Critical illness impacts GH secretion in a biphasic pattern. The initial stress response consists of activated growth hormone (GH) release, GH secretion is reduced in the chronic phase of critical illness. High levels of GH causes severe insulin resistance and proinflammation, which may contribute to the morbidity and mortality of acute critical illness. The molecular mechanisms subserving these insulin antagonistic effects are unknown, but in vitro studies suggest that insulin and GH share postreceptor signalling pathways. This study was preformed to investigate if there is a crosslink between the two signalling pathways in human striated muscle in vivo.