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    <title>Ergebnis für Versionen - 4003654</title>
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      <title>Nachweis für eine unzulängliche Hyperventilation, die bei submaximaler Belastung bei allen hochtrainierten Ausdauersportlern eine arterielle Hypoxämie bewirkt</title>
      <pubDate>Sat, 01 Jan 2000 04:40:25 +0100</pubDate>
      <link>https://sponet.de/sponet/Record/3031608</link>
      <guid>https://sponet.de/sponet/Record/3031608</guid>
      <author>Durand, F.</author>
      <author>Mucci, P.</author>
      <author>Prefaut, C.</author>
      <dc:format>Artikel</dc:format>
      <dc:subject>Ausdauer</dc:subject>
      <dc:subject>Training</dc:subject>
      <dc:subject>Hypoxie</dc:subject>
      <dc:subject>Atmung</dc:subject>
      <dc:subject>Ventilationsschwelle</dc:subject>
      <dc:format>Artikel</dc:format>
      <dc:creator>Durand, F.</dc:creator>
      <dc:creator>Mucci, P.</dc:creator>
      <dc:creator>Prefaut, C.</dc:creator>
      <content:encoded><![CDATA[In einer Untersuchung nachgewiesen, dass hochtrainierte Ausdauersportler, die keine belastungsinduzierte Hypoxämie (EIH) entwickeln, die gleiche ausgeprägte Hypoxie bei submaximaler Belastung wie Sportler mit EIH aufweisen. Das verweist darauf, dass das gleiche Phänomen - eine Mangel an ausgleichender Hyperpnoe durch Ausdauertraining - im ersten Teil der EIH auftritt. Bei maximaler Belastung kann jedoch ein ausgleichender Mechanismus bei den Sportlern ohne EIH postuliert werden, da die submaximale Hypoxämie rückläufig war. Im Gegenstz dazu zeigten Sportlern mit EIH nach der zweiten Ventilationsschwelle ein nichtventilatorisches Phänomen, das vom Trainingsumfang abhängig zu sein scheint.]]></content:encoded>
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      <title>Nachweis für eine unadäquate Hyperventilation, die arterielle Hypoxie bei submaximaler Belastung bei hochtrainierten Ausdauersportlern bewirkt</title>
      <pubDate>Sat, 01 Jan 2000 04:40:25 +0100</pubDate>
      <link>https://sponet.de/sponet/Record/4003654</link>
      <guid>https://sponet.de/sponet/Record/4003654</guid>
      <author>Durand, F.</author>
      <author>Mucci, P.</author>
      <author>Prefaut, C.</author>
      <dc:format>Artikel</dc:format>
      <dc:subject>Ventilationsschwelle</dc:subject>
      <dc:subject>Training</dc:subject>
      <dc:subject>Hypoxie</dc:subject>
      <dc:subject>Gasstoffwechsel</dc:subject>
      <dc:subject>Blut</dc:subject>
      <dc:subject>Ausdauer</dc:subject>
      <dc:subject>Atmung</dc:subject>
      <dc:format>Artikel</dc:format>
      <dc:creator>Durand, F.</dc:creator>
      <dc:creator>Mucci, P.</dc:creator>
      <dc:creator>Prefaut, C.</dc:creator>
      <content:encoded><![CDATA[Purpose: The majority of highly trained endurance athletes with a maximal oxygen uptake greater than 60 mL·min-1·kg-1 develop exercise-induced hypoxemia (EIH). Yet some of them apparently do not. The pathophysiology of EIH seems to be multifactorial, and one explanatory hypothesis is a relative hypoventilation. Nevertheless, conflicting results have been reported concerning its contribution to EIH. The aim of this study was to compare the cardiorespiratory responses to maximal exercise of highly trained endurance athletes demonstrating the same aerobic capacity without EIH (N athletes) and with EIH (H athletes). Methods: Ten N athletes and twelve H athletes performed an incremental exercise test. Measurements of arterial blood gases and cardiorespiratory parameters were performed at rest and during exercise. Results: All athletes presented a significant decrease in PaO2 (P < 0.05) from rest up to 80% V(dot)O2max associated with an increase in PaCO2, both findings consistent with a relative hypoventilation. Then the H athletes, who had a greater training volume per week and a higher second ventilatory threshold than the N athletes (respectively, 17 ± 1.1 vs 13.1 ± 0.7 h·wk-1; 91.8 ± 1.7 vs 86.1 ± 1.8% V(dot)O2max), presented a continuous PaO2 decrease up to V(dot)O2max. This was associated with a widening (Ai-a)DO2. Conclusion: This study showed that a relative hypoventilation, probably induced by a high level of endurance training, induced hypoxemia in all athletes. However, a nonventilatory mechanism, perhaps related to the volume of training, seemed to affect gas exchanges beyond the second ventilatory threshold in the H athletes, thereby enhancing EIH.]]></content:encoded>
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