Breathing Dry Air Research Articles

Effect of breathing dry warm air on respiratory water loss at rest and during exercise

The changes in respiratory water loss with time, expressed as the mass of water vapour lost per liter BTPS of ventilation (M H 2O ) and expired temperature (T e), used to calculate the relative humidity (ERH), were investigated in ten normal while breathing warm dry air by mouth ( P i H 2 O = 0 kPa; T i = 30° C ); (i) at rest for a period of 35 min; (ii) during 15 min light muscular exercise (50 W); (iii) at increasing work load from 50 to 100 W between the 5th and 10th min of he exercise. The data collected were compared to those obtained in room air conditions ( P i = H 2 O = 0.68–1.3 kPa ) and under conditions with slightly heated inspired air ( T i = 28–30° C ). At rest, when breathing dry warm air M H 2O and ERH fell during the first 15 min, while they recovered their initial values during the last 20 min. In contrast no differences in M H 2O or ERH were ovserved when breathing ambient warm air. At constant and moderate work load for 15 min, the respiratory water loss fell significantly (compared to the 5th min) at the 10th and the 15th min when breathing warm dry air. The added hyperpnea which was obtained by increasing work load from 50 to 100 W between the 5th and 10th min of exercise did not further reduced M H 2O and ERh. The transient fall in M H 2O and ERH, which lasted at least 15 min either at rest or during muscular exercise, suggested that the mechanism underlying humidification of expired gas is overwhelmed by thermal stress, suggested that the mechanism underlying humidification of expired gas is overwhelmed by thermal stress. Since the upper airways mucosa is unable to saturate expired gas, this also suggested that the mucosa is dehydrated and probably hyperosmotic. The progressive recovey in M H 2O and ERh after 15 min of warm dry air breathing at rest, suggest operation of a slow adaptive mechanism.

Comparison of PY 108-068, a New Calcium Antagonist, with Nifedipine in Exercise-Induced Asthma

Several calcium antagonists, each with significantly different chemical structures, have demonstrated variable attenuation of exercise-induced asthma. Quantitative comparisons have been hampered by differences in the intensity of challenge and the severity of the underlying disease between groups of patients. In 12 asthmatic adults with relatively severe exercise-induced asthma, we compared the effect of a new calcium antagonist, PY 108-068, in doses of 75 mg and 150 mg with nifedipine (30 mg) and placebo on resting flow rates and flow rates after exercise. Over a three-week period, each patient completed a four-day, randomized, double-blind Latin-square study. After receiving one of four oral drugs, spirometry was repeated every 30 minutes for two hours, followed by a six-minute treadmill exercise test breathing dry air. The exercise tests were well matched for work rate, ventilation, heart rate, and oxygen uptake. Spirometry was then repeated seven times over the next 30 minutes after exercise. Though both 150 mg of PY 108-068 and nifedipine were associated with mild bronchodilation before exercise, only the latter was significant (p less than 0.05). Exercise-induced asthma (expressed as maximal percent fall in the forced expiratory volume in one second from before baseline) was significantly attenuated only by 150 mg of PY 108-068 compared to placebo (24 +/- 13 vs 40 +/- 16; p less than 0.05). Headache, which occurred in six subjects after nifedipine, five after 150 mg of PY 108-068, one after 75 mg of PY 108-068, and none after placebo, was subjectively more severe after nifedipine. We conclude that in these patients, there was a tendency for mild bronchodilation before exercise with both 150 mg of PY 108-068 and nifedipine, but only the 150-mg dose provided significant protection against exercise-induced asthma two hours after the drug.

Effect of breathing dry air on structure and function of airways

We compared the effect of breathing dry air (0.70 mg H2O/l) with that of breathing room air (8.62 mg H2O/l) in guinea pigs anesthetized with urethane. The data showed that breathing dry air caused a reduction of extravascular water (EVW) in the trachea (P less than 0.01) but not the lung. Structural analysis showed that this water loss occurred from the loose connective tissue of the submucosa. Histamine dose response curves performed on the animals showed that breathing dry air caused an increase in the maximum response (delta max RL) (P less than 0.01) without changing either the dose required to produce 50% of the delta max RL or the ratio of delta max RL to this dose. We conclude that breathing dry air produces an acute reduction of EVW of the loose connective tissue of the airways and an increase in the maximum response to histamine.

Magnitude of the interaction between the bronchomotor effects of sulfur dioxide and those of dry (cold) air.

We studied the interaction between airway drying (cooling) and inhalation of sulfur dioxide (SO2) causing bronchoconstriction in 8 subjects with mild asthma. On 3 separate days, we measured specific airway resistance (SRaw) before and after the subject performed voluntary eucapnic hyperpnea at a constant minute ventilation (30 to 40 L/min) for successive 3-min periods with doubling concentrations of SO2 in dry cold air (-20 degrees C, 0% relative humidity), in dry warm air (22 degrees C, 0% relative humidity), and in partially humidified warm air (22 degrees C, 70% relative humidity). On another day, we measured SRaw before and after the subject performed each of 6 successive 3-min periods of voluntary eucapnic hyperpnea at the same minute ventilation breathing dry cold air without SO2. The concentration of SO2 that caused a 100% increase in SRaw was significantly lower in dry cold air and in dry warm air than it was in humidified warm air. Repeated hyperpnea with dry cold air without SO2 at the same ventilation had no effect on SRaw. We then had the same subjects perform voluntary eucapnic hyperpnea at successively increasing levels of ventilation on 3 different days with dry air alone, dry air with 0.1 ppm SO2, or dry air with 0.25 ppm SO2. The minute ventilation that caused an 80% increase in SRaw was significantly lower for hyperpnea with 0.1 and with 0.25 ppm SO2 than for dry air without SO2, but these differences were small.(ABSTRACT TRUNCATED AT 250 WORDS)

Simplified eucapnic voluntary hyperventilation challenge

A simplified scheme for eucapnic voluntary hyperventilation (EVH) is described that requires only that a source of dry gas containing 5% CO 2, 21% O 2, and 74% N 2 be hyperventilated at 40 L/min or greater. Refrigeration or measurement of end tidal CO 2 is not required. When the ventilation pattern of a standardized treadmill exercise challenge in a group of exercise-sensitive asthmatics breathing dry air was matched according to this EVH procedure, the magnitude of the resultant bronchospasm and the exclusive nature of the postchallenge refractory period were similar, since patients in both cases were still fully responsive to methacholine. It is concluded that such an EVH challenge may be used to reproduce the bronchial heat and water fluxes that occur with exercise challenge as well as the consequential challenge-specific refractoriness that follows.

Refractory period after exercise-induced asthma unexplained by respiratory heat loss.

Fifteen asthmatic children and young adults each exercised for 6 min by cycling on a cycle ergometer while breathing either cold (4.1 degrees C +/- 0.5 SEM) and dry (2.05 mg/L +/- 0.05) air or warm (37.2 degrees C +/- 0.3) fully saturated air. Each subject performed 4 tests arranged in pairs. Test pair A consisted of cold dry exercise followed by another cold dry exercise and test pair B consisted of a warm humid exercise followed by a cold dry exercise. Ventilation, heart rate, and gas exchange were closely matched in all 4 tests in each subject with a mean oxygen consumption of 34.8 +/- 0.8 ml/min/kg. In test pair A, all subjects were rendered refractory by the first cold dry exercise as manifested by a significant attenuation of their exercise-induced asthma (EIA) after the second cold dry test (per cent decrease in FEV1, delta FEV1 = 16 +/- 4 compared with 38 +/- 4). In 3 subjects, the warm humid exercise did not cause EIA and did not render them refractory to the second cold dry exercise. The 12 remaining subjects exhibited a refractory period similar to that shown in test pair A. They did not develop EIA after the warm humid test (delta FEV1 = 1 +/- 2), but after the subsequent cold dry exercise the per cent decrease in FEV1 was 19 +/- 3, similar to that in the second of the 2 cold dry exercise tests. These experiments suggest that in the majority of subjects exercise per se appears to be the cause for refractoriness and not airway cooling or bronchoconstriction.

Respiratory heart exchange with varying temperature and humidity of inspired air.

ARTICLESRespiratory Heat Exchange with Varying Temperature and Humidity of Inspired AirJoseph W. McCutchan, and Craig L. TaylorJoseph W. McCutchan, and Craig L. TaylorPublished Online:01 Aug 1951https://doi.org/10.1152/jappl.1951.4.2.121MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByA two-part model for evaluation of thermal neutrality for sleeping peopleBuilding and Environment, Vol. 132Airway DehydrationChest, Vol. 121, No. 6Changing heat and moisture exchangers after 96 hours rather than after 24 hours: A clinical and microbiological evaluationCritical Care Medicine, Vol. 28, No. 3Relationship between the humidity and temperature of inspired gas and the function of the airway mucosaCritical Care Medicine, Vol. 24, No. 11Respiratory heat loss during work at various ambient temperaturesRespiration Physiology, Vol. 79, No. 2Inhalation of salt aerosol particles—i. Estimation of the temperature and relative humidity of the air in the human upper airwaysJournal of Aerosol Science, Vol. 19, No. 3Thermal sensation of the body as influenced by the thermal microclimate in a face mask31 May 2007 | Ergonomics, Vol. 30, No. 12Effect of breathing dry warm air on respiratory water loss at rest and during exerciseRespiration Physiology, Vol. 67, No. 2Respiratory water loss as a function of ventilatory or environmental factorsRespiration Physiology, Vol. 56, No. 1Respiratory water lossRespiration Physiology, Vol. 39, No. 3Temperature distributions in normal and neoplastic tissues during hyperthermia: lumped parameter analysisJournal of Thermal Biology, Vol. 4, No. 2Humidification of Respired Gas by Nasal Mucosa29 June 2016 | Annals of Otology, Rhinology & Laryngology, Vol. 82, No. 3The effect of environmental temperature on respiratory ventilation in the pigRespiration Physiology, Vol. 8, No. 1A MODEL DESCRIPTION OF THERMAL EXCHANGE FOR THE NUDE MAN IN HOT ENVIRONMENTS25 April 2007 | Ergonomics, Vol. 8, No. 2Heat and water exchange in the respiratory tractThe American Journal of Medicine, Vol. 30, No. 2 More from this issue > Volume 4Issue 2August 1951Pages 121-135 https://doi.org/10.1152/jappl.1951.4.2.121PubMed14888622History Published online 1 August 1951 Published in print 1 August 1951 Metrics

Vital capacity: A study of the effect of breathing dry air: Leas, R. D.: Arch. Int. Med., 1927, xxxix, 475

Vital capacity: A study of the effect of breathing dry air: Leas, R. D.: Arch. Int. Med., 1927, xxxix, 475