Exercise-induced oxyhemoglobin desaturation and pulmonary diffusing capacity during high-intensity exercise

Turcotte, R.; Kiteala, Lori; Marcotte, Jacques-Édouard; Perrault, Hélène

doi:10.1007/s004210050183

Cited by 16 publications

(19 citation statements)

References 35 publications

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“…Powers et al (1992) have collected data between 10% and 100% O 2max and while they focussed their analysis on results obtained at O 2max , inspection of their data suggests that in many subjects a signi®cant reduction appeared at intensities as low as approximately 30% O 2max which is in agreement with the results from the present study. In searching for an explanation for the progressive hypoxaemia during incremental exercise, consideration must be given to mechanisms which have been suggested to change with intensity, such as inadequate hyperventilation (Dempsey et al 1984;Miyachi and Tabata 1992;Harms and Stager 1995;Turcotte et al 1997;Gavin et al 1998), an oxygen diusion limitation (Hammond et al 1986) and ventilation-perfusion ( A a ) mismatch Hopkins et al 1994).…”

Section: Discussionmentioning

confidence: 99%

“…While several subsequent studies in endurance athletes have reported a signi®cant fall in arterial oxyhaemoglobin saturation (S a O 2 ) with exercise intensities at or close to maximal oxygen uptake ( O 2max ; Williams et al 1986;Powers et al 1992;Harms and Stager 1995) the mechanism of EIH remains uncertain. Several hypotheses have been suggested including intra-and extra-pulmonary shunts (Dempsey et al 1984;Powers et al 1992), inadequate hyperventilation (Dempsey et al 1984;Powers et al 1984;Miyachi and Tabata 1992;Harms and Stager 1995;Turcotte et al 1997; Gavin et al 1998), an oxygen diusion limitation based on low pulmonary capillary blood transit time or interstitial oedema (Dempsey et al 1982;Wagner et al 1986;Schaartzik et al 1992) and ventilation-perfusion inequalities (Torre-Bueno et al 1985;Hammond et al 1986;Wagner et al 1986;Schaartzik et al 1992;Hopkins and McKenzie 1993;Hopkins et al 1994).…”

Section: Introductionmentioning

confidence: 99%

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Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Rice

Scroop

Gore³

et al. 1999

European Journal of Applied Physiology

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A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Rice

Scroop

Gore³

et al. 1999

European Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…Thirdly, the increased airflow velocity carries pollutants deeper into the respiratory tract. Furthermore, pulmonary diffusion capacity has been shown to increase with exercise [3][4][5][6] ; it may therefore be postulated that the diVusion of pollutant gases increases with exercise. For several days after strenuous exercise, nasal mucociliary clearance has been shown to be impaired in long distance runners, 7 and this is possibly attributable to exposure to air pollution, as stressed by Atkinson.…”

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confidence: 99%

Exercise and outdoor ambient air pollution

Carlisle

Sharp²

2001

Br J Sports Med

188

150

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Objectives-To establish by literature survey: (a) levels at which air pollutants are considered damaging to human health and to exercisers in particular; (b) the current ambient levels experienced in the United Kingdom; (c) whether athletes are especially at risk. Methods-Six major urban air pollutants were examined: carbon monoxide (CO); nitrogen oxides (NO X ); ozone (O 3 ); particulate matter (PM 10 ); sulphur dioxide (SO 2 ); volatile organic compounds (VOCs). Results-CO is detrimental to athletic performance. NO 2 is of concern to human health, but outdoor levels are low. O 3 poses a potentially serious risk to exercising athletes. Decrements in lung function result from exposure, and there is evidence that athletic performance may be aVected. Detrimental eVects may occur at low ambient levels, but there is no scientific consensus on this matter. PM 10 is causing concern in the scientific community. Blood lead accumulation during exercise indicates that personal exposure to toxic compounds associated with PM 10 may be magnified. Generally, outdoor ambient levels of SO 2 are too low to cause a problem to the athlete, except the asthmatic athlete. The few studies on exposure of exercisers to VOCs are reviewed.Conclusions-Athletes and exercisers should avoid exercising by the road side even though levels of the more noxious air pollutants have been controlled in the United Kingdom. O 3 is particularly damaging to athletes; it reaches its highest concentrations on hot bright days in rural areas. (Br J Sports Med 2001;35:214-222)

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“…It does appear, though, that a large portion of male master athletes exhibit exercise‐induced arterial hypoxaemia (Anselme et al, 1994; Prefaut et al, 1994, 1997; Aguilaniu et al, 1995, 1998; Mucci et al, 1998; McClaran et al, 1995). In summary, exercise‐induced hypoxaemia has been reported to have a prevalence of about 50% (Powers et al, 1988), with athletes divided into those who desaturate and those who do not (Turcotte et al, 1997; Chapman et al, 1999; Sheel et al, 2000). There appears to be no difference in height, weight and lung volume between these two groups (Durand et al, 2000).…”

Section: Exercise‐induced Arterial Hypoxaemiamentioning

confidence: 99%

Arterial desaturation during exercise in man: implication for O₂ uptake and work capacity

Nielsen

2003

Scandinavian Med Sci Sports

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Exercise-induced arterial hypoxaemia is defined as a reduction in the arterial O2 pressure (PaO2) by more than 1 kPa and/or a haemoglobin O2 saturation (SaO2) below 95%. With blood gas analyses ideally reported at the actual body temperature, desaturation is a consistent finding during maximal ergometer rowing. Arterial desaturation is most pronounced at the end of a maximal exercise bout, whereas the reduction in PaO2 is established from the onset of exercise. Exercise-induced arterial hypoxaemia is multifactorial. The ability to maintain a high alveolar O2 pressure (PAO2) is critical for blood oxygenation and this appears to be difficult in large individuals. A large lung capacity and, in turn, diffusion capacity seem to protect PaO2. A widening of the PAO2-PaO2 difference does indicate that a diffusion limitation, a ventilation-perfusion mismatch and/or a shunt influence the transport of O2 from alveoli to the pulmonary capillaries. An inspired O2 fraction of 0.30 reduces the widened PAO2-PaO2 difference by 75% and prevents a reduction of PaO2 and SaO2. With a marked increase in cardiac output, diffusion limitation combined with a fast transit time dominates the O2 transport problem. Furthermore, a postexercise reduction in pulmonary diffusion capacity suggests that the alveolo-capillary membrane is affected. An antioxidant attenuates oxidative burst by neutrophilic granulocytes, but it does not affect PaO2, SaO2 or O2 uptake (VO2), and the ventilatory response to maximal exercise also remains the same. It is proposed, though, that increased concentration of certain cytokines correlates to exercise-induced hypoxaemia as cytokines stimulate mast cells and basophilic granulocytes to degranulate histamine. The basophil count increases during maximal rowing. Equally, histamine release is associated with hypoxaemia and when the release of histamine is prevented, the reduction in PaO2 is attenuated. During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2. When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation. It is proposed that other organs benefit from enhanced O2 availability, and especially the brain appears to increase its oxygenation during maximal exercise with hyperoxia.

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Exercise-induced oxyhemoglobin desaturation and pulmonary diffusing capacity during high-intensity exercise

Cited by 16 publications

References 35 publications

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Exercise and outdoor ambient air pollution

Arterial desaturation during exercise in man: implication for O₂ uptake and work capacity

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Exercise-induced oxyhemoglobin desaturation and pulmonary diffusing capacity during high-intensity exercise

Cited by 16 publications

References 35 publications

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Exercise and outdoor ambient air pollution

Arterial desaturation during exercise in man: implication for O2 uptake and work capacity

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Arterial desaturation during exercise in man: implication for O₂ uptake and work capacity