Heart rate and blood pressure variability in obese normotensive subjects.
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.
Piccirillo
G
G
I Clinica Medica, University of Rome, La Sapienza, Italy.
Vetta
F
F
Viola
E
E
Santagada
E
E
Ronzoni
S
S
Cacciafesta
M
M
Marigliano
V
V
D019540:Area Under Curve; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D003430:Cross-Sectional Studies; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D009765:Obesity / Q000503:physiopathology*; D009767:Obesity, Morbid / Q000503:physiopathology*; D012044:Regression Analysis; D012083:Renin / Q000097:blood; D012119:Respiration; D012146:Rest / Q000502:physiology; D012815:Signal Processing, Computer-Assisted; D018667:Tilt-Table Test
D001786:Blood Glucose; D007328:Insulin; D012083:Renin; D009638:Norepinephrine