Cardiovascular
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12503/31252
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Browsing Cardiovascular by Author "White, Daniel"
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Item A CASE FOR A STANDARDIZED METHOD FOR THE NORMALIZATION OF MUSCLE SYMPATHETIC NERVE ACTIVITY AMPLITUDE(2013-04-12) White, DanielPurpose: MSNA has no agreed upon standard for analysis. For example, mean burst strength (MBS), total activity (TA) and total MSNA (TMSNA) rely on amplitude measurements assigned arbitrary units which are highly dependent on the method of normalization. We investigated the hypothesis that computer algorithms used for automatic normalization of MSNA amplitudes differ from those obtained with manual normalization leading to erroneous interpretations. Methods: MSNA from healthy human subjects (n=8, 2 female) was obtained by microneurography of the peroneal nerve while resting quietly in a 30* semi-recumbent position. Data was analyzed by 3 different normalization methods (Min-Max Auto (MM), Mean Auto (MA), and Rectified Manual (RM)). MSNA is quantified as burst frequency (BF), burst incidence (BI), MBS, TA, and TMSNA. Results: There were no differences in BF or BI between the three analysis methods. However, significant differences were detected between MM and RM in MBS, TA and TMSNA (p=0.002, p=0.009, and p=0.004). Rankings according to activity were not different between MM and RM but were different in MA compared to either MM or RM. Conclusions: There is an overwhelming need to standardize the analysis of MSNA. The current study points out that the variables BF and BI can be compared across studies. However, our data identify that the RM normalization is the only method to quantify MBS, TA and TMSNA for cross-study comparisons.Item COMPREHENSIVE MODEL OF AUTONOMIC CONTROL OF HEART RATE DURING EXERCISE(2013-04-12) White, DanielPurpose: Exercise Physiology textbooks illustrate the autonomic control of heart rate (HR) at the beginning of dynamic exercise as an immediate and selective withdrawal of parasympathetic (PS) control of the Sino-Atrial node resulting in a rise in HR up to 100 beats per min. The appearance of norepinephrine in the blood after 100 bpm was interpreted as the time at which the sympathetic nervous system was activated. In the past ten years animal investigations indicate that increases in sympathetic outflow are involved in the increase in HR at exercise onset. Therefore, we hypothesized that re-analysis of previous investigations utilizing pharmacologic blockade of the autonomic nervous system and our carotid baroreflex modeling techniques of humans during dynamic exercise would identify the role of sympathetic activity in exercise. Methods: Comprehensive analysis of HR data presented in 8 "autonomic neural control of heart rate" research articles and book chapters in both humans and animals coupled with our own neck pressure/neck suction published data was used to generate a novel model of the autonomic control of HR during exercise. Results: Throughout the progression of exercise (HR = 100, 117, 150), neck pressure stimuli induce reflexive increases in HR (+6, 3, 1), and pharmacological blockade with glycopyrrolate induces increases in HR (+24, 21, 12). Comprehensive regression modeling of the increases in heart rate during exercise identified that sympathetic activity establishes the exercise intensity related HR and it is the PS control of the heart that expresses the baroreflex response. Conclusions: These data provide compelling evidence that cardiac sympathetic and PS activities were continuously active throughout exercise. Furthermore, there was no evidence of an abrupt shift from PS withdrawal to sympathetic activation in autonomic control of HR during exercise but rather a steady rise in HR due to increasing cardiac sympathetic tone. Contrary to there being a PS withdrawal at the onset of exercise previous work identify that during exercise onset increases in PS tone dampen the sharp rise in HR in response to the immediate increase in cardiac sympathetic activity.