Exercise-induced lactate accumulation regulates intramuscular triglyceride metabolism via transforming growth factor-β1 mediated pathways

• The roles of lactate and TGF-β1 on IMTG lipolysis during recovery form strenuous exercise was examined.
• There was a temporal association between elevation in muscle TGF-β1 abundance and IMTG lipolysis indexes.
• Inhibition of TGF-β1 signaling in muscle attenuated IMTG lipolysis in response to acute exercise.
• Acute and chronic intramuscular injection of lactate increased TGF-β1 abundance and IMTG lipolysis indexes.
• Lactate regulates IMTG metabolism via TGF-β1 mediated pathways during recovery form strenuous exercise.

The mechanism regulating the utilization of intramuscular triacylglycerol (IMTG) during high-intensity interval training (HIIT) and post-exercise recovery period remains elusive. In this study, the acute and long-term effects of HIIT on transforming growth factor beta 1 (TGF-β1) abundance in rat skeletal muscle and role of lactate and TGF-β1 in IMTG lipolysis during post-exercise recovery period were examined. TGF-β1 and Adipose triacylglycerol lipase (ATGL) abundance as well as total lipase activity in the gastrocnemius muscle significantly increased to a maximum value 10 h after acute bout of HIIT. Inhibition of TGF-β1 signaling by intramuscular injection of SB431542 30 min prior to the acute exercise attenuated ATGL abundance and total lipase activity in the gastrocnemius muscle in response to acute exercise. Intramuscular acute injection of lactate increased TGF-β1 and ATGL abundance in the gastrocnemius muscle and there were a significant increase in Muscle TGF-β1 and ATGL abundance after 5 weeks of HIIT/lactate treatment. These results indicate that exercise-induced lactate accumulation regulates intramuscular triglyceride metabolism via transforming growth factor-β1 mediated pathways during post-exercise recovery from strenuous exercise.