Exhaled nitric oxide after high-intensity exercise at 2800 m altitude.

BACKGROUND: Nitric oxide (NO) concentration in exhaled gas is a marker of some inflammatory processes in the lung, and endogenous NO plays a role in the physiological responses to exercise and altitude. The aim of this study was to compare changes in exhaled NO concentration 5-60 mins after high-intensity exercise at 2800 m and at 180 m altitude. METHODS: Twenty trained healthy volunteers (12 men), aged 19-28 years, were included in this open, crossover study. Subjects performed two exercise tests at different altitudes, 2800 m and 180 m, in a randomized order. The fraction of NO in exhaled gas (FE(NO)) was measured 5 mins before and 5-60 mins after 8 mins of running on a treadmill at a heart rate (HR) of 90% of peak HR. Peak HR was assessed during a pretest at 180 m. Ambient temperature was 20.1°C (SD = 1.2) and relative humidity 40.2% (SD = 3.2). FE(NO) measurements were corrected for altitude gas density effects and converted to partial pressure of NO (PE(NOcorr)). RESULTS: PE(NOcorr) was reduced from 1.47 (1.21, 1.73) millipascal (mPa) at baseline to 1.11 (0.87, 1.34) mPa 5 mins after exercise at 2800 m and from 1.54 (1.24, 1.84) to 1.04 (0.87, 1.22) mPa 5 mins after exercise at 180 m. There was no difference in PE(NOcorr) between exercise at 2800 m and 180 m, and PE(NOcorr) was normalized within 20 mins. CONCLUSIONS: Exercise at 2800 m induces a similar acute reduction in exhaled nitric oxide concentration as compared with 180 m in healthy subjects.

Exhaled nitric oxide and lung function after moderate normobaric hyperoxic exposure.

INTRODUCTION: Pulmonary oxygen toxicity is associated with inflammatory responses in the airways and alveoli. The purpose of this study was to investigate whether the changes in exhaled nitric oxide (FE(NO)) after exposure to normobaric hyperoxia (NBO), 100% oxygen (O2) at 1 atmosphere absolute (atm abs) for 90 minutes, are associated with changes in lung function. METHODS: Eighteen healthy non-smoking subjects were exposed to NBO breathing 100% oxygen and to breathing ambient air, both for 90 minutes on separate days and in random order. Dynamic and static lung volumes, maximal expiratory flow rates, distribution of ventilation including closing volume and slope of phase III of the nitrogen washout curve (delta N2), diffusion capacity (D(L)CO) and FE(NO) were measured before and after the exposures. RESULTS: The mean reduction in FE(NO) was 20% (SD = 20) after the NBO exposure (p < 0.001). Static and dynamic lung volumes, maximal expiratory flow rates, DLCO and distribution of ventilation were unchanged. No association was found between the changes in the lung function variables and the change in FE(NO). DISCUSSION: Unchanged indices of distribution of ventilation and maximal expiratory flow rates indicate no small airways' dysfunction, and unchanged DLCO suggests preserved gas transfer in the lung despite a significant reduction in FE(NO). FE(NO) might be an index of oxygen exposure, but further studies over a wide range of oxygen exposures are necessary to establish the role of FE(NO) as a marker of pulmonary oxygen toxicity.

Bronchial nitric oxide flux and alveolar nitric oxide concentration after exposure to hyperoxia.

BACKGROUND: The fraction of nitric oxide in exhaled gas (FE(NO)) is reduced by 30-70% after exposure to partial pressures of oxygen (Po2) of 200-240 kPa for 90 min. The purpose of this study was to partition FE(NO) into its flow-independent alveolar and bronchial components. A reduced bronchial NO flux (JawNO) is associated with induced bronchoconstriction, while increased alveolar NO concentration (C(A)NO) is associated with increased alveolar dead space. METHODS: There were 12 patients undergoing hyperbaric oxygen (HBO) therapy for 90 min at a Po2 of 240 kPa and 20 healthy subjects exposed to normobaric hyperoxia (NBO) breathing 100% oxygen for 90 min who were compared to a control group of 6 subjects breathing ambient air. FE(NO) was measured at flow rates from 30 to 250 ml x s(-1) before and after the exposures and the Högman Märilainen algorithm was used to calculate JawNO and C(A)NO. RESULTS: FE(NO) at an expiratory flow rate of 50 ml x s(-1) was reduced from 17.6 +/- 8.3 to 12.3 +/- 6.3 ppb after HBO exposure and from 17.8 +/- 6.2 to 13.3 +/- 5.2 ppb after NBO exposure. There was a significant reduction in JawNO, but unchanged C(A)NO. There were no changes in the control experiment. DISCUSSION: The reduction in FE(NO) after exposure to normobaric and hyperbaric hyperoxia appears to be predominantly an airway effect. An unchanged and low C(A)NO indicate preserved integrity of the gas exchange units without increased alveolar dead space at rest.

Added mass in human swimmers: age and gender differences.

In unstationary swimming (changing velocity), some of the water around the swimmer is set in motion. This can be thought of as an added mass (M(a)) of water. The purpose of this study was to find added mass on human swimmers and investigate the effect of shape and body size. Thirty subjects were connected to a 2.8m long bar with handles, attached with springs (stiffness k = 318 N/m) and a force cell. By oscillating this system vertically and registering the period of oscillations it was possible to find the added mass of the swimmer, given the known masses of the bar and swimmer. Relative added mass (M(a)%) for boys, women and men were, respectively, 26.8 +/- 2.9%, 23.6 +/- 1.6% and 26.8 +/- 2.3% of the subjects total mass. This study reported significantly lower added mass (p < 0.001) and relative added mass (p < 0.002) for women compared to men, which indicate that the possible body shape differences between genders may be an important factor for determining added mass. Boys had significantly lower (p < 0.001) added mass than men. When added mass was scaled for body size there were no significant differences (p = 0.996) between boys and men, which indicated that body size is an important factor that influences added mass. The added mass in this study seems to be lower and within a smaller range than previously reported (Klauck, 1999; Eik et al., 2008). It is concluded that the added mass in human swimmers, in extended gliding position, is approximately 1/4 of the subjects' body mass.