RESUMO
OBJECTIVE: The purpose of this study was to investigate the effects of a single bout of high-intensity interval exercise (HIIE) on high-sensitivity cardiac troponin T (hs-cTnT) release and to explore the potential influencing factors. METHODS: Twenty-one experienced marathon runners completed HIIE on treadmill. Each bout of HIIE included a hard run (15.8 ± 1.3 km·h-1) at 90% vVO2max for 2 min followed by an easy run (8.8 ± 0.7 km·h-1) at 50% vVO2max for 2 min performed 23 times within 92 min. Heart rate (HR) was recorded every 2 min during HIIE. The hs-cTnT level was measured before (pre), immediately after (0 h), and at 4 and 24 h after exercise. RESULTS: The hs-cTnT level was elevated at 0 h, peaked at 4 h, and had not returned to the baseline value at 24 h after exercise. The response of hs-cTnT at 4 h was positively related to exercise HR. Subjects with a greater increase in hs-cTnT level had a higher exercise HR under fixed exercise intensity. CONCLUSION: HIIE at 90% vVO2max interspersed with 50% vVO2max for recovery can elicit hs-cTnT elevation. HR is a good predictor of exercise-induced cardiac troponin (cTn) release under fixed exercise intensity. Further study should consider to correct for HR when constructing impact factors contributing to exercise-induced cTn release.
RESUMO
PURPOSE: To investigate the effects of hypoxic training on redox status and cardiac troponin (cTn) release after intermittent exercise. METHOD: Nine well-trained male marathon runners (age, 21.7 ± 2.3 year; body mass, 64.7 ± 4.8 kg; height, 177.9 ± 3.8 cm; and VO2max, 64.3 ± 6.7 ml kg(-1) min(-1)) completed intermittent exercise under normoxic [trial N; fraction of inspiration oxygen (FIO2), 21.0 %] and hypoxic (trial H; FIO2, 14.4 %) conditions in random order. Each bout of intermittent exercise included hard run (16.2 ± 0.8 km h(-1)) at 90 % VO2max for 2 min followed by easy run (9.0 ± 0.4 km h(-1)) at 50 % VO2max for 2 min and 23 bouts in 92 min totally. Malondialdehyde, reduced glutathione (GSH), superoxide dismutase, an estimate of total antioxidant capacity (T-AOC), high-sensitivity cardiac troponin T (hs-cTnT), and cardiac troponin I (cTnI) were measured before, immediately after (0 h), and 2, 4, and 24 h after the completion of trials N and H. RESULT: GSH was increased immediately after trial N. T-AOC was lower 4 h after trial H than trial N. Hs-cTnT was elevated from 0 to 4 h and returned to baseline 24 h after both trials. CTnI was increased after trial H; peaked at 2-4 h and returned to below the detection by 24 h. CONCLUSION: The overall redox status was balanced under normoxic conditions, and exercise-induced cTn release did not deviate. However, the protective effects of antioxidant were weaker in the hypoxic state than normoxic, and the stress on the myocardium induced by intermittent exercise was transiently aggravated.
