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Erschienen in:
01.05.2008 | ORIGINAL CONTRIBUTION
Skeletal muscle myofibrillar protein oxidation and exercise capacity in heart failure
Erschienen in: Basic Research in Cardiology | Ausgabe 3/2008
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Background
Heart failure is characterized by limited exercise tolerance and by a skeletal muscle myopathy with atrophy and shift toward fast fibres. An inflammatory status with elevated pro-inflammatory cytokines and exaggerated free radicals production can worsen muscle damage. We have previously demonstrated in a model of heart failure, the monocrotaline treated rat, that oxidation of skeletal muscle actin, tropomyosin and myosin produces a reduction of contractile efficiency, which may further depress muscle function and exercise capacity.
Aims
To investigate the presence of oxidized myofibrillar proteins in skeletal muscle of CHF patients by means of the Oxyblot technique and to correlate it with exercise capacity.
Methods
We have analyzed skeletal muscle biopsies taken from six patients with class III–IV NYHA CHF and four control patients (peak VO2 12.8 ± 1.9 vs. 29.7 ± 1.7 ml/kg/min, p < 0.0001).
Results and conclusions
A correlation between degree of myofibrillar oxidation and exercise capacity measured as peak VO2 was obtained. In the skeletal muscle of CHF patient there was a much higher level of myofibrillar protein oxidation as expressed by the Oxyblot/Red Ponceau (Oxy/RP) ratio as compared to controls (2.1 ± 0.3 vs. 1.02 ± 0.09, p < 0.0001). The VO2/Oxy/RP was significantly lower in the CHF patients. Higher levels of muscle oxidation were found in patients with lower exercise capacity with an inverse correlation between Oxyblot and VO2 values (r
2 = 0.83).