Arterial hypoxemia and performance during intense exercise

Koskolou, Maria; McKenzie, Donald C.

doi:10.1007/bf00599246

Cited by 56 publications

(30 citation statements)

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“…These authors concluded that maximal performance was impaired at a % SaO 2 level of 87%, but not under a milder desaturation level of 90%. In our study the mean SaO 2 of the hypoxemic rowers was a little higher (88.6%) than the lower level (87%) set by Koskolou and McKenzie (1994) in which decreases in performance was found, a fact that may in part explain this difference in performance between the two studies. Perhaps, the potential adverse effects of hypoxemia on exercise performance would be measurable in conditions of more severe O 2 arterial desaturation.…”

Section: Comparison Of Blood Redox Status Between the Normoxemic And contrasting

confidence: 62%

“…Our finding on exercise performance was not in agreement with previous reports that arterial hypoxemia induced by an artificial reduction in the inspired O 2 fraction during maximal cycle test to exhaustion impaired the total work output in well-trained male cyclists (Koskolou and McKenzie 1994). These authors concluded that maximal performance was impaired at a % SaO 2 level of 87%, but not under a milder desaturation level of 90%.…”

Section: Comparison Of Blood Redox Status Between the Normoxemic And contrasting

confidence: 58%

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The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

et al. 2011

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Exercise-induced arterial hypoxemia (EIAH), characterized by decline in arterial oxyhemoglobin saturation (SaO(2)), is a common phenomenon in endurance athletes. Acute intensive exercise is associated with the generation of reactive species that may result in redox status disturbances and oxidation of cell macromolecules. The purpose of the present study was to investigate whether EIAH augments oxidative stress as determined in blood plasma and erythrocytes in well-trained male rowers after a 2,000-m rowing ergometer race. Initially, athletes were assigned into either the normoxemic (n = 9, SaO(2) >92%, [Formula: see text]: 62.0 ± 1.9 ml kg(-1) min(-1)) or hypoxemic (n = 12, SaO(2) <92%, [Formula: see text]: 60.5 ± 2.2 ml kg(-1 )min(-1), mean ± SEM) group, following an incremental [Formula: see text] test on a wind resistance braked rowing ergometer. On a separate day the rowers performed a 2,000-m all-out effort on the same rowing ergometer. Following an overnight fast, blood samples were drawn from an antecubital vein before and immediately after the termination of the 2,000-m all-out effort and analyzed for selective oxidative stress markers. In both the normoxemic (SaO(2): 94.1 ± 0.9%) and hypoxemic (SaO(2): 88.6 ± 2.4%) rowers similar and significant exercise increase in serum thiobarbituric acid-reactive substances, protein carbonyls, catalase and total antioxidant capacity concentration were observed post-2,000 m all-out effort. Exercise significantly increased the oxidized glutathione concentration and decreased the ratio of reduced (GSH)-to-oxidized (GSSG) glutathione in the normoxemic group only, whereas the reduced form of glutathione remained unaffected in either groups. The increased oxidation of GSH to GSSG in erythrocytes of normoxemic individuals suggest that erythrocyte redox status may be affected by the oxygen saturation degree of hemoglobin. Our findings indicate that exercise-induced hypoxemia did not further affect the increased blood oxidative damage of lipids and proteins observed after a 2,000-m rowing ergometer race in highly-trained male rowers. The present data do not support any potential link between exercise-induced hypoxemia, oxidative stress increase and exercise performance.

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Section: Comparison Of Blood Redox Status Between the Normoxemic And contrasting

confidence: 62%

Section: Comparison Of Blood Redox Status Between the Normoxemic And contrasting

confidence: 58%

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

et al. 2011

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“…EIH has been defined as % SaO # 91 % [24], and the development of hypoxaemia during severe exercise has been shown to have physiological limitations on work performance [9]. We hypothesized that, if the delivery of oxygen was being compromised by episodes of hypoxaemia during exercise, a dose-dependent physiological stimulus for adaptation of the oxygen carrying system may have been generated.…”

Section: Discussionmentioning

confidence: 99%

“…Mild hypoxaemia has been reported to occur during intense exercise in some well-trained individuals [8], and the degree of hypoxaemia can be exacerbated by decreasing the partial pressure of oxygen in inspired air [9,10]. The development of hypoxaemia has been shown recently to be a requirement for stimulation of Epo with exercise [11], which may account for some of the variability of the post-exercise Epo responses reported in the literature.…”

Section: Introductionmentioning

confidence: 96%

Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

ROBERTS¹,

SMITH²,

Donnelly³

et al. 2000

Clinical Science

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This study examined exercise-induced hypoxaemia (EIH) and plasma volume contraction as modulators of serum erythropoietin (Epo) production. Five athletes cycled for 3 min at supra-maximal power outputs, at each of two different elevations (1,000 m and 2,100 m). Five subjects were exposed to normobaric hypoxia (F(I)O(2)=0.159), seven subjects underwent plasmapheresis to reduce plasma volume and eight subjects were time controls for Epo levels. Oxyhaemoglobin saturation was significantly reduced during exercise and during normobaric hypoxia. The time period of haemoglobin oxygen saturation <91% was 24+/-29 s (mean+/-S.D., n=5) for exercise at 1000 m, 136+/-77 s (mean+/-S.D., n=5) for exercise at 2100 m and 178+/-255 s (mean+/-S.D., n=5) with resting hypoxic exposure. However, significantly increased serum Epo levels were observed only following exercise (24+/-3%; mean+/-S.D., n=5 at 1,000 m and 36+/-5%; mean+/-S.D., n=5 at 2,100 m). Volume contraction also resulted in increased serum Epo (35+/-6%; mean+/-S.D., n=7) in spite of a significant rise in haematocrit of 2.2%. Despite similar degrees of arterial desaturation, only the hypoxaemia induced by exercise was associated with an increase in serum Epo. This finding indicates that other factors, in addition to hypoxaemia, are important in modulating the production of Epo in response to exercise. Volume depletion in the absence of exercise resulted in increases in Epo levels that were comparable with those observed in response to exercise. The paradoxical responses of the increased haematocrit and the increase in Epo in subjects undergoing plasmapheresis suggests that plasma volume may also modulate the production of Epo.

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“…In fact, V O 2 appears to decrease by 2 % for each 1 % decrease of SpO 2 , at least when SpO 2 falls below 95 % [ 13 ] . Other studies have shown that even when V O 2max is maintained during exercise, a reduction of the SpO 2 reduces work capacity [ 18 ] . However, in our study, this was not the case for the white runners, who were able to outperform the black runners despite their signifi cantly lower SpO 2 values under hypoxic conditions ( • ▶ Fig.…”

mentioning

confidence: 99%

Greater Performance Impairment of Black Runners than White Runners when Running in Hypoxia

et al. 2014

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This study aimed to compare the response of performance-matched black and white runners during maximal and sub-maximal running in normoxic and hypoxic conditions. 14 well-trained runners (8 black, 6 white) performed 2 incremental maximal exercise tests and 2 fatigue resistance tests at 21% O2 (normoxia) or 14% O2 (hypoxia). Respiratory parameters, heart rate (HR), lactate concentration ([La(-)]) as well as arterial saturation (SpO2) were measured. Enzyme activities and myosin heavy chain content (MHC) were also measured. White runners reached a significantly greater peak treadmill speed and a higher HRmax than black runners in hypoxia (p<0.05). Additionally, White runners achieved a greater time to fatigue than black runners (p<0.05), with black runners displaying a greater decline in performance in hypoxia compared to normoxia (20.3% vs. 13.4%, black vs. white, respectively). However, black runners presented lower [La(-)] and higher SpO2 than white runners in hypoxia (p<0.05). Black runners had a higher proportion of MHC IIa and higher lactate dehydrogenase activity (p<0.05). The greater performance impairment observed in black runners in hypoxia suggests a greater performance sensitivity to this condition, despite the maintenance of physiological variables such as SpO2 and [La (-) ] within a smaller range than white runners.

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Arterial hypoxemia and performance during intense exercise

Cited by 56 publications

References 77 publications

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

Greater Performance Impairment of Black Runners than White Runners when Running in Hypoxia

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