Skeletal Muscle Glycogen Breakdown According to Duration of Endurance Training

Sang Hyun Kim

doi:10.5763/kjsm.2016.34.2.101

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Kim: Skeletal Muscle Glycogen Breakdown According to Duration of Endurance Training

Review Article

Korean J Sports Med 2016;34(2):101-106.

Published online: 20 January 2016

DOI: https://doi.org/10.5763/kjsm.2016.34.2.101

Skeletal Muscle Glycogen Breakdown According to Duration of Endurance Training

Sang Hyun Kim

Department of Sports Science, Chonbuk National University, Jeonju, Korea

Correspondence: Sang Hyun Kim Department of Sports Science, Chonbuk National University, 567 Baekje-daero, Deokjin-gu, Jeonju 54896, Korea Tel: +82-63-270-2853, Fax: +82-63-270-4234 E-mail: sh5275@jbnu.ac.kr

Received 31 October 2016 Revised 26 November 2016 Accepted 26 November 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Endurance exercise training such as marathon can increase the ability of exercise performance. Muscle glycogen is associated with an exercise performance, because glycogen depletion is primary causes of muscle fatigue. This review summarizes the glycogen saving effect according to duration of endurance exercise training. Long-term endurance exercise-induced mitochondrial biogenesis contributes to glycogen saving effect that is reduced glycogen breakdown and lactate accumulation. Glycogen sparing is due to a smaller decrease in adenosine triphosphate and phosphocreatine and a smaller increase in inorganic phosphate in the working muscles. It takes required endurance exercise training for about 4 weeks or more. Single bout or short-term endurance exercise is not sufficient to bring an increase in functional mitochondria. But peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) increases rapidly after single bout of endurance exercise. PGC-1α downregulates glycogenolytic and glycolytic enzymes to reduce muscle glycogen breakdown and lactic acid accumulation after short-term endurance exercise.

Keywords: Exercise, Glycogen, Mitochondria, Peroxisome proliferator-activated receptor-γ, coactivator-1α, Glycogenolysis

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Fig. 1.

Glucose-fatty acid cycle (Randle cycle). G-6-P, glucose 6-phosphate; PFK, phosphofructokinase; PDH, pyruvate dehydrogenase.

Fig. 2.

Inorganic phosphate (Pi) mediates the slowing of glycogenolysis and lactate production. G-6-P, glucose 6-phosphate; FFA, free fatty acids; ATP, adenosine triphosphate; ADP, adenosine diphosphate; PCr, phosphocreatine.

Fig. 3.

Peroxisome proliferator-activated receptor-γ coacti-vator-1α (PGC-1α) mediates downregulation of glycogenolytic and glycolytic enzymes to reduce glycogen breakdown and lactate production. Pi, Inorganic phosphate; ATP, adenosine triphosphate; ADP, adenosine diphosphate; G-1-P, glucose 1-phosphate; PFK, phosphofructokinase; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; LDH, lactate dehydrogenase; PDH, pyruvate dehydrogenase.

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