Hemodynamic response to work at simulated altitude, 4,000 m.

Stenberg, Jesper; Ekblom, Björn; Messin, R

doi:10.1152/jappl.1966.21.5.1589

Cited by 172 publications

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“…2,3) Although under acute hypoxia at higher altitude (corresponding to 4000 -5000 m) CO increases during low to submaximal exercise, [24][25][26][27] the increase is probably due to a difference in the degree of hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

et al. 2010

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SummaryIt has been unclear how acute hypoxia at moderate altitude affects stroke volume (SV), an index of cardiac function, during exercise. The present study was conducted to reveal whether acute normobaric hypoxia might alter SV during exercise.Nine healthy male subjects performed maximal exercise testing under normobaric normoxic, and normobaric hypoxic conditions (O 2 : 14.4%) in a randomized order. A novel thoracic impedance method was used to continuously measure SV and cardiac output (CO) during exercise.Acute hypoxia decreased maximal work rate (hypoxia; 247 ± 6 [SE] versus normoxia; 267 ± 8 W, P < 0.005) and VO 2 max (hypoxia; 2761 ± 99 versus normoxia; 3039 ± 133 mL/min, P < 0.005). Under hypoxic conditions, SV and CO at maximal exercise decreased (SV: hypoxia; 145 ± 11 versus normoxia; 163 ± 11 mL, P < 0.05, CO: hypoxia; 26.7 ± 2.1 versus normoxia; 30.2 ± 1.8 L/min, P < 0.05). In acute hypoxia, SV during submaximal exercise at identical work rate decreased. Furthermore, in hypoxia, 4 of 9 subjects attained their highest SV at maximal exercise, while in normoxia, 8 of 9 subjects did.Acute normobaric hypoxia attenuated the increment of SV and CO during exercise, and SV reached a plateau earlier under hypoxia than in normoxia. Cardiac function during exercise at this level of acute normobaric hypoxia might be attenuated. (Int Heart J 2010; 51: 170-175) Key words: Normobaric hypoxia, Cardiac output, Oxygen uptake, Exercise testing D uring ascent to a moderate to high altitude, individuals are exposed to progressive decreases in atmospheric pressure that lead to a reduction in inspired, alveolar, and arterial oxygen pressures. Training at moderate altitude (corresponding to 2000 -3000 m) is associated with relatively severe hypoxemia during submaximal and maximal exercise, 1) and acute hypoxia of this level decreases VO 2 max as well as exercise capacity.2-4) Thus, hypoxia at moderate altitude limits training intensity, which leads to relative deconditioning in elite athletes, although endurance athletes often use hypoxic training to improve sea-level performance. 5) Because VO 2 is the product of cardiac output (CO) and the arterio-venous oxygen content difference (C(a-v)O 2 ), a decrease in VO 2 max at maximal exercise may be due to a decrease of either factor, or both.Acute hypoxia may induce abnormalities in cardiac function and redistribution of CO not only at rest but also during exercise. In an animal study, CO at rest increased during acute severe hypoxia (FiO 2 10% and 5%), and blood flow to all organs increased except for the skin and muscle.6) In humans under acute hypoxia, heart rate (HR) and CO increase while systemic vascular resistance decreases. 7)Echocardiography also reveals altered mitral flow patterns, suggestive of mild LV diastolic dysfunction.8) Subacute hypoxia (FiO 2 12%, simulating an altitude of approximately 4000 m) induced mild diastolic dysfunction in young healthy individuals. 9)Stroke volume (SV) increases as the work rate increases at low to moderate intensity exercise, ...

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Section: Discussionmentioning

confidence: 99%

Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

et al. 2010

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“…Cerretelli & di Prampero, 1987). Admitted exceptions are the upward shift of the Q vs. Vo0 line observed in acute hypoxia (Stenberg, Ekblom & Messin, 1966; Hughes, Clode, Edwards, Goodwin & Jones, 1968) and after moderate CO poisoning (Vogel & Gleser, 1972). These exceptions have been explained in terms of an 'error signal', related to reduced Ca 02 influencing the control system of Q (Cerretelli & di Prampero, 1987 Preliminary reports of this study have previously been published (Ferretti, Kayser, Schena, Turner & Hoppeler, 1991;Ferretti, Kayser, Moia, Schena & Turner, 1991).…”

Section: Ferretti An\d Othersmentioning

confidence: 99%

Regulation of perfusive O2 transport during exercise in humans: effects of changes in haemoglobin concentration.

Ferretti

Kayser

Schena

et al. 1992

The Journal of Physiology

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SUMMARY1. Recently it was suggested that submaximal cardiac output (Q) could vary in response to changes in arterial 02 concentration (Ca,02) so that arterial 02 delivery QaIo2 = Q X Ca O2 in ml min-) is kept constant.2. This hypothesis was tested on eight healthy male subjects, at rest and during exercise (50, 100 and 150 W) in three conditions: normaemia (N), after 6 weeks of endurance training (T), and 2 days after subsequent autologous blood reinfusion (P). 6. In conclusion, the tested hypothesis was supported by the present results. The observed constancy of Qv 2 suggested that Qv 2 may play a key role in regulating the cardiovascular response to exercise.

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“…Elliot et al (10) reported a 14% reduction the first day after arrival at 406 mmHg at 84% VO 2 max in eight subjects. Stenberg et al (31) showed a 14% reduction upon acute Fig. 6.…”

Section: Discussionmentioning

confidence: 95%

V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

Loeppky

Sheard

Salgado

et al. 2016

Physiology International

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This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈4,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the V E STPD at RER <1.0 was significantly lower and the V E BTPS was higher because of higher breathing frequency; at VO 2 max, both V E STPD and V E BTPS were not significantly different. As percent of VO 2 max, the V E BTPS was nearly identical and V E STPD was 30% lower throughout the exercise at 455 mmHg. The lower V E STPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where V E STPD at submaximal workloads was maintained or increased above that at sea level. The lower V E STPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO 2 (≈0.17 pHa units), reduction in PACO 2 (≈5 mmHg) and higher PAO 2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict V E STPD from VO 2 and P B in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in V E STPD at low workloads after arrival at altitude.

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Hemodynamic response to work at simulated altitude, 4,000 m.

Cited by 172 publications

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Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

Regulation of perfusive O2 transport during exercise in humans: effects of changes in haemoglobin concentration.

V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

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Hemodynamic response to work at simulated altitude, 4,000 m.

Cited by 172 publications

References 0 publications

Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

Effects of Acute Hypoxia at Moderate Altitude on Stroke Volume and Cardiac Output During Exercise

Regulation of perfusive O2 transport during exercise in humans: effects of changes in haemoglobin concentration.

VESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

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V_ESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia