The effects of exercise at high altitude on high-sensitivity cardiac troponin release and associated biventricular cardiac function

Background It has been consistently shown that heavy exercise leads to cardiac troponin (cTn) release and variable changes in post exercise cardiac function. This relationship has not been explored at increasing or significant high altitude (HA). This study assessed the effects of exercise at progressively increasing HA on high-sensitivity (hs)-cTnT levels and their relationship to biventricular cardiac function and severity of acute mountain sickness (AMS). Transthoracic echocardiograms, hs-cTnT levels and AMS scores were measured at rest at 1,300 m then repeated post exercise and 12 h later after progressive trekking to 3,440, 4,270 m and at 5,150 m (after trekking to 5,643 m) on 19 healthy subjects (age 35.4 +/- A years, 52.6 % males). There was a detectable increase (> 5 ng/L) in post exercise hs-cTnT with exercise at HA which became significant at 5,150 m (5.84 % at 3,440 m, 5.2 % at 4,270 m and 56.3 % at 5,150 m; p = 0.0005). Compared with baseline, HA to 5,150 m led to a significant rise in post exercise Lake Louis AMS scores (p < 0.001) pulmonary artery systolic pressure (PASP) (23.7 +/- A 3.8 vs 37.9 +/- A 11.7 mmHg: p < 0.001), cardiac output (5.2 +/- A 1.2 vs 7.5 +/- A 1.3 l/min; p < 0.001) and a fall in SpO(2) (96.1 +/- A vs 77.4 +/- A 12.0 %; p < 0.001). There was no change in stroke volume (p = 0.10) or estimated filling pressures (E/E') of the left (p = 0.50) and right ventricles (p = 0.4). On multivariate analysis increasing cardiac output (p = 0.02) and PASP (p = 0.04) and decreasing SpO(2) (p = 0.01) were the only independent predictors of increasing cTnT levels (overall R (2) = 0.23, p < 0.0001). Moderate intensity exercise at significant HA influences the post exercise increase in hs-cTnT without overt deleterious effects on cardiac function.