Evidence map›Paper›PMID 16051629›Full record

Trial reportThe Journal of physiology2005

Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen.

Glenn K McConell, Robert S Lee-Young, Zhi-Ping Chen, Nigel K Stepto, Ngan N Huynh, Terry J Stephens, Benedict J Canny, Bruce E Kemp

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

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  5. Intensive training and reduced volume increases muscle FXYD1 expression and phosphorylation at rest and during exercise in athletes.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Glenn K McConellDepartment of Physiology, University of Melbourne, Parkville, Victoria, Australia. mcconell@unimelb.edu.au
Robert S Lee-Young
Zhi-Ping Chen
Nigel K Stepto
Ngan N Huynh
Terry J Stephens
Benedict J Canny
Bruce E Kemp
Monash University · AUCommonwealth Scientific and Industrial Research Organisation · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We examined the effect of short-term exercise training on skeletal muscle AMP-activated protein kinase (AMPK) signalling and muscle metabolism during prolonged exercise in humans. Eight sedentary males completed 120 min of cycling at 66 +/- 1% , then exercise trained for 10 days, before repeating the exercise bout at the same absolute workload. Participants rested for 72 h before each trial while ingesting a high carbohydrate diet (HCHO). Exercise training significantly (P < 0.05) attenuated exercise-induced increases in skeletal muscle free AMP: ATP ratio and glucose disposal and increased fat oxidation. Exercise training abolished the 9-fold increase in AMPK alpha2 activity observed during pretraining exercise. Since training increased muscle glycogen content by 93 +/- 12% (P < 0.01), we conducted a second experiment in seven sedentary male participants where muscle glycogen content was essentially matched pre- and post-training by exercise and a low CHO diet (LCHO; post-training muscle glycogen 52 +/- 7% less than in HCHO, P < 0.001). Despite the difference in muscle glycogen levels in the two studies we obtained very similar results. In both studies the increase in ACCbeta Ser(221) phosphorylation was reduced during exercise after training. In conclusion, there is little activation of AMPK signalling during prolonged exercise following short-term exercise training suggesting that other factors are important in the regulation of glucose disposal and fat oxidation under these circumstances. It appears that muscle glycogen is not an important regulator of AMPK activation during exercise in humans when exercise is begun with normal or high muscle glycogen levels.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesBlood GlucoseDietary CarbohydratesExerciseGlucoseGlycogenHumansLipid MetabolismMaleMultienzyme ComplexesMuscle, SkeletalPhosphorylationProtein Serine-Threonine KinasesSerineSignal TransductionAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesBlood GlucoseDietary CarbohydratesGlucoseGlycogenMultienzyme ComplexesPRKAA2 protein, humanProtein Serine-Threonine KinasesSerine

Identifiers

PMID16051629
PMCPMC1474728
OpenAlexW1583686565

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.