Abstract-Excess weight is established as a major risk factor for cardiovascular diseases, particularly in young individuals.To get a better understanding of the pathophysiology underlying increased cardiovascular disease risk, we evaluated early signs of organ damage and their possible relationship to sympathetic nervous activity. Eighteen lean (body mass index Ͻ25 kg/m 2 ) and 25 overweight or obese (body mass index Ͼ25 kg/m 2 ) healthy university students were included in the study. We comprehensively assessed subclinical target organ damage, including the following: (1) assessment of renal function; (2) left ventricular structure and systolic and diastolic function; and (3) O besity is an established risk factor for cardiovascular disease (CVD) development. 1 Although excess adiposity is frequently linked with metabolic abnormalities such as elevated triglycerides, low levels of high-density lipoprotein (HDL), elevated glucose, elevated blood pressure (BP), insulin resistance, and a proinflammatory state, most likely contributing to excess CVD, 2 large scale epidemiological studies have shown that the CVD risk associated with obesity remains appreciable even after correction for these factors. 1,3 Perhaps surprising is the finding that the obesity-related relative risk of death from stroke and all of the CVDs combined is higher in younger than in older subjects, 4,5 indicating that excess adiposity is likely to have deleterious effects on the cardiovascular system already at an early age, well before clinical manifestations of CVD become apparent. In agreement with this view, recent studies have demonstrated that the presence of obesity since childhood was the only consistent and significant determinant of adverse cardiac remodeling 6 and that being overweight at age 20 years or obese at any time in life was linked with a 3-fold increased risk of developing chronic renal failure. 7 Moreover, functional and structural abnormalities of the endothelium are already evident in obese children aged 9 to 12 years. 8 Given that the sympathetic nervous system (SNS) is an important regulatory mechanism of both metabolic and cardiovascular functions, altered SNS may likely play a role in the etiology and complications of obesity. 9 It is now well established that obesity is associated with elevated SNS Continuing medical education (CME) credit is available for this article. Go to http://cme.ahajournals.org to take the quiz.

A new measure of the MBPS, BP(Power) which is based on a mathematical estimate of the rate and amplitude of the rise, is higher in hypertensives, white coat hypertensives, and is modifiable by some specific antihypertensive therapies suggests that it may be theoretically useful to highlight those subjects at greatest risk of cardiovascular events and for determining the most benefit of antihypertensive therapy.

These results suggest that the central nervous system mechanisms influencing the increase in MSNA burst amplitude during arousal may also be fundamental in determining the rate and power of BP rise during the morning period.

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We determined whether the reactivity of the sympathetic nervous system (SNS) is related to the morning surge in blood pressure. Ambulatory blood pressure recordings were obtained from 33 subjects (14 males / 19 females ) and the amplitude, the rate of rise (RoR) and the rate x amplitude product (BPPower) of morning mean arterial pressure (MAP) were determined mathematically. Subjects were average age 41 + 4 years (range 18 ‐ 83), BMI 26+1 and 24% of whom were taking antihypertensive therapy. The reactivity of the SNS to an aversive stimulus was assessed on a separate day by microneurographic recording of multiunit, postganglionic muscle sympathetic nerve activity (MSNA), measured from the peroneal nerve. MAP and MSNA were measured concurrently at rest and during a cold pressor test (hand in ice water for 2 min). The cold pressor test increased MSNA and MAP by 24.0 + 2.4 mmHg. MSNA was adjusted for age and BMI. BPPower and RoR were positively correlated to the cold pressor induced increase in total MSNA (r=0.4, P=0.02) and MSN burst amplitude (r=0.5, P=0.01) but were not related to the increase in MSNA frequency. These results suggest that the CNS mechanisms influencing the increase in MSN burst amplitude during arousal may also be fundamental in determining the rate of blood pressure rise during the morning period.Supported by NHMRC project grant 317826