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Skeletal muscle AMPK is not activated during 2 h of moderate intensity exercise at ∼65% V ̇ O 2 peak in endurance trained men
Author(s) -
McConell Glenn K.,
Wadley Glenn D.,
Le plastrier Kieran,
Linden Kelly C.
Publication year - 2020
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp277619
Subject(s) - ampk , skeletal muscle , medicine , endocrinology , endurance training , amp activated protein kinase , regulator , exercise physiology , protein kinase a , chemistry , kinase , biochemistry , gene
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 peakin 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 peakin 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 peakin 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 peakin 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 peakin 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 αThr 172 phosphorylation (2‐fold) and ACCβ Ser 222 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 peakin endurance trained men.