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Ibuprofen inhibits skeletal muscle hypertrophy in rats
Quinlyn A Soltow1, Jenna L Betters, Jeff E Sellman
1Center for Exercise Science, University of Florida, Gainesville, 32611, USA.
Purpose:
We sought to determine whether cyclooxygenase (COX) activity is necessary for overload-induced growth of adult rat skeletal muscle, and whether nitric oxide synthase (NOS) activity is involved in upregulation of COX messenger RNA (mRNA) expression in skeletal muscle.
Methods:
Unilateral surgical removal of the gastrocnemius and soleus was performed on the right hindlimb of 16 female Sprague-Dawley rats (approximately 230 g) to induce chronic overload (OL) of the plantaris for 14 d, with sham surgeries performed on the contralateral leg as a normally loaded (NL) control. Half of the rats were treated with the nonspecific COX inhibitor, ibuprofen (0.2 mg.mL(-1) in drinking water; approximately 20 mg.kg(-1).d(-1)). In a second experiment, the plantaris was unilaterally overloaded for 5 or 14 d in male rats (approximately 350 g; N = 16 rats per time point) and half of the animals were treated with the NOS inhibitor, L-NAME (0.75 mg.mL(-1) in drinking water; approximately 90 mg.kg(-1).d(-1)).
Results:
Ibuprofen treatment inhibited plantaris hypertrophy by approximately 50% (P < 0.05) following 14 d of OL, as did L-NAME treatment (P < 0.05). COX-1 and COX-2 mRNA did not differ between any groups at 5 d. At 14 d, however, L-NAME caused a 30-fold increase in plantaris COX-1 mRNA expression independent of loading condition. Additionally, OL induced a 20-fold increase in COX-2 mRNA expression compared with NL (P < 0.05) at 14 d, without affecting COX-1 mRNA level. L-NAME treatment significantly inhibited OL-induced expression of COX-2 mRNA.
Conclusion:
COX activity is important for in vivo muscle hypertrophy, and plantaris overload is associated with NOS activity-dependent COX-2 expression.
Insights
Cyclooxygenase (COX) activity is crucial for muscle growth following overload. Nitric oxide synthase (NOS) activity influences the expression of COX-2 during this process.
Area of Science:
- Skeletal Muscle Physiology
- Molecular Biology
- Pharmacology
Background:
- Skeletal muscle hypertrophy results from overload.
- The roles of cyclooxygenase (COX) and nitric oxide synthase (NOS) in this process are not fully understood.
Purpose of the Study:
- To investigate if COX activity is essential for overload-induced skeletal muscle growth in adult rats.
- To determine if NOS activity affects COX messenger RNA (mRNA) expression in skeletal muscle during overload.
Main Methods:
- Adult rats underwent surgical induction of chronic overload (OL) on the plantaris muscle.
- Animals were treated with either a COX inhibitor (ibuprofen) or a NOS inhibitor (L-NAME).
- COX-1 and COX-2 mRNA levels were analyzed in plantaris muscles after 5 and 14 days of OL.
Main Results:
- Ibuprofen treatment reduced plantaris hypertrophy by approximately 50%.
- L-NAME treatment also significantly inhibited hypertrophy.
- Overload increased COX-2 mRNA expression, which was blunted by L-NAME treatment. L-NAME also increased COX-1 mRNA expression.
Conclusions:
- COX activity plays a significant role in skeletal muscle hypertrophy in vivo.
- Overload-induced skeletal muscle growth is associated with NOS activity-dependent COX-2 expression.
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