Effects of non-insulin-dependent diabetes on oxygen consumption during treadmill exercise

Regensteiner, Judith G.; Sippel, Jeffrey M.; McFarling, Eric T.; Wolfel, Eugene E.; Hiatt, William R.

doi:10.1249/00005768-199506000-00012

Cited by 134 publications

(142 citation statements)

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“…At 0400 hours of each inpatient period, a priming dose of L-[1,2-13 C]leucine (1.8 mg͞kg of FFM) was administered through a peripheral forearm vein. This was followed by a continuous infusion of L- [1,[2][3][4][5][6][7][8][9][10][11][12][13] C]leucine (1.8 mg͞kg of FFM per h). Insulin [1.5 milliunits (mU)͞kg of FFM per min] or normal saline infusion was randomized and began at 0700 hours.…”

Section: Methodsmentioning

confidence: 99%

“…However, the effect of insulin on skeletal muscle mitochondrial function and oxidative capacity have not been defined. Previous studies have suggested a relationship between insulin action and the oxidative capacity of skeletal muscle (3)(4)(5)(6)(7)(8)(9)(10). For example, the ratio between oxidative and glycolytic enzyme activities is decreased in skeletal muscle from type 2 diabetic subjects compared with nondiabetic subjects (6).…”

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confidence: 99%

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Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts

Stump

Short

Bigelow

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

418

369

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Mitochondria are the primary site of skeletal muscle fuel metabolism and ATP production. Although insulin is a major regulator of fuel metabolism, its effect on mitochondrial ATP production is not known. Here we report increases in vastus lateralis muscle mitochondrial ATP production capacity (32-42%) in healthy humans (P < 0.01) i.v. infused with insulin (1.5 milliunits͞kg of fat-free mass per min) while clamping glucose, amino acids, glucagon, and growth hormone. Increased ATP production occurred in association with increased mRNA levels from both mitochondrial (NADH dehydrogenase subunit IV) and nuclear [cytochrome c oxidase (COX) subunit IV] genes (164 -180%) encoding mitochondrial proteins (P < 0.05). In addition, muscle mitochondrial protein synthesis, and COX and citrate synthase enzyme activities were increased by insulin (P < 0.05). Further studies demonstrated no effect of low to high insulin levels on muscle mitochondrial ATP production for people with type 2 diabetes mellitus, whereas matched nondiabetic controls increased 16 -26% (P < 0.02) when four different substrate combinations were used. In conclusion, insulin stimulates mitochondrial oxidative phosphorylation in skeletal muscle along with synthesis of gene transcripts and mitochondrial protein in human subjects. Skeletal muscle of type 2 diabetic patients has a reduced capacity to increase ATP production with high insulin levels.cytochrome c oxidase ͉ NADH dehydrogenase subunit IV ͉ amino acids ͉ citrate synthase

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts

Stump

Short

Bigelow

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

418

369

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show abstract

“…108 These are increased 2-and 4-fold in male and female patients with type 2 diabetes respectively 109 and 3-10-fold in those with type 1 diabetes. [110][111][112][113][114][115] Complications include reduced left ventricular function, higher resting heart rates, reduced cardiac reserve, reduced cardiac return, orthostatic hypotension, and coronary artery stenosis. [116][117][118][119][120] In addition, hypoglycaemia may promote prolongation of PR and QT intervals, promoting arrhythmias during exercise.…”

Section: Exercise Prescriptionmentioning

confidence: 99%

Diabetes and exercise.

Peirce

1999

Br J Sports Med

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Exercise is frequently recommended in the management of type 1 and 2 diabetes mellitus and can improve glucose uptake by increasing insulin sensitivity and lowering body adiposity. Both alone and when combined with diet and drug therapy, physical activity can result in improvements in glycaemic control in type 2 diabetes. In addition, exercise can also help to prevent the onset of type 2 diabetes, in particular in those at higher risk, and has an important role in reducing the significant worldwide burden of this type of diabetes. Recent studies have improved our understanding of the acute and long term physiological benefits of physical activity, although the precise duration, intensity, and type of exercise have yet to be fully elucidated. However, in type 1 diabetes, the expected improvements in glycaemic control with exercise have not been clearly established. Instead significant physical and psychological benefits of exercise can be achieved while careful education, screening, and planning allow the metabolic, microvascular, and macrovascular risks to be predicted and diminished. (Br J Sports Med 1999;33:161-173)

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“…Subsequently, 7-day low-level PAR questionnaire responses were used to assess habitual physical activity. 21 This questionnaire has been used and validated in population studies as well as in our laboratory in people with DM and peripheral arterial disease. 22 During this visit, subjects were instructed to discontinue aspirin and nonsteroidal anti-inflammatory medications 1 week before testing and to avoid exercise for 36 hours before testing.…”

Section: Methodsmentioning

confidence: 99%

Impaired Fibrinolysis in Premenopausal Women and Age-matched Men with Type 2 Diabetes Mellitus: A Pilot Study

Brandenburg

Reusch

Felder

et al. 2002

Journal of Investigative Medicine

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Effects of non-insulin-dependent diabetes on oxygen consumption during treadmill exercise

Cited by 134 publications

References 0 publications

Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts

Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts

Diabetes and exercise.

Impaired Fibrinolysis in Premenopausal Women and Age-matched Men with Type 2 Diabetes Mellitus: A Pilot Study

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