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Study · Measured the body's own peptide · 2024

4 results

Temporal expression of mitochondrial life cycle markers during acute and chronic overload of rat plantaris muscles.

Hyatt JK, Lu EJ, McCall GE

Frontiers in physiology30 Aug 2024Cited by 2 (Europe PMC)

PMID39282091 (opens in a new tab)PMCIDPMC11392739 (opens in a new tab)DOI10.3389/fphys.2024.1420276 (opens in a new tab)PepBankPUB-39282091
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Summary

Skeletal muscle hypertrophy is generally associated with a fast-to-slow phenotypic adaptation in both human and rodent models. Paradoxically, this phenotypic shift is not paralleled by a concomitant increase in mitochondrial content and aerobic markers that would be expected to accompany a slow muscle phenotype. To understand the temporal response of the mitochondrial life cycle (i.e., biogenesis, oxidative phosphorylation, fission/fusion, and mitophagy/autophagy) to hypertrophic stimuli, in this study, we used the functional overload (FO) model in adult female rats and examined the plantaris muscle responses at 1 and 10 weeks. As expected, the absolute plantaris muscle mass increased by ∼12 and 26% at 1 and 10 weeks following the FO procedure, respectively. Myosin heavy-chain isoform types I and IIa significantly increased by 116% and 17%, respectively, in 10-week FO plantaris muscles. Although there was a general increase in protein markers associated with mitochondrial biogenesis in acute FO muscles, this response was unexpectedly sustained under 10-week FO conditions after muscle hypertrophy begins to plateau. Furthermore, the early increase in mito/autophagy markers observed under acute FO conditions was normalized by 10 weeks, suggesting a cellular environment favoring mitochondrial biogenesis to accommodate the aerobic demands of the plantaris muscle. We also observed a significant increase in the expression of mitochondrial-, but not nuclear-, encoded oxidative phosphorylation (OXPHOS) proteins and peptides (i.e., humanin and MOTS-c) under chronic, but not acute, FO conditions. Taken together, the temporal response of markers related to the mitochondrial life cycle indicates a pattern of promoting biogenesis and mitochondrial protein expression to support the energy demands and/or enhanced neural recruitment of chronically overloaded skeletal muscle.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

No result from this study comes from a test of the peptide.

Natural levels measured4

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Other

    In rats, MOTS‑c expression increased in plantaris muscle after 10 weeks of functional overload.

    In plain wordsIn rats, the body's own MOTS‑c rose in muscle that was overloaded for a long time.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c expression under chronic overload
    Study

    ratn: not reported in source

    Functional overload of plantaris muscle
    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    We also observed a significant increase in the expression of mitochondrial-, but not nuclear-, encoded oxidative phosphorylation (OXPHOS) proteins and peptides (i.e., humanin and MOTS-c) under chronic, but not acute, FO conditions.
    1 context sentence
    Summary · context
    To understand the temporal response of the mitochondrial life cycle (i.e., biogenesis, oxidative phosphorylation, fission/fusion, and mitophagy/autophagy) to hypertrophic stimuli, in this study, we used the functional overload (FO) model in adult female rats and examined the plantaris muscle responses at 1 and 10 weeks.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Other

    In rats, MOTS‑c expression did not increase in plantaris muscle at 1 week of functional overload.

    In plain wordsIn rats, the body's own MOTS‑c did not rise in muscle after short-term overload.

    Peptide
    MOTS-c
    Outcome
    No significant changeMOTS-c expression under acute overload
    Study

    ratn: not reported in source

    Functional overload of plantaris muscle
    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    We also observed a significant increase in the expression of mitochondrial-, but not nuclear-, encoded oxidative phosphorylation (OXPHOS) proteins and peptides (i.e., humanin and MOTS-c) under chronic, but not acute, FO conditions.
    1 context sentence
    Summary · context
    To understand the temporal response of the mitochondrial life cycle (i.e., biogenesis, oxidative phosphorylation, fission/fusion, and mitophagy/autophagy) to hypertrophic stimuli, in this study, we used the functional overload (FO) model in adult female rats and examined the plantaris muscle responses at 1 and 10 weeks.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  3. 03AnimalEndogenous levelAnimal study (in vivo)Other

    In rats, the muscle's own humanin expression increased in plantaris muscle under chronic (10-week) functional overload.

    In plain wordsIn rats, the muscle's own humanin levels rose after 10 weeks of heavy muscle overload.

    Peptide
    Humanin
    Outcome
    IncreaseHumanin expression under chronic functional overload
    Study

    ratn: not reported in source

    Functional overload of the plantaris muscle
    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    We also observed a significant increase in the expression of mitochondrial-, but not nuclear-, encoded oxidative phosphorylation (OXPHOS) proteins and peptides (i.e., humanin and MOTS-c) under chronic, but not acute, FO conditions.
    1 context sentence
    Summary · context
    To understand the temporal response of the mitochondrial life cycle (i.e., biogenesis, oxidative phosphorylation, fission/fusion, and mitophagy/autophagy) to hypertrophic stimuli, in this study, we used the functional overload (FO) model in adult female rats and examined the plantaris muscle responses at 1 and 10 weeks.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

  4. 04AnimalEndogenous levelAnimal study (in vivo)Other

    In rats, the muscle's own humanin expression did not increase in plantaris muscle under acute (1-week) functional overload.

    In plain wordsIn rats, the muscle's own humanin levels did not rise after 1 week of heavy muscle overload.

    Peptide
    Humanin
    Outcome
    No significant changeHumanin expression under acute functional overload
    Study

    ratn: not reported in source

    Functional overload of the plantaris muscle
    Outcome group
    Mitochondrial function · Musculoskeletal

    Source sentences

    Summary
    We also observed a significant increase in the expression of mitochondrial-, but not nuclear-, encoded oxidative phosphorylation (OXPHOS) proteins and peptides (i.e., humanin and MOTS-c) under chronic, but not acute, FO conditions.
    1 context sentence
    Summary · context
    To understand the temporal response of the mitochondrial life cycle (i.e., biogenesis, oxidative phosphorylation, fission/fusion, and mitophagy/autophagy) to hypertrophic stimuli, in this study, we used the functional overload (FO) model in adult female rats and examined the plantaris muscle responses at 1 and 10 weeks.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Versions 4 to 18Current

    28 Oct 2026, 02:02 UTC

    The same notice was added 15 times, first on 13 Oct 2026, 21:44 UTC. The status did not change between them.

    Study results updated

  2. Version 3

    13 Oct 2026, 16:31 UTC

    Study data updated · source update from Europe PMC

  3. Version 2

    10 Oct 2026, 08:19 UTC

    Study results updated

  4. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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