Sandoval Darleen A, Guy Deanna L Aftab, Richardson M Antoinette, Ertl Andrew C, Davis Stephen N
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6303, USA.
Diabetes. 2004 Jul;53(7):1798-806. doi: 10.2337/diabetes.53.7.1798.
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. Twenty-seven type 1 diabetic patients (13 women and 14 men) were studied during a single-step, 2-h hyperinsulinemic (9 pmol x kg(-1) x min(-1))-hypoglycemic (approximately 2.8 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.
既往研究表明，适度强度的运动可减弱非糖尿病个体对随后低血糖的自主神经、神经内分泌及代谢性反调节反应。本研究的目的是确定：1）1型糖尿病患者是否也存在这种情况；2）反应减弱的程度是否取决于运动强度。27例1型糖尿病患者（13例女性和14例男性）在进行两次90分钟运动试验后1天，接受单步、持续2小时的高胰岛素血症（9 pmol·kg⁻¹·min⁻¹）-低血糖（约2.8 mmol/L）钳夹试验，运动强度分别为30%（n = 11）或50%（n = 11）的最大摄氧量（Vo₂max），或不进行任何前期应激（对照组，n = 25）。在30%和50% Vo₂max的前期运动后，与对照组相比，对随后低血糖的肾上腺素反应（分别为1,959±553和1,528±424 vs. 3,420±424 pmol/L；P < 0.05）和胰多肽反应（分别为97±32和98±8 vs. 223±32 pmol/L；P < 0.05）显著降低。与对照组相比，两种运动强度后内源性葡萄糖生成均显著降低，而葡萄糖利用率以及因此维持低血糖所需的外源性葡萄糖输注率均显著增加。与对照组相比，两种强度的前期运动在基线时（16±4和22±4 vs. 31±3次/分钟）以及低血糖期间（22±4和27±5 vs. 41±3次/分钟）均使肌肉交感神经活动显著降低（P < 0.05）。与对照组相比，两个运动组的总低血糖症状也显著减少（P < 0.05）。总之，1型糖尿病患者进行低强度和中等强度的多次长时间运动可减弱对次日低血糖的关键自主神经（肾上腺素和胰多肽）和代谢（内源性葡萄糖生成和外周葡萄糖摄取）反调节反应。
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