The results of this study demonstrate that CHD patients with T2DM under a suboptimal metabolic control display accelerated muscle protein loss compared with a matched group of non-DM CHD patients.
Antecedent moderate-intensity exercise has been shown to blunt autonomic, neuroendocrine, and metabolic counterregulatory responses to subsequent hypoglycemia in nondiabetic individuals. The aims of the current study were to determine 1) whether this occurs in type 1 diabetic patients and 2) whether the degree of blunting is dependent on exercise intensity. Twentyseven type 1 diabetic patients (13 women and 14 men) were studied during a single-step, 2-h hyperinsulinemic (9 pmol ⅐ kg ؊1 ⅐ min ؊1 )-hypoglycemic (ϳ2.8 mmol/l) clamp 1 day after two 90-min exercise bouts at 30% (n ؍ 11) or at 50% (n ؍ 11) VO 2max or after no prior stress (control subjects, n ؍ 25). After prior exercise at both 30 and 50% VO 2max , epinephrine (1,959 ؎ 553 and 1,528 ؎ 424 vs. 3,420 ؎ 424 pmol/l, respectively; P < 0.05) and pancreatic polypeptide (97 ؎ 32 and 98 ؎ 8 vs. 223 ؎ 32 pmol/l, respectively; P < 0.05) responses to subsequent hypoglycemia were significantly lower compared with those of control subjects. Endogenous glucose production was significantly lower, while glucose utilization and, consequently, the exogenous glucose infusion rate needed to maintain hypoglycemia were significantly greater after both exercise intensities compared with that of control subjects. Muscle sympathetic nerve activity was significantly reduced by prior exercise of both intensities at baseline (16 ؎ 4 and 22 ؎ 4 vs. 31 ؎ 3 bursts/min) and during hypoglycemia (22 ؎ 4 and 27 ؎ 5 vs. 41 ؎ 3 bursts/min) compared with that of control subjects (P < 0.05). Total hypoglycemic symptoms were also significantly lower (P < 0.05) in both exercise groups compared with the control group. In summary, repeated episodes of prolonged exercise of both low and moderate intensities blunted key autonomic (epinephrine and pancreatic polypeptide) and metabolic (endogenous glucose production and peripheral glucose uptake) counterregulatory responses to next-day hypoglycemia in type 1 diabetes. Diabetes 53: 1798 -1806, 2004 I ntensive maintenance of normal glucose levels delays or prevents the development of microvascular complications associated with diabetes (1,2). Unfortunately, an approximate threefold increase in severe hypoglycemia in these intensively treated patients (1) limits the widespread implementation of this treatment paradigm. Although excess insulin is an important contributing factor to increased hypoglycemia, with increased duration of the disease, glucagon responses to hypoglycemia in type 1 diabetes are absent (3). This leaves type 1 diabetic patients dependent on epinephrine to counter falling glucose levels. However, recent antecedent episodes of hypoglycemia have significantly reduced autonomic counterregulatory responses to subsequent hypoglycemia in nondiabetic and type 1 diabetic patients (4 -7). This has been termed hypoglycemia-associated autonomic failure (8,9) and is proposed to create a vicious cycle of hypoglycemia for the type 1 diabetic patient.Exercise has numerous therapeutic benefits. Despite this, exercise often results in hypogly...
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