Abstract
Recent studies of the ketogenic diet, an extremely high-fat diet with extremely low carbohydrates, suggest that it changes the energy metabolism properties of skeletal muscle. However, ketogenic diet effects on muscle metabolic characteristics are diverse and sometimes countervailing. Furthermore, ketogenic diet effects on skeletal muscle performance are unknown. After male Wistar rats (8 weeks of age) were assigned randomly to a control group (CON) and a ketogenic diet group (KD), they were fed for 4 weeks respectively with a control diet (10% fat, 10% protein, 80% carbohydrate) and a ketogenic diet (90% fat, 10% protein, 0% carbohydrate). After the 4-week feeding period, the extensor digitorum longus (EDL) muscle was evaluated ex vivo for twitch force, tetanic force, and fatigue. We also analyzed the myosin heavy chain composition, protein expression of metabolic enzymes and regulatory factors, and citrate synthase activity. No significant difference was found between CON and KD in twitch or tetanic forces or muscle fatigue. However, the KD citrate synthase activity and the protein expression of Sema3A, citrate synthase, succinate dehydrogenase, cytochrome c oxidase subunit 4, and 3-hydroxyacyl-CoA dehydrogenase were significantly higher than those of CON. Moreover, a myosin heavy chain shift occurred from type IIb to IIx in KD. These results demonstrated that the 4-week ketogenic diet improves skeletal muscle aerobic capacity without obstructing muscle contractile function in sedentary male rats and suggest involvement of Sema3A in the myosin heavy chain shift of EDL muscle.
Highlights
The ketogenic diet, a high-fat diet with low or absent carbohydrate, mimics the fasting state of the body [1]
No significant difference in the expression of PFK was found between control group (CON) and ketogenic diet group (KD) (Fig 2F)
Because we found increased expression of Citrate synthase (CS), COX-IV, and HAD in addition to fast-to-slow shift of myosin heavy chain (MyHC) type II isoforms, we analyzed the expressions of PGC-1α, PPAR-α, Mef2C, and key proteins related to those changes as potential mechanisms (Fig 4)
Summary
The ketogenic diet, a high-fat diet with low or absent carbohydrate, mimics the fasting state of the body [1]. This diet increases ketone production from the liver and shifts energy sources to fat instead of carbohydrate [2,3,4,5,6]. The generated ketone is used eventually as an energy substrate in different organs such as the brain and skeletal muscles.
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