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N‐acetylcysteine improves skeletal muscle fatigue resistance in a model of peripheral arterial insufficiency
Author(s) -
Roseguini Bruno,
Souccar Caden,
Han Sang
Publication year - 2013
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.27.1_supplement.940.24
Subject(s) - acetylcysteine , skeletal muscle , saline , medicine , soleus muscle , muscle fatigue , endocrinology , peripheral , femoral artery , hindlimb , sed , anesthesia , chemistry , antioxidant , electromyography , biochemistry , physical medicine and rehabilitation
Oxidative stress plays a major role in the genesis of skeletal muscle dysfunction in patients with Peripheral Arterial Disease (PAD). We tested the hypothesis that administration of the antioxidant N‐acetylcysteine (NAC) would improve isolated skeletal muscle fatigue resistance in a mice model of PAD. Male Balb/c mice (n=15) were subjected to bilateral ligation of the femoral artery and after 2 weeks of recovery, received daily intraperitoneal injections of either NAC (150 mg/kg, n=7) or saline (n=8) for 15 days. At the end of the treatment, the extensor digitorium longus (EDL) and soleus (SOL) muscles were excised for analysis of the contractile function and fatigue resistance in vitro (32°C). Maximal specific force was not different between groups for both the EDL (NAC: 37.3±1.4 N/cm 2 ; Saline: 36.1±1.5 N/cm 2 ) and the soleus (NAC: 35.5±1.2 N/cm 2 ; Saline: 34.1±1.2 N/cm 2 ). In the soleus muscle, force after 10 min of submaximal tetanic stimulation (60 Hz, 300 ms trains, 0.3 trains/s) was higher (p<0.05) in NAC‐treated animals (45±3% of the initial value) when compared to controls (30.3 ±3%). No differences were found in fatigue development between groups in the EDL muscle (NAC:35.7±1.9%; Saline 37.5±1.1%). These results indicate that NAC treatment substantially improves fatigue resistance in the soleus muscle in a model of peripheral arterial insufficiency. Support‐ Fapesp 2011/18197–0 (B.R.), 2010/51344–3 (CS)

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