Exercise reduces airway sodium ion reabsorption in cystic fibrosis but not in exercise asthma.

When ventilating large volumes of air during exercise, airway fluid secretion is essential for airway function. Since these are impaired in cystic fibrosis and exercise-induced asthma, it was the aim of this study to determine how exercise affects airway Na(+) and Cl(-) transport and whether changes depend on exercise intensity. Nasal potential was measured in Ringer's solution, with amiloride to block Na(+) transport, and in low chloride-containing isoproterenol to assess Cl(-) channels. Nasal potential was measured at rest and during submaximal and maximal bicycle ergometer exercise in individuals with cystic fibrosis, exercise-induced asthma and controls. At rest, nasal potential was significantly higher in cystic fibroses than in the others. Maximal exercise decreased nasal potentials in cystic fibrosis and controls but not in exercise asthma. Submaximal exercise decreased nasal potentials only in cystic fibrosis. Cl(-) transport was not affected. Our results indicate that nasal potentials and Na(+) transport were decreased by maximal exercise in healthy and cystic fibrosis, whereas submaximal exercise decreased potentials in cystic fibrosis only. Exercise did not affect nasal potentials in asthmatics. Decreased reabsorption during exercise might favour airway fluid secretion during hyperpnoea. This protective effect appears blunted in patients with exercise-induced asthma.

No evidence for interstitial lung oedema by extensive pulmonary function testing at 4,559 m.

The aim of the present study was to better understand previously reported changes in lung function at high altitude. Comprehensive pulmonary function testing utilising body plethysmography and assessment of changes in closing volume were carried out at sea level and repeatedly over 2 days at high altitude (4,559 m) in 34 mountaineers. In subjects without high-altitude pulmonary oedema (HAPE), there was no significant difference in total lung capacity, forced vital capacity, closing volume and lung compliance between low and high altitude, whereas lung diffusing capacity for carbon monoxide increased at high altitude. Bronchoconstriction at high altitude could be excluded as the cause of changes in closing volume because there was no difference in airway resistance and bronchodilator responsiveness to salbutamol. There were no significant differences in these parameters between mountaineers with and without acute mountain sickness. Mild alveolar oedema on radiographs in HAPE was associated only with minor decreases in forced vital capacity, diffusing capacity and lung compliance and minor increases in closing volume. Comprehensive lung function testing provided no evidence of interstitial pulmonary oedema in mountaineers without HAPE during the first 2 days at 4,559 m. Data obtained in mountaineers with early mild HAPE suggest that these methods may not be sensitive enough for the detection of interstitial pulmonary fluid accumulation.

Intermittent hypoxia at rest for improvement of athletic performance.

Two modalities of applying hypoxia at rest are reviewed in this paper: intermittent hypoxic exposure (IHE), which consists of hypoxic air for 5-6 min alternating with breathing room air for 4-5 min during sessions lasting 60-90 min, or prolonged hypoxic exposure (PHE) to normobaric or hypobaric hypoxia over up to 3 h/day. Hypoxia with IHE is usually in the range of 12-10%, corresponding to an altitude of about 4000-6000 m. Normobaric or hypobaric hypoxia with PHE corresponds to altitudes of 4000-5500 m. Five of six studies applying IHE and all four well-controlled studies using PHE could not show a significant improvement with these modalities of hypoxic exposure for sea level performance after 14-20 sessions of exposure, with the exception of swimmers in whom there might be a slight improvement by PHE in combination with a subsequent tapering. There is no direct or indirect evidence that IHE or PHE induce any significant physiological changes that might be associated with improving athletic performance at sea level. Therefore, IHE and PHE cannot be recommended for preparation of competitions held at sea level.

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude.

Individuals susceptible to high-altitude pulmonary oedema (HAPE) are characterised by an abnormal increase of pulmonary artery systolic pressure (PASP) in hypoxia and during normoxic exercise, reduced hypoxic ventilatory response, and smaller lung volume. In 37 mountaineers with well-documented altitude tolerance, it was investigated whether any combination of these noninvasive measurements, including exercise in hypoxia, could improve the identification of HAPE-susceptible subjects at low altitude. HAPE-susceptible subjects showed a significant higher increase of PASP during hypoxia at rest (48+/-10 mmHg) compared with controls (38+/-3 mmHg), as well as during normoxic exercise (57+/-14 versus 38+/-7 mmHg) and hypoxic exercise (69+/-13 versus 49+/-8 mmHg). PASP could not be assessed in three and eight subjects during normoxic or hypoxic exercise, respectively, due to insufficient Doppler profiles or systemic arterial hypertension. Sensitivity (77-94%) and specificity (76-93%) were not significantly different between the various testing conditions. Additional assessment of hypoxic ventilatory response and lung function parameters did not improve identification of HAPE-susceptible subjects in a multivariate analysis. Due to the greater number of missing values in pulmonary artery systolic pressure measurements during hypoxic exercise, it was concluded that pulmonary artery systolic pressure measurements at rest during hypoxia or exercise in normoxia are most feasible for the identification of high-altitude pulmonary oedema-susceptible subjects.

Erythropoiesis and performance after two weeks of living high and training low in well trained triathletes.

The purpose of our study was to evaluate hematologic acclimatization during 2 weeks of intensive normoxic training with regeneration at moderate altitude (living high-training low, LHTL) and its effects on sea-level performance in well trained athletes compared to another group of equally trained athletes under control conditions (living low - training low, CONTROL). Twenty-one triathletes were ascribed either to LHTL (n = 11; age: 23.0 +/- 4.3 yrs; VO 2 max: 62.5 +/- 9.7 [ml x min -1 x kg -1]) living at 1956 m of altitude or to CONTROL (n = 10; age: 18.7 +/- 5.6 yrs; VO 2 max: 60.5 +/- 6.7 ml x min -1 x kg -1) living at 800 m. Both groups performed an equal training schedule at 800 m. VO 2 max, endurance performance, erythropoietin in serum, hemoglobin mass (Hb tot, CO-rebreathing method) and hematological quantities were measured. A tendency to improved performance in LHTL after the camp was not significant (p < 0.07). Erythropoietin concentration increased temporarily in LHTL (Delta 14.3 +/- 8.7 mU x ml -1; p < 0.012). Hb tot remained unchanged in LHTL whereas was slightly decreased from 12.5 +/- 1.3 to 11.9 +/- 1.3g x kg -1 in CONTROL (p < 0.01). As the reticulocyte number tended to higher values in LHTL than in CONTROL, it seems that a moderate stimulation of erythropoiesis during regeneration at altitude served as a compensation for an exercise-induced destruction of red cells.

Effect of exercise intensity on the changes in alveolar slopes of carbon dioxide and oxygen expiratory profiles in humans.

The slope of the expired alveolar partial pressure of carbon dioxide profile increases during exercise. Its relationship to metabolic rate, however, remains to be determined at high exercise intensities. We therefore determined the slope of alveolar partial pressures of carbon dioxide and oxygen (PACO2, PAO2, respectively) during incremental cycle ergometer exercise (an increment of 40 W each minute) to exhaustion in 11 normal subjects. The PACO2 and PAO2 increased as linear functions of carbon dioxide production and oxygen uptake (VO2), respectively, up to the estimated lactate threshold (thetaLa-). At higher intensities PACO2 increased disproportionately but PAO2 continued to increase at the same rate in 7 subjects but increased more rapidly in the remainder. The rate of change in PACO2 per unit rate of change in VO2 averaged 3.15 (SD 1.05) (mmHg.s(-1)). (l.min(-1))-1 while the rate of change in PAO2 per unit rate of change in VO2 averaged -3.53 (SD 0.79) (mmHg.s(-1)) (l.min(-1))-1 over this range. The more rapid increase in PACO2 above thetaLa- was consistent with an accelerated CO2 exchange, whereas the more rapid rate of change in PAO2 in 3 of the subjects may have reflected the development of an increased distribution of the ventilation perfusion ratio in addition to the effects of hyperventilation.

Assessment of high altitude tolerance in healthy individuals.

The most reliable prediction of high altitude tolerance can be derived from the clinical history of previous comparable exposures. Unfortunately, there are no reliable tests for prediction prior to first-time ascents. Although susceptibility to AMS is usually associated with a low hypoxic ventilatory response (HVR), there is too much overlap with the range of normal values, which precludes measuring HVR or O(2) saturation during brief hypoxia for reliable identification of susceptibility to AMS. A low HVR and an exaggerated rise in pulmonary artery pressure with (prolonged) hypoxia, or exercise in normoxia, are markers of susceptibility to high altitude pulmonary edema (HAPE). These tests can not be recommended for routinely determining high altitude tolerance because the prevalence of susceptibility to HAPE is low and because specificity and sensitivity of these tests are not sufficiently established. On the other hand, HAPE may be avoided in susceptible individuals by ascent rates of 300 m per day above an altitude of 2000 m. Since prediction of risk of mountain sickness is difficult, it is important during the physician consultation prior to ascent to consider the altitude profile, the type of ascent, the performance capacity, the history of previous exposures, and the medical infrastructure of the area.

Effect of "living high-training low" on the cardiac functions at sea level.

Living high-training low (LHTL), living at high altitude and training at sea level, is reported to be beneficial in enhancing physical performance. Effect of LHTL on cardiac function which is one of major determinants in performance, however, was not examined. To address this issue, 21 well-trained triathletes divided into control (n = 10, living and training at sea level) and LHTL group (living at 1980 m altitude > or = 12 hrs/day and training at sea level) were Doppler echocardiographically examined before and at the end of the two-week program. Heart rate and blood pressure did not change in both groups. At end of the training, left ventricular endsystolic diameter of LHTL group was smaller than that of controls (32 vs 34 mm, P < 0.05). Shortening fraction and ejection fraction in LHTL group increased by 9% and 17 %, respectively, P < 0.05. Preejection period/ejection time was more greatly reduced in LHTL group (P < 0.05). Stroke volume and cardiac output in LHTL increased. Diastolic function was not significantly affected by LHTL. These results suggest that LHTL produced an improvement of systolic function underlined by incremented left ventricular contractility, which might be associated with increased beta-adrenergic receptor or an improved myocardial energy utilization.