| Autor: |
Nardone M; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Incognito AV; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Kathia MM; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Omazic LJ; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Lee JB; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Teixeira AL; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada., Xie S; Global Management Studies, Ted Rogers School of Management, Ryerson University, Toronto, Ontario, Canada., Vianna LC; NeuroV̇ASQ̇ - Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasilia, Brasilia, Federal District, Brazil., Millar PJ; Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.; Toronto General Research Institute, Toronto General Hospital, Toronto, Ontario, Canada. |
| Abstrakt: |
Calculating the blood pressure (BP) response to a burst of muscle sympathetic nerve activity (MSNA), termed sympathetic transduction, may be influenced by an individual's resting burst frequency. We examined the relationships between sympathetic transduction and MSNA in 107 healthy males and females and developed a normalized sympathetic transduction metric to incorporate resting MSNA. Burst-triggered signal averaging was used to calculate the peak diastolic BP response following each MSNA burst (sympathetic transduction of BP) and following incorporation of MSNA burst cluster patterns and amplitudes (sympathetic transduction slope). MSNA burst frequency was negatively correlated with sympathetic transduction of BP ( r = -0.42; P < 0.01) and the sympathetic transduction slope ( r = -0.66; P < 0.01), independent of sex. MSNA burst amplitude was unrelated to sympathetic transduction of BP in males ( r = 0.04; P = 0.78), but positively correlated in females ( r = 0.44; P < 0.01) and with the sympathetic transduction slope in all participants ( r = 0.42; P < 0.01). To control for MSNA, the linear regression slope of the log-log relationship between sympathetic transduction and MSNA burst frequency was used as a correction exponent. In subanalysis of males (38 ± 10 vs. 14 ± 4 bursts/min) and females (28 ± 5 vs. 12 ± 4 bursts/min) with high versus low MSNA, sympathetic transduction of BP and sympathetic transduction slope were lower in participants with high MSNA (all P < 0.05). In contrast, normalized sympathetic transduction of BP and normalized sympathetic transduction slope were similar in males and females with high versus low MSNA (all P > 0.22). We propose that incorporating MSNA burst frequency into the calculation of sympathetic transduction will allow comparisons between participants with varying levels of resting MSNA. |
