Beneficial metabolic adaptations due to endurance exercise training in the fasted state

Abstract

Training with limited carbohydrate availability can stimulate adaptations in muscle cells to facilitate energy production via fat oxidation. Here we investigated the effect of consistent training in the fasted state, vs. training in the fed state, on muscle metabolism and substrate selection during fasted exercise. Twenty young male volunteers participated in a 6-wk endurance training program (1-1.5 h cycling at ∼70% Vo(₂max), 4 days/wk) while receiving isocaloric carbohydrate-rich diets. Half of the subjects trained in the fasted state (F; n = 10), while the others ingested ample carbohydrates before (∼160 g) and during (1 g·kg body wt⁻¹·h⁻¹) the training sessions (CHO; n = 10). The training similarly increased Vo(₂max) (+9%) and performance in a 60-min simulated time trial (+8%) in both groups (P < 0.01). Metabolic measurements were made during a 2-h constant-load exercise bout in the fasted state at ∼65% pretraining Vo(₂max). In F, exercise-induced intramyocellular lipid (IMCL) breakdown was enhanced in type I fibers (P < 0.05) and tended to be increased in type IIa fibers (P = 0.07). Training did not affect IMCL breakdown in CHO. In addition, F (+21%) increased the exercise intensity corresponding to the maximal rate of fat oxidation more than did CHO (+6%) (P < 0.05). Furthermore, maximal citrate synthase (+47%) and β-hydroxyacyl coenzyme A dehydrogenase (+34%) activity was significantly upregulated in F (P < 0.05) but not in CHO. Also, only F prevented the development exercise-induced drop in blood glucose concentration (P < 0.05). In conclusion, F is more effective than CHO to increase muscular oxidative capacity and at the same time enhances exercise-induced net IMCL degradation. In addition, F but not CHO prevented drop of blood glucose concentration during fasting exercise.

Fig. 1.

Effects of training in the fasted state (F) vs. training in the carbohydrate-fed state (CHO) on intramyocellular lipid (IMCL) content during a 2-h constant-load exercise bout. Data provided are means ± SE (F: n = 9; CHO: n = 9) and represent values before (pretest) and after (posttest) a 6-wk training period in either the fasted state (F) or with ample carbohydrate intake before and during the training sessions (CHO). Intramyocellular lipid content was measured before and at the end of a 2-h constant-load cycling bout. The workload was 175 ± 6 W and corresponded to 65% of V̇o_2max in the pretest vs. 60% of V̇o_2max in the posttest. Panel Basal IMCL content (A) and net IMCL breakdown (B) in type I (top) and type IIa (bottom) fibers. Fiber type-specific IMCL content was determined by fluorescence microscopy on Oil-Red-O-stained muscle cross sections [arbitrary units (AU)]. *P < 0.05 vs. pretest. #P < 0.05, significant IMCL breakdown during exercise.

Fig. 2.

Intramyocellular lipid content visualized by Oil-Red-O staining before and after a 2-h constant-load exercise bout in one subject before and after training in the fasted state. Pictures show cross sections of a human vastus lateralis muscle before (pretest; A and B) and after (posttest; C and D) a 6-wk training period in the fasted state. Intramyocellular lipid content was measured before (A and C) and at the end of a 2-h constant-load cycling bout (B and D). Intramyocellular lipid droplets are stained red by the Oil-red-O assay. Type I and type IIx muscle fibers are identified; all other fibers are type IIa fibers.

Fig. 3.

Effects of training in the fasted state vs. training in the carbohydrate-fed state on AMPKα phosphorylation during a 2-h constant-load exercise bout. Data provided are means ± SE (F: n = 10; CHO: n = 10) and represent values before (pretest) and after (posttest) a 6-wk training period in either the fasted state (F) or with ample carbohydrate intake before and during the training sessions (CHO). AMPKα phosphorylation was measured before and at the end of a 2-h constant-load cycling bout. The workload was 175 ± 6 W and corresponded to 65% of V̇o_2max in the pretest vs. 60% of V̇o_2max in the posttest. A: basal AMPKα phosphorylation. B: net AMPKα phosphorylation change. AMPKα phosphorylation was determined by Western blotting and expressed relative to total AMPKα protein content (AU). *P < 0.05 vs. pretest.

Fig. 4.

Effects of training in the fasted state vs. training in the carbohydrate-fed state on blood glucose concentration during a 2-h constant-load exercise bout. Data provided are means ± SE (F: n = 10; CHO: n = 10) and represent values before (pretest) and after (posttest) a 6-wk training period in either the fasted state (F) or with ample carbohydrate intake before and during the training sessions (CHO). Concentrations of blood glucose were measured before and at the end of a 2-h constant-load cycling bout. The workload was 175 ± 6 W and corresponded to 65% of V̇o_2max in the pretest vs. 60% of V̇o_2max in the posttest. *P < 0.05 vs. pretest. †P < 0.05 vs. CHO. #P = 0.07 vs. pretest.