Respiratory muscle damage biomarkers in response to inspiratory pressure-threshold loading in healthy young adults

Abstract

Elevated inspiratory muscle work is encountered during strenuous exercise, exacerbations of COPD and during inspiratory pressure-threshold loading (ITL). It is unclear whether elevated inspiratory muscle work results in muscle damage and if this can be detected using blood biomarkers. This study investigated respiratory muscle damage in response to ITL using a novel muscle damage biomarker panel. Seven healthy men (33+2 yrs) performed 60 min of ITL at a resistance equivalent to 0% and 70% of their maximal inspiratory pressure, with conditions performed two weeks apart. Blood was collected before and 1, 24, and 48 h after each ITL session. Serum creatine kinase muscle-type (CKM), myoglobin, fatty acid-binding protein 3 (FABP3), myosin light chain 3 (MLC3), and fast and slow skeletal troponin I (sTnI) were measured using ELISAs. None of the biomarkers increased following 0% ITL. After 70% ITL, CKM increased at 1 h (71+6%, P=0.001) and remained elevated at 24 h (51+6%, P=0.006) compared to baseline. Myoglobin (39+6%, P=0.001) and fast sTnI (47+13%, P=0.014) increased at 1 h after ITL. FABP3 increased at 24 h (29+7%, P=0.02) and slow sTnI at 24 (34+8%, P=0.05) and 48 h (44+6%, P=0.034) after ITL. MLC3 did not increase after 70% ITL. In conclusion, elevated inspiratory muscle work using ITL in healthy young men resulted in muscle damage as evidenced by increases in CKM, myoglobin, fast and slow sTnI and FABP3. CKM, myoglobin and fast sTnI could be used to assess respiratory muscle damage immediately (1 h), while CKM, FABP3 and slow sTnI could be used to assess respiratory muscle damage 24 and 48 h following conditions that cause elevated inspiratory muscle work.