Cited by 225Cardiovascular and exercise physiologyMuscle metabolism and nutritionMuscle Physiology and Disorders

Role of glycogen availability in sarcoplasmic reticulum Ca2+ kinetics in human skeletal muscle

Open access
Ørtenblad, Niels, Nielsen, Joachim, Saltin, Bengt, Holmberg, Hans‐Christer·2011·The Journal of Physiology

Abstract

Non‐technical summary: Glucose is stored as glycogen in skeletal muscle. The importance of glycogen as a fuel during exercise has been recognized since the 1960s; however, little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. We show that low muscle glycogen is associated with an impairment of muscle ability to release Ca 2+, which is an important signal in the muscle activation. Thus, depletion of glycogen during prolonged, exhausting exercise may contribute to muscle fatigue by causing decreased Ca 2+ release inside the muscle. These data provide indications of a signal that links energy utilization, i.e. muscle contraction, with the energy content in the muscle, thereby inhibiting a detrimental depletion of the muscle energy store.

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Registry

Crossref · 10.1113/jphysiol.2010.195982

Cites

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  • Commencing exercise with < 200 mmol/kg dw is likely to impair training intensity due to the lack of muscle substrate and impact on the contractile capacity of muscle cells via impaired calcium regulation.

    “However, it should be noted that commencing exercise with < 200 mmol/kg dw is likely to impair training intensity due to the lack of muscle substrate and impact on the contractile capacity of muscle cells via impaired calcium regulation [50–52].”

    From Fuel for the Work Required: A Theoretical Framework for Carbohydrate Periodization and the Glycogen Threshold Hypothesis (2018) · cites this paper as [50]

    The Association of glycogen and SR Ca²⁺ release rate section (page not supplied) reports impaired calcium release when arm glycogen fell below 200 mmol/kg dry weight after exhaustive exercise. The Introduction links glycogen availability to exercise performance. However, this study did not test whether commencing exercise below 200 mmol/kg dry weight impairs training intensity or directly measure contractile capacity under that starting condition. (LLM, conf=0.86)

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  • An increase in Ca2+ concentration in the cells, via activation of phosphorylase kinase, triggers glycogen degradation.

    “An increase in Ca2+ concentration in the cells, via activation of phosphorylase kinase, triggers glycogen degradation [65,66].”

    From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [66]

    The section “Association between SR and the glycogenolytic complex” says that phosphorylase activation is controlled by sarcoplasmic-reticulum calcium flux. It does not state that calcium activates phosphorylase kinase or explicitly establish the claimed sequence leading to glycogen degradation. Page numbers are unavailable in our copy. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • Low muscle glycogen levels influence both force and power production by modulating muscle activation through effects on muscle excitability and sarcoplasmic reticulum Ca2+ release rate.

    “Thus, low muscle glycogen levels influence both force and power production by modulating muscle activation through effects on muscle excitability and sarcoplasmic reticulum Ca2+ release rate [3, 14, 15], which becomes evident when muscle glycogen concentration falls below an apparent level of 250–200 mmol kg−1 dw in most [15, 16, 17], but not all studies [18].”

    From Carbohydrate Storage and Supplementation Strategies for Peak Performance in Cross-Country Skiing (2026) · cites this paper as [15]

    The Introduction links low glycogen with reduced force and altered excitation–contraction coupling, and the ‘Association of glycogen and SR Ca2+ release rate’ section reports impaired Ca2+ release at low glycogen levels. The cited paper does not establish an effect on power production or muscle excitability specifically. It also suggests a critical level of 280–300 mmol kg−1 dry weight for impaired Ca2+ release, rather than the sentence’s 250–200 range. Page numbers are unavailable in our copy. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • In a shorter, ~1 h ski race with junior elite cross-country skiers involving mainly double poling, glycogen was on average reduced to 31% (from 540 to 167 mmol kg−1 dw) in the arms and 71% (from 485 to 331 mmol kg−1 dw) in the legs directly after the race.

    “In a shorter, ~1 h ski race with junior elite cross‐country skiers, involving mainly double poling technique, glycogen was on average reduced to 31% (from 540 to 167 mmol kg−1 dw) in the arms and 71% (from 485 to 331 mmol kg−1 dw) in the legs directly after the race [15].”

    From Carbohydrate Storage and Supplementation Strategies for Peak Performance in Cross-Country Skiing (2026) · cites this paper as [15]

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    Experimental — accuracy not yet measured
  • Glycogen utilization rates varied from 21% (arm) and 16% (leg) during a 4 min sprint; 66% (arm) and 39% (leg) during a 1-h ski race; to 86% (leg) during a race lasting 7 h 30 min in recreational skiers.

    “Glycogen utilization rates varied from 21% (arm) and 16% (leg) during a 4 min sprint; 66% (arm) and 39% (leg) during a 1‐h ski race; to 86% (leg) during a race lasting 7 h 30 min in recreational skiers.”

    From Carbohydrate Storage and Supplementation Strategies for Peak Performance in Cross-Country Skiing (2026) · cites this paper as [15]

    The Glycogen content section (page unavailable) reports greater glycogen utilization in arms than legs during a roughly 57-minute race, but its figures imply about 69% arm and 29% leg utilization—not the claimed 66% and 39%. The Subjects and Cross country race performance sections describe elite skiers in that race; our copy does not report the claimed 4-minute sprint or 7-hour-30-minute race in recreational skiers. (LLM, conf=0.88)

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Research works printed but not linked: 1

  1. [33]33. Kruszynska YT, Ciaraldi TP & Henry RR (2001). In Handbook of Physiology. A Critical, Comprehensive Presentation of Physiological Knowledge and Concepts, section 7, The Endocrine System, ed. Jefferson LS & Cherrington A, pp. 579-607. Oxford University Press, New York.

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Authors
Ørtenblad, N., Nielsen, J., Saltin, B., & Holmberg, H.
Affiliations
  • University of Southern Denmark (DK)
  • University of Copenhagen (DK)
  • Swedish Olympic Committee (SE)
Venue
The Journal of Physiology
Publisher
Wiley
Published
2011-01-28
Volume
589
Issue
3
Pages
711-725
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W1558831010
Cited by
225
References
54
Citations by year
2026: 14 · 2025: 18 · 2024: 14 · 2023: 12 · 2022: 16 · 2021: 25 · 2020: 21 · 2019: 19 · 2018: 18 · 2017: 7 · 2016: 9 · 2015: 12 · 2014: 12 · 2013: 9 · 2012: 13
FWCI
23.98
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
Funders
Kulturministeriet
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
skeletal muscle glycogen, sarcoplasmic reticulum calcium release, calcium kinetics, muscle fatigue, glycogen depletion, muscle contraction, energy metabolism, physical activity
MeSH terms
Adult, Biopsy, Needle, Calcium, Cresols, Dietary Carbohydrates, Glycogen, Humans, Kinetics, Male, Myofibrils, Sarcoplasmic Reticulum, Skiing, Muscle, Skeletal, Muscle Fibers, Skeletal, Muscle Fatigue, Myosin Heavy Chains, Lactic Acid, Microscopy, Electron, Transmission, Quadriceps Muscle, Young Adult, Athletes

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