RESUMO
We investigated the acute myogenic response to resistance exercise with and without blood-flow restriction (BFR). Six men and women (age, 22 ± 1 years) performed unilateral knee extensions at 40% of 1-repetition maximum with or without (CNTRL) BFR applied via pressure cuff inflated to 220 mm Hg. Muscle biopsies were collected at 4 h and 24 h postexercise. Addition of BFR increased myoD and c-Met messenger RNA expression relative to CNTRL. Expression of hepatocyte growth factor protein was significantly higher following CNTRL.
Assuntos
Fator de Crescimento de Hepatócito/metabolismo , Desenvolvimento Muscular , Proteína MyoD/metabolismo , Proteínas Proto-Oncogênicas c-met/metabolismo , Músculo Quadríceps/metabolismo , Treinamento Resistido/métodos , Regulação para Cima , Adolescente , Adulto , Biomarcadores/metabolismo , Biópsia por Agulha , Constrição , Estudos Cross-Over , Feminino , Regulação da Expressão Gênica , Fator de Crescimento de Hepatócito/genética , Humanos , Masculino , Proteína MyoD/genética , Proteínas Proto-Oncogênicas c-met/genética , Músculo Quadríceps/crescimento & desenvolvimento , RNA Mensageiro/metabolismo , Fatores de Tempo , Adulto JovemRESUMO
Fatigue is a symptom of many diseases, but it can also manifest as a unique medical condition, such as idiopathic chronic fatigue (ICF). While the prevalence of ICF increases with age, mitochondrial content and function decline with age, which may contribute to ICF. The purpose of this study was to determine whether skeletal muscle mitochondrial dysregulation and oxidative stress is linked to ICF in older adults. Sedentary, old adults (n = 48, age 72.4 ± 5.3 years) were categorized into ICF and non-fatigued (NF) groups based on the FACIT-Fatigue questionnaire. ICF individuals had a FACIT score one standard deviation below the mean for non-anemic adults > 65 years and were excluded according to CDC diagnostic criteria for ICF. Vastus lateralis muscle biopsies were analyzed, showing reductions in mitochondrial content and suppression of mitochondrial regulatory proteins Sirt3, PGC-1α, NRF-1, and cytochrome c in ICF compared to NF. Additionally, mitochondrial morphology proteins, antioxidant enzymes, and lipid peroxidation were unchanged in ICF individuals. Our data suggests older adults with ICF have reduced skeletal muscle mitochondrial content and biogenesis signaling that cannot be accounted for by increased oxidative damage.