Skeletal Muscle Glycogen Breakdown According to Duration of Endurance Training.
10.5763/kjsm.2016.34.2.101
- Author:
Sang Hyun KIM
1
Author Information
1. Department of Sports Science, Chonbuk National University, Jeonju, Korea. sh5275@jbnu.ac.kr
- Publication Type:Review
- Keywords:
Exercise;
Glycogen;
Mitochondria;
Peroxisome proliferator-activated receptor-γ coactivator-1α;
Glycogenolysis
- MeSH:
Adenosine Triphosphate;
Glycogen*;
Glycogenolysis;
Lactic Acid;
Mitochondria;
Muscle Fatigue;
Muscle, Skeletal*;
Muscles;
Organelle Biogenesis;
Peroxisomes;
Phosphocreatine
- From:The Korean Journal of Sports Medicine
2016;34(2):101-106
- CountryRepublic of Korea
- Language:Korean
-
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.
