Mechanisms of blood pressure regulation that differ in men repeatedly exposed to high-G acceleration.
The purpose of this study was to test the hypothesis that repeated exposure to high acceleration (G) would be associated with enhanced functions of specific mechanisms of blood pressure regulation. We measured heart rate (HR), stroke volume (SV), cardiac output (), mean arterial blood pressure, central venous pressure, forearm and leg vascular resistance, catecholamines, and changes in leg volume (%DeltaLV) during various protocols of lower body negative pressure (LBNP), carotid stimulation, and infusions of adrenoreceptor agonists in 10 males after three training sessions on different days over a period of 5-7 days using a human centrifuge (G trained). These responses were compared with the same measurements in 10 males who were matched for height, weight, and fitness but did not undergo G training (controls). Compared with the control group, G-trained subjects demonstrated greater R-R interval response to equal carotid baroreceptor stimulation (7.3 +/- 1.2 vs. 3.9 +/- 0.4 ms/mmHg, P = 0.02), less vasoconstriction to equal low-pressure baroreceptor stimulation (-1.4 +/- 0.2 vs. -2.6 +/- 0.3 U/mmHg, P = 0.01), and higher HR (-1.2 +/- 0.2 vs. -0.5 +/- 0.1 beats. min(-1). mmHg(-1), P = 0.01) and alpha-adrenoreceptor response (32.8 +/- 3.4 vs. 19.5 +/- 4.7 U/mmHg, P = 0.04) to equal dose of phenylephrine. During graded LBNP, G-trained subjects had less decline in and SV, %DeltaLV, and elevation in thoracic impedance. G-trained subjects also had greater total blood (6,497 +/- 496 vs. 5,438 +/- 228 ml, P = 0.07) and erythrocyte (3,110 +/- 364 vs. 2,310 +/- 96 ml, P = 0.06) volumes. These results support the hypothesis that exposure to repeated high G is associated with increased capacities of mechanisms that underlie blood pressure regulation.
United States Army Institute of Surgical Research Library, 3400 Rawley E. Chambers Ave., Bldg. 3611, Fort Sam Houston, TX 78234, USA. victor.convertino@amedd.army.mil
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D000064:Acclimatization / Q000502:physiology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002302:Cardiac Output; D002339:Carotid Arteries / Q000502:physiology; D004837:Epinephrine / Q000097:blood; D004911:Erythrocyte Volume; D005542:Forearm / Q000098:blood supply; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D018471:Hypergravity; D007262:Infusions, Intravenous; D007545:Isoproterenol / Q000494:pharmacology; D007866:Leg / Q000098:blood supply; D008150:Lower Body Negative Pressure; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects; D013318:Stroke Volume; D014655:Vascular Resistance; D014661:Vasoconstriction
D000316:Adrenergic alpha-Agonists; D010656:Phenylephrine; D007545:Isoproterenol; D009638:Norepinephrine; D004837:Epinephrine