We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).

Background-Portable peak flow meters are used in clinical practice for measurement of peak expiratory flow (PEF) at many different altitudes throughout the world. Some PEF meters are affected by gas density. This study was undertaken to establish which type of meter is best for use above sea level and to determine changes in spirometric measurements at altitude. Methods-The variable orifice mini-Wright peak flow meter was compared with the fixed orifice Micro Medical Microplus turbine microspirometer at sea level and at Everest Base Camp (5300 m). Fifty one members of the 1994 British Mount Everest Medical Expedition were studied (age range, 19-55). Results-Mean forced vital capacity (FVC) fell by 5% and PEF rose by 25*5%. However , PEF recorded with the mini-Wright peak flow meter underestimated PEF by 31%, giving readings 6-6% below sea level values. FVC was lowest in the mornings and did not improve significantly with ac-climatisation. Lower PEF values were observed on morning readings and were associated with higher acute mountain sickness scores, although the latter may reflect decreased effort in those with acute mountain sickness. There was no change in forced expiratory volume in one second (FEVy) at altitude when measured with the turbine microspirometer. Conclusions-The cause of the fall in FVC at 5300 m is unknown but may be attributed to changes in lung blood volume, interstitial lung oedema, or early airways closure. Variable orifice peak flow meters grossly underestimate PEF at altitude and fixed orifice devices are therefore preferable where accurate PEF measurements are required above sea level. Portable peak flow meters are widely used in clinical practice for measurement of peak ex-piratory flow (PEF) at many different altitudes throughout the world. At altitude the decrease in air density mechanically causes variable orifice meters, such as the mini-Wright, to underestimate flow."l An under-reading of 26% at a simulated altitude of 5455m has been demonstrated in hypobaric chamber experiments .3 However, fixed orifice spirometers such as the Micro Medical Microplus turbine spirometer have recently been evaluated in a hypobaric chamber and are unaffected by barometric pressure.4 In the same way that decreased air density causes variable orifice meters to under-read, by decreasing resistance to respiratory gas flow5 it causes true PEF to rise at altitude.36 Forced vital capacity (FVC) falls with ascent to al-titude"9 and a decrease of 3% at 5500 m simulated altitude has been recorded.6 We compared the mini-Wright peak flow meter with the a hand held turbine spirometer to assess the performance of the two meters in a field study at altitude. FVC, PEF, and forced expiratory volume in one second (FEV1) were documented using a turbine spirometer, and PEF using the mini-Wright peak flow meter, in a large study of members of the 1994 British Mount Everest Medical Expedition. Methods After obtaining informed consent, spirometric data were collected from 51 members of the 1994 British Mount Everest Medic...

The aims of the present study were to determine the changes in forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and peak expiratory flow (PEF), during an ascent to 5,300 m in the Nepalese Himalayas, and to correlate the changes with arterial oxygen saturation measured by pulse oximetry (SpO2) and symptoms of acute mountain sickness (AMS). Forty-six subjects were studied twice daily during an ascent from 2,800 m (mean barometric pressure 550.6 mmHg) to 5,300 m (mean barometric pressure 404.3 mmHg) during a period of between 10 and 16 days. Measurements of FVC, FEV1, PEF, SpO2, and AMS were recorded. AMS was assessed using a standardized scoring system. FVC fell with altitude, by a mean of 4% from sea level values [95% confidence intervals (CI) 0.9% to 7.4%] at 2,800 m, and 8.6% (95% CI 5.8 to 11.4%) at 5,300 m. FEV1 did not change with increasing altitude. PEF increased with altitude by a mean of 8.9% (95% CI 2.7 to 15.1%) at 2,800 m, and 16% (95% CI 9 to 23%) at 5,300 m. These changes were not significantly related to SpO2 or AMS scores. These results confirm a progressive fall in FVC and increase in PEF with increasing hypobaric hypoxia while FEV1 remains unchanged. The increase in PEF is less than would be predicted from the change in gas density. The fall in FVC may be due to reduced inspiratory force producing a reduction in total lung capacity; subclinical pulmonary edema; an increase in pulmonary blood volume, or changes in airway closure. The absence of a correlation between the spirometric changes and SpO2 or AMS may simply reflect that these measurements of pulmonary function are not sufficiently sensitive indicators of altitude-related disease. Further studies are required to clarify the effects of hypobaric hypoxia on lung volumes and flows in an attempt to obtain a unifying explanation for these changes.

Mason, Nicholas P., Merete Petersen, Christian Mé lot, Bakyt Imanow, Olga Matveykine, Marie-Therese Gautier, Akpay Sarybaev, Almaz Aldashev, Mirsaid M. Mirrakhimov, Brian H. Brown, Andrew D. Leathard, and Robert Naeije. Serial changes in nasal potential difference and lung electrical impedance tomography at high altitude. J Appl Physiol 94: 2043-2050, 2003. First published December 6, 2002 10.1152 10. /japplphysiol.00777.2002 work suggests that treatment with inhaled ␤2-agonists reduces the incidence of high-altitude pulmonary edema in susceptible subjects by increasing respiratory epithelial sodium transport. We estimated respiratory epithelial ion transport by transepithelial nasal potential difference (NPD) measurements in 20 normal male subjects before, during, and after a stay at 3,800 m. NPD hyperpolarized on ascent to 3,800 m (P Ͻ 0.05), but the change in potential difference with superperfusion of amiloride or isoprenaline was unaffected. Vital capacity (VC) fell on ascent to 3,800 m (P Ͻ 0.05), as did the normalized change in electrical impedance (NCI) measured over the right lung parenchyma (P Ͻ 0.05) suggestive of an increase in extravascular lung water. EchoDoppler-estimated pulmonary artery pressure increases were insufficient to cause clinical pulmonary edema. There was a positive correlation between VC and NCI (R 2 ϭ 0.633) and between NPD and both VC and NCI (R 2 ϭ 0.267 and 0.418). These changes suggest that altered respiratory epithelial ion transport might play a role in the development of subclinical pulmonary edema at high altitude in normal subjects. pulmonary edema; hypobaric hypoxia ALTHOUGH ONLY A MINORITY OF those who go to high altitude develop the potentially fatal condition of highaltitude pulmonary edema (HAPE), there is increasing evidence that the majority of people ascending to altitude may develop subclinical pulmonary edema (9). Forced vital capacity (FVC) falls on ascent to high altitude and is thought to be primarily due to subclinical pulmonary edema (32). The control of pulmonary extravascular lung water (EVLW) has traditionally been attributed to the interplay of Starling forces, with the pulmonary capillary pressure attributed the major regulatory role. It is now realized that sodium transport across the respiratory epithelium plays an important role in the removal of alveolar water (34) and that an intact epithelial barrier is necessary for the resolution of alveolar edema (35). Hypoxia reduces epithelial sodium transport in cultured rat alveolar epithelial monolayers (29) and decreases the expression of alveolar epithelial ion transport proteins (8). In addition, treatment of HAPE-susceptible individuals with inhaled ␤ 2 -agonists, which are known to increase transepithelial sodium transport, decreases pulmonary edema without any effect on pulmonary hemodynamics (44).Measurement of alveolar ion transport in vivo in human subjects is not feasible; however, measurement of the potential difference (PD) generated by ion transport in the nasal mucosa can be used as a marker...