Determinants of maximal oxygen uptake in severe acute  hypoxia

Calbet, José A. L.; Boushel, Robert; Rådegran, Göran; Söndergaard, Hans Peter; Wagner, Peter D.; Saltin, Bengt

doi:10.1152/ajpregu.00155.2002

Cited by 205 publications

(252 citation statements)

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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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“…Perhaps the reduction of muscle mass fibre size at very high altitude is the explanation for the failure to see an increase in VO 2max after exposure to these extreme environments [63,64]. Failure to recover VO 2max after acclimatization despite normalization of arterial O 2 concentration is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues [65].…”

Section: Discussionmentioning

confidence: 99%

Physiological and Kinanthropometrical Parameters of an Elite Climber. Single case study.

et al. 2012

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“…Because fatigue is a perception, it is likely to be influenced by many sensory inputs; thus the increase in performance may have been moderated by other oxygen-sensing tissues, such as peripheral chemoreceptors or even the pulmonary vasculature (22). Alternatively, increased heart rate during hyperoxia raises the possibility that exercise before the gas switch may have been limited, at least in part, by a hypoxia-induced limitation to cardiac output (10,11). While switching from acute hypoxia to hyperoxia does not affect heart rate when work rate remains constant (4), heart rate may continue to rise if work rate is increased (10).…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, increased heart rate during hyperoxia raises the possibility that exercise before the gas switch may have been limited, at least in part, by a hypoxia-induced limitation to cardiac output (10,11). While switching from acute hypoxia to hyperoxia does not affect heart rate when work rate remains constant (4), heart rate may continue to rise if work rate is increased (10). In the present study, peak heart rate before the gas switch was lower in CH than AH, yet maximal heart rate during hyperoxia was not different between conditions.…”

Section: Discussionmentioning

confidence: 99%

Cerebrovascular Responses To Incremental Exercise During Hypobaric Hypoxia: Effect Of Oxygenation On Maximal Performance

Lorenz

Subudhi

Fulco

et al. 2008

Medicine &Amp; Science in Sports &Amp; Exercise

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Standard Form 298 (Rev. 8/98) REPORT DOCUMENTATION PAGEPrescribed by ANSI Std. Z39.18 Form Approved OMB No. 0704-0188The public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing the burden, Approved for public release; distribution unlimited. SPONSORING/MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) SPONSOR/MONITOR'S REPORT NUMBER(S)While performing demanding physical activity for long durations, fluid and electrolyte imbalance is common in athletes, military personnel, and recreational hikers. The military and civilian communities have introduced extensive heat mitigation measures to manage heat strain and reduce the risk of serious exertional heat illnesses (EHI). These heat mitigation measures include fluid and electrolyte replacement guidelines, vigilance, and identifying high-risk individuals. Despite these measures, exercise in hot weather continues to result in preventable injuries and deaths in young, healthy individuals. With existing emphasis on appropriate fluid intake during exercise for the avoidance of dehydration, heat illness, and associated performance decrements, there has been a subsequent increase in reported exertional hyponatremia (HYPO) cases related to excessive water intake, elevated sweating rates, excessive sodium losses in sweat, and inadequate sodium intake in soldiers (1), athletes (2,3,4), and recreational hikers (5,6). The primary purpose of this article is to systemically examine the epidemiological literature of fluid and electrolyte imbalances that occur during physical activity. The secondary purpose of this article is to examine signs and symptoms of HYPO and EHI cases from the literature (1,2,5,7Y26) and the U.S. Army Research Institute of Environmental Medicine (USARIEM) Total Army Injury and Health Outcomes Database (TAIHOD). While it is acknowledged that the populations at risk for HYPO and EHI may differ, reasonable comparisons are made by examining incidence rates to better understand relative magnitude of each condition. It has been reported that these two conditions have several overlapping clinical features, which has led to misdiagnosis in some rare cases. This article is not intended to persuade the reader of the relative importance of either condition.altitude; near infrared spectroscopy; cerebral blood flow; fatigue; muscle oxygenation intact animal to the cellular, subcellular, and molecular levels. It is published 12 times a year (monthly) by the American lymphatics, including experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the publishes original investigations on the physiology of the heart, blood vessels, and AJP -...

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Determinants of maximal oxygen uptake in severe acute hypoxia

Cited by 205 publications

References 45 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

Physiological and Kinanthropometrical Parameters of an Elite Climber. Single case study.

Cerebrovascular Responses To Incremental Exercise During Hypobaric Hypoxia: Effect Of Oxygenation On Maximal Performance

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