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    Skeletal muscle AMPK is not activated during 2 h of moderate intensity exercise at similar to 65%V?O2peakin endurance trained men

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    Author
    McConell, GK; Wadley, GD; Le Plastrier, K; Linden, KC
    Date
    2020-07-27
    Source Title
    The Journal of Physiology
    Publisher
    WILEY
    University of Melbourne Author/s
    Wadley, Glenn
    Affiliation
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    McConell, G. K., Wadley, G. D., Le Plastrier, K. & Linden, K. C. (2020). Skeletal muscle AMPK is not activated during 2 h of moderate intensity exercise at similar to 65%V?O2peakin endurance trained men. JOURNAL OF PHYSIOLOGY-LONDON, 598 (18), pp.3859-3870. https://doi.org/10.1113/JP277619.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251501
    DOI
    10.1113/JP277619
    Abstract
    KEY POINTS: AMP-activated protein kinase (AMPK) is considered a major regulator of skeletal muscle metabolism during exercise. However, we previously showed that, although AMPK activity increases by 8-10-fold during ∼120 min of exercise at ∼65% V ̇ O 2 peak in untrained individuals, there is no increase in these individuals after only 10 days of exercise training (longitudinal study). In a cross-sectional study, we show that there is also a lack of activation of skeletal muscle AMPK during 120 min of cycling exercise at 65% V ̇ O 2 peak in endurance-trained individuals. These findings indicate that AMPK is not an important regulator of exercise metabolism during 120 min of exercise at 65% V ̇ O 2 peak in endurance trained men. It is important that more energy is directed towards examining other potential regulators of exercise metabolism. ABSTRACT: AMP-activated protein kinase (AMPK) is considered a major regulator of skeletal muscle metabolism during exercise. Indeed, AMPK is activated during exercise and activation of AMPK by 5-aminoimidazole-4-carboxyamide-ribonucleoside (AICAR) increases skeletal muscle glucose uptake and fat oxidation. However, we have previously shown that, although AMPK activity increases by 8-10-fold during ∼120 min of exercise at ∼65% V ̇ O 2 peak in untrained individuals, there is no increase in these individuals after only 10 days of exercise training (longitudinal study). In a cross-sectional study, we examined whether there is also a lack of activation of skeletal muscle AMPK during 120 min of cycling exercise at 65% V ̇ O 2 peak in endurance-trained individuals. Eleven untrained (UT; V ̇ O 2 peak = 37.9 ± 5.6 ml.kg-1  min-1 ) and seven endurance trained (ET; V ̇ O 2 peak = 61.8 ± 2.2 ml.kg-1  min-1 ) males completed 120 min of cycling exercise at 66 ± 4% V ̇ O 2 peak (UT: 100 ± 21 W; ET: 190 ± 15 W). Muscle biopsies were obtained at rest and following 30 and 120 min of exercise. Muscle glycogen was significantly (P < 0.05) higher before exercise in ET and decreased similarly during exercise in the ET and UT individuals. Exercise significantly increased calculated skeletal muscle free AMP content and more so in the UT individuals. Exercise significantly (P < 0.05) increased skeletal muscle AMPK α2 activity (4-fold), AMPK αThr172 phosphorylation (2-fold) and ACCβ Ser222 phosphorylation (2-fold) in the UT individuals but not in the ET individuals. These findings indicate that AMPK is not an important regulator of exercise metabolism during 120 min of exercise at 65% V ̇ O 2 peak in endurance trained men.

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