Carbohydrate improves exercise capacity but does not affect subcellular lipid droplet morphology, AMPK and p53 signalling in human skeletal muscle
| Autor: | Julien Louis, J. Marc Fell, Sam O. Shepherd, James P. Morton, Emily Jevons, Matthew Cocks, James E. P. Moran, Daniel J. Owens, Daniel G. Ellis, Mark A. Hearris, Juliette A. Strauss |
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| Rok vydání: | 2021 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Physiology AMP-Activated Protein Kinases RC1200 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Lipid droplet Internal medicine Dietary Carbohydrates medicine Humans Muscle Skeletal Meal Exercise Tolerance Glycogen Chemistry Lactate threshold Skeletal muscle AMPK Lipid Droplets Carbohydrate 030104 developmental biology medicine.anatomical_structure Endocrinology Mitochondrial biogenesis Tumor Suppressor Protein p53 030217 neurology & neurosurgery |
| Zdroj: | The Journal of Physiology. 599:2823-2849 |
| ISSN: | 1469-7793 0022-3751 |
| Popis: | We examined the effects of carbohydrate (CHO) feeding on lipid droplet (LD) morphology, muscle glycogen utilisation and exercise‐induced skeletal muscle cell signalling. After a 36 h CHO loading protocol and pre‐exercise meal (12 and 2 g kg–1, respectively), eight trained males ingested 0, 45 or 90 g CHO h–1 during 180 min cycling at lactate threshold followed by an exercise capacity test (150% lactate threshold). Muscle biopsies were obtained pre‐ and post‐completion of submaximal exercise. Exercise decreased (P < 0.01) glycogen concentration to comparable levels (∼700 to 250 mmol kg–1 DW), though utilisation was greater in type I (∼40%) versus type II fibres (∼10%) (P < 0.01). LD content decreased in type I (∼50%) and type IIa fibres (∼30%) (P < 0.01), with greater utilisation in type I fibres (P < 0.01). CHO feeding did not affect glycogen or IMTG utilisation in type I or II fibres (all P > 0.05). Exercise decreased LD number within central and peripheral regions of both type I and IIa fibres, though reduced LD size was exclusive to type I fibres. Exercise induced (all P < 0.05) comparable AMPKThr172 (∼4‐fold), p53Ser15 (∼2‐fold) and CaMKIIThr268 phosphorylation (∼2‐fold) with no effects of CHO feeding (all P > 0.05). CHO increased exercise capacity where 90 g h–1 (233 ± 133 s) > 45 g h–1 (156 ± 66 s; P = 0.06) > 0 g h–1 (108 ± 54 s; P = 0.03). In conditions of high pre‐exercise CHO availability, we conclude CHO feeding does not influence exercise‐induced changes in LD morphology, glycogen utilisation or cell signalling pathways with regulatory roles in mitochondrial biogenesis. |
| Databáze: | OpenAIRE |
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