There are several limitations in this study. First, because this was a community-based trial conducted within YMCAs and led by their staff, we were not able to obtain the type of quantitative data from the exercise training sessions that would enable us to examine dose-response effects. Second, the sample was largely older women, which did not permit us to examine sex effects, although we did control for sex in the analyses. Third, the sample was not recruited on the basis of elevated levels of inflammatory markers; there is evidence that exercise reduces inflammation, but only among those with elevated levels at baseline.31
Conclusions
The results of this study reinforce a central role for physical activity in weight management, particularly for older adults with chronic health conditions such as MetS and CVD. Not only does physical activity improve the magnitude of lost weight, but it also improves the inflammatory profile, particularly for CRP. In this regard, while both WL+RT and WL+AT promote additional weight loss as compared to WL, only WL+RT was found to be superior to WL in reducing CRP at 18 months. Further study is needed to examine what changes in muscle are responsible for the effect that RT has on CRP with attention given to potential dose-response effects.
What is already known about this subject?
Chronic inflammation is a major health problem in aging.
Weight loss is known to reduce biomarkers of inflammation.
Evidence suggests that aerobic exercise and resistance exercise reduce inflammation, but for aerobic exercise the effect appears dependent upon loss in fat mass.
What does this study add?
First study to compare weight loss with and without aerobic or resistance exercise on inflammation in older adults.
A community-based randomized trial of older adults with the metabolic syndrome and/or cardiovascular disease.
This weight loss trial was long-term, lasting 18-months.
Acknowledgements
Since there were no funds allocated at the time of the grant award for a data sharing plan, we are not able to provide de-identified, individual participant data to other researchers. The study protocol is available from the corresponding author.
We are indebted to our participants, our project manager and Registered Dietitian Beverly Nesbit, our lead interventionist Jillian Gaukstern, and our lead assessor Jessica Sheedy for their contributions related to the supervision and conduct of the trial.
Funding Agencies: This study was funded by a grant from National Institutes of Health/National Heart, Lung and Blood Institute, R18 HL076441, awarded to Drs. Rejeski and Marsh. Partial support was also provided by National Institutes on Aging grants, P30 AG021332 & R01AG051624.
Footnotes
Clinical Trial Registration: Registered with ClinicalsTrials.gov ().
Disclosures: None of the authors declare any conflict of interest related to this manuscript.
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