Nerve conduction study and heart rate variability in obese persons

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCC170

Poster Communications: Nerve conduction study and heart rate variability in obese persons

R. L. Yadav1, R. Khadka1, D. Thakur1, K. Agrawal1, B. Paudel1

1. Department of Basic and Clinical Physiology, B.P.Koirala Institute of Health Sciences, Dharan, Nepal.

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Obesity increased worldwide (35.5% obese & 66% overweight in USA, 2012; 30%- Mexico, 2009) and in other South Asian countries, including Nepal & Bangladesh (from 1.6% – 10% & from 2.7% – 8.9% respectively, 2006). Studies have indicated an increase in all cause mortality (>300,000 deaths/year) with increased obesity, especially death from cardiovascular disease. Hence, obesity is considered as a major public health problem. Though measurement of body fat is too complex, body mass index (BMI, kg/m2) & waist-hip ratio (WHR) are used in daily practice. According to WHO, BMI≥30 kg/m2 is classified as obese & WHR cut-off being 0.9. There are controversial results of different studies regarding effects of obesity on autonomic nervous system and peripheral somatic nerves. Thus, our objective is to study the nerve conduction (NCS) and heart rate variability (HRV) in adult obese persons. The study was conducted on 30 adult obese persons (BMI>30, kg/m2) and 29 healthy normal weight persons (BMI, 18-24, kg/m2). In all subjects, short-term heart rate variability (HRV) and nerve conduction were assessed using standard protocol. The data obtained were analysed between the groups using Mann Whitney U test and presented as median (inter-quartile range). P value < 0.05 were considered as statistically significant. In comparison to normal weight persons, obese had lower compound muscle action potential (CMAP) amplitudes of right median [9.09(7.62-10.20) Vs 10.75(8.71-12.2), mV, p=0.025], and right [8.5(7.04-11.18) Vs 12.1(10.55-15), mV, p=0.000] and left tibial [9.08(6.58-11.65) Vs 13.05(10.2-15.6), mV, p=0.002] nerves. Whereas, obese persons had prolonged CMAP durations of right [10.5(9.62-12) Vs 10(8.4-10.3), mV, p=0.02] and left median 10.85(10-11.88) Vs 10(9-10.57), mV, p=0.019] nerves, and right tibial [10(9-11) 8.5(7.92-10), mV, p=0.032] nerve. Sensory NCS showed similar results. Among HRV variables, SDNN [35.55(26.77-49.25) Vs 46.15(37.22-58.57) ms, p=0.038], RMSSD [28.75(16.72-38.35) Vs 41.55(30.6-56.75), ms, p=0.018], NN50 count [15.5(2-39) Vs 83.5(32.75-116.25), p=0.010], pNN50, HF power and SD1, which reflect cardiac parasympathetic activities were significantly lower whereas, sympathetic marker LF/HF [1.2(0.65-2.20) Vs 0.79(0.5-1.02), p=0.045] was higher in obese persons than in the normal weight persons. Thus, we conclude that obesity affected autonomic modulation with an increase in sympathetic tone coupled with a reduction in vagal tone, indicating poor cardiac rhythm control. However, nerve conduction study showed a tendency of poorer amplitudes and lengthened CMAP and SNAP durations, which might lead to future somatic neuropathy in obese persons. The obesity affected predominantly parasympathetic function and the parasympathetic fibers are usually myelinated. Thus, both the NCS & HRV indicates that obesity might alter the myelination of both somatic & autonomic nerve fibers.



Where applicable, experiments conform with Society ethical requirements.

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