Showing papers by "Michael Kjaer published in 1998"
TL;DR: E endurance trained athletes have a higher epinephrine secretion capacity compared to sedentary individuals, which indicates a development of a so-called "sports adrenal medulla" as a result of a long term adaptation of an endocrine gland to physical training.
Abstract: The adrenaline release from the adrenal medulla increases during exercise, but at a given absolute work intensity the magnitude of this response is less pronounced in endurance trained vs sedentary individuals most likely due to a lower sympathetic stimulation of the adrenal medulla. However, when trained and untrained subjects are compared at identical relative work loads as well as in response to numerous non-exercise stimuli. endurance trained athletes have a higher epinephrine secretion capacity compared to sedentary individuals. This indicates a development of a so-called "sports adrenal medulla" as a result of a long term adaptation of an endocrine gland to physical training. Such an adaptation is parallel to adaptations taking place in other tissues like skeletal muscle and the heart. and can be advantageous in relation to both exercise performance in the competing athlete and cause a biological rejuvenation in relation to aging.
91 citations
TL;DR: The data suggest that caffeine had direct effects on both the adipose tissue and the active muscle, and it is proposed that the ergogenic action of caffeine is occurring, at least in part, by a direct action of the drug on muscle.
Abstract: Normally, caffeine ingestion results in a wide spectrum of neural and hormonal responses, making it difficult to evaluate which are critical regulatory factors. We examined the responses to caffein...
86 citations
TL;DR: A decline in plasma insulin is important for the rise in glucose production during exercise in a variety of species, whereas an increase in plasma glucagon is probably more important in other species than man, where glucagon plays a role only in prolonged exercise.
Abstract: Hepatic glucose production increases during exercise as a sum of liver glycogenolysis and gluconeogenesis. Whereas the former dominates during intense exercise, the latter contributes substantially with prolonged exercise and the concomitant decline in liver glycogen stores and with increased gluconeogenic precursor supply. Afferent neural feedback signals from contracting muscle and feedback signals mediated via the blood stream, can stimulate glucose production to maintain euglycemia. A rise in blood glucose directly inhibits hepatic glucose production, whereas a decline in blood glucose enhances liver glucose production via release of glucoregulatory hormones. In addition to this, central mechanisms coupled to the degree of motor center activity can be responsible for part of the increase in glucose mobilization, especially during intense exercise where hepatic glucose release exceeds peripheral glucose uptake and plasma glucose rises. A decline in plasma insulin is important for the rise in glucose production during exercise in a variety of species, whereas an increase in plasma glucagon is probably more important in other species than man, where glucagon plays a role only in prolonged exercise. Sympathetic nervous activity to the liver and circulating norepinephrine has been demonstrated to be without any role in glucose production, whereas epinephrine has a minor stimulating effect on hepatic glucose mobilization during intense exercise. Growth hormone and cortisol contribute only minimally to the exercise induced rise in liver glucose output.
70 citations
TL;DR: In adrenalectomized patients an increase in muscle neutral lipase activity was found at the end of prolonged exercise only if epinephrine was infused, and HSL adapts differently to training in muscle compared with adipose tissue.
Abstract: Because the enzymatic regulation of muscle triglyceride metabolism is poorly understood we explored the character and activation of neutral lipase in muscle. Western blotting of isolated rat muscle fibers demonstrated expression of hormone-sensitive lipase (HSL). In incubated soleus muscle epinephrine increased neutral lipase activity by beta-adrenergic mechanisms involving cyclic AMP-dependent protein kinase (PKA). The increase was parallelled by an increase in glycogen Phosphorylase activity and could be abolished by antiserum against HSL. Electrical stimulation caused a transient increase in activity of both neutral lipase and glycogen Phosphorylase. The increase in lipase activity during contractions was not influenced by sympathectomy or Propranolol.
55 citations