The haemodynamics of obesity: a theoretical analysis.
BACKGROUND
Obesity and hypertension are frequently associated with one another, and changes in body weight are usually accompanied by consensual changes in blood pressure.


OBJECTIVE
To examine formally the haemodynamic conditions required for a weight gain to cause a rise in blood pressure in the resting state.


METHODS
The relevant equations were developed, and then used in a simulation to predict blood pressure and peripheral vascular resistance in response to changes in body weight. The model was tested on data taken from published reports. Furthermore, the impact of the composition of the excess weight, i.e. fat versus muscle tissue, on the haemodynamics of obesity was incorporated into the simulation by using a range of tissue-specific blood flow rates taken from published reports.


RESULTS
The key determinant of weight-induced increases in blood pressure is a disproportional increase in cardiac output, which is not fully accounted for by the haemodynamic contribution of new tissues. An increase in muscle tissue relative to fat in newly gained weight is a further factor in the blood pressure increase arising from any given level of excess weight.


CONCLUSIONS
The disproportional increase in cardiac output in obesity is best attributed to stimulation of cardiac dynamics by the adrenergic nervous system. The low resistance of adipose tissue relative to muscle may be the physiologic basis for the dominance of fat-free mass in multiple regression analyses of blood pressure determinants in the population; it further suggests that in the obese hypertensive, fat tissue may provide protection against cardiovascular disease by limiting increases in total peripheral resistance.
Ferrannini
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Metabolism Unit, University of Pisa, Italy.
D001794:Blood Pressure / Q000502:physiology; D001823:Body Composition / Q000502:physiology*; D001835:Body Weight / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D003198:Computer Simulation; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D008955:Models, Cardiovascular; D009765:Obesity / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology