Inspiratory flow-resistive breathing, respiratory muscle-induced systemic oxidative stress, and diaphragm fatigue in healthy humans

We examined whether the respiratory muscles of humans contribute to systemic oxidative stress following inspiratory flow-resistive breathing, whether the amount of oxidative stress is influenced by the level of resistive load, and whether the amount of oxidative stress is related to the degree of diaphragm fatigue incurred. It is only when sufficiently strenuous that inspiratory flow-resistive breathing elevates plasma F2-isoprostanes, and our novel data show that this is not related to a reduction in transdiaphragmatic twitch pressure.

Exercise-induced diaphragm fatigue in a Paralympic champion rower with spinal cord injury

The aim of this case report was to determine whether maximal upper body exercise was sufficient to induce diaphragm fatigue in a Paralympic champion adaptive rower with low-lesion spinal cord injury (SCI). An elite arms-only oarsman (age: 28 yr; stature: 1.89 m; and mass: 90.4 kg) with motor-complete SCI (T12) performed a 1,000-m time trial on an adapted rowing ergometer. Exercise measurements comprised pulmonary ventilation and gas exchange, diaphragm EMG-derived indexes of neural respiratory drive, and intrathoracic pressure-derived indexes of respiratory mechanics. Diaphragm fatigue was assessed by measuring pre- to postexercise changes in the twitch transdiaphragmatic pressure (Pdi,tw) response to anterolateral magnetic stimulation of the phrenic nerves. The time trial (248 ± 25 W, 3.9 min) elicited a peak O2 uptake of 3.46 l/min and a peak pulmonary ventilation of 150 l/min (57% MVV). Breath-to-stroke ratio was 1:1 during the initial 400 m and 2:1 thereafter. The ratio of inspiratory transdiaphragmatic pressure to diaphragm EMG (neuromuscular efficiency) fell from rest to 600 m (16.0 vs. 3.0). Potentiated Pdi,tw was substantially reduced (−33%) at 15–20 min postexercise, with only partial recovery (−12%) at 30–35 min. This is the first report of exercise-induced diaphragm fatigue in SCI. The decrease in diaphragm neuromuscular efficiency during exercise suggests that the fatigue was partly due to factors independent of ventilation (e.g., posture and locomotion). NEW & NOTEWORTHY This case report provides the first objective evidence of exercise-induced diaphragm fatigue in spinal cord injury (SCI) and, for that matter, in any population undertaking upper body exercise. Our data support the notion that high levels of exercise hyperpnea and factors other than ventilation (e.g., posture and locomotion) are responsible for the fatigue noted after upper body exercise. The findings extend our understanding of the limits of physiological function in SCI.

Influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training on the plasma cytokine response to maximum sustainable voluntary ventilation

The influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training (IMT) on the cytokine response to maximum sustainable voluntary ventilation (MSVV) is unknown. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1 h of ( 1) passive rest and ( 2) MSVV, whereby participants undertook volitional hyperpnea at rest that mimicked the breathing and respiratory muscle recruitment patterns commensurate with heavy cycling exercise. Plasma cytokines remained unchanged during passive rest. There was a main effect of time ( P < 0.01) for plasma interleukin-1β (IL-1β) and interleukin-6 (IL-6) concentrations and a strong trend ( P = 0.067) for plasma interleukin-1 receptor antagonist concentration during MSVV. Plasma IL-6 concentration was reduced after IMT by 27 ± 18% (main effect of intervention, P = 0.029), whereas there was no change after PLA ( P = 0.753). There was no increase in a systemic marker of oxidative stress [DNA damage in peripheral blood mononuclear cells (PBMC)], and diaphragm fatigue was not related to the increases in plasma IL-1β and IL-6 concentrations. A dose-response relationship was observed between respiratory muscle work and minute ventilation and increases in plasma IL-6 concentration. In conclusion, increases in plasma IL-1β and IL-6 concentrations during MSVV were not due to diaphragm fatigue or DNA damage in PBMC. Increases in plasma IL-6 concentration during MSVV are attenuated following IMT, and the plasma IL-6 response is dependent upon the level of respiratory muscle work and minute ventilation.