MECHANISMS OF CARDIOVASCULAR ADJUSTMENTS ASSOCIATED WITH PRESYNCOPAL-LIMITED LOWER BODY NEGATIVE PRESSURE TOLERANCE (ORTHOSTASIS).

Persistent Link:
http://hdl.handle.net/10150/188096
Title:
MECHANISMS OF CARDIOVASCULAR ADJUSTMENTS ASSOCIATED WITH PRESYNCOPAL-LIMITED LOWER BODY NEGATIVE PRESSURE TOLERANCE (ORTHOSTASIS).
Author:
SATHER, TOM MALVIN.
Issue Date:
1985
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
In man, tolerance to an orthostatic stress varies widely. Compensatory cardiovascular responses to orthostatic stressors such as head-up tilt, +Gz acceleration, and lower body negative pressure (LBNP) have been identified. However, physiologic reactions associated with the capacity to withstand a presyncopal- limited orthostatic exposure requires additional clarification. The relationship between maximal oxygen uptake (‘VO₂ max) and presyncopal-limited LBNP tolerance was examined in adult male subjects categorized into high (HAC) and low (LAC) aerobic capacity groups. In addition to similar (N.S.) cardiovascular responses, the (mean) and cumulative LBNP stress indices (CS)) observed in the HAC (722 torr•min) and LAC (784 torr•min) groups were also similar (N.S.). These data fail to support a relationship between LBNP tolerance and ‘VO₂ max. Cardiovascular responses associated with LBNP tolerance were measured during the control period (pre-LBNP) and final minute (peak LBNP) of decompression. The CSI criterion distinguished high (HT, n = 10) and low (LT, n = 8) LBNP tolerant groups was 640 torr•min. A greater (p < 0.05) end-diastolic volume and cardiac output was observed in the HT subjects during pre-LBNP may have provided a larger reserve to utilize throughout exposure to LBNP. At peak LBNP, both groups demonstrated similar (N.S.) cardiac outputs despite a higher (p < 0.05) HT heart rate. These data suggest that a major mechanism in prolonging LBNP tolerance may have been a greater LBNP-induced tachycardia. Blood samples were drawn to determine group differences in vasoactive neuroendocrine response. During peak LBNP, concentrations of norepinephrine increased (p < 0.05) in both groups. The HT group displayed greater (p < 0.05) LBNP-induced increases in vasopressin and plasma renin activity. These data suggest that HT subjects may have supplemented the catecholamine pressor response by involving the vasopressin and renin-angiotensin systems. The affect of cholenergic and beta-adrenergic blockades on cardiovascular responses to LBNP were examined in six HT and five LT subjects. CSI in both groups were unchanged (N.S.) by administration of atropine as compared to a placebo LBNP exposure. Propranolol however, reduced (p < 0.05) LBNP tolerance in both groups. This CSI reduction was greater (p < 0.05) in the HT subjects. The reduction in LBNP tolerance appeared closely associated with the negative chronotropic effect.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Exercise -- Physiological aspects.; Blood -- Circulation -- Regulation.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Animal Physiology; Graduate College
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleMECHANISMS OF CARDIOVASCULAR ADJUSTMENTS ASSOCIATED WITH PRESYNCOPAL-LIMITED LOWER BODY NEGATIVE PRESSURE TOLERANCE (ORTHOSTASIS).en_US
dc.creatorSATHER, TOM MALVIN.en_US
dc.contributor.authorSATHER, TOM MALVIN.en_US
dc.date.issued1985en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractIn man, tolerance to an orthostatic stress varies widely. Compensatory cardiovascular responses to orthostatic stressors such as head-up tilt, +Gz acceleration, and lower body negative pressure (LBNP) have been identified. However, physiologic reactions associated with the capacity to withstand a presyncopal- limited orthostatic exposure requires additional clarification. The relationship between maximal oxygen uptake (‘VO₂ max) and presyncopal-limited LBNP tolerance was examined in adult male subjects categorized into high (HAC) and low (LAC) aerobic capacity groups. In addition to similar (N.S.) cardiovascular responses, the (mean) and cumulative LBNP stress indices (CS)) observed in the HAC (722 torr•min) and LAC (784 torr•min) groups were also similar (N.S.). These data fail to support a relationship between LBNP tolerance and ‘VO₂ max. Cardiovascular responses associated with LBNP tolerance were measured during the control period (pre-LBNP) and final minute (peak LBNP) of decompression. The CSI criterion distinguished high (HT, n = 10) and low (LT, n = 8) LBNP tolerant groups was 640 torr•min. A greater (p < 0.05) end-diastolic volume and cardiac output was observed in the HT subjects during pre-LBNP may have provided a larger reserve to utilize throughout exposure to LBNP. At peak LBNP, both groups demonstrated similar (N.S.) cardiac outputs despite a higher (p < 0.05) HT heart rate. These data suggest that a major mechanism in prolonging LBNP tolerance may have been a greater LBNP-induced tachycardia. Blood samples were drawn to determine group differences in vasoactive neuroendocrine response. During peak LBNP, concentrations of norepinephrine increased (p < 0.05) in both groups. The HT group displayed greater (p < 0.05) LBNP-induced increases in vasopressin and plasma renin activity. These data suggest that HT subjects may have supplemented the catecholamine pressor response by involving the vasopressin and renin-angiotensin systems. The affect of cholenergic and beta-adrenergic blockades on cardiovascular responses to LBNP were examined in six HT and five LT subjects. CSI in both groups were unchanged (N.S.) by administration of atropine as compared to a placebo LBNP exposure. Propranolol however, reduced (p < 0.05) LBNP tolerance in both groups. This CSI reduction was greater (p < 0.05) in the HT subjects. The reduction in LBNP tolerance appeared closely associated with the negative chronotropic effect.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectExercise -- Physiological aspects.en_US
dc.subjectBlood -- Circulation -- Regulation.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineAnimal Physiologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.identifier.proquest8603154en_US
dc.identifier.oclc696816739en_US
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