Obesity characterized by increased mass of adipose tissue leads to systemic inflammation. Calorie restriction (CR) improves parameters associated with immune response and antioxidant defense. We hypothesized that CR with a high fat diet (HFCR) regulates local and systemic inflammation and oxidative stress damage in a high fat diet induced obesity (HF group). We investigated effect of HFCR on inflammation and oxidative stress-related markers in liver and adipose tissues as well as adipokines in plasma. HFCR lowered liver triglyceride levels, total cholesterol levels, and the plasma leptin/adiponectin ratio to normal levels and improved glucose tolerance. HFCR also improved fatty liver and normalized adipocyte size and morphology. HFCR reduced lipid peroxidation and decreased the expression levels of inducible nitric oxide synthetase, cyclooxygenase-2, NF-E2-related factor, and heme oxygenase-1 in the liver. Moreover, HFCR suppressed the expression levels of C- reactive protein and manganese superoxide dismutase in the adipose tissue in the HF group. These results suggest that HFCR may have beneficial effects on inflammation and oxidative stress as well as lipid profiles in the HF diet induced obesity. Moreover, HFCR may be a good way to increase compliance in obese patients and to prevent obesity induced complications without changes in dietary pattern.

Purpose: We investigated the effects of group III mechanoreceptors to cardiovascular responses in both pre-menopausal woman and post-menopausal woman during passive ankle dorsiflexion (PAD). Methods: Twenty healthy volunteers (10 postmenopausal women and 10 pre-menopausal women) were recruited for this study. Stroke volume (SV), heart rate (HR), cardiac output (CO), and total vascular conductances (TVC) were measured continuously throughout the experiment. To stimulate the group III mechanoreceptors, PAD was performed for one minute. Results: The results showed that mean arterial pressure (MAP) mediated by the mechanoreflex activation was significantly increased in both groups. However, this pressor response was significantly higher in post-menopausal women. This reflex significantly increased both SV and CO in pre-menopausal women, while there were no differences in post-menopausal women. There was no difference in HR in either group. The mechanoreflex significantly decreased TVC in post-menopausal woman, while there was no difference in pre-menopausal woman. Conclusion: The results indicate that the excessive pressor response mediated by the mechanoreflex occurs due to overactivity of group III mechanorecptors and the mechanism is produced mainly via peripheral vasoconstriction in postmenopausal women.

Previous studies strongly indicate that the arterial baroreflex plays an important role in cardiovascular responses to dynamic exercise. However, the effect of arterial baroreflex on the hemodynamic responses to dynamic exercise is not well understood after menopause. Therefore, we investigated the cardiovascular responses during cycle exercise (30 W and 60 W) in healthy premenopausal and postmenopausal women. Thirty premenopausal and postmenopausal women were instrumented to measure heart rate (HR), cardiac output (CO) and mean arterial pressure (MAP). MAP was significantly increased with exercise intensity in postmenopausal women, while there was no difference in premenopausal women. CO, HR, total vascular conductance (TVC) and stroke volume increased with increasing workloads in both premenopausal and postmenopausal women. However, TVC was significantly lower after menopause at moderate workload compared to the premenopausal women (107.3±13.4 vs. 91.4±5.2 mm/min/Hg). The results indicate that higher MAP after menopause occurred due to combining increase in CO as well as substantial decrease in peripheral vascular conductance. We conclude that menopause altered normal cardiovascular responses to graded dynamic exercise. Additionally, after menopause significantly a higher increase in arterial blood pressure may be due to a depression in arterial baroreflex function during exercise.

Group III muscle afferent mechanoreflex evokes excessive blood pressure response in hypertensive rats. However, hemodynamic responses to the mechanoreflex are not well understood in prehypertensive women. Therefore, we investigated the effect of mechanoreceptors to physiological responses during passive ankle dorsiflexion in both normotension and prehypertension. Thirty healthy women (10 prehypertension and 10 normotension) were recruited for this study. Subjects were continuously instrumented to measure stroke volume (SV), heart rate (HR), cardiac output (CO), mean arterial pressure (MAP) throughout the experiment. To stimulate group III mechanoreceptors, passive ankle dorsiflexion was performed by a Cybex Norm for one minute. The results indicate that MAP was significantly increased during ankle dorsiflexion in both groups; however, this pressor response was significantly higher in prehypertensive women (9.8±1.7 vs. 13.7±1.5 mmHg). SV and CO were significantly increased in normotensive women, while no differences in prehyperentsive women. There was no difference in HR in both groups. Total vascular conductance was significantly decreased in prehypertensive women. It is concluded that excessive pressor response mediated by ankle dorsiflexion is occurred by overactivity of group III mechanorecptors and the mechanism is produced via peripheral vasoconstriction in prehypertensive women.