Exhaustive exercise under moderate normobaric hypoxia did not augment cardiac biomarker release compared to normoxia, but attenuated increases in Mb, NT-proBNP, and IMA.
Does moderate normobaric hypoxia alter the release kinetics of cardiac biomarkers following exhaustive exercise in trained and untrained men?
High-intensity exhaustive exercise under moderate normobaric hypoxia does not exacerbate cardiac biomarker release compared to normoxia, supporting its cardiovascular safety.
Post-exercise release of cardiac biomarkers reflects physiological adaptations of the myocardium to exercise; however, data on their kinetics after exhaustive exercise under hypoxia remain scarce. We determined the kinetics of cardiac biomarker changes following a single bout of exercise to volitional exhaustion under normoxia and moderate normobaric hypoxia (2000 m and 3000 m a.s.l.) in trained (n = 12; VO2max 64.2 ± 2.9 mL·kg−1·min−1) and untrained (n = 12; VO2max 44.1 ± 7.4 mL·kg−1·min−1) men. Participants performed a graded exercise test (GXT) followed by a constant-workload exercise test (CXT) at the lactate threshold under three conditions (FiO2 = 20.9%, 16.5%, 14.4%). Venous blood was sampled at rest, immediately post-exercise, and at 2, 6, and 24 h of recovery for determination of cardiac troponin T (cTnT) and I (cTnI), myoglobin (Mb), creatine kinase MB isoform (CK-MB), heart-type fatty acid-binding protein (H-FABP), ischemia-modified albumin (IMA), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) by ELISA. Exhaustive exercise induced significant elevations in all biomarkers, peaking at 2–6 h post-exercise and largely returning to resting values by 24 h. Moderate normobaric hypoxia did not augment the cardiac biomarker response; rather, it attenuated the increases in Mb, NT-proBNP, and IMA, likely due to earlier peripheral fatigue and lower absolute mechanical work. The inhibitory effect of hypoxia on cTnI release was observed exclusively in trained men, suggesting an interaction between training-related cardiac adaptations and the hypoxic stimulus. These findings support the safety of high-intensity exercise at simulated altitudes of 2000–3000 m a.s.l.
Czuba et al. (Tue,) conducted a other in Healthy trained and untrained men (n=24). Exercise to volitional exhaustion under moderate normobaric hypoxia vs. Normoxia (FiO2 = 20.9%) was evaluated on Kinetics of cardiac biomarker changes (cTnT, cTnI, Mb, CK-MB, H-FABP, IMA, NT-proBNP). Exhaustive exercise under moderate normobaric hypoxia did not augment cardiac biomarker release compared to normoxia, but attenuated increases in Mb, NT-proBNP, and IMA.
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