Research ArticleEffect of aerobic exercise training dose on liver fat and visceral adiposity
Introduction
It is now recognized that the topography of body fat distribution predicts the adverse cardiovascular and metabolic consequences of obesity independent of fat quantity. For instance, high levels of visceral adipose tissue (VAT) are an independent predictor of hypertension [1], myocardial infarction [2], and insulin resistance [3], [4]. Likewise, excess liver fat, as seen in non-alcoholic fatty liver disease (NAFLD), has emerged as an independent risk factor for cardiometabolic disease that may be more strongly associated with risk than VAT [5], [6]. Hence, reducing ectopic fat deposits is a suitable target for interventions to prevent disease.
Since there are limited pharmacological agents to specifically reduce ectopic fat, the efficacy of lifestyle therapies has become a focus of research. In this regard, weight loss via diet and exercise reduces VAT [7], [8] and liver fat [9], [10], [11] but reductions of ⩾3% of body weight are generally required for hepatic benefit, with greater weight loss (5–10%) producing superior benefits [12]. However, these levels of weight loss are inherently difficult to sustain [13]. Given that NAFLD afflicts one third of adults [14] and most obese individuals [15], the efficacy of lifestyle interventions that do not rely on weight loss (such as moderate exercise) warrants investigation.
Several trials have examined the effect of exercise interventions on liver fat, but their interpretation is limited by small sample sizes, lack of non-exercise control groups and heterogeneity in exercise modality and dose. These studies employed exercise doses ranging from 2 to 6 days per week, lasting for 20–60 min per session, with intensities ranging between low (45% VO2peak) and strenuous (85% of VO2peak) [9], [10], [16], [17], [18], [19], [20], [21], [22]. Therefore, establishing practical recommendations for exercise prescription is difficult based on the current evidence.
The purpose of this study was to investigate the efficacy of regular aerobic exercise at one of three doses requiring different levels of effort and time commitment vs. a sham exercise placebo control (PLA) in reducing liver fat and VAT in overweight/obese adults using gold standard, double-blind, randomized placebo-controlled design. We also measured the effects of these interventions on other markers of cardiometabolic risk in order to advise practical recommendations.
Section snippets
Experimental protocol
Intrahepatic lipid (IHL) and abdominal adiposity, including VAT, were assessed before and after 8 weeks of exercise training or PLA intervention. Cardiorespiratory fitness/work capacity, anthropometric measurements (body weight, BMI, and waist circumference), blood lipids, serum aminotransferases, hs-CRP and resting blood pressure were also measured at baseline and post-intervention. The primary aim of the study was assessed by comparing the mean change in liver fat and VAT between the PLA group
Results
One hundred and twenty-two individuals were screened by telephone interview, with 48 eligible volunteers (17 men and 31 women) undergoing initial assessment and randomization (Fig. 1). The study population had an average BMI of 33.4 ± 1.3 kg/m2 and mean age of 43.6 ± 3.0 years. Baseline participant characteristics are described in Table 1. All participants completed the training and PLA interventions. Post-intervention dietary and habitual physical activity data were unavailable for some participants
Discussion
We investigated the effectiveness of commonly prescribed doses of aerobic exercise training compared with a PLA group, independent of dietary intervention or weight loss, on fat distribution including liver fat and VAT in previously inactive adults. We observed a significant reduction in liver fat in all aerobic exercise intervention groups, with the effect size when compared with PLA being large (ES = 1.42, 1.23, and 0.96 for the HI:LO, LO:HI, and LO:LO groups, respectively). These benefits were
Financial support
This research was supported by funding from the Diabetes Australia Research Trust. (Establishment Grant: N.A. Johnson). JG is supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and a Project grant (1049857). AS is supported by fellowships from the University of Sydney/Sydney Medical School and the National Health and Medical Research Council. The funding
Conflict of interest
S.E. Keating, D.A. Hackett, H.M. Parker, M.K Baker, V.H. Chuter, H.T. O’Connor, J.A. Gerofi, and A. Sainsbury declare no conflict of interest. N.A. Johnson: has received honoraria for speaking engagements for Merck Sharp & Dohme. I.D. Caterson: has performed and still performs clinical trials of obesity treatment and prevention some of which have been funded by government, but others by the pharmaceutical industry. Current trials are funded by the NHMRC [3], NovoNordisk, Amylin Corporation, the
Authors’ contributions
Study concept and design (JGeorge, NJ), acquisition of data (SK, DH), analysis and interpretation of data (SK, NJ, JGeorge and HP), drafting and critical revision of manuscript (all authors), statistical analysis (SK, NJ). All authors approved the final draft for submission.
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