Exercise metabolism was examined in 13 endurance athletes who exercised on three occasions for 40 min at 70% of maximal O2 uptake in an environmental chamber at either 20 degrees C and 20% relative humidity (RTT) or 40 degrees C and 20% relative humidity before (PRE ACC) or after (POST ACC) 7 days of acclimation. Exercise in the heat resulted in a lower (P < 0.05) mean O2 uptake (0.13 l/min) and higher (P < 0.01) heart rate and respiratory exchange ratio. Acclimation resulted in a lower (P < 0.01) mean heart rate and respiratory exchange ratio. Postexercise rectal temperature, muscle temperature, muscle and blood lactate, and blood glucose were higher (P < 0.01) in the PRE ACC than in the RTT trial, but all were reduced (P < 0.01) in the POST ACC compared with the PRE ACC trial. Muscle glycogenolysis and percentage of type I muscle fibers showing glycogen depletion were greater (P < 0.05) in the PRE ACC than in the RTT trial. Muscle glycogenolysis was unaffected by acclimation during exercise in the heat, although the percentage of depleted type I fibers was higher (P < 0.05) in the unacclimated state. Plasma epinephrine was higher (P < 0.01) during exercise in the heat in the unacclimated individual relative to RTT but was lower (P < 0.01) in the POST ACC than in the PRE ACC trial. The greater reliance on carbohydrate as a fuel source during exercise in the heat appears to be partially reduced after acclimation. These alterations are consistent with the observed changes in plasma epinephrine concentrations.

To characterize splanchnic and muscle metabolism during exercise in non-insulin-dependent diabetes mellitus (NIDDM), eight male nonobese patients and seven healthy control subjects (CON) were studied during 40 min of bicycle exercise at 60% of maximal oxygen uptake. Biopsies were obtained from the quadriceps femoris muscle at rest and immediately after exercise. Arterial glucose concentration in NIDDM had declined by 10% (P < 0.01) at the end of exercise, whereas in CON it had risen by 21% (P < 0.05). Leg glucose uptake rose from 0.19 +/- 0.06 mmol/min at rest to 2.25 +/- 0.61 mmol/min at the end of exercise in NIDDM and from 0.13 +/- 0.05 to 1.17 +/- 0.34 mmol/min in CON. Splanchnic glucose output increased from 0.52 +/- 0.06 to 2.37 +/- 0.26 mmol/min in NIDDM and from 0.79 +/- 0.12 to 2.44 +/- 0.38 mmol/min in CON. Leg lactate output during exercise was twofold higher in NIDDM. Muscle contents of lactate and glycogen were similar in both groups at rest, whereas after exercise lactate tended to be higher (19.5 +/- 1.7 vs. 12.7 +/- 5.9 mmol/kg dry wt) and glycogen lower (154 +/- 35 vs. 251 +/- 41 mmol glucosyl units/kg dry wt) in NIDDM. Whole body respiratory exchange ratio during exercise was higher in NIDDM (0.84 +/- 0.02 vs. 0.78 +/- 0.02, P < 0.05). Exercise-induced changes in other muscle metabolites were similar in NIDDM and CON. These data indicate that the decline in blood glucose during exercise in nonobese NIDDM is due to enhanced peripheral glucose utilization rather than to an attenuated increase in splanchnic glucose output.

This large audit has shown that the glucose stimulation test is well tolerated and can easily be performed in an out-patient setting with minimal medical supervision. The 240 minute sample added little additional information and could be omitted.

Both insulin secretion and insulin sensitivity are important in the development of diabetes but current methods used for their measurements are complex and cannot be used for epidemiological surveys. This study describes a simplified approach for the estimation of first phase insulin release and insulin sensitivity from a standard 40-min intravenous glucose tolerance test (IVGTT), and compares these parameter estimations with the sophisticated minimal model analysis of a frequently sampled 3-h IVGTT and the euglycaemic clamp technique. For the simplified IVGTT, first phase insulin release was measured as the insulin area above basal post glucose load unit-1 incremental change (i.e. peak rise) in plasma glucose over 0-10 min, and insulin sensitivity as a rate of glucose disappearance (Kg) unit-1 insulin increase above basal from 0-40 min post-glucose load in 18 subjects who were studied twice, either basally or in a perturbed pathophysiological state (i.e. pre- and post-ultramarathon race, n = 5; pre- and post-20 h pulsatile hyperinsulinaemia, n = 8; pre- and post-thyrotoxic state, n = 5). A further 12 subjects were compared by IVGTT, and glucose clamp. In addition, seven dogs were studied three times by IVGTT during normal saline infusion and after short-term (1/2 hour) or long-term (72 hour) adrenaline infusions. First phase insulin release and insulin sensitivity estimated from the simplified IVGTT as calculated by the two methods correlated closely (rs = 0.89 and rs = 0.87, respectively), although less precisely in markedly insulin-resistant subjects and the slopes and y intercepts of the linear regression lines were similar in the basal and perturbed states.(ABSTRACT TRUNCATED AT 250 WORDS)