The regulation of post prandial glucose metabolism is primarily mediated by insulin. Insulin acts via a membrane receptor to signal the uptake of glucose from the blood to the tissue by a facilitated glucose transporter mechanism. It has been shown that insulin facilitated glucose uptake by skeletal muscle and hypoxia facilitated glucose transport are separate and additive. Thus, it would appear that the chemical pathways associated with glucose uptake under hypoxic conditions is different to that of insulin. Recently, it has been shown that a decrease in glucose disposal in active healthy young men during euglycemic clamps performed under hypoxic conditions at an altitude of 4500m at 2 and 7 days. These data suggest the men became insulin resistant with hypoxia at altitude. It appears that under hypoxic conditions at altitude insulin mediated glucose metabolism in vivo is decreased, while in vitro studies with skeletal muscle preparations show an increase in insulin/hypoxia mediated glucose metabolism. We hypothesize that 6 hours at a stimulated altitude of 4000m will result in increases in glucose metabolism which will be evident in the glucose, insulin and c-peptide responses to an oral glucose tolerance test. Data from this study will provide information on the acute metabolic responses to altitude which are important to our understanding of the physiologic stresses imposed on professional and recreational pursuits performed at high elevations.
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