Evidence map›Paper›PMID 28332118›Full record

ReviewSports medicine (Auckland, N.Z.)2017

Nutrition and Training Influences on the Regulation of Mitochondrial Adenosine Diphosphate Sensitivity and Bioenergetics.

Graham P Holloway

Open access · hybridAbstract readReview
In one paragraph

Review in Sports medicine (Auckland, N.Z.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. A High-Fat Diet Induces Oxidative Stress in OPA1Antioxidants (Basel, Switzerland) · 2025
    Article
  5. Review
  6. Mitochondrial Biogenesis in Skeletal Muscle.Advances in experimental medicine and biology · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Recent advances in mitochondrial diseases: From molecular insights to therapeutic perspectives.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Review
  11. Article
  12. Article
  13. Sarcopenia: Etiology, Nutritional Approaches, and miRNAs.International journal of molecular sciences · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
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.

Graham P HollowayDepartment of Human Health and Nutritional Sciences, University of Guelph, 491 Gordon St., Guelph, ON, N1G 2W1, Canada. ghollowa@uoguelph.ca.
University of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the seminal finding almost 50 years ago that exercise training increases mitochondrial content in skeletal muscle, a considerable amount of research has been dedicated to elucidate the mechanisms inducing mitochondrial biogenesis. The discovery of peroxisome proliferator-activated receptor γ co-activator 1α as a major regulator of exercise-induced gene transcription was instrumental in beginning to understand the signals regulating this process. However, almost two decades after its discovery, our understanding of the signals inducing mitochondrial biogenesis remain poorly defined, limiting our insights into possible novel training modalities in elite athletes that can increase the oxidative potential of muscle. In particular, the role of mitochondrial reactive oxygen species has received very little attention; however, several lifestyle interventions associated with an increase in mitochondrial reactive oxygen species coincide with the induction of mitochondrial biogenesis. Furthermore, the diminishing returns of exercise training are associated with reductions in exercise-induced, mitochondrial-derived reactive oxygen species. Therefore, research focused on altering redox signaling in elite athletes may prove to be effective at inducing mitochondrial biogenesis and augmenting training regimes. In the context of exercise performance, the biological effect of increasing mitochondrial content is an attenuated rise in free cytosolic adenosine diphosphate (ADP), and subsequently decreased carbohydrate flux at a given power output. Recent evidence has shown that mitochondrial ADP sensitivity is a regulated process influenced by nutritional interventions, acute exercise, and exercise training. This knowledge raises the potential to improve mitochondrial bioenergetics in the absence of changes in mitochondrial content. Elucidating the mechanisms influencing the acute regulation of mitochondrial ADP sensitivity could have performance benefits in athletes, especially as these individuals display high levels of mitochondria, and therefore are subjects in whom it is notoriously difficult to further induce mitochondrial adaptations. In addition to changes in ADP sensitivity, an increase in mitochondrial coupling would have a similar bioenergetic response, namely a reduction in free cytosolic ADP. While classically the stoichiometry of the electron transport chain has been considered rigid, recent evidence suggests that sodium nitrate can improve the efficiency of this process, creating the potential for dietary sources of nitrate (e.g., beetroot juice) to display similar improvements in exercise performance. The current review focuses on these processes, while also discussing the biological relevance in the context of exercise performance.

Indexed as

Energy MetabolismAdenosine DiphosphateExerciseHumansMitochondriaMitochondria, MuscleMuscle, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTranscription FactorsAdenosine DiphosphatePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTranscription Factors

Identifiers

PMID28332118
PMCPMC5371621
OpenAlexW2599053467

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.