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Endurance exercise attenuates mechanical ventilation‐induced diaphragm weakness
Author(s) -
Smuder Ashley J,
Min Kisuk,
Hudson Matthew B,
Kwon OhSung,
Nelson W Bradley,
Kavazis Andreas N,
Powers Scott K
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1059.20
Subject(s) - diaphragm (acoustics) , weakness , oxidative stress , medicine , ventilation (architecture) , diaphragmatic breathing , lipid peroxidation , endurance training , cardiology , anesthesia , chemistry , endocrinology , surgery , pathology , mechanical engineering , loudspeaker , engineering , physics , alternative medicine , acoustics
Mechanical ventilation (MV) is used to maintain alveolar ventilation in patients incapable of doing so on their own. However, MV renders the diaphragm inactive leading to weakness due to increased proteolysis and contractile dysfunction. It is established that MV‐induced oxidative stress is required for diaphragm weakness to occur. In contrast, endurance exercise training improves diaphragmatic antioxidant capacity and protects against oxidative stress. Therefore, we hypothesized that exercise training prior to MV would protect the diaphragm from MV‐induced oxidative stress and contractile dysfunction. To test this hypothesis animals were randomly assigned to one of three groups: 1) acutely anesthetized control; 2) 12 hours MV; and 3) endurance exercise trained prior to 12 hours MV. Following MV, diaphragm maximal specific force production was significantly decreased compared to control. Further, MV promoted an increase in both lipid peroxidation and protease activation in the diaphragm. In contrast, exercise training prior to MV increased diaphragmatic antioxidant capacity and attenuated MV‐induced diaphragm lipid peroxidation, protease activation, and contractile dysfunction. Collectively, these findings support the hypothesis that exercise training prior to MV protects the diaphragm from MV‐induced weakness. Supported by NIH RO1 HL087839 awarded to SKP and T32 HD043730 awarded to AJS