RESUMO
One characteristic of ageing skeletal muscle is a decline in mitochondrial function. Activation of AMP-activated protein kinase (AMPK) occurs in response to an increased AMP/ATP ratio, which is one potential result of mitochondrial dysfunction. We have previously observed higher AMPK activity in old (O; 30 months) vs young adult (YA; 8 months) fast-twitch muscle in response to chronic overload. Here we tested the hypothesis that AMPK would also be hyperactivated in O vs YA fast-twitch extensor digitorum longus muscles from Fischer(344) x Brown Norway (FBN) rats (n = 8 per group) in response to high-frequency electrical stimulation of the sciatic nerve (HFES) or injection of AICAR, an activator of AMPK. Muscles were harvested immediately after HFES (10 sets of six 3-s contractions, 10 s rest between contractions, 1 min rest between sets) or 1 h after AICAR injection (1 mg (g body weight)(-1) subcutaneously). The phosphorylations of AMPKalpha and acetyl-CoA carboxylase (ACC2; a downstream AMPK target) were both greatly increased (P Assuntos
Proteínas Quinases Ativadas por AMP/efeitos dos fármacos
, Proteínas Quinases Ativadas por AMP/metabolismo
, Envelhecimento/fisiologia
, Aminoimidazol Carboxamida/análogos & derivados
, Contração Muscular/fisiologia
, Ribonucleotídeos/administração & dosagem
, Transdução de Sinais/fisiologia
, Envelhecimento/efeitos dos fármacos
, Aminoimidazol Carboxamida/administração & dosagem
, Animais
, Ativação Enzimática/efeitos dos fármacos
, Contração Muscular/efeitos dos fármacos
, Ratos
, Ratos Endogâmicos F344
, Transdução de Sinais/efeitos dos fármacos