Moderate intensity physical activity prevents increased blood glucose concentrations, fat pad deposition and cardiac action potential prolongation following diet-induced obesity in a juvenile-adolescent rat model

Alannah van Waveren; Mitch J Duncan; Fiona R Coulson; Andrew Fenning

doi:10.1186/2052-9538-1-11

Moderate intensity physical activity prevents increased blood glucose concentrations, fat pad deposition and cardiac action potential prolongation following diet-induced obesity in a juvenile-adolescent rat model

BMC Obes. 2014 Aug 20:1:11. doi: 10.1186/2052-9538-1-11. eCollection 2014.

Authors

Alannah van Waveren¹, Mitch J Duncan², Fiona R Coulson³, Andrew Fenning⁴

Affiliations

¹ Central Queensland University, Institute of Health and Social Science Research, Rockhampton, Queensland 4702 Australia.
² School of Medicine & Public Health, Priority Research Centre in Physical Activity and Nutrition, The University of Newcastle, Newcastle, Australia.
³ School of Medical and Applied Sciences, Central Queensland University, Rockhampton, Queensland 4702 Australia.
⁴ Central Queensland University, Institute of Health and Social Science Research, Rockhampton, Queensland 4702 Australia ; School of Medical and Applied Sciences, Central Queensland University, Rockhampton, Queensland 4702 Australia.

Abstract

Background: Both obesity and a lack of physical activity have been associated with an elevated risk of cardiovascular disease (CVD). The incidence of obesity is increasing, especially in juvenile-adolescents. While there is limited research examining the chronic effects of obesity in adolescent humans and animal models of this condition, little is also known concerning how moderate physical activity might prevent or attenuate secondary cardiovascular complications induced by obesity during adolescence. We investigated the effects of diet-induced obesity (consisting of a high-fat, high-carbohydrate diet (HFHC)) on biometric indices, vascular and airway function, cardiovascular function, systemic oxidative stress and markers of inflammation in a juvenile-adolescent rodent model. Four groups were used: control (CON), physical activity (PA) treated, HFHC and HFHC + PA (n = 16 per group). HFHC feeding started at 4 weeks of age for a period of 12 weeks. Physical activity treatment was initiated (PA and HFHC + PA groups) when the animals were 8 weeks of age, for 8 weeks.

Results: Physical activity in juvenile-adolescent healthy rats showed no change in comparison to the CON group in all experimental parameters except for increases in lipid peroxidation, decreases in inflammatory cytokines, improvements in vascular reactivity and decreased atrial responses to positive chronotropic agents. The HFHC animals were mildly hyperglycemic, hypertensive, displayed renal hypertrophy and showed increased retroperitoneal fat pad deposition compared to the CON group. HFHC + PA rats were also hypertensive, however showed improvements in cardiac electrophysiology, body weight, fat pad deposition and inflammatory signaling, in comparison to the HFHC fed rats and CON animals.

Conclusion: In conclusion, in a juvenile-adolescent animal model of diet-induced obesity engagement in physical activity is beneficial in reducing the inflammatory effects of obesity.

Keywords: Cardiac arrhythmia; Hypertension; Inflammation; Juvenile obesity; Metabolic syndrome; Oxidative stress; Physical activity; Vascular reactivity; Western obese diets.