Obesity is associated with sympathetic neural activation and elevated blood pressure(1,2). However, it is unclear whether modest elevations in body weight are sufficient to induce increases sympathetic activity (3). Furthermore, there is a large amount of individual variability in the blood pressure response to weight change (4). The reason(s) for this inter-individual variability are still uncertain, but body fat distribution and cardiorespiratory fitness may play a role (5,6). To address these and other issues regarding the relation between adiposity, sympathetic neural activity and blood pressure, we first examined the effects of modest, diet-induced weight gain on muscle sympathetic nervous system activity (MSNA) in healthy, lean, normotensive individuals. We hypothesized that modest weight gain would increase MSNA in these individuals, and that this neural activation would be accompanied by increases in blood pressure. Concordant with this hypothesis, MSNA and resting blood pressure were significantly elevated following weight gain. The increase in MSNA was correlated with the magnitude of body weight and fat gain, but was not obviously related to increases in visceral fat. We next examined the ability of cardiorespiratory fitness (CRF) to modulate the weight gain-induced increase in blood pressure in the same cohort of young, nonobese and normotensive individuals. We hypothesized that the increase in blood pressure would be attenuated in individuals with higher- compared with lower CRF (HCRF and LCRF, respectively). Indeed, we found that HCRF experienced significantly smaller increases in resting and ambulatory blood pressure compared to LCRF. In the pooled sample, baseline fitness was inversely related to the changes in resting systolic and diastolic pressure, and this relation was not diminished after statistically controlling for changes in abdominal visceral fat. The results of the present investigation suggest that even modest weight gain increases sympathetic activity and blood pressure, which, if left untreated, may contribute to the development of hypertension and other cardiovascular disorders. Maintenance of higher levels of CRF during periods of weight gain may reduce cardiovascular disease risk by mitigating the increases in blood pressure. Collectively, these findings may have important implications for understanding the link between obesity and hypertension.

References

1. Davy KP. The global epidemic of obesity: are we becoming more sympathetic? Curr Hypertens Rep. 2004;6:241-6.

2. Grassi G, Seravalle G, Cattaneo BM, et al. Sympathetic activation in obese normotensive subjects. Hypertension. 1995;25:560-3.

3. Huggett RJ, Scott EM, Gilbey SG, Bannister J, Mackintosh AF, Mary DA. Disparity of autonomic control in type 2 diabetes mellitus. Diabetologia. 2005;48:172-9.

4. Masuo K, Mikami H, Ogihara T, Tuck ML. Weight gain-induced blood pressure elevation. Hypertension. 2000;35:1135-40.

5. Hayashi T, Boyko EJ, Leonetti DL, et al. Visceral adiposity is an independent predictor of incident hypertension in Japanese Americans. Ann Intern Med. 2004;140:992-1000.

6. Barlow CE, LaMonte MJ, Fitzgerald SJ, Kampert JB, Perrin JL, Blair SN. Cardiorespiratory fitness is an independent predictor of hypertension incidence among initially normotensive healthy women. Am J Epidemiol. 2006;163:142-50.