Component

Core (rectal) body temperature

Core (rectal) body temperature. Species, exposure and limitations are retained in each linked claim.

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

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. M8-B decreased deep body temperature in Trpm8-positive mice and rats but not in Trpm8-null mice, and intravenous administration was more effective than intrathecal or intracerebroventricular, indicating a peripheral action.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/22323721.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0", "start_char": 0, "end_char": 1784, "text_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0"}
    experimental_model
    Rats and mice with a selective TRPM8 antagonist given by several routes
    exposure
    M8-B intravenously, intrathecally or intracerebroventricularly, at constant or changing ambient temperature
    limitations
    On-target action is supported by the absence of effect in Trpm8-null mice. The peripheral site of action is inferred from route comparison, not from direct measurement at the nerve ending.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Rat, mouse and human channels in vitro
    plain_language
    Blocking the skin cold sensor makes the body cool down, because it never learns it is cold.
    primary_references
    [cold-p22323721] Pharmacological blockade of the cold receptor TRPM8 attenuates autonomic and behavioral cold defenses and decreases deep body temperature. (2012). https://pubmed.ncbi.nlm.nih.gov/22323721/ DOI: 10.1523/jneurosci.5606-11.2012
    tissue_or_cell_type
    Skin sensory neurons and thermoeffectors
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 91–102

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats and mice with a selective TRPM8 antagonist given by several routes · source_derived_draft · unverified_draft

    ### cold-trpm8-blockade-temperature M8-B decreased deep body temperature in Trpm8-positive mice and rats but not in Trpm8-null mice, and intravenous administration was more effective than intrathecal or intracerebroventricular, indicating a peripheral action. Condition category: machinery_impairment nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Blocking the skin cold sensor makes the body cool down, because it never learns it is cold. organism: Rat, mouse and human channels in vitro tissue_or_cell_type: Skin sensory neurons and thermoeffectors experimental_model: Rats and mice with a selective TRPM8 antagonist given by several routes limitations: On-target action is supported by the absence of effect in Trpm8-null mice. The peripheral site of action is inferred from route comparison, not from direct measurement at the nerve ending. exposure: M8-B intravenously, intrathecally or intracerebroventricularly, at constant or changing ambient temperature evidence_span: {"source_cache": "artifacts/cold-research/22323721.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0", "start_char": 0, "end_char": 1784, "text_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0"} [cold-p22323721] Pharmacological blockade of the cold receptor TRPM8 attenuates autonomic and behavioral cold defenses and decreases deep body temperature. (2012). https://pubmed.ncbi.nlm.nih.gov/22323721/ DOI: 10.1523/jneurosci.5606-11.2012
    Complete structured claim and evidence
  2. A low intravenous dose did not affect body temperature at a constantly high or constantly low ambient temperature, but readily decreased it when rats were kept warm during infusion and transferred to cold immediately after, and below 23 degrees C tail-skin temperature the effect was inversely related to skin temperature.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/22323721.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0", "start_char": 0, "end_char": 1784, "text_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0"}
    experimental_model
    Rats and mice with a selective TRPM8 antagonist given by several routes
    exposure
    M8-B intravenously, intrathecally or intracerebroventricularly, at constant or changing ambient temperature
    limitations
    On-target action is supported by the absence of effect in Trpm8-null mice. The peripheral site of action is inferred from route comparison, not from direct measurement at the nerve ending.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Rat, mouse and human channels in vitro
    plain_language
    The sensor only matters while the skin is actually cooling.
    primary_references
    [cold-p22323721] Pharmacological blockade of the cold receptor TRPM8 attenuates autonomic and behavioral cold defenses and decreases deep body temperature. (2012). https://pubmed.ncbi.nlm.nih.gov/22323721/ DOI: 10.1523/jneurosci.5606-11.2012
    tissue_or_cell_type
    Skin sensory neurons and thermoeffectors

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 117–128

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats and mice with a selective TRPM8 antagonist given by several routes · source_derived_draft · unverified_draft

    ### cold-trpm8-skin-delivery-requirement A low intravenous dose did not affect body temperature at a constantly high or constantly low ambient temperature, but readily decreased it when rats were kept warm during infusion and transferred to cold immediately after, and below 23 degrees C tail-skin temperature the effect was inversely related to skin temperature. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The sensor only matters while the skin is actually cooling. organism: Rat, mouse and human channels in vitro tissue_or_cell_type: Skin sensory neurons and thermoeffectors experimental_model: Rats and mice with a selective TRPM8 antagonist given by several routes limitations: On-target action is supported by the absence of effect in Trpm8-null mice. The peripheral site of action is inferred from route comparison, not from direct measurement at the nerve ending. exposure: M8-B intravenously, intrathecally or intracerebroventricularly, at constant or changing ambient temperature evidence_span: {"source_cache": "artifacts/cold-research/22323721.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0", "start_char": 0, "end_char": 1784, "text_sha256": "c0ead3b0097eaa75bf74d806e7f40bc61da4275cdd0af92735be9cad681ed3f0"} [cold-p22323721] Pharmacological blockade of the cold receptor TRPM8 attenuates autonomic and behavioral cold defenses and decreases deep body temperature. (2012). https://pubmed.ncbi.nlm.nih.gov/22323721/ DOI: 10.1523/jneurosci.5606-11.2012
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Brown adipose volume correlated with the change in metabolic heat production during the mild cold phase, and positively correlated with rectal temperature at the end of that phase, which in turn correlated with shivering onset time.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/32948898.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "699fc07665c5f8800951348b6948dba539ed6aed5d1d354d4793be8f9f731b6a", "start_char": 0, "end_char": 1697, "text_sha256": "699fc07665c5f8800951348b6948dba539ed6aed5d1d354d4793be8f9f731b6a"}
    experimental_model
    Eighteen men with measured brown adipose volume during gradual cold exposure
    exposure
    Gradual cooling to 18.6 degrees C for non-shivering thermogenesis and 11.6 degrees C for shivering onset
    limitations
    Correlational human physiology. It tests whether muscle compensates for low brown fat, and finds an earlier shivering onset instead.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Human
    plain_language
    People with more of the tissue made more heat without shivering and started shivering later.
    primary_references
    [cold-p32948898] Multiorgan contribution to non-shivering and shivering thermogenesis and vascular responses during gradual cold exposure in humans. (2020). https://pubmed.ncbi.nlm.nih.gov/32948898/ DOI: 10.1007/s00421-020-04496-1
    tissue_or_cell_type
    Brown adipose tissue and skeletal muscle

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 507–518

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eighteen men with measured brown adipose volume during gradual cold exposure · source_derived_draft · unverified_draft

    ### cold-bat-volume-nst Brown adipose volume correlated with the change in metabolic heat production during the mild cold phase, and positively correlated with rectal temperature at the end of that phase, which in turn correlated with shivering onset time. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: People with more of the tissue made more heat without shivering and started shivering later. organism: Human tissue_or_cell_type: Brown adipose tissue and skeletal muscle experimental_model: Eighteen men with measured brown adipose volume during gradual cold exposure limitations: Correlational human physiology. It tests whether muscle compensates for low brown fat, and finds an earlier shivering onset instead. exposure: Gradual cooling to 18.6 degrees C for non-shivering thermogenesis and 11.6 degrees C for shivering onset evidence_span: {"source_cache": "artifacts/cold-research/32948898.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "699fc07665c5f8800951348b6948dba539ed6aed5d1d354d4793be8f9f731b6a", "start_char": 0, "end_char": 1697, "text_sha256": "699fc07665c5f8800951348b6948dba539ed6aed5d1d354d4793be8f9f731b6a"} [cold-p32948898] Multiorgan contribution to non-shivering and shivering thermogenesis and vascular responses during gradual cold exposure in humans. (2020). https://pubmed.ncbi.nlm.nih.gov/32948898/ DOI: 10.1007/s00421-020-04496-1
    Complete structured claim and evidence
  2. Immersion at 14 degrees C lowered rectal temperature and increased metabolic rate by 350%, with heart rate and systolic and diastolic blood pressure rising by 5, 7 and 8%.

    Cold water immersion → Whole-body metabolic rate source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/10751106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291", "start_char": 0, "end_char": 2332, "text_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291"}
    experimental_model
    Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C
    exposure
    One hour head-out immersion at three water temperatures
    limitations
    The thermoneutral arm separates hydrostatic pressure from cold. Cortisol did not rise at any temperature, which bears directly on calling immersion a stress response.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Human
    plain_language
    At 14 degrees the body burns roughly four and a half times as much energy as at rest.
    primary_references
    [cold-p10751106] Human physiological responses to immersion into water of different temperatures. (2000). https://pubmed.ncbi.nlm.nih.gov/10751106/ DOI: 10.1007/s004210050065
    tissue_or_cell_type
    Whole body

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 182–193

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C · source_derived_draft · unverified_draft

    ### cold-cold-metabolic-rate Immersion at 14 degrees C lowered rectal temperature and increased metabolic rate by 350%, with heart rate and systolic and diastolic blood pressure rising by 5, 7 and 8%. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: At 14 degrees the body burns roughly four and a half times as much energy as at rest. organism: Human tissue_or_cell_type: Whole body experimental_model: Young men during 1-hour head-out immersions at 32, 20 and 14 degrees C limitations: The thermoneutral arm separates hydrostatic pressure from cold. Cortisol did not rise at any temperature, which bears directly on calling immersion a stress response. exposure: One hour head-out immersion at three water temperatures evidence_span: {"source_cache": "artifacts/cold-research/10751106.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291", "start_char": 0, "end_char": 2332, "text_sha256": "d018fda7c67dc61bb0d4a38ddfd7850e7252897587c5a4477607271b10d42291"} [cold-p10751106] Human physiological responses to immersion into water of different temperatures. (2000). https://pubmed.ncbi.nlm.nih.gov/10751106/ DOI: 10.1007/s004210050065
    Complete structured claim and evidence
  3. Pharmacological reduction of creatine decreased whole-body energy expenditure after beta-3 agonist administration and reduced beige and brown adipose metabolic rate, and creatine metabolism genes were compensatorily induced when UCP1-dependent thermogenesis was ablated, with creatine reduction in Ucp1-deficient mice lowering core body temperature.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/26496606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7", "start_char": 0, "end_char": 1097, "text_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7"}
    experimental_model
    Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction
    exposure
    Cold exposure, beta-3 agonist administration, and creatine depletion
    limitations
    Identifies a UCP1-independent route. Pharmacological creatine reduction is a blunt tool, and the compensatory induction in UCP1-deficient mice is an expression finding.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Mouse
    plain_language
    Take creatine away and the burn falls, most visibly when the usual heat protein is already gone.
    primary_references
    [cold-p26496606] A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. (2015). https://pubmed.ncbi.nlm.nih.gov/26496606/ DOI: 10.1016/j.cell.2015.09.035
    tissue_or_cell_type
    Beige and brown adipose tissue
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 455–466

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction · source_derived_draft · unverified_draft

    ### cold-creatine-depletion-energy Pharmacological reduction of creatine decreased whole-body energy expenditure after beta-3 agonist administration and reduced beige and brown adipose metabolic rate, and creatine metabolism genes were compensatorily induced when UCP1-dependent thermogenesis was ablated, with creatine reduction in Ucp1-deficient mice lowering core body temperature. Condition category: machinery_impairment nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Take creatine away and the burn falls, most visibly when the usual heat protein is already gone. organism: Mouse tissue_or_cell_type: Beige and brown adipose tissue experimental_model: Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction limitations: Identifies a UCP1-independent route. Pharmacological creatine reduction is a blunt tool, and the compensatory induction in UCP1-deficient mice is an expression finding. exposure: Cold exposure, beta-3 agonist administration, and creatine depletion evidence_span: {"source_cache": "artifacts/cold-research/26496606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7", "start_char": 0, "end_char": 1097, "text_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7"} [cold-p26496606] A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. (2015). https://pubmed.ncbi.nlm.nih.gov/26496606/ DOI: 10.1016/j.cell.2015.09.035
    Complete structured claim and evidence
  4. Cold-exposed Dio2-disrupted mice became hypothermic due to impaired brown adipose thermogenesis despite normal plasma T3 and normal basal UCP1, and survived by compensatory shivering with acute weight loss.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"}
    experimental_model
    Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue
    exposure
    Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection
    limitations
    The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Mouse
    plain_language
    Normal hormone in the blood was not enough; the tissue had to make its own.
    primary_references
    [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    tissue_or_cell_type
    Brown adipose tissue
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 390–401

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue · source_derived_draft · unverified_draft

    ### cold-dio2-null-hypothermia Cold-exposed Dio2-disrupted mice became hypothermic due to impaired brown adipose thermogenesis despite normal plasma T3 and normal basal UCP1, and survived by compensatory shivering with acute weight loss. Condition category: nutrient_deficiency nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Normal hormone in the blood was not enough; the tissue had to make its own. organism: Mouse tissue_or_cell_type: Brown adipose tissue experimental_model: Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue limitations: The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone. exposure: Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection evidence_span: {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"} [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    Complete structured claim and evidence
  5. In winter swimmers the thermoregulatory threshold for inducing cold thermogenesis was lowered by 0.34 degrees C while apparent hypothalamic thermosensitivity was unchanged, and the magnitude of cold thermogenesis related solely to rectal temperature, indicating predominance of central temperature input.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/10825419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62", "start_char": 0, "end_char": 2308, "text_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62"}
    experimental_model
    Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C
    exposure
    One hour of cold water immersion at 13 degrees C
    limitations
    A comparison of adapted and unadapted people. The adrenaline contribution to thermogenesis is the authors’ estimate from their thermoregulation data, not a direct measurement of a hormone-driven heat fraction.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Human
    plain_language
    Repeated exposure moves the set point at which the body decides to make heat.
    primary_references
    [cold-p10825419] Thermoregulation in winter swimmers and physiological significance of human catecholamine thermogenesis. (2000). https://pubmed.ncbi.nlm.nih.gov/10825419/ DOI: 10.1111/j.1469-445x.2000.01909.x
    tissue_or_cell_type
    Whole body thermoregulation

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 637–648

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C · source_derived_draft · unverified_draft

    ### cold-winter-swimmer-threshold In winter swimmers the thermoregulatory threshold for inducing cold thermogenesis was lowered by 0.34 degrees C while apparent hypothalamic thermosensitivity was unchanged, and the magnitude of cold thermogenesis related solely to rectal temperature, indicating predominance of central temperature input. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Repeated exposure moves the set point at which the body decides to make heat. organism: Human tissue_or_cell_type: Whole body thermoregulation experimental_model: Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C limitations: A comparison of adapted and unadapted people. The adrenaline contribution to thermogenesis is the authors’ estimate from their thermoregulation data, not a direct measurement of a hormone-driven heat fraction. exposure: One hour of cold water immersion at 13 degrees C evidence_span: {"source_cache": "artifacts/cold-research/10825419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62", "start_char": 0, "end_char": 2308, "text_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62"} [cold-p10825419] Thermoregulation in winter swimmers and physiological significance of human catecholamine thermogenesis. (2000). https://pubmed.ncbi.nlm.nih.gov/10825419/ DOI: 10.1111/j.1469-445x.2000.01909.x
    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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