Exercise Responses in Patients With IDDM

Nugent, A. M.; Steele, I. C.; Al-Modaris, F.; Vallely, Stephen; Moore, A.; Campbell, N. P. S.; Bell, P. M.; Buchanan, K.D.; Trimble, E.R.; Nicholls, D. P.

doi:10.2337/diacare.20.12.1814

Cited by 38 publications

(20 citation statements)

References 32 publications

(59 reference statements)

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“…These abnormalities could thus be related to increased dead space ventilation, as previously described in diabetic patients. 31 In summary, our study showed that the severity of microalbuminuria in type 2 diabetic patients was correlated with impaired cardiovascular function and oxygen transport during exercise. A unified hypothesis may herein be generated that microalbuminuria may signal a state of generalized microvascular dysfunction, with increased capillary permeability to macromolecules, such as plasma proteins.…”

Section: Discussionmentioning

confidence: 90%

Altered Exercise Gas Exchange as Related to Microalbuminuria in Type 2 Diabetic Patients

Lau

Leung

et al. 2004

Chest

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Section: Discussionmentioning

confidence: 90%

Altered Exercise Gas Exchange as Related to Microalbuminuria in Type 2 Diabetic Patients

Lau

Leung

et al. 2004

Chest

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“…However, although heart rate and systolic blood pressure increased as expected during exercise, diastolic blood pressure decreased by ϳ10 mmHg. Diastolic dysfunction during exercise, not accompanied by systolic dysfunction or altered cardiac output response, has been reported by several authors (32)(33)(34) in type 1 diabetic patients with no evidence of autonomic neuropathy, leading to the hypothesis that alterations in diastolic filling may represent the earliest functional defect of diabetic cardiomyopathy. Surprisingly, however, an exercise-induced reduction in diastolic blood pressure in type 1 diabetes has not been previously reported.…”

Section: Discussionmentioning

confidence: 91%

“…We believe that the experimental design used in previous exercise studies obscured recognition of this finding. The large majority of previous exercise studies in type 1 diabetes used incremental maximal tests (33,35,36) or brief periods of submaximal exercise (37); furthermore, diastolic blood pressure was seldom reported, and glycemic levels during exercise were never controlled (introducing the confounding effect of concomitant hypoglycemia, which may independently lower blood pressure and stimulate the ANS).…”

Section: Discussionmentioning

confidence: 99%

Effect of Antecedent Hypoglycemia on Counterregulatory Responses to Subsequent Euglycemic Exercise in Type 1 Diabetes

et al. 2003

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Exercise-related hypoglycemia is common in intensively treated patients with type 1 diabetes. The underlying mechanisms are not clearly defined. In nondiabetic subjects, hypoglycemia blunts counterregulatory responses to subsequent exercise. It is unknown whether this also occurs in type 1 diabetes. Therefore, the goal of this study was to test the hypothesis that prior hypoglycemia could result in acute counterregulatory failure during subsequent exercise in type 1 diabetes. A total of 16 type 1 diabetic patients (8 men and 8 women, HbA 1c 7.8 ؎ 0.3%) were investigated during 90 min of euglycemic cycling exercise, following either two 2-h periods of previous-day hypoglycemia (2.9 mmol/l) or previous-day euglycemia. Patients' counterregulatory responses (circulating levels of counterregulatory hormones, intermediary metabolites, substrate flux via indirect calorimetry, tracer-determined glucose kinetics, and cardiovascular measurements) were comprehensively assessed during exercise. Identical euglycemia and basal insulin levels were successfully maintained during all exercise studies, regardless of blood glucose levels during the previous day. After resting euglycemia, patients displayed normal counterregulatory responses to exercise. Conversely, when identical exercise was repeated after hypoglycemia, the glucagon response to exercise was abolished, and the epinephrine, norepinephrine, cortisol, endogenous glucose production, and lipolytic responses were reduced by 40 -80%. This resulted in a threefold increase in the amount of exogenous glucose needed to maintain euglycemia during exercise. Our results demonstrate that antecedent hypoglycemia, in type 1 diabetes, can produce acute counterregulatory failure during a subsequent episode of prolonged moderate-intensity exercise. The metabolic consequence of the blunted neuroendocrine and autonomic nervous system counterregulatory responses was an acute failure of endogenous glucose production to match the increased glucose requirements during exercise. These data indicate that counterregulatory failure may be a significant in vivo mechanism responsible for exercise-associated hypoglycemia in type 1 diabetes.

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“…In this study, VO 2max was similar between the groups. This is in keeping with previous studies in which patients with uncomplicated type 1 diabetes had a normal aerobic exercise capacity (40). We chose the intensity of isometric exercise based on individual muscular strengths, rather than on VO 2max , because use of the latter would lead to different work loads if groups differed with respect to VO 2max .…”

mentioning

confidence: 85%

Resistance to Exercise-Induced Increase in Glucose Uptake During Hyperinsulinemia in Insulin-Resistant Skeletal Muscle of Patients With Type 1 Diabetes

et al. 2001

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Insulin and exercise have been shown to activate glucose transport at least in part via different signaling pathways. However, it is unknown whether insulin resistance is associated with a defect in the ability of an acute bout of exercise to enhance muscle glucose uptake in vivo. We compared the abilities of insulin and isometric exercise to stimulate muscle blood flow and glucose uptake in 12 men with type 1 diabetes (age 24 ؎ ; normal subjects versus patients with type 1 diabetes, NS), and exercise increased oxygen consumption similarly in both groups (25.3 ؎ 4.3 vs. 20.1 ؎ 3.0 ml ⅐ kg ؊1 muscle ⅐ min ؊1 , respectively, NS). Rates of insulin-stimulated muscle blood flow and the increments in muscle blood flow induced by exercise were also similar in normal subjects (129 ؎ 14 ml ⅐ kg ؊1 ⅐ min ؊1) and in patients with type 1 diabetes (115 ؎ 12 ml ⅐ kg ؊1 ⅐ min ؊1). The patients with type 1 diabetes exhibited resistance to both insulin stimulation of glucose uptake (34 ؎ 6 vs. 76 ؎ 9 mol ⅐ kg ؊1 muscle ⅐ min ؊1 , P < 0.001) and also to the exercise-induced increment in glucose uptake (82 ؎ 15 vs. 162 ؎ 29 mol ⅐ kg ؊1 muscle ⅐ min ؊1 , P < 0.05). We conclude that the ability of exercise to increase insulin-stimulated glucose uptake in vivo is blunted in patients with insulin-resistant type 1 diabetes compared with normal subjects. This could be caused by either separate or common defects in exercise-and insulinstimulated pathways.

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Exercise Responses in Patients With IDDM

Abstract: There is no evidence of impairment of the exercise response in subjects with long-standing diabetes, and the apparent fall in left ventricular EF at peak exercise could be related to hemodynamic adaptation.

Cited by 38 publications

References 32 publications

Altered Exercise Gas Exchange as Related to Microalbuminuria in Type 2 Diabetic Patients

Altered Exercise Gas Exchange as Related to Microalbuminuria in Type 2 Diabetic Patients

Effect of Antecedent Hypoglycemia on Counterregulatory Responses to Subsequent Euglycemic Exercise in Type 1 Diabetes

Resistance to Exercise-Induced Increase in Glucose Uptake During Hyperinsulinemia in Insulin-Resistant Skeletal Muscle of Patients With Type 1 Diabetes

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