A low-calorie diet with or without interval exercise training improves adiposopathy in obese women

Abstract

The objective of this study was to test if a low-calorie diet plus interval exercise (LCD+INT) improves adiposopathy, an endocrine dysfunction, when compared with an energy-deficit-matched LCD in obese women. Subjects (age: 48.2 ± 2.4 years, body mass index: 37.8 ± 1.3 kg/m²) were randomized to a 13-day LCD (<i>n</i> = 12; mixed meals of ∼1200 kcal/day) or LCD+INT (<i>n</i> = 12; 12 sessions of 60 min/day alternating 3 min at 50% and 90% peak heart rate). Exercise was estimated to expend 350 kcal per oxygen uptake-heart rate regression analysis and individuals were refed calories expended to match energy availability between groups. Absolute (post - pre caloric intake) and relative (total daily and exercise energy expenditure relative to calorie intake) energy deficits were calculated. Fitness (peak oxygen uptake) and body composition (BodPod; Cosmed USA Inc.) were measured and a 120-min, 75g oral glucose tolerance test was performed at pre- and post-intervention to assess adiposopathy (i.e., ratio of high molecular weight-adiponectin to leptin) and estimate insulin sensitivity. LCD and LCD+INT had similar absolute (<i>P</i> = 0.55) and relative (<i>P</i> = 0.76) energy deficits. LCD and LCD+INT had similar reductions in fat mass (both <i>P</i> < 0.001), despite LCD inducing greater weight loss (<i>P</i> = 0.02) than LCD+INT. Both treatments improved adiposopathy (<i>P</i> = 0.003) and peripheral insulin sensitivity (<i>P</i> = 0.02). Absolute energy deficit correlated to improved adiposopathy (<i>r = -</i>0.41, <i>P</i> = 0.05), and absolute and relative energy deficits were associated with increased insulin sensitivity (<i>r =</i> -0.47, <i>P</i> = 0.02; and <i>r =</i> -0.40, <i>P</i> = 0.05, respectively), independent of body composition changes and increased peak oxygen uptake. Taken together, LCD, with or without INT, improves adiposopathy in relation to insulin sensitivity in obese women, suggesting that a short-term energy deficit is key for reducing risk of type 2 diabetes.