The effects of different types of aquatic exercise training interventions on a high-fructose diet-fed mice.

Gradual weight gain in modern people and a lowering onset age of metabolic disease are highly correlated with the intake of sugary drinks and sweets. Long-term excessive fructose consumption can lead to hyperglycemia, hyperlipidemia and accumulation of visceral fat. Abdominal obesity is more severe in females than in males. In this study, we used a high-fructose-diet-induced model of obesity in female mice. We investigated the effects of aquatic exercise training on body weight and body composition. After 1 week of acclimatization, female ICR mice were randomly divided into two groups: a normal group (n=8) fed standard diet (control), and a high-fructose diet (HFD) group (n=24) fed a HFD. After 4 weeks of induction followed by 4 weeks of aquatic exercise training, the 24 obese mice were divided into 3 groups (n=8 per group): HFD with sedentary control (HFD), HFD with aquatic strength exercise training (HFD+SE), and HFD with aquatic aerobic exercise training (HFD+AE). We conducted serum biochemical profile analysis, weighed the white adipose tissue, and performed organ histopathology. After 4 weeks of induction and 4 weeks of aquatic exercise training, there was no significant difference in body weight among the HFD, HFD+SE and HFD+AE groups. Serum triglyceride (TG), AST, ALT, and uric acid level were significantly lower in the HFD+SE and HFD+AE groups than in the HFD group. The weight of the perirenal fat pad was significantly lower in the HFD+AE group than in the HFD group. Hepatic TG and total cholesterol (TC) were significantly lower in the HFD+AE group than in the other groups. Long-term intake of a high-fructose diet can lead to obesity and increase the risk of metabolic disease. Based on our findings, we speculate that aquatic exercise training can effectively promote health and fitness. However, aquatic aerobic exercise training appears to have greater benefits than aquatic strength exercise training. © The author(s).