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• W2004649495 abstract "In the present issue of Clinical Autonomic Research, Rodriguez-Colon et al. [1] examine the behavior of 24-h heart rate profile in a large cohort of adolescents recruited in the follow-up of the Penn State Children Cohort Study. Specifically, the authors performed power spectral analysis of the 24-h heart rate signal in order to determine whether and to what extent the high-frequency/low-frequency components of the R–R interval, which are well known to represent reliable indices of parasympathetic/sympathetic cardiac drive, respectively [2], are altered in these subjects. Data that were analyzed by adjustments for confounders (specifically age and gender) were compared to those obtained in non-obese children and adolescents. The results expand previous information collected on this topic [3–6], by showing that the circadian pattern of parasympathetic and sympathetic control of the heart rate signal is altered in these young groups of obese. They also provide evidence that the alterations in vagal modulation of sinus node activity are manifest in both genders, independently of the subject’s age and over the whole 24-h period. However, when circadian curves of estimated high-frequency components detected in obese and control subjects are compared, it becomes clear that the difference in the two curves is greater for magnitude in the daytime period between 6.00 a.m. and 2.00 p.m. This time window includes the early morning hours known to be associated with a pronounced adrenergic overdrive to the heart and peripheral vessels, and with a greater risk of sudden arrhythmic death, particularly in obese patients [2, 7]. Although technically well performed and founded on a solid database, the study by Rodriguez-Colon et al. [1] has a number of limitations. First, unfortunately, no data are available on the relationships between the high-frequency/ low-frequency heart rate patterns and waist-to-hip ratio, which is a sensitive marker of body fat distribution [7]. This information is needed to determine whether the observed cardiac autonomic dysregulation was more pronounced in people with visceral fat obesity, or people with peripheral fat obesity, as it has been reported in obese adults [8, 9]. More importantly, these missing data would have given the researchers an opportunity to more closely link the autonomic dysfunction to the metabolic alteration, which is a hallmark of the central type of body fat depot, i.e., insulin resistance [7, 8]. The second limitation refers to the fact that the neural alterations reported in the present study strictly refer to cardiac autonomic drive and not to the overall cardiovascular autonomic function. In other words, the data collected by Rodriguez-Colon et al. [1] do not provide any insight on the behavior of sympathetic neural function in cardiovascular districts other than the heart. This is because no relationship exists between the data collected by the power spectral analysis and those obtained via direct measures of sympathetic drive, such as those collected via the microneurographic recording of efferent postganglionic muscle sympathetic nerve traffic in the peroneal nerve [10]. Finally, in the study by Rodriguez-Colon et al. [1], information is available on the presence, as well as the severity, of the sleep apnea syndrome in the obese adolescents studied, and thus, on the independent effects, this obesityrelated complication may have on parasympathetic and sympathetic neural function [2, 11, 12]. G. Grassi Clinica Medica, Istituto di Ricerca Clinica Carattere Scientifico Multimedica, Universita Milano Bicocca, Sesto San Giovanni, Milano, Italy" @default.
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• W2004649495 date "2014-11-01" @default.
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• W2004649495 title "“Broken” autonomic cardiac circadian clock in obese adolescents: evidence and implications" @default.
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• W2004649495 doi "https://doi.org/10.1007/s10286-014-0260-z" @default.
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