-transparent.png){kind=logo}
OBJECTIVE To assess autonomic modulation of cardiovascular activity in massively obese subjects. METHODS Cross-sectional clinical study. METHODS 43 age-matched normotensive subjects: 15 moderately obese (body mass index (BMI) < 40); 14 massively obese (BMI > 40) and 14 nonobese controls (BMI < 26). METHODS Using power spectral analysis, heart rate and arterial pressure variability were determined at rest and after sympathetic stress (tilt). Two spectral components were analysed: a low-frequency (LF) component at around 0.1 Hz, predominantly reflecting sympathetic modulation and a high-frequency (HF) component at around 0.26 Hz, reflecting parasympathetic modulation. RESULTS Spectral data for heart rate showed that the massively obese subjects had lower LF [mean +/- s.e.m.] normalized units (NUs) at rest (35.1 +/- 0.9) and after tilt (56.1 +/- 2.1), than the moderately obese subjects (LF NUs at rest 53.9 +/- 4.2, P < 0.001; LF NUs tilt: 66.8 +/- 5.6, P < 0.001) and nonobese control subjects (LF NUs at rest, 56.6 +/- 3.0, P < 0.001); (LF NUs tilt: 81.7 +/- 1.7, P < 0.001). Data for systolic arterial pressure variability measured at rest exhibited the inverse pattern, the massively obese group having higher mean LF values (LF mm Hg2 rest: 15.0 +/- 1.4; LF mm Hg2 tilt: 15.7 +/- 1.5) than the moderately obese group (LF mm Hg2 rest 3.2 +/- 0.7, P < 0.001; LF mm Hg2 tilt: 7.2 +/- 2.0, P < 0.001) and than the nonobese control subjects (LF mm Hg2 rest 3.5 +/- 0.5, LF mm Hg2 tilt 8.5 +/- 0.8, P < 0.001). Regression detected a significant association between BMI and LF of systolic pressure (beta = 0.364; P = 0.0007), In LF of heart rate (beta = -5.555; P = 0.00001) and very low frequency (VLF) of diastolic pressure (beta = -3.305; P = 0.0020). CONCLUSIONS Obesity seems to increase sympathetic modulation of arterial pressure, but diminishes modulation of heart rate. Because our obese subjects had high plasma noradrenaline levels, their low LF power of heart rate could reflect diminished adrenoceptor responsiveness.
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
July 1990,
Clinical physiology (Oxford, England),
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
October 2011,
Journal of alternative and complementary medicine (New York, N.Y.),
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
February 1993,
Angiology,
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
March 2011,
Physiological measurement,
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
April 1992,
Journal of hypertension. Supplement : official journal of the International Society of Hypertension,
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
July 2004,
Clinical science (London, England : 1979),
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
October 1987,
Clinical physiology (Oxford, England),
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
February 2000,
The Journal of laboratory and clinical medicine,
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
June 1986,
Journal of hypertension,
G Piccirillo, and
F Vetta, and
E Viola, and
E Santagada, and
S Ronzoni, and
M Cacciafesta, and
V Marigliano
January 2011,
Indian journal of physiology and pharmacology,
