Background:
It is generally accepted that body weight is maintained when there is energy balance between intake and expenditure. Energy balance can be achieved at different rates of expenditure through exercise and caloric intake which has been referred to as energy flux: high flux reflects high expenditure and high intake while low flux describes low energy expenditure and intake. Overweight, obesity, and diabetes are major risk factors for cardiovascular disease and CVD risk factors tend to increase with hyperglycemia and BMI. Exercise is a viable way to achieve weight maintenance, however, there is limited data about the role of energy flux on CVD risk factors when individuals maintain their body weight. We investigated the effect of energy flux and change in energy flux on CVD risk factors in when body weight is maintained.
Methods:
One hundred and thirteen overweight or obese class I adults ages 21 to 45 were randomized to a control group, moderate exercise (17.5 kcal/kg/week) or high exercise group (35 kcal/kg/week). The exercise groups performed supervised exercise at and intensity of 70-75% of their heart rate maximum. Impaired fasting glucose was defined as a fasting glucose of 100-125 mg/dL. General linear models were used to test the relationship of exercise intensity and impaired fasting glucose on change in energy flux from baseline to six months, as well as the relationship of 6-month change in energy flux with change in CVD risk factors, namely, HDLc, LDLc, vLDLc, total cholesterol, triglycerides, Apolipoprotein B (ApoB), and C-reactive protein.
Results:
Seventy-two percent of the population was overweight and 22% were obese. Mean change in energy flux from baseline to month six was 128.8 kcal/day. In multivariable analyses including age, sex, BMI, impaired fasting glucose, and energy expenditure group assignment, neither exercise group assignment nor baseline obesity status had any effect on change in energy flux, lipids, or inflammatory markers. Impaired fasting glucose was associated with a significantly greater increase in energy flux from baseline to six months (p=0.03). There was a stepwise change in C-reactive protein from baseline to six months, with a decrease (-2.46 mg/dL) in controls, a moderate increase (+0.32 mg/dL) in the moderate intensity exercise group and a larger increase (+0.82 mg/dL) in the very intensive exercise group, p= 0.03 for moderate intensity and p=0.02 for very intensive exercise groups compared to controls. Finally, increases in energy flux from baseline to six months were associated with increased ApoB (p=0.04), though there were no significant changes in energy flux by group assignment.
Conclusion:
Intensification of exercise and increases in energy flux while maintaining stable weight is associated with increases in certain cardiovascular risk factors, namely C-reactive protein and ApoB.
Siphon-Controlled Automation on a Lab-on-a-Disc Using Event-Triggered Dissolvable Film Valves