Resting Energy Expenditure and Blood Pressure: Evidence of Perpetual Association

Abstract

A myriad of cross-sectional and prospective studies have evaluated the interrelationship between blood pressure (BP) levels and different traditional metabolic surrogates including body mass index (BMI). In addition, clinically meaningful conditions such as hypertension and the metabolic syndrome independently of treatment for either condition have shown a prospective bidirectional association among different ethnicities and age burdens. However, along with the positive association between BP and adverse metabolic phenotypes, the exact underlying pathophysiological background has not yet been fully elucidated. Resting energy expenditure (REE), a quantitative measurement of metabolic processes at rest, was found to be correlated with BP levels in different ethnicities after adjustment for potential confounders. The arising clinical question is whether the measurement of REE might be a predictor of increasing BP levels or incident hypertension later in life independently of confounders including body adiposity and common pathophysiological pathways such as enhanced sympathetic nervous drive and subclinical inflammatory processes. To address the above clinical question, a longitudinal study has to be projected. However, it is also important to validate the reproducibility of the association over time, ie, sequential longitudinal evaluation of REE and BP levels. In the current issue of The Journal of Clinical Hypertension, Sriram and colleagues evaluated the association of systolic BP with REE in a cohort of 229 originally overweight premenopausal women without comorbidities who were recruited to participate in a weight loss program to normalize their BMI. After BMIrelated target achievement, the cohort of “newly normoweight” women was observed annually for 4 years and different adiposity surrogates were assessed in combination with BP and REE measurements during each individual investigational visit. The constant association of REE with BP at several follow-up timeframes after adjustment for confounders highlighted the consistency of the results over time. As a general comment, and beyond the purpose of the study by Sriram and colleagues, a successful weight loss intervention of limited time once again was not able to retain BMI within normal levels during the follow-up period. Indeed, the subset of women returned at the last visit had the same weight as before the intervention. However, we should point out that the rate of women who returned for follow-up visits was progressively reduced. Only 30 women returned for the last follow-up laboratory visit compared with 140 women with normalized BMI after weight loss intervention. Thus, prospective changes of body adiposity and REE in relation to BP changes could not be addressed by the design of the present study mainly as a result of reduced power for longitudinal evaluation. Curiously, only systolic BP was used as a principal outcome in the investigational approach of Sriram and colleagues. Although previous reports have demonstrated a mild relationship between REE and diastolic BP, the present study did not explain whether even this mild association persists overtime. Moreover, from a clinical point of view, diastolic BP might be more important compared with systolic BP in middle-aged patients. Additionally, bias regarding the exact methodology for measuring laboratory BP should not be neglected. It would be interesting to know the 24-hour profile of BP and measures of BP variability across visits. Although 24-hour BP measurements might be far different than laboratory resting BP, the former better reflects the overall hemodynamic load and may overcome eventual white-coat phenomena. A step further, does variability in laboratory BP correlate with REE variability across the 3 days of each individual followup laboratory visit? The answer to this question might enable us to better understand the reciprocal temporal changes of BP and REE. Although the procedure of REE assessment seems adequate because it is performed in laboratory conditions of “complete quiescence” after an overnight stay at a general clinical research center, neither the duration nor the quality of sleep the night before testing are reported. Under the hypothesis that participants did not demonstrate respiratory disorders during sleep, REE at awaking could be modulated by sleep characteristics. The role of the sympathetic nervous system in the pathophysiology of obesity-related hypertension is well established. We believe that a more sophisticated measurement of sympathetic nervous system activity, namely muscle nerve sympathetic activity, might better define its confounding effect compared with the measurement of urinary catecholamines alone. Over and under the above methodological remarks, the study by Sriram and colleagues set the basis for the prospective evaluation of REE either on BP levels or on Address for correspondence: Costas Thomopoulos, MD, 2, Helena Venizelou sqr, 11521 Athens, Greece E-mail: thokos@otenet.gr