Abstract
[Purpose]Strenuous exercise often induces skeletal muscle damage, which results in impaired performance. Sphingolipid metabolism contributes to various cellular processes, including apoptosis, stress response, and inflammation. However, the relationship between exercise-induced muscle damage and ceramide (a key component of sphingolipid metabolism), is rarely studied. The present study aimed to explore the regulatory role of sphingolipid metabolism in exercise-induced muscle damage.[Methods]Mice were subjected to strenuous exercise by treadmill running with gradual increase in intensity. The blood and gastrocnemius muscles (white and red portion) were collected immediately after and 24 h post exercise. For 3 days, imipramine was intraperitoneally injected 1 h prior to treadmill running.[Results]Interleukin 6 (IL-6) and serum creatine kinase (CK) levels were enhanced immediately after and 24 h post exercise (relative to those of resting), respectively. Acidic sphingomyelinase (A-SMase) protein expression in gastrocnemius muscles was significantly augmented by exercise, unlike, serine palmitoyltransferase-1 (SPT-1) and neutral sphingomyelinase (N-SMase) expressions. Furthermore, imipramine (a selective A-SMase inhibitor) treatment reduced the exercise-induced CK and IL-6 elevations, along with a decrease in cleaved caspase-3 (Cas-3) of gastrocnemius muscles.[Conclusion]We found the crucial role of A-SMase in exercise-induced muscle damage.
Highlights
Sphingolipids, including ceramide (Cer), are important bioactive molecules that are involved in diverse biological processes, including apoptosis, proliferation, differentiation, growth arrest, and inflammation[1,2,3,4,5]
We explored whether the rate-limiting enzymes of sphingolipid metabolism, such as SPT-1 and SMases contribute to Exercise-induced muscle damage (EIMD) in gastrocnemius muscle after acute strenuous exercise
The current study demonstrated that EIMD might be partly responsible for cellular Cer production by enhancing Acidic sphingomyelinase (A-SMase) expression against strenuous exercise
Summary
Sphingolipids, including ceramide (Cer), are important bioactive molecules that are involved in diverse biological processes, including apoptosis, proliferation, differentiation, growth arrest, and inflammation[1,2,3,4,5]. In vitro and animal studies have demonstrated Cer-induced lipotoxicity in cardiomyocytes This is evidenced by the oxidative stress and cell death caused by the enhanced activity of ceramide synthase (-2 or -5)-provoked myocytic Cer accumulation[13,14]. The gastrocnemius muscle of aerobic exercised (5-week) rats exhibited enhanced activities of SPT and SMases, whereas that of ceramidase was reduced without alterations in Cer levels[16]. Based on this information, it is speculated that sphingolipid metabolism may contribute to exercise-induced skeletal muscle damage similar to strenuous exercise-produced cell death caused by sphingolipid metabolism and myocyte inflammation
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