Abstract
An acute bout of exercise imposes a major challenge on whole-body metabolism and metabolic adjustments are needed in multiple tissues during recovery to reestablish metabolic homeostasis. It is currently unresolved how this regulation is orchestrated between tissues. This study was undertaken to clarify the role of skeletal muscle derived interleukin 6 (IL-6) in the coordination of the metabolic responses during recovery from acute exercise. Skeletal muscle specific IL-6 knockout (IL-6 MKO) and littermate Control mice were rested or ran on a treadmill for 2h. Plasma, skeletal muscle, liver and adipose tissue were obtained after 6 and 10h of recovery. Non-exercised IL-6 MKO mice had higher plasma lactate and lower plasma non-esterified fatty acids than Controls. The activity of pyruvate dehydrogenase in the active form was, in skeletal muscle, higher in IL-6 MKO mice than Controls in non-exercised mice and 6h after exercise. IL-6 MKO mice had lower glucose transporter 4 protein content in inguinal adipose tissue (WAT) than Control in non-exercised mice and 10h after treadmill running. Epididymal WAT hormone sensitive lipase phosphorylation and inguinal WAT mitogen activated kinase P38 phosphorylation were higher in IL-6 MKO than Control mice 6h after exercise. These findings indicate that skeletal muscle IL-6 may play an important role in the regulation of substrate utilization in skeletal muscle, basal and exercise-induced adaptations in adipose tissue glucose uptake and lipolysis during recovery from exercise. Together this indicates that skeletal muscle IL-6 contributes to reestablishing metabolic homeostasis during recovery from exercise by regulating WAT and skeletal muscle metabolism.
Highlights
A single bout of exercise has profound effects on whole-body metabolism, increasing insulin sensitivity [1], fatty acid oxidation [2] and activating metabolic pathways and gene transcription in skeletal muscle, adipose tissue and liver during recovery [3,4,5,6,7]
This suggests that lack of skeletal muscle Interleukin 6 (IL-6) reduced the ability to increase inguinal white adipose tissue (iWAT) glucose transporter 4 (GLUT4) protein after exercise and resulted in increased stress kinase signaling in adipose tissue late in recovery from prolonged exercise
The results confirm that knockout of skeletal muscle IL-6 can increase pyruvate dehydrogenase (PDHa) activity in skeletal muscle and supports the hypothesis that skeletal muscle IL-6 may play a role in the regulation of carbohydrate and fat metabolism late in recovery from exercise
Summary
A single bout of exercise has profound effects on whole-body metabolism, increasing insulin sensitivity [1], fatty acid oxidation [2] and activating metabolic pathways and gene transcription in skeletal muscle, adipose tissue and liver during recovery [3,4,5,6,7]. The molecular mechanisms underlying the coordination of whole-body metabolism and tissue specific gene transcription during recovery from exercise are unclear Circulating factors such as myokines may contribute to the regulation of these changes. In fed mice injection of IL-6 has been shown to reduce pyruvate dehydrogenase (PDHa) activity in skeletal muscle [11] while lack of skeletal muscle IL-6 has been demonstrated to increase skeletal muscle PDHa activity in mice [12]. Together this indicates that IL-6 is involved in decreasing carbohydrate metabolism in skeletal muscle
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