Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise

• Published in: Journal of applied physiology (1985) Vol. 94; no. 6; pp. 2181 - 2187
• Main Authors: Baldwin, Jacinta, Snow, Rodney J, Gibala, Martin J, Garnham, Andrew, Howarth, Krista, Febbraio, Mark A
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01.06.2003; American Physiological Society
• Subjects: Adenine Nucleotides - metabolism; Adenosine diphosphate; Adult; Amino Acids - metabolism; Biological and medical sciences; Blood Glucose - analysis; Citric Acid Cycle - physiology; Exercise; Exercise - physiology; Fatigue; Fatigue - etiology; Fundamental and applied biological sciences. Psychology; Glycogen - metabolism; Heart Rate; Humans; Hypoxanthine - blood; Hypoxanthine - metabolism; Inosine Monophosphate - metabolism; Lactic Acid - blood; Lactic Acid - metabolism; Male; Metabolism; Muscle, Skeletal - metabolism; Muscular system; Oxygen Consumption; Oxygen uptake; Pyruvates - metabolism; Stress; Striated muscle. Tendons; Time Factors; Vertebrates: osteoarticular system, musculoskeletal system; Physical exercise; Human; Glycogen; Bicycle ergometer; Fatigue; Bioavailability; Metabolism; citric acid cycle; hypoxanthine; Carbohydrate; metabolic stress; Adenine nucleotide; Tricarboxylic acid
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00866.2002

1  Department of Physiology, University of Melbourne, Parkville 3010, Victoria; 2  School of Health Sciences, Deakin University, Burwood 3125, Victoria; 4  Skeletal Muscle Research Laboratory, School of Medical Sciences, Royal Melbourne Institute of Technology, Bundoora 3083, Victoria, Australia; and 3  Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S4K1 The hypothesis that fatigue during prolonged exercise arises from insufficient intramuscular glycogen, which limits tricarboxylic acid cycle (TCA) activity due to reduced TCA cycle intermediates (TCAI), was tested in this experiment. Seven endurance-trained men cycled at ~70% of peak O 2 uptake ( O 2 peak ) until exhaustion with low (LG) or high (HG) preexercise intramuscular glycogen content. Muscle glycogen content was lower ( P  < 0.05) at fatigue than at rest in both trials. However, the increase in the sum of four measured TCAI (>70% of the total TCAI pool) from rest to 15 min of exercise was not different between trials, and TCAI content was similar after 103 ± 15 min of exercise (2.62   ± 0.31 and 2.59 ± 0.28 mmol/kg dry wt for LG and HG, respectively), which was the point of volitional fatigue during LG. Subjects cycled for an additional 52 ± 9 min during HG, and although glycogen was markedly reduced ( P  < 0.05) during this period, no further change in the TCAI pool was observed, thus demonstrating a clear dissociation between exercise duration and the size of the TCAI pool. Neither the total adenine nucleotide pool (TAN = ATP + ADP   + AMP) nor IMP was altered compared with rest in either trial, whereas creatine phosphate levels were not different when values measured at fatigue were compared with those measured after 15   min of exercise. These data demonstrate that altered glycogen availability neither compromises TCAI pool expansion nor affects the TAN pool or creatine phosphate or IMP content during prolonged exercise to fatigue. Therefore, our data do not support the concept that a decrease in muscle TCAI during prolonged exercise in humans compromises aerobic energy provision or is the cause of fatigue. citric acid cycle; metabolic stress; hypoxanthine