Carbohydrate is a crucial energy fuel for exercise, and carbohydrate supplementation as peri-exercise has beneficial effects on exercise performance. However, recent studies have indicated the possibility that periodized carbohydrate restriction improves exercise performance. Carbohydrate restriction before exercise increases fatty-acid oxidation (FAO) and alternatively prevents carbohydrate consumption during exercise. This may contribute to the prevention of muscle glycogen depletion during endurance exercise competition. Additionally, acute and chronic studies have shown that peri-exercise carbohydrate restriction enhances molecular and functional adaptation related to FAO. Similarly, exercise training in a low-muscle glycogen state accompanied by carbohydrate restriction was reported to enhance mitochondrial biogenesis and improve FAO capacity, aerobic capacity, and endurance performance in untrained and highly trained subjects. The potential mechanism of these metabolic adaptations may be related to elevated circulating fatty-acid and adrenaline concentration during exercise with carbohydrate restriction and/or a low-muscle glycogen state. In addition, a decrease in muscle glycogen content may trigger signaling pathways related to FAO and mitochondria biogenesis by activating proteins with a glycogen-binding domain. This article reviews the effects of exercise with carbohydrate restriction and/or low-muscle glycogen state on metabolic adaptation and exercise performance and describes the molecular mechanisms and availability.

The decrease of muscle glycogen may be useful for the improvement of endurance performance. Intense anaerobic exercise requires a high rate of glycogen utilization, but consecutive intense anaerobic exercises induce a pronounced decline of external power and muscle glycogen consumption. We hypothesized that a long rest period between consecutive intense anaerobic exercises may aid in sustaining external power and glycogen consumption. Secondly, we hypothesized that active rest (AR) during the long resting period may be more effective than passive rest (PR).Six subjects performed four 30-second Wingate tests (WAnT) with a 4-minute recovery between each bout (Consecutive method). The subjects also performed a similar exercise procedure, but with a 30-minute seated resting period after the second bout (PR method).The other six male subjects performed four 30-second WAnTs with a 4-minute recovery between each bout, with 30-minutes of cycling at 40% VO₂max after the second bout (AR method). The subjects also performed PR method.The total work during the third and fourth bouts was greatest under the AR condition, followed by the PR condition, and finally the Consecutive method (p<0.05 for all comparisons). Blood lactate concentration during resting period was significantly lower, while muscle glycogen consumption was greater AR method than PR method (p<0.05 for both).A long resting period between consecutive intense anaerobic exercises may prevent the decline in external power and work. Additionally, AR has more favorable effects on muscle glycogen consumption, resulting in very low muscle glycogen levels, even with a small total amount of exercise.

Recent studies indicate that exercise with a low muscle glycogen state enhances exercise-induced metabolic adaptation. However, it is unclear whether metabolic adaptation is involved with muscle glycogen depletion level. In this study, we investigated the effects of prior muscle glycogen depletion level on metabolic response during acute continuous exercise. Seven men completed two experimental trials consisting of two exercise sessions per day. During the first session, participants performed either intermittent exercise (IE) at VO₂max (the IE-CE trial) or continuous exercise (CE) at lactate threshold (the CE-CE trial). During the second session, participants performed 60 minutes of CE at lactate threshold. During this second session, fatty acid oxidation (FAO) was calculated. To determine muscle glycogen content and PGC-1α and PDK-4 mRNA abundance, muscle biopsies were taken at rest after the first session and 2 hours after the second session. After the first session, muscle glycogen content was significantly lower in the IE-CE trial (38.1±5.0 mmol/kg w.w.) than in the CE-CE trial (56.7±10.2 mmol/kg w.w.), P<0.05. FAO was higher in the IE-CE trial than the CE-CE trial at baseline and 15 minutes after the second session (both P<0.05). PGC-1α mRNA abundance increased after exercise (IE-CE, 5.9±2.5; CE-CE, 2.6±1.3-fold; P<0.1). PDK-4 mRNA abundance increased significantly after exercise (IE-CE, 22.2±8.8; CE-CE, 31.5±10.6-fold; P<0.05). PGC-1α and PDK-4 mRNA were not significantly different between the trials. In conclusion, continuous exercise with a slightly muscle glycogen-depleted state induced similar level of PGC-1α and PDK-4 mRNA expression, but attenuated FAO, compared to exercise with a moderate muscle glycogen-depleted state.