The effects of increased respiratory muscle work on biomarkers of muscle damage

The effects of increased respiratory muscle work on biomarkers of muscle damage

The current techniques to measure respiratory muscle damage are invasive and/or costly. A simple and minimally invasive approach to identify the presence of muscle damage that can accommodate the internal location of the respiratory muscles is the use of blood biomarkers. The overall aim of this research was to investigate whether damage to the respiratory muscles occurs after increased respiratory muscle work and to determine if serum biomarkers can be used to measure respiratory muscle damage. Study 1 investigated respiratory muscle damage following inspiratory pressure threshold loading (ITL). Seven healthy men (33 ± 2 years) undertook 60 minutes of ITL at a resistance equivalent to ~0% (Sham ITL) and 70% of their maximal inspiratory mouth pressure (PImax) two weeks apart. Serum was collected before and at 1, 24, and 48 h after each ITL session. Creatine kinase muscle-type (CKM) was higher at 1 and 24 hours, fast skeletal troponin-I (sTnI) at 1 hour, while slow sTnI was higher at 48 hours post-ITL. Study 2 investigated the effects of volitional hyperpnea (VH) on biomarkers of respiratory muscle damage. Eight healthy men (33 ± 2 years) undertook 10 min of volitional hyperpnea (VH) and rest (control) two weeks apart. VH involved mimicking the breathing and diaphragm recruitment patterns in a square wave manner to a level equivalent to those at 85% of their maximum minute ventilation produced during a maximal incremental cycling test. Serum was collected before and at 1, 24, and 48 hours after both control and VH trials. Only slow sTnI was significantly higher at 24 h post VH as compared to same time point of control trial. Study 3 investigated the effects of inspiratory muscle training (IMT) on muscle damage biomarkers, respiratory function, and functional capacity in coronavirus disease (COVID-19) recovered young adults, successfully weaned from mechanical ventilation. The IMT group performed 30 dynamic inspiratory efforts twice daily at 50% of their PImax while the Control group performed 60 inspiratory efforts at 10% of PImax daily. Serum was collected at baseline, week two, and week four. CKM and slow sTnI were lower at two and four weeks for the IMT compared to the control group. This thesis provides evidence that serum CKM and fast sTnI could be used to assess respiratory muscle damage immediately, while CKM and slow sTnI could be used to assess respiratory muscle damage at later stages following conditions or diseases that elevate respiratory muscle work or activity and cause respiratory muscle damage.

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