| Summary: | Increased respiratory muscle work is encountered during strenuous whole-body exercise, and at rest in older adults and those with pulmonary limitations such as chronic obstructive pulmonary disease (COPD). When sufficiently strenuous it can result in diaphragmatic fatigue, increased blood lactate concentrations, and an alteration in respiratory muscle recruitment patterns. Increased respiratory muscle work also elevates cytokines interleukin-6 (IL-6) and interleukin-1β (IL-1β) within the respiratory muscles and systemically. There is mounting evidence that inflammation contributes significantly to the ageing process and age related diseases. Enhanced oxidative stress, glycogen depletion and diaphragmatic fatigue are all potential stimuli for this production. Whole-body exercise training can attenuate systemic inflammation and oxidative stress in younger adults during exercise, and in older adults who experience this at rest. An attenuation of muscle glycogen or increases in antioxidant enzymes may explain such reductions. Inspiratory muscle training (IMT) may also elicit similar adaptations in the inspiratory muscles, and thus also attenuate these markers. Accordingly, this thesis evaluated in younger adults whether: (I) the respiratory muscles contribute to exercise-induced increases in plasma cytokines and/or systemic oxidative stress measured by DNA damage to peripheral blood mononuclear cells (PBMC) during 1 h of steady-state cycling exercise (EX) and volitional hyperpnoea at rest which mimicked the breathing and respiratory muscle recruitment patterns achieved during EX (HYPEX) and heavy exercise (VH); (II) an increase in these inflammatory markers was related to diaphragmatic fatigue; (III) IMT attenuates these markers during EX, HYPEX and EX; and (IV) IMT changes an estimation of the maximum lactate steady-state and respiratory muscle recruitment patterns during the lactate minimum test. This thesis also evaluated in older adults at rest whether: (V) IMT attenuates plasma cytokines and DNA damage to PBMC. It was found in younger adults that: (I) plasma IL-6 concentrations increased during EX, HYPEX and VH and plasma IL-1β increased during VH. Plasma interleukin-1 receptor antagonist concentration and oxidative DNA damage to PBMC remained unchanged during VH; (II) the increase in IL-6 and IL-1β during VH was not related to the induction of diaphragmatic fatigue; (III) following IMT, plasma IL-6 concentrations were reduced by 33% during EX, 24% during VH, but were unchanged during HYPEX; and (V) following IMT, an estimation of the maximum lactate steady-state and respiratory muscle recruitment patterns remained unchanged during the lactate minimum test. It was found in older adults that: (IV) following IMT, nine plasma cytokines and DNA damage to PBMC remained unchanged. This thesis provides novel evidence that the respiratory muscles contribute to exercise-induced increases in plasma IL-6 and IL-1β concentration and that this increase is not related to diaphragmatic fatigue. IMT attenuates plasma IL-6 concentration during exercise, but not in a range of plasma cytokines in older adults at rest. It is attractive to speculate that the respiratory muscles contribute to the systemic inflammation observed in COPD patients and IMT may reduce the dysregulated cytokine response observed during exercise of COPD patients.
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