The effects of reduced muscle perfusion pressure on dynamic exercise performance and cardiovascular and respiratory functions were investigated. Eight subjects were studied during supine cycle ergometry at stepwise increasing workloads until exhaustion with and without the legs exposed to a supra-atmospheric pressure of 50 mmHg (Leg Positive Pressure, LPP), a novel and convenient means of reducing the perfusion pressure in the working muscles. In the LPP condition exercise performance was reduced by 40% which, judging from assessments of perceived exertion, was due to premature muscle fatigue, indicating local or overall underperfusion of the working muscles. At any given work load, the arterial pressure response was considerably stronger during LPP than in the control condition. LPP also caused greater increases in blood lactate concentration and pulmonary ventilation, the differences from control increasing with the work load. Furthermore, the ventilatory equivalent for O2 at a given work load was markedly higher in the LPP than in the control condition, while exercise-induced decreases in end-tidal PCO2 were considerably exaggerated by LPP. The augmented pressor response during flow-restricted exercise, together with the strong ventilatory response which was out of proportion to overall O2 uptake, suggests increased activation of muscle chemoreflexes by accumulation of metabolic end products, the increased pressor response tending to reduce the local flow error in the working muscles.
BJURSTEDT, H., C. M. HESSER, G. LILJESTRAND and G. MATELL. Effects of posture on alveolar-arterial CO, and 0, differences and on alveolar dead space in man. Acta physiol. scand. 1962. 54. 65-82. -The increase in ventilation and lowering of the end-tidal Pco, after changing from the supine to the standing position were observed to be associated with a significant rise in the arterial to end-tidal CO, tension difference (average + 2.1 mm Hg) in addition to an increased effective alveolar to arterial 0, tension difference (+ 4.8 mm Hg). All dead spaces increased, the alveolar dead space (= the physiological minus the anatomical dead space) on an average by 28 ml. Assuming an unchanged distribution of ventilation this can be expressed as corresponding to 6 per cent of the alveoli being unperfused. A lowering of the alveolar Pco2 during standing is thus in part due to an increased arterial to end-tidal GO, tension difference. The end result is also influenced by a certain metabolic acidosis (average decrease in BHCO,B, 7 0.6 mM/l), in addition to peripheral retention of CO,. The Eff. VA/VE ratio decreased in all subjects, indicating a decline in the respiratory gas exchange efficiency by an average of 6 per cent. The changes observed may be explained as a consequence of the influence of gravityon the blood flow and its distribution not only in the systemic but also in the pulmonary circulation. Already in 1914 LILJESTRAND a n d WOLLIN showed that the alveolar CO, tension in m a n is lower during motionless standing than in the supine position. These authors had also confirmed a n d extended the old observation that assuming the up-right position calls forth a n increase in the pulmonary ventilation (cf. LILJESTRAND and WOLLIN 1913). Both the lowered alveolar 5-623015. Acta physiol. scand. Vol. 54. 65 66 H. BJURSTEDT ET A L .C:O, tension and the increase in pulmonary ventilation have been confirmed in numerous investigations (d. The mechanisms underlying the fall in the alveolar (20, and the increase in pulmonary ventilation after changing from the supine to the standing position are not fully understood. T h e former effect cannot be explained xilelj-b y an increased blowing off of CO, b y the hyperventilation, since the amount of C 0 2 eliminated during several minutes of motionless standing does not exceed the 0, uptake, as demonstrated b y HITCHCOCK and FER-GUSON as well as by RAHS and AXENT. These authors referred the lowered alveolar Pc:p2 during standing to impaired CO, elimination from the lungs, caused by the decrease in cardiac output with a concomitant CO, retention in the tissues and in venous blood, especially in the lo\ver portion of the body.By using special tecliniqucs for the continuous and simultaneous recording of blood gas changes 011 the centrifuge, rather drastic changes in the pulmonary circulation and gas exchange have been observed, both in the dog ;BARK, BJVRSTEDT and COLERIDGE 1959) and in man (BARR 1961 a). I n the espcriments to be reported beloiv, using similar techniques on the tilt-tabl...
We studied the responses of six healthy volunteers to standard 70 degrees head-up tilt tests before exhaustive exercise of short duration (control) and after 5, 25, 50, 80, and 110 min of recovery, all tests lasting for 6 min except when impending syncope (IS) necessitated premature termination of a test. Marked impairment of orthostatic tolerance was apparent during the first half-hour of recovery as manifested by symptoms of IS in five subjects in one or both of the first two postexercise tilt tests. In none of the subjects who developed symptoms of IS did central venous pressure fall to a lower level than it did in the control test. From the central venous and arterial pressure reactions we conclude that when IS developed, declining systematic resistance rather than diminished cardiac filling was the responsive factor. The increased tendency for orthostatic collapse occurred during a period of recovery marked by persistent postexercise acidemia and hyperthermia suggesting interference of these conditions and associated events with the normal ability to vasoconstrict during orthostasis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.