Beta2-adrenoceptor agonists (beta2-agonists) acutely elevate insulin-independent muscle glucose uptake in rodents and augment insulin sensitivity after chronic treatment in humans. With the development and future projection of the global prevalence of type II diabetes, the interest in leveraging pharmacological manipulation of the beta2-adrenoceptor to treat type II diabetes has increased. However, reports in obese rodents demonstrate that beta2-agonists acutely impair insulin and glucose tolerance, which, if translatable to humans, could significantly reduce the therapeutic potential of activating the beta2-adrenoceptor in insulin resistant humans. Furthermore, the acute effects of beta2-adrenoceptor agonists on muscle glucose uptake and metabolism and the underlying mechanism(s) both at basal conditions and during metabolic challenges such as exercise, recovery and insulin stimulation remains incompletely understood in humans. Thus, the purpose of the current PhD thesis is to delineate the impact of beta2-agonist on acute glucometabolic regulation during different conditions to enable a better understanding of the therapeutic potential of beta2-agonists including its’ pitfalls. This purpose has been pursued in three different studies investigating the impact of beta2-agonist on muscle glucose uptake and metabolism at the basal condition, during and in recovery from a single bout of exercise and during hyperinsulinemic isoglycemic conditions. The results from the three studies demonstrate that beta2-adrenoceptor agonist elevates basal muscle glucose uptake (Study I) in line with that observed in in vitro rodent studies, but that the elevation in vivo might be confounded by increased insulin secretion, which makes the impact of muscle beta2-adrenergic signalling on basal muscle glucose uptake difficult to delineate. During exercise, beta2-agonist decreased muscle glucose uptake (Study II), an effect that shifted to an increase in muscle glucose uptake in recovery from exercise (Study II). Lastly, beta2-agonist markedly impaired insulin-stimulated muscle glucose uptake in insulin resistant subjects (Study III). The muscle biopsies sampled throughout the studies suggest that beta2-agonist primarily impairs exercise- and insulin-stimulated muscle glucose uptake through alterations in glycogen metabolism. Conversely, the increases in muscle glucose uptake at basal conditions and in recovery from exercise likely occurs due to increased glycolytic flux and elevated glucose transport which, perhaps, occurs in an insulin-independent manner. Collectively, this thesis demonstrates that beta2-agonist elicits some intriguing acute effects on muscle glucose uptake in humans as seen in Study I and II that potentially could be harnessed to combat insulin resistance and type II diabetes. However, Study III clearly highlights that beta2- agonist markedly impairs insulin-stimulated muscle glucose uptake in insulin resistant subjects. Thus, administration of beta2-agonist in people with type II diabetes could result in acutely aggravated postprandial hyperglycemia, which would severely reduce the therapeutic potential of beta2-agonists in type II diabetes. How this translates to long term treatment with beta2-agonists and whether or not it supresses the beneficial impact of beta2-agonists effect on insulin sensitivity in people with type II diabetes should be examined in future studies.