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Published on: February 25, 2016
Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post-infarction, compensated chronic
J W E Rush1, H J Green, D A Maclean
1Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada. jwerush@uwaterloo.ca
Aim:
Involvement of oxidative stress and nitric oxide synthase (NOS) isoforms in skeletal muscle cellular adaptations to chronic heart failure (CHF) is controversial, and possible muscle fibre-type heterogeneity in the oxidative stress and NOS responses to CHF have not been examined. Consequently, we hypothesized that the changes in determinants of elevated oxidative and nitrosylative stress associated with CHF would occur in skeletal muscle and would be similar in predominantly type I slow twitch muscle (soleus) and type II fast twitch muscle (plantaris) of rats.
Methods:
The purpose of this study was to measure NOS isoforms (endothelial, inducible and neuronal NOS) and antioxidant enzymes (SOD-1, SOD-2, catalase) by protein immunoblot as well as markers of oxidative stress by biochemical assays in soleus and plantaris muscle sections of the rat hind limb. This was performed for control and post-infarction, compensated CHF rats.
Results:
Twelve weeks after coronary artery ligation-induced moderate CHF, soleus exhibited decreased SOD-1, SOD-2 and eNOS, but increased iNOS and nNOS isoforms assessed by immunoblot. This was associated with elevated lipid and DNA oxidative damage assessed by biochemical assays. In contrast, plantaris muscle exhibited no changes in antioxidant enzymes or NOS isoforms, and had lower lipid and DNA oxidative damage.
Conclusion:
These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.
Insights
Chronic heart failure (CHF) causes oxidative stress and alters nitric oxide synthase (NOS) isoforms differently in slow-twitch (soleus) versus fast-twitch (plantaris) muscles, impacting skeletal muscle function.
Area of Science:
- Cardiovascular Physiology
- Skeletal Muscle Biology
- Oxidative Stress Research
Background:
- The role of oxidative stress and nitric oxide synthase (NOS) isoforms in skeletal muscle adaptations to chronic heart failure (CHF) remains unclear.
- Potential differences in these responses between slow-twitch (type I) and fast-twitch (type II) muscle fibers in CHF have not been investigated.
Purpose of the Study:
- To investigate skeletal muscle fiber-type-specific changes in oxidative stress and NOS isoforms in a rat model of CHF.
- To test the hypothesis that oxidative and nitrosylative stress markers would change similarly in soleus (type I) and plantaris (type II) muscles during CHF.
Main Methods:
- Protein immunoblotting was used to quantify NOS isoforms (eNOS, iNOS, nNOS) and antioxidant enzymes (SOD-1, SOD-2, catalase) in soleus and plantaris muscles.
- Biochemical assays measured lipid and DNA oxidative damage in muscle sections from control and CHF rats.
Main Results:
- In soleus muscle, CHF led to decreased SOD-1, SOD-2, and eNOS, but increased iNOS and nNOS, accompanied by elevated oxidative damage.
- Plantaris muscle showed no significant changes in antioxidant enzymes or NOS isoforms and exhibited lower oxidative damage compared to soleus.
- These findings indicate distinct responses between slow and fast-twitch muscle fibers to CHF.
Conclusions:
- Skeletal muscle exhibits a fiber-type-specific response to oxidative stress and NOS alterations in CHF.
- These differential responses are crucial for understanding the mechanisms underlying skeletal muscle dysfunction in CHF.
- The study highlights the importance of considering muscle fiber heterogeneity in CHF-related pathophysiology.
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