Journal of applied physiology
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Randomized Controlled Trial
Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes.
Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4°C, 37% relative humidity) and warm humid (25°C, 94% relative humidity) air on separate days. ⋯ Bronchoconstriction occurred in eight athletes in the cold dry environment and was completely blocked by inhalation of warm humid air [maximal fall in forced expiratory volume in 1 s = 18.1 ± 2.1% (SD) in cold dry air and 1.7 ± 0.8% in warm humid air, P < 0.01]. Exercise caused an increase in urinary excretion of CC16 in all subjects (P < 0.001), but this rise in CC16 was blunted following inhalation of warm humid air [median CC16 increase pre- to postchallenge = 1.91 and 0.35 ng/μmol in cold dry and warm humid air, respectively, in athletes with EIB (P = 0.017) and 1.68 and 0.48 ng/μmol in cold dry and warm humid air, respectively, in athletes without EIB (P = 0.002)]. The results indicate that exercise hyperpnea transiently disrupts the airway epithelium of all athletes (not only in those with EIB) and that inhalation of warm moist air limits airway epithelial cell perturbation and injury.
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Higher oscillations of cerebral blood velocity and arterial pressure (AP) induced by breathing with inspiratory resistance are associated with delayed onset of symptoms and increased tolerance to central hypovolemia. We tested the hypothesis that subjects with high tolerance (HT) to central hypovolemia would display higher endogenous oscillations of cerebral blood velocity and AP at presyncope compared with subjects with low tolerance (LT). One-hundred thirty-five subjects were exposed to progressive lower body negative pressure (LBNP) until the presence of presyncopal symptoms. ⋯ However, low frequency (0.04-0.15 Hz) oscillations of mean MCAv and MAP were higher at presyncope in HT subjects compared with LT subjects (MCAv: HT, 7.2 ± 0.7 vs. LT, 5.3 ± 0.6 (cm/s)(2), P = 0.075; MAP: HT, 15.3 ± 1.4 vs. 7.9 ± 1.2 mmHg(2), P < 0.001). Consistent with our previous findings using inspiratory resistance, high oscillations of mean MCAv and MAP are associated with HT to central hypovolemia.
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Intermittent hypoxia (IH) resulting from sleep apnea can lead to pulmonary hypertension. IH causes oxidative stress that may limit bioavailability of the endothelium-derived vasodilator nitric oxide (NO) and thus contribute to this hypertensive response. We therefore hypothesized that increased vascular superoxide anion (O(2)(-)) generation reduces NO-dependent pulmonary vasodilation following IH. ⋯ Finally, both H-IH and E-IH increased arterial O(2)(-) levels, although this response was more pronounced following H-IH, and H-IH exposure resulted in greater protein tyrosine nitration indicative of increased NO scavenging by O(2)(-). We conclude that IH increases pulmonary VSM sensitivity to NO and cGMP. Furthermore, endogenous O(2)(-) limits NO-dependent vasodilation following H-IH through an apparent reduction in bioavailable NO.
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Deep inspirations modulate airway caliber and airway closure and their effects are impaired in asthma. The association between asthma and obesity raises the question whether the deep inspiration (DI) effect is also impaired in the latter condition. We assessed the DI effects in obese and nonobese nonasthmatics. ⋯ Given that DI has bronchodilatory and bronchoprotective effects, we further assessed these components separately. In the obese subjects, DI prior to Mch enhanced Mch-induced bronchoconstriction, but DI after Mch resulted in bronchodilation that was of similar magnitude as in the nonobese. We conclude that obesity is characterized by increased Mch responsiveness, predominantly of the small airways, due to a DI effect that renders the airways more sensitive to the stimulus.
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Cardiac output measurement from arterial pressure waveforms presumes a defined relationship between the arterial pulse pressure (PP), vascular compliance (C), and resistance (R). Cardiac output estimates degrade if these assumptions are incorrect. We hypothesized that sepsis would differentially alter central and peripheral vasomotor tone, decoupling the usual pressure wave propagation from central to peripheral sites. ⋯ However, aortic PP exceeded both femoral and radial arterial PP. Although Z, R, and C derived from aortic and radial pressure and aortic flow were similar during baseline, Z increases and C decreases when derived from aortic pressure whereas Z decreases and C increases when derived from radial pressure, while R decreased similarly with both pressure signals. This central-to-peripheral vascular tone decoupling, as quantified by the difference in calculated Z and C from aortic and radial artery pressure, may explain the decreasing precision of peripheral arterial pressure profile algorithms in assessing cardiac output in septic shock patients and suggests that different algorithms taking this vascular decoupling into account may be necessary to improve their precision in this patient population.