Increased aerobic capacity reduces susceptibility to acute high-fat diet-induced weight gain

Abstract

Objective: Aerobic capacity is the most powerful predictor of all-cause mortality in humans; however, its role in the development of obesity and susceptibility for high-fat diet (HFD)-induced weight gain is not completely understood.

Methods: Herein, a rodent model system of divergent intrinsic aerobic capacity [high capacity running (HCR) and low capacity running (LCR)] was utilized to evaluate the role of aerobic fitness on 1-week HFD-induced (45% and 60% kcal) weight gain. Food/energy intake, body composition analysis, and brown adipose tissue gene expression were assessed as important potential factors involved in modulating HFD-induced weight gain.

Results: HCR rats had reduced 1-week weight gain on both HFDs compared with LCR. Reduced HFD-induced weight gain was associated with greater adaptability to decrease food intake following initiation of the HFDs. Further, the HCR rats were observed to have reduced feeding efficiency and greater brown adipose mass and expression of genes involved in thermogenesis.

Conclusions: Rats with high intrinsic aerobic capacity have reduced susceptibility to 1-week HFD-induced weight gain, which is associated with greater food intake adaptability to control intake of energy-dense HFDs, reduced weight gain per kcal consumed, and greater brown adipose tissue mass and thermogenic gene expression.

Figure 1

High intrinsic aerobic capacity reduces HFD-induced weight gain. Body weight and composition was determined prior to and following one week of HFD. One week weight gain (A), one week change in fat mass (B, n=8–16), and one week change in percent body fat (C, n=8–16) are presented as means ± SEM. § p<0.05 interaction, * p<0.05 main effect HCR vs. LCR, † p<0.05 main effect LFD vs. HFD, & p<0.05 main effect 45% HFD vs 60% HFD.

Figure 2

High intrinsic aerobic capacity is associated with food intake adaptability and reduced feeding efficiency following HFD. Change in food and energy intake were calculated as the difference between the LFD lead-in week and one week of HFD, and feeding efficiency is the weight gain in milligrams for the week divided by the total weekly energy intake: A) change in food intake, B) change in energy intake, C) feeding efficiency, and D) estimated feeding efficiency adjusted for final body weight (ANCOVA) (n=16–24) are presented as means ± SEM. § p<0.05 interaction,* p<0.05 main effect HCR vs. LCR, † p<0.05 main effect LFD vs. HFD, & p<0.05 main effect 45% HFD vs 60% HFD, †† p<0.05 LFD vs. HFD within strain, && p<0.05 45% HFD vs 60% HFD within strain.

Figure 3

Change in food/energy intake versus weight gain. Linear regression of on week body weight gain versus B) change in food intake and D) change in energy intake (blue = HCR, red = LCR, LFD = ●, 45% = ■, 60% = ▲) are presented with p-value and r² when appropriate.

Figure 4

White adipose tissue. Epididymal (A) and retroperitoneal (B) fat pad masses at the time of sacrifice. Morphometric analysis of the retroperitoneal fat pad are presented as (C) cell area and (D) cell number are presented as means ± SEM (n=8). (E) Representative H&E images of retroperitoneal fat pad. * p<0.05 main effect HCR vs. LCR, †† p<0.05 LFD vs. HFD within strain.

Figure 5

Brown adipose tissue. Representative H&E images of brown adipose tissue are presented in panel A. (B) Fat pad mass was determined at sacrifice and estimated mass of brown fat pad adjusted for final body weight (ANCOVA) is shown in panel E. Gene expression in brown adipose was determined by RT-PCR and western blot analysis: relative mRNA expression of (C) UCP1 and (D) PGC1a were normalized to CycA, and western blot analysis of brown adipose homogenate for (F) UCP1. Brown adipose mitochondrial content was assessed by (G) citrate synthase activity. All data are presented as means ± SEM (n=8). § p<0.05 interaction,* p<0.05 main effect HCR vs. LCR, † p<0.05 main effect LFD vs. HFD, & p<0.05 main effect 45% HFD vs 60% HFD, †† p<0.05 LFD vs. HFD within strain, && p<0.05 45% HFD vs 60% HFD within strain.