High-intensity exercise hyperpnea places substantial demands upon the respiratory muscles, but whether this causes respiratory muscle damage is unknown. We investigated respiratory muscle damage following volitional hyperpnea (equivalent to 85% of participants maximum minute ventilation produced during a maximal incremental cycling test) using a skeletal muscle damage biomarker panel. Eight healthy men (33 + 2 years) underwent 10-min trials of volitional hyperpnea and rest (control) two weeks apart. Serum was collected before and at 1, 24, and 48 h after both volitional hyperpnea and control trials. Creatine kinase muscle-type (CKM), fast skeletal troponin I (sTnI) and slow sTnI were measured using enzyme-linked immunosorbent assay. Two-way analysis of variance revealed time × trial interaction effects for slow sTnI (p = 0.018), but not for CKM (p = 0.072) and fast sTnI (p = 0.140). Slow sTnI was significantly higher at +24 h post volitional hyperpnea (p < 0.001) as compared to the same time point of the control trial. These results indicate that high-intensity exercise hyperpnea may induce a small amount of respiratory muscle damage as evidenced by the increases in slow sTnI. Future studies including more time points, different respiratory muscle exercise protocols, and examining the differences between sexes could provide additional insights into the utility of blood biomarkers for identifying respiratory muscle damage.
Keywords: biomarkers; respiratory muscle damage; skeletal troponin I; volitional hyperpnea.
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