Glucoregulatory and metabolic response to exercise in obese noninsulin-dependent diabetes

Abstract

The metabolic response to exercise in obese postabsorptive noninsulin-dependent diabetics was compared to that of obese nondiabetics. Exercise consisted of 45 min on a cycle ergometer at 60% maximum oxygen consumption. Six diabetic subjects were studied during oral hypoglycemic therapy and four on diet alone. The sulfonylurea therapy had no effect on the response. Glycemia was elevated at rest in both diabetic subgroups (192 +/- 24 mg/dl for diet alone, 226 +/- 36 mg/dl for sulfonylurea treatment) and a similar fall (35 and 37 mg/dl, respectively) occurred with exercise. In control subjects, glycemia was 86 +/- 4 mg/dl and did not change with exercise. In the diabetics at rest, glucose production was elevated (220 +/- 25 mg/min), whereas the metabolic clearance of glucose was suppressed. During exercise the increase in glucose utilization was similar to that in controls, but glucose production failed to increase significantly, thus accounting for the decline in plasma glucose. At rest, plasma immunoreactive insulin (IRI) was elevated to 0.90 ng/ml in the controls and decreased to 0.65 ng/ml with exercise. In the diabetics IRI was similarly elevated (0.89 ng/ml) but failed to decrease normally with exercise. Lactate, pyruvate, alanine, and free fatty acids increased similarly in diabetics and controls, whereas the increase in 3-hydroxybutyrate during recovery was less in diabetics. The sustained insulinemia, the basal overproduction of glucose, and hyperglycemia itself may all contribute to the observed differences in glucose flux during exercise in noninsulin-dependent diabetics.

Substrate source utilisation in long-term diagnosed type 2 diabetes patients at rest, and during exercise and subsequent recovery

“…The exercise-induced decline in blood glucose concentrations continued during subsequent recovery, blood glucose Rd remaining well above its Ra (114±1%). These data extend the observations made in previous studies [17,23,24,42] and demonstrate that exercise forms a potent strategy to acutely improve glycaemic control in type 2 diabetes.…”

“…Though this has been observed before [15,17,18,23,41], the present study shows that this can be attributed to an improved plasma glucose disposal rate, with plasma glucose Rd representing 118±6% of its Ra during exercise ( Table 2). The exercise-induced decline in blood glucose concentrations continued during subsequent recovery, blood glucose Rd remaining well above its Ra (114±1%).…”

“…This can be attributed to a blunted increase in hepatic glucose output [23] and/or an increase in whole-body glucose uptake rate [15,17,18,24]. The latter has been shown to result in greater carbohydrate oxidation rates during exercise in type 2 diabetes patients in some [24] but not all studies [15][16][17][18].…”

A Minimal Exercise Extension for Models of the Glucoregulatory System

“…Trying to model all these effects simultaneously results in a model that is difficult to identify, as time constants of these effects are similar. Therefore, the effect of exercise is modeled as an increase in glucose effectiveness at zero insulin , in accordance with observations of [9]. The proposed sub-model can, thus, be used as an extension for all models incorporating the concept of insulin independent glucose uptake.…”

“…Therefore, the effect of insulin is considered constant during this period and can be combined with the glucose effectiveness at zero insulin into the new parameter . Endogenous glucose production is assumed to be constant during exercise [9]. The complete model extension corresponds to equations (1) and (2).…”