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9.L6 Nitric oxide levels in exercise<br />

<strong>The</strong> effects <strong>of</strong> exercise on levels <strong>of</strong> exhaled NO in healthy, athletic adults, and those with<br />

respiratory and/or cardiac disease has been investigated, with a few studies also done in<br />

children. In healthy adults, the measurement <strong>of</strong> exhaled NO with exercise (treadmill or<br />

bicycle) showed a decrease when measuring the absolute levels in single breaths, but there<br />

was a two to three fold increase in NO output taking into account the increased ventilatory<br />

minute volume @ersson, Wiklund et al. 1993; Iwamoto, Pendergast et al. 1994; Trolin, Anden<br />

et al. 1994; Phillips, Giraud et al. 1996; Yasuda, Itoh et al. L997). <strong>The</strong> increased output more<br />

closely related to increased ventilation than increased blood flow @hillips, Giraud et al. 1996)<br />

and significantly correlated with CO2 production (Iwamoto, Pendergast et al. 1994). Two<br />

studies assessed the contribution from nasal or oral exhalations showing that most <strong>of</strong> the NO<br />

coming from the lower airways (Lundberg, Rinder et al. 1997; Yasuda, Itoh et al. 1997) and<br />

from the airway rather than alveolar compartment @ersson, Wiklund et al. 1993). <strong>The</strong> nasal<br />

cavity NO reduced by 47Vo after one minute and 76Vo after five minutes <strong>of</strong> exercise<br />

(Lundberg, Rinder et al. 1997).<br />

<strong>The</strong>re have been many studies done in elite athletes. When compared to those with lower<br />

levels <strong>of</strong> fitness, the athletes had a significantly more linear increase in NO output (Maroun,<br />

Mehta et al. 1995; Chirpaz-Oddou, Favre-Juvin et al. L997; Sheel, Edwards et al. 2000;<br />

Verges, Flore et al. 2005). This output correlated well with oxygen consumption, COz<br />

production, minute ventilation and heart rate (Chirpaz-Oddou, Favre-Juvin et al. 1997).In one<br />

study, athletes that developed exercise induced hypoxemia had lower levels <strong>of</strong> NO compared<br />

to those who did not seen (Kippelen, Caillaud et al. 2N2), but this was not confirmed in<br />

another (Sheel, Edwards et al. 2000). Exercise in cold challenge conditions resulted in lower<br />

levels <strong>of</strong> exhaled NO output being achieved and a slower time to recovery with lower FEVr<br />

(<strong>The</strong>rminarias, Flore et al. 1998; Pendergast, Krasney et al. 1999). <strong>The</strong>se results suggested<br />

that physical conditioning increases expiratory NO output during exercise and this may be due<br />

to an increased vascular and/or epithelial production <strong>of</strong> NO. <strong>The</strong> enhanced vascular NO<br />

production may be the result <strong>of</strong> increased share stress or <strong>of</strong> an up regulation <strong>of</strong> the endothelial<br />

NOS gene expression (Maroun, Mehta et al. 1995).<br />

Can NO predict development <strong>of</strong> exercise induced bronchospasm? Higher baseline levels were<br />

significantly associated with bronchoconstriction and histamine responsiveness in atopic<br />

rather than non-atopic steroid naive healthy conscripts (Rouhos, Ekroos et al. 2005). In 50<br />

consecutive subjects, a ROC curve yielded a value <strong>of</strong> 0.636 when comparing those who did<br />

250

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