TO FIND OUT THE VARIATION OF SYMPATHETIC & PARASYMPATHETIC TESTS BETWEEN MALE & MENSTRUAL PHASE OF MENSTRUAL CYCLE IN FEMALE.

The hormonal fluctuations that occur during normal menstrual cycle has profound influence on autonomic functions. This influence on autonomic nervous system may affect cardiovagal control. The aim of the study is to find out the variation of Parasympathetic function tests during different phases of menstrual cycle in young healthy females. The mean E:I ratio in Menstrual Phase of menstrual cycle in females is 1.34 ± 0.06. The mean E:I ratio in males is 1.41 ± 0.12. The mean Postural SBP in Menstrual Phase of menstrual cycle in females is 97.76 ± 5.13 mmHg. The mean Postural SBP in males is 103.24 ± 6.88 mmHg. The study concludes that there was statistically significant heart rate variability during three phases of the menstrual cycle, as observed by the increased sympathetic discharge in the luteal phase compared to the increased parasympathetic discharge in the follicular phase. The results of our study have emphasized the complexity of the relationship between ovarian steroids and various hemodynamic regulatory systems. Keywords: Sympathetic, Parasympathetic & Menstrual.

Cardiac and Vascular Sympathetic Baroreflex Control during Orthostatic Pre-Syncope

We hypothesized that sympathetic baroreflex mediated uncoupling between neural sympathetic discharge pattern and arterial pressure (AP) fluctuations at 0.1 Hz during baroreceptor unloading might promote orthostatic pre-syncope. Ten volunteers (32 ± 6 years) underwent electrocardiogram, beat-to-beat AP, respiratory activity and muscle sympathetic nerve activity (MSNA) recordings while supine (REST) and during 80° head-up tilt (HUT) followed by -10 mmHg stepwise increase of lower body negative pressure until pre-syncope. Cardiac and sympathetic baroreflex sensitivity were quantified. Spectrum analysis of systolic and diastolic AP (SAP and DAP) and calibrated MSNA (cMSNA) variability assessed the low frequency fluctuations (LF, ~0.1 Hz) of SAP, DAP and cMSNA variability. The squared coherence function (K2) quantified the coupling between cMSNA and DAP in the LF band. Analyses were performed while supine, during asymptomatic HUT (T1) and at pre-syncope onset (T2). During T2 we found that: (1) sympathetic baroreceptor modulation was virtually abolished compared to T1; (2) a progressive decrease in AP was accompanied by a persistent but chaotic sympathetic firing; (3) coupling between cMSNA and AP series at 0.1 Hz was reduced compared to T1. A negligible sympathetic baroreceptor modulation during pre-syncope might disrupt sympathetic discharge pattern impairing the capability of vessels to constrict and promote pre-syncope.

Central vs. peripheral determinants of sympathetic neural recruitment: insights from static handgrip exercise and postexercise circulatory occlusion

Sympathetic outflow is modified during acute homeostatic stress through increased firing of low-threshold axons, recruitment of latent axons, and synaptic delay modifications. However, the role of central mechanisms versus peripheral reflex control over sympathetic recruitment remains unknown. Here, we examined sympathetic discharge patterns during fatiguing static handgrip (SHG) exercise and postexercise circulatory occlusion (PECO) to study the central vs. peripheral reflex elements of sympathetic neural coding. Muscle sympathetic nerve activity (MSNA; microneurography) was measured in six males (25 ± 3 yr) at baseline (3 min) and during 5 min of SHG exercise completed at 20% maximal voluntary contraction. Isolation of the peripheral metaboreflex component was achieved by PECO for 3 min. Action potential (AP) patterns were studied using wavelet-based methodology. Compared with baseline, total MSNA increased by minute 3 of SHG, remaining elevated throughout the duration of exercise and PECO (all P < 0.05). The AP content per burst increased above baseline by minute 4 of SHG (Δ4 ± 2), remaining elevated at minute 5 (Δ6 ± 4) and PECO (Δ4 ± 4; all P < 0.05). Similarly, total AP clusters increased by minute 4 of SHG (Δ5 ± 5) and remained elevated at minute 5 (Δ6 ± 3) and PECO (Δ7 ± 5; all P < 0.01), indicating recruitment of latent subpopulations. Finally, the AP cluster size-latency profile was shifted downward during minutes 4 (−32 ± 22 ms) and 5 (−49 ± 17 ms; both P < 0.05) of SHG but was not different than baseline during PECO ( P > 0.05). Our findings suggest that central perceptual factors play a specific role in the synaptic delay aspect of sympathetic discharge timing, whereas peripheral reflex mechanisms affect recruitment of latent axons.