Component

Human skeletal-muscle ATP synthetic flux by 31P-MRS

Human skeletal-muscle ATP synthetic flux by 31P-MRS. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Higher reported phosphate intake was associated with lower resting ATP synthesis (r=−0.62, p=0.03) in the 13-person pilot.

    Dietary phosphate intake normalized to total energy intake → Human skeletal-muscle ATP synthetic flux by 31P-MRS source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/38482570.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11f6599b477ce87228e00e4d562eb0c70615dceebb82a983188e9b0fcd8e730f", "start_char": 0, "end_char": 2164, "text_sha256": "11f6599b477ce87228e00e4d562eb0c70615dceebb82a983188e9b0fcd8e730f"}
    experimental_model
    Small cross-sectional diet-recall and 31P-MRS association study
    exposure
    24-hour dietary recall normalized to energy; calf-muscle MRS at rest/exercise
    limitations
    Observational pilot with n=13, not a controlled excess-phosphate intervention. The source uses a phosphocreatinine wording error; PCr is represented as phosphocreatine.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    More reported dietary phosphorus did not imply better energetics; this association does not establish causation.
    primary_references
    [phosphorus-p38482570] Association between dietary phosphate intake and skeletal muscle energetics in adults without cardiovascular disease. (2024). https://pubmed.ncbi.nlm.nih.gov/38482570/ DOI: 10.1152/japplphysiol.00818.2023
    tissue_or_cell_type
    Thirteen adults without cardiopulmonary disease

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 1245–1256

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small cross-sectional diet-recall and 31P-MRS association study · source_derived_draft · unverified_draft

    ### phosphorus-high-intake-atp-association Higher reported phosphate intake was associated with lower resting ATP synthesis (r=−0.62, p=0.03) in the 13-person pilot. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: More reported dietary phosphorus did not imply better energetics; this association does not establish causation. organism: Human tissue_or_cell_type: Thirteen adults without cardiopulmonary disease experimental_model: Small cross-sectional diet-recall and 31P-MRS association study limitations: Observational pilot with n=13, not a controlled excess-phosphate intervention. The source uses a phosphocreatinine wording error; PCr is represented as phosphocreatine. exposure: 24-hour dietary recall normalized to energy; calf-muscle MRS at rest/exercise evidence_span: {"source_cache": "artifacts/phosphorus-research/38482570.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11f6599b477ce87228e00e4d562eb0c70615dceebb82a983188e9b0fcd8e730f", "start_char": 0, "end_char": 2164, "text_sha256": "11f6599b477ce87228e00e4d562eb0c70615dceebb82a983188e9b0fcd8e730f"} [phosphorus-p38482570] Association between dietary phosphate intake and skeletal muscle energetics in adults without cardiovascular disease. (2024). https://pubmed.ncbi.nlm.nih.gov/38482570/ DOI: 10.1152/japplphysiol.00818.2023
    Complete structured claim and evidence

  2. The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux.

    SLC34A3-associated phosphate wasting in the 2016 ATP-flux patient → Human skeletal-muscle ATP synthetic flux by 31P-MRS source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"}
    experimental_model
    31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments
    exposure
    Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case
    limitations
    ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The study found a similar pattern in one person with inherited renal phosphate wasting.
    primary_references
    [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    tissue_or_cell_type
    Skeletal muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 607–618

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments · source_derived_draft · unverified_draft

    ### phosphorus-human-atp-defect The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study found a similar pattern in one person with inherited renal phosphate wasting. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments limitations: ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold. exposure: Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case evidence_span: {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"} [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    Complete structured claim and evidence

  3. After oral phosphate repletion normalized serum phosphate, measured muscle ATP synthetic flux normalized in the single patient.

    Study-specific phosphate repletion interventions → Human skeletal-muscle ATP synthetic flux by 31P-MRS source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"}
    experimental_model
    31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments
    exposure
    Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case
    limitations
    ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    Correcting the shortage restored the measured flux in this individual.
    primary_references
    [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    tissue_or_cell_type
    Skeletal muscle

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 620–631

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments · source_derived_draft · unverified_draft

    ### phosphorus-human-atp-rescue After oral phosphate repletion normalized serum phosphate, measured muscle ATP synthetic flux normalized in the single patient. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the shortage restored the measured flux in this individual. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments limitations: ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold. exposure: Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case evidence_span: {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"} [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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