Exercise in the fasted state facilitates fibre type‐specific intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans

Feb 12, 2005The Journal of physiology

Exercise without eating first helps break down specific muscle fat and rebuilds muscle energy stores in people

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Abstract

Fasted exercise reduced intramyocellular triglyceride (IMTG) content in type I muscle fibers from 18% to 6%.

Exercise in the fasted state led to a significant decrease in IMTG content in type I fibers, while the carbohydrate-fed state maintained IMTG levels.
During recovery, IMTG in type I fibers decreased in the carbohydrate condition but remained unchanged in the fasted state.
The rate of muscle glycogen resynthesis was three times greater in the fasted state compared to the carbohydrate-fed state.
Post-exercise oral glucose loading resulted in a significantly higher increase in plasma insulin levels after fasted exercise than after carbohydrate intake.
IMTG breakdown during prolonged exercise primarily occurs in type I fibers when fasted, and this process is inhibited in the presence of carbohydrates.

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The effects were compared of exercise in the fasted state and exercise with a high rate of carbohydrate intake on intramyocellular triglyceride (IMTG) and glycogen content of human muscle. Using a randomized crossover study design, nine young healthy volunteers participated in two experimental sessions with an interval of 3 weeks. In each session subjects performed 2 h of constant-load bicycle exercise ( approximately 75% ), followed by 4 h of controlled recovery. On one occasion they exercised after an overnight fast (F), and on the other (CHO) they received carbohydrates before ( approximately 150 g) and during (1 g (kg bw)(-1) h(-1)) exercise. In both conditions, subjects ingested 5 g carbohydrates per kg body weight during recovery. Fibre type-specific relative IMTG content was determined by Oil red O staining in needle biopsies from m. vastus lateralis before, immediately after and 4 h after exercise. During F but not during CHO, the exercise bout decreased IMTG content in type I fibres from 18 +/- 2% to 6 +/- 2% (P = 0.007) area lipid staining. Conversely, during recovery, IMTG in type I fibres decreased from 15 +/- 2% to 10 +/- 2% in CHO, but did not change in F. Neither exercise nor recovery changed IMTG in type IIa fibres in any experimental condition. Exercise-induced net glycogen breakdown was similar in F and CHO. However, compared with CHO (11.0 +/- 7.8 mmol kg(-1) h(-1)), mean rate of postexercise muscle glycogen resynthesis was 3-fold greater in F (32.9 +/- 2.7 mmol kg(-1) h(-1), P = 0.01). Furthermore, oral glucose loading during recovery increased plasma insulin markedly more in F (+46.80 microU ml(-1)) than in CHO (+14.63 microU ml(-1), P = 0.02). We conclude that IMTG breakdown during prolonged submaximal exercise in the fasted state takes place predominantly in type I fibres and that this breakdown is prevented in the CHO-fed state. Furthermore, facilitated glucose-induced insulin secretion may contribute to enhanced muscle glycogen resynthesis following exercise in the fasted state.

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Exercise in the fasted state facilitates fibre type‐specific intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans

Abstract

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