Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen

Yeo, Wee Kian, McGee, Sean L., Carey, Andrew L., Paton, Carl D., Garnham, Andrew P., Hargreaves, Mark and Hawley, John A. 2010, Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen, Experimental physiology, vol. 95, no. 2, pp. 351-358, doi: 10.1113/expphysiol.2009.049353.

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Title Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen
Author(s) Yeo, Wee Kian
McGee, Sean L.ORCID iD for McGee, Sean L.
Carey, Andrew L.
Paton, Carl D.
Garnham, Andrew P.
Hargreaves, Mark
Hawley, John A.
Journal name Experimental physiology
Volume number 95
Issue number 2
Start page 351
End page 358
Total pages 8
Publisher Wiley
Place of publication Oxford, England
Publication date 2010-02
ISSN 0958-0670
Summary We have previously demonstrated that well-trained subjects who completed a 3 week training programme in which selected high-intensity interval training (HIT) sessions were commenced with low muscle glycogen content increased the maximal activities of several oxidative enzymes that promote endurance adaptations to a greater extent than subjects who began all training sessions with normal glycogen levels. The aim of the present study was to investigate acute skeletal muscle signalling responses to a single bout of HIT commenced with low or normal muscle glycogen stores in an attempt to elucidate potential mechanism(s) that might underlie our previous observations. Six endurance-trained cyclists/triathletes performed a 100 min ride at ∼70% peak O2 uptake (AT) on day 1 and HIT (8 × 5 min work bouts at maximal self-selected effort with 1 min rest) 24 h later (HIGH). Another six subjects, matched for fitness and training history, performed AT on day 1 then 1–2 h later, HIT (LOW). Muscle biopsies were taken before and after HIT. Muscle glycogen concentration was higher in HIGH versus LOW before the HIT (390 ± 28 versus 256 ± 67 μmol (g dry wt)−1). After HIT, glycogen levels were reduced in both groups (P < 0.05) but HIGH was elevated compared with LOW (229 ± 29 versus 124 ± 41 μmol (g dry wt)−1; P < 0.05). Phosphorylation of 5'AMP-activated protein kinase (AMPK) increased after HIT, but the magnitude of increase was greater in LOW (P < 0.05). Despite the augmented AMPK response in LOW after HIT, selected downstream AMPK substrates were similar between groups. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was unchanged for both groups before and after the HIT training sessions. We conclude that despite a greater activation AMPK phosphorylation when HIT was commenced with low compared with normal muscle glycogen availability, the localization and phosphorylation state of selected downstream targets of AMPK were similar in response to the two interventions.
Language eng
DOI 10.1113/expphysiol.2009.049353
Field of Research 060114 Systems Biology
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
HERDC collection year 2010
Copyright notice ©2009, Wiley
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Document type: Journal Article
Collection: School of Medicine
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Created: Fri, 12 Mar 2010, 12:05:01 EST by Sean McGee

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