Evidence map›Paper›PMID 26792336›Full record

ReviewThe Journal of experimental biology2016

Mitochondria to motion: optimizing oxidative phosphorylation to improve exercise performance.

Kevin E Conley

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of experimental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 77 citations in OpenAlex.

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  14. Diurnal variation in skeletal muscle mitochondrial function dictates time-of-day-dependent exercise capacity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  17. Non-lethal sampling for assessment of mitochondrial function does not affect metabolic rate and swimming performance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kevin E ConleyDepartments of Radiology, Physiology & Biophysics, and Bioengineering, University of Washington Medical Center, Seattle, WA 98195, USA kconley@uw.edu.
University of Washington Medical Center · US

Funding

MR &Optical Diagnosis of Muscle Metabolism and FunctionR01AR041928 · NIAMS · UNIVERSITY OF WASHINGTON · PI CONLEY, KEVIN E · 1993 to 2011
$6.8M
Translational Center for In Vivo Mitochondrial MedicineRC2AG036606 · NIA · UNIVERSITY OF WASHINGTON · PI CONLEY, KEVIN E, MARCINEK, DAVID J. · 2009 to 2010
$1.5M
RESPIRATION AND GLYCOLYSIS--INTEGRATION IN ACTIVE MUSCLER01AR045184 · NIAMS · UNIVERSITY OF WASHINGTON · PI CONLEY, KEVIN E · 1998 to 2002
$872k
NIAMS NIH HHS R01 AR41928NIAMS NIH HHS R01 AR45184NIA NIH HHS RC2 AG036606PHS HHS R01 AGAR10853
6 · The paper itself

Abstract

Mitochondria oxidize substrates to generate the ATP that fuels muscle contraction and locomotion. This review focuses on three steps in oxidative phosphorylation that have independent roles in setting the overall mitochondrial ATP flux and thereby have direct impact on locomotion. The first is the electron transport chain, which sets the pace for oxidation. New studies indicate that the electron transport chain capacity per mitochondria declines with age and disease, but can be revived by both acute and chronic treatments. The resulting higher ATP production is reflected in improved muscle power output and locomotory performance. The second step is the coupling of ATP supply from O2 uptake (mitochondrial coupling efficiency). Treatments that elevate mitochondrial coupling raise both exercise efficiency and the capacity for sustained exercise in both young and old muscle. The final step is ATP synthesis itself, which is under dynamic control at multiple sites to provide the 50-fold range of ATP flux between resting muscle and exercise at the mitochondrial capacity. Thus, malleability at sites in these subsystems of oxidative phosphorylation has an impact on ATP flux, with direct effects on exercise performance. Interventions are emerging that target these three independent subsystems to provide many paths to improve ATP flux and elevate the muscle performance lost to inactivity, age or disease.

Indexed as

MotionAnimalsElectron TransportExerciseHumansMitochondria, MuscleOxidative PhosphorylationPhosphorylationExercise capacityExercise efficiencyMagnetic resonance spectroscopyMitochondrial couplingMuscle energeticsP/O

Identifiers

PMID26792336
PMCPMC6514472
OpenAlexW2401970375

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.