Cardiovascular Reactivity to Acute Mental Stress in Post Ovulatory Females.

BACKGROUND: Female hormones fluctuate with the phases of menstrual cycle. Estrogen, which has attributes in cardio-protection, is secreted less during luteal phase. In post-ovulatory phase, days 1-2 before menstruation has minimal female hormone influence due to less secretion. Mental stress subjected at this phase might enhance sympathetic activation which in long run may precipitate cardiovascular diseases. Hence, to explore the autonomic activity to mental stress during this phase of menstrual cycle the study was undertaken. METHODS: Thirty apparently healthy young postovulatory female medical students of B. P. Koirala Institute of Health Sciences, Nepal of age 19.93 (± 0.91) years with BMI of 20.70 kg/m2 (± 2.49) kg/m2 were recruited for the present study. Their short term heart rate variability (HRV) of 5 min was recorded during rest at sitting position. Then each subject was given a mental stress (nine questions selected from MENSA workout questionnaire) for 5 min. During the stress, HRV was recorded simultaneously. Data was statistically analyzed using Friedman test followed by multiple comparisons. The p<0.005 was considered statistically significant. RESULTS: Mental stress significantly decreased RMSSD (p= 0.001), NN50 (p= 0.001) and PNN50 (p=0.001) in time domain and HF nu (p=0.012) in frequency domain parameters of HRV. CONCLUSIONS: Young healthy post ovulatory females responded to acute mental stress by withdrawing cardiac parasympathetic activity.

Association between obesity and heart rate variability indices: an intuition toward cardiac autonomic alteration - a risk of CVD.

BACKGROUND: Obese people have a higher prevalence of cardiovascular disease, which is supposed to be due to autonomic dysfunction and/or metabolic disorder. The alterations in cardiac autonomic functions bring out the changes in the heart rate variability (HRV) indicators, an assessing tool for cardiac autonomic conditions. OBJECTIVE: To compare the cardiac autonomic activity between obese and normal weight adults and find out the highest association between the indices of HRV and obesity. METHODS: The study was conducted in 30 adult obese persons (body mass index [BMI] >30 kg/m2) and 29 healthy normal weight controls (BMI 18-24 kg/m2). Short-term HRV variables were assessed using standard protocol. Data were compared between groups using Mann-Whitney U test. Obesity indices such as waist circumference, hip circumference, waist-hip ratio (WHR), and BMI were measured and calculated, and they were correlated with HRV indices using Spearman's correlation analysis. RESULTS: In the obese group, there was a significant increase in the mean heart rate, whereas the HRV parasympathetic indicators were less (eg, root mean square of differences of successive RR intervals [28.75 {16.72-38.35} vs 41.55 {30.6-56.75} ms, p=0.018], number of RR intervals that differ by >50 ms, that is, NN50 [15.5 {2-39} vs 83.5 {32.75-116.25}, p=0.010], etc) and the sympathetic indicator low frequency (LF)/high frequency (HF) ratio (1.2 [0.65-2.20] vs 0.79 [0.5-1.02], p=0.045) was more than that of the normal weight group. Spearman's correlation between HRV and obesity indices showed significant positive correlation of WHR with LF in normalized unit (r=0.478, p<0.01) and LF/HF ratio (r=0.479, p<0.01), whereas it had significant negative correlation with high frequency power ms2 (r=-0.374, p<0.05) and HF in normalized unit (r=-0.478, p<0.01). There was a nonsignificant correlation of BMI with HRV variables in obese individuals. CONCLUSION: Increased WHR, by far an indicator of visceral adiposity, was strongly associated with reduced cardiac parasympathetic and increased sympathetic activity in obese individuals defined by BMI. However, BMI itself has a weak relationship with HRV cardiac autonomic markers. Thus, even with a slight increase in WHR in an individual, there could be a greater risk of cardiovascular morbidity and mortality brought about by cardiac autonomic alterations.

Somatic neural alterations in non-diabetic obesity: a cross-sectional study.

BACKGROUND: Reports on alterations in somatic neural functions due to non-diabetic obesity, a major risk factor for diabetes, are few and still a matter of debate. Nevertheless, to our knowledge, reports lack any comments on the type of somatic nerve fibers affected in non-diabetic obesity. Therefore, this study aimed to find out the alteration in somatic neural functions in non-diabetic obese persons if any. METHODS: The study was conducted on 30 adult non-diabetic obese persons (mean age 32.07 ± 7.25 years) with BMI > 30 Kg/m2 (mean BMI 30.02 ± 2.89 Kg/m2) and 29 age- and sex-matched normal weight controls (mean age 30.48 ± 8.01 years) with BMI: 18-24Kg/m2 (mean BMI 21.87 ± 2.40 Kg/m2). Nerve conduction study (NCS) variables of median, tibial and sural nerves were assessed in each subject using standard protocol. The data were compared by Mann Whitney 'U' test. RESULTS: 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 bilateral tibial nerves [Right: 8.5(7.04-11.18) Vs 12.1(10.55-15) mV, p < 0.001 and left 9.08(6.58-11.65) Vs 13.05(10.2-15.6) mV, p = 0.002]. Furthermore, obese persons had prolonged CMAP durations of right and left median [10.5(9.62-12) Vs 10(8.4-10.3) ms, p = 0.02 and 10.85(10-11.88) Vs 10(9-10.57) ms, p = 0.019] and right tibial [10(9-11) 8.5(7.92-10) ms, p = 0.032] nerves. Sensory NCS (sural nerve) also showed diminished sensory nerve action potential (SNAP) amplitude [16(12.08-18.21) vs 22.8(18.3-31.08) µV, p < 0.001] and prolonged duration. However, onset latencies and conduction velocities for all nerves were comparable between the groups. CONCLUSION: This study documents subclinical peripheral nerve damage in non-diabetic obese with abnormal NCS parameters; shorter amplitudes and prolonged CMAP and SNAP durations. The reduced amplitudes of mixed and sensory nerves might be due to decreased axonal number stimulation or actual decrease in number of axonal fibers, or defect at NMJ in non-diabetic obese. Prolonged durations but normal onset latencies and conduction velocities strongly suggest involvement of slow conducting fibers.

Pre- and postovulatory auditory brainstem response in normal women.

Studies with ovarian hormones on auditory brainstem response (ABR) have conflicting reports although women have ABR shorter than men. This study compared ABR between pre- and postovulatory phases of menstrual cycle in consenting 40 healthy female volunteers (age 19 ± 2.35 years). The study was conducted under standard laboratory conditions (room temperature 26 ± 2°C) using Neuropack (Nihon Kohden machine, NM-420S; H636, Japan) and earphone dynamic receiver ELEGA (Type DR-531; no.237, Japan) in sound proof room. Ears were stimulated simultaneously using standard protocol. ABR was recorded in pre- and postovulatory phases. Ovulation was estimated by measuring basal body temperature. The ABR wave latencies (WLs) I, II, III, IV, V and inter-peak latencies (IPLs) I-III, III-V, I-V were compared between the two phases of menstrual cycle using paired t test. The postovulatory phase had shorter WL V (5.71 ± 0.18 ms vs. 5.81 ± 0.19 ms, p < 0.01), IPL III-V (1.89 ± 0.16 ms vs. 1.94 ± 0.19 ms, p < 0.05), and I-V (3.88 ± 0.16 ms vs. 3.95 ± 0.18 ms, p < 0.05) than in preovulatory. Other WLs and IPLs showed decreasing trend in postovulatory phase. ABR is better in postovulatory phase as compared to preovulatory phase probably due to progesterone hormone which might be involved in modulating auditory hearing pathway at postovulatory phase.