Background: In pulmonary hypertension right ventricular pressure overload leads to abnormal left ventricular (LV) diastolic function. Acute high altitude exposure is associated with hypoxia-induced elevation of pulmonary artery pressure particularly in the setting of high altitude pulmonary edema. Tissue Doppler Imaging (TDI) allows assessment of LV diastolic function by direct measurements of myocardial velocities independently of cardiac preload. We hypothesized that in healthy mountaineers, hypoxia-induced pulmonary artery hypertension at high altitude is quantitatively related to LV diastolic function as assessed by conventional and TDI Doppler methods. Methods: 41 healthy subjects (11 women; mean age 41±12 years) underwent transthoracic echocardiography at low altitude (550m) and after a rapid ascent to high altitude (4559 m). Measurements included the right ventricular to right atrial pressure gradient (P_RV-RA), transmitral early (E) and late (A) diastolic flow velocities and mitral annular early (E_m) and late A_m) diastolic velocities obtained by TDI at four locations: septal, inferior, lateral and anterior. Results: At high altitude, P_RV-RA increased from 16±7 to 44±15 mmHg (p<0.0001), whereas transmitral E/A ratio was significantly lower (1.11±0.27 vs1.41±0.35; p<0.0001) due to a significant increase of A from (52±15 cm/s) to (65p±16 cm/s) (p=0.0001). P_RV-RA and transmitral E/A ratio were inversely correlated (r²=0.16; p=0.0002) for the whole spectrum of measured values (low and high altitude). Diastolic mitral annular motion interrogation showed similar findings for spatially averaged (4 locations) as well as for the inferior and septal locations: A_m increased from low to high altitude (all p<0.01); consequently, E_m/A_m ratio was lower at high vs low altitude (all p<0.01). These intraindividual changes were reflected interindividually by an inverse correlation between P_RV-RA and E_m/A_m (all p<0.006) and a positive association between P_RV-RA and A_m (all p<0.0009). Conclusion: High altitude exposure led to a two-to-three fold increase in pulmonary artery pressure in healthy mountaineers. This acute increase in pulmonary artery pressure led to a change in LV diastolic function that was directly correlated with the severity of pulmonary hypertension. However, in contrast to patients suffering from some form of cardiopulmonary disease and pulmonary hypertension, in these healthy subjects, overt LV diastolic dysfunction was not observed, because it was prevented by augmented atrial contraction. We propose the new concept of compensated diastolic (dys)function.