Immobilization Leads to Alterations in Intracellular Phosphagen and Creatine Transporter Content in Human Skeletal Muscle.
Atrophy
Creatine Metabolism
Imobilization
Skeletal Muscle
Journal
American journal of physiology. Cell physiology
ISSN: 1522-1563
Titre abrégé: Am J Physiol Cell Physiol
Pays: United States
ID NLM: 100901225
Informations de publication
Date de publication:
06 May 2020
06 May 2020
Historique:
entrez:
7
5
2020
pubmed:
7
5
2020
medline:
7
5
2020
Statut:
aheadofprint
Résumé
The role of dysregulated intracellular creatine metabolism in disuse atrophy is unknown. In this study, skeletal muscle biopsy samples were obtained after 7-days of unilateral leg immobilization (IMMOB) and the non-immobilized control limb (CTRL) of 15 healthy males (23.1 ± 3.5 yrs). Samples were analyzed for fibre-type cross-sectional area (CSA) and creatine transporter (CreaT) at the cell membrane periphery (MEM) or intracellular (INT) areas, via immunoflouresence microscopy. Creatine kinase (CK) and AMP-activated protein kinase (AMPK) were determined via immunoblot. PCr, Cr and ATP were measured via enzymatic analysis. Body composition and maximal isometric knee extensor strength were assessed before and after disuse. Leg strength and fat-free mass were reduced in IMMOB (~32% and 4%, respectively; P<0.01 for both). Type II fibre CSA was smaller (~12%; P=0.028) and intramuscular PCr lower (~13%; P=0.015) in IMMOB vs. CTRL. CreaT protein was greater in Type I fibres in both limbs (P<0.01). CreaT was greater in IMMOB vs. CTRL (P < 0.01) and inversely associated with PCr concentration in both limbs (P < 0.05). MEM CreaT was greater than the INT CreaT in Type I and II fibres of both limbs (~14% for both; P<0.01 for both). Type I fibre CreaT tended to be greater in IMMOB vs. CTRL (P=0.074). CK was greater, and phospho-to-total AMPK
Identifiants
pubmed: 32374680
doi: 10.1152/ajpcell.00072.2020
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Allen Foundation
ID : 2015.223
Organisme : BBSRC
ID : BB/N018214/1