While the importance of regulating arterial blood pressure within a 'normal' range is widely appreciated, the definition of 'normal' and the means by which humans and other species regulate blood pressure under various conditions remain hotly debated. The effects of diverse physiological, pathological and environmental challenges on blood pressure and the mechanisms that attempt to maintain it at an optimal level are reviewed and critically analyzed in a series of articles published in this themed issue of the European Journal of Applied Physiology. We summarize here the major points made in these reviews, with emphasis on unifying concepts of regulatory mechanisms and future directions for research.
[Show abstract][Hide abstract] ABSTRACT: Muscle sympathetic nerve activity (MSNA) is not increased during leg cycling at light and mild intensities, despite activation of central command and the exercise pressor reflex. We determined whether increasing central blood volume and loading the cardiopulmonary baroreceptors modulate sympathetic vasomotor outflow during leg cycling. To this end, we changed the pedaling frequency to enhance skeletal muscle pump. Subjects performed two leg cycle exercises at differential pedal rates of 60 and 80 rpm (60EX and 80EX trials) for two conditions (with and without MSNA measurement). In each trial, subjects completed leg cycling with a differential workload to maintain constant oxygen consumption (VO2). MSNA was recorded via microneurography at the right median nerve of the elbow. Without MSNA measurement, thoracic impedance, stroke volume (SV), and cardiac output (CO) were measured non-invasively using impedance cardiography. Heart rate and VO2 during exercise did not differ between the 60EX and 80EX trials. Changes in thoracic impedance, SV, and CO during the 80EX trial were greater than during the 60EX trial. MSNA during the 60EX trial was unchanged compared with that at rest (25.8 ± 3.1 [rest] to 28.3 ± 3.4 [exercise] bursts/min), whereas a significant decrease in MSNA was observed during the 80EX trial (25.8 ± 2.8 [rest] to 19.7 ± 2.0 [exercise] bursts/min). These results suggest that a muscle pump-induced increase in central blood volume, and thereby loading of cardiopulmonary baroreceptors, could inhibit sympathetic vasomotor outflow during mild dynamic leg exercise, despite activation of central command and the exercise pressor reflex.
[Show abstract][Hide abstract] ABSTRACT: Introduction: The goal of this study was to determine which anthropometric factors measured via air displacement plethysmography (ADP) play a significant role in augmenting orthostatic stability during sustained acceleration G-force (+G) exposure in a short arm human centrifuge (SAHC). The authors hypothesized that test subjects with a greater normalized fat free mass in percentage of total body mass (FFM%) would exhibit greater orthostatic stability during consecutive þG loads.
Methods: Twenty +G naive test subjects (10 female, 10 male), were recruited for this study, in which they underwent 2 rounds of 1/2/1 G-force profile in a SAHC. Before being exposed to +G, each subject underwent anthropometric analysis via ADP to ascertain total body mass (BM, kg), body volume (BV, L), body surface area (BSA, m²), normalized fat mass/fat free mass in percentage of total body mass (FM% and FFM%). During SAHC exposure, hemodynamic parameters were continuously obtained from each test subject. The measured anthropometric parameters were compared against baseline mean arterial pressure (MAP, mmHg), heart rate (HR, bpm), stroke volume (SV, mL) cardiac output (CO, L min -1) and systemic vascular resistance (SVR, dyn s cm -5) to determine correlations.
Results: From the 20 subjects, 13 test subjects (5 F, 8 M) completed all phases of +G exposure, and were therefore classified as having high +G tolerance (NALOC). From the 7 remaining test subjects (5 F, 2 M); 6 aborted or reduced their +G exposure, and were therefore classified as exhibiting low +G tolerance (ALOC). One subject dropped out prior to testing, and is not included in the data. Total BM, BV, and BSA were significantly higher (p o 0.05) in the NALOC group. Significant correlations between baseline SV/CO and these parameters were also determined. FFM% showed no differences between the two groups, and did not exhibit any correlations with baseline hemodynamics. NALOC subjects tended to have a higher CO and SV at baseline, whereas ALOC subjects tended to exhibit higher SVR at baseline.
Discussion: Total BM, BV, and BSA were the anthropometric factors associated with orthostatic stability during +G. The higher these parameters, the higher the baseline SV, which combined contributed to greater orthostatic stability during +G. Male test subjects had an overall advantage over females via increased body dimensions and augmented cardiac function. Anthropometric analysis via ADP thus reveals critical information regarding how anthropometry influences hemodynamic function and further studies on this topic are warranted.
[Show abstract][Hide abstract] ABSTRACT: Blood pressure homeostasis is maintained by several mechanisms regulating cardiac output, vascular resistances, and blood volume. At cellular levels, reactive oxygen species (ROS) signaling is involved in multiple molecular mechanisms controlling blood pressure. Among ROS producing systems, NADPH oxidases (NOXs), expressed in different cells of the cardiovascular system, are the most important enzymes clearly linked to the development of hypertension. NOXs exert a central role in cardiac mechanosensing, endothelium-dependent relaxation, and Angiotensin-II (Ang-II) redox signaling regulating vascular tone. The central role of NOXs in redox-dependent cardiovascular cell functions renders these enzymes a promising pharmacological target for the treatment of cardiovascular diseases, including hypertension. The aim of the present review is to focus on the physiological role of the cardiovascular NOX-generating ROS in the molecular and cellular mechanisms affecting blood pressure.
Frontiers in Physiology 07/2015; 6:194. DOI:10.3389/fphys.2015.00194 · 3.53 Impact Factor
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