Journal of Applied Physiology AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 97: 579-584, 2004. First published April 30, 2004; doi:10.1152/japplphysiol.01344.2003
8750-7587/04 $5.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
97/2/579    most recent
01344.2003v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Howarth, K. R.
Right arrow Articles by Gibala, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Howarth, K. R.
Right arrow Articles by Gibala, M. J.

Effect of endurance training on muscle TCA cycle metabolism during exercise in humans

Krista R. Howarth,1 Paul J. LeBlanc,2 George J. F. Heigenhauser,2 and Martin J. Gibala1

1Exercise Metabolism Research Group, Department of Kinesiology, and 2Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8S 4K1

Submitted 16 December 2003 ; accepted in final form 19 April 2004

We tested the theory that links the capacity to perform prolonged exercise with the size of the muscle tricarboxylic acid (TCA) cycle intermediate (TCAI) pool. We hypothesized that endurance training would attenuate the exercise-induced increase in TCAI concentration ([TCAI]); however, the lower [TCAI] would not compromise cycle endurance capacity. Eight men (22 ± 1 yr) cycled at ~80% of initial peak oxygen uptake before and after 7 wk of training (1 h/day, 5 days/wk). Biopsies (vastus lateralis) were obtained during both trials at rest, after 5 min, and at the point of exhaustion during the pretraining trial (42 ± 6 min). A biopsy was also obtained at the end of exercise during the posttraining trial (91 ± 6 min). In addition to improved performance, training increased (P < 0.05) peak oxygen uptake and citrate synthase maximal activity. The sum of four measured TCAI was similar between trials at rest but lower after 5 min of exercise posttraining [2.7 ± 0.2 vs. 4.3 ± 0.2 mmol/kg dry wt (P < 0.05)]. There was a clear dissociation between [TCAI] and endurance capacity because the [TCAI] at the point of exhaustion during the pretraining trial was not different between trials (posttraining: 2.9 ± 0.2 vs. pretraining: 3.5 ± 0.2 mmol/kg dry wt), and yet cycle endurance time more than doubled in the posttraining trial. Training also attenuated the exercise-induced decrease in glutamate concentration (posttraining: 4.5 ± 0.7 vs. pretraining: 7.7 ± 0.6 mmol/kg dry wt) and increase in alanine concentration (posttraining: 3.3 ± 0.2 vs. pretraining: 5.6 ± 0.3 mmol/kg dry wt; P < 0.05), which is consistent with reduced carbon flux through alanine aminotransferase. We conclude that, after aerobic training, cycle endurance capacity is not limited by a decrease in muscle [TCAI].

metabolic regulation; amino acids; acetyl CoA



Address for reprint requests and other correspondence: M. J. Gibala, Exercise Metabolism Research Group, Dept. of Kinesiology, IWC Rm. AB122, McMaster University, Hamilton, Ontario, Canada L8S 4K1 (E-mail: gibalam{at}mcmaster.ca).




This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
Y. Li, R. K. Dash, J. Kim, G. M. Saidel, and M. E. Cabrera
Role of NADH/NAD+ transport activity and glycogen store on skeletal muscle energy metabolism during exercise: in silico studies
Am J Physiol Cell Physiol, January 1, 2009; 296(1): C25 - C46.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
M. Mourtzakis, T. E. Graham, J. Gonzalez-Alonso, and B. Saltin
Glutamate availability is important in intramuscular amino acid metabolism and TCA cycle intermediates but does not affect peak oxidative metabolism
J Appl Physiol, August 1, 2008; 105(2): 547 - 554.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
G. D. Lewis, A. Asnani, and R. E. Gerszten
Application of Metabolomics to Cardiovascular Biomarker and Pathway Discovery
J. Am. Coll. Cardiol., July 8, 2008; 52(2): 117 - 123.
[Abstract] [Full Text] [PDF]


Home page
Exp PhysiolHome page
N. R. Stob, D. R. Seals, J. Jensen, M. A. van Baak, A. J. Steig, R. C. Lindstrom, B. T. Bikman, and C. Bell
Autonomic Neuroscience: Increased thermogenic responsiveness to intravenous {beta}-adrenergic stimulation in habitually exercising humans is not related to skeletal muscle {beta}2-adrenergic receptor density
Exp Physiol, September 1, 2007; 92(5): 823 - 830.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
K. D. Dawson, D. J. Baker, P. L. Greenhaff, and M. J. Gibala
An acute decrease in TCA cycle intermediates does not affect aerobic energy delivery in contracting rat skeletal muscle
J. Physiol., June 1, 2005; 565(2): 637 - 643.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.