Insulin action on heart and skeletal muscle glucose uptake in weight lifters and endurance athletes

There are no studies comparing myocardial metabolism between endurance- and resistance-trained athletes. We used 2-deoxy-2-[18F]fluoro-d-glucose and positron emission tomography combined with the euglycemic hyperinsulinemic clamp technique to compare the ability of insulin to stimulate myocardial, skeletal muscle, and whole body glucose uptake between weight lifters ( n = 8), endurance athletes ( n = 8), and sedentary men ( n = 9). Maximal aerobic power (ml ⋅ kg− 1⋅ min− 1) was higher in the endurance athletes (71 ± 2, P < 0.001) than the weight lifters (42 ± 2) and the sedentary men (42 ± 2). Skeletal muscle glucose uptake (μmol ⋅ kg muscle− 1⋅ min− 1) was enhanced in the endurance athletes (125 ± 16, P < 0.01) but was similar in weight lifters (59 ± 12) and sedentary (63 ± 7) men. The rate of glucose uptake per unit mass of myocardium (μmol ⋅ kg− 1⋅ min− 1) was similarly decreased in endurance athletes (544 ± 50) and weight lifters (651 ± 45) compared with sedentary men (1,041 ± 78, P < 0.001 vs. endurance athletes and weight lifters). Both groups of athletes had increased left ventricular mass. Consequently, total left ventricular glucose uptake was comparable in all groups. These data demonstrate that aerobic but not resistance training is associated with enhanced insulin sensitivity in skeletal muscle. Despite this, cardiac changes are remarkably similar in weight lifters and endurance athletes and are characterized by an increase in left ventricular mass and diminished insulin-stimulated glucose uptake per heart mass.

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Leptin administration improves skeletal muscle insulin responsiveness in diet-induced insulin-resistant rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2001.280.1.e130 ◽

2001 ◽

Vol 280 (1) ◽

pp. E130-E142 ◽

Cited By ~ 44

Author(s):

Ben B. Yaspelkis ◽

James R. Davis ◽

Maziyar Saberi ◽

Toby L. Smith ◽

Reza Jazayeri ◽

...

Keyword(s):

Skeletal Muscle ◽

Insulin Secretion ◽

Glucose Tolerance ◽

Glucose Uptake ◽

Whole Body ◽

Glucose Disposal ◽

High Fat ◽

Insulin Resistant ◽

Skeletal Muscle Glucose Uptake ◽

Uptake And Transport

In addition to suppressing appetite, leptin may also modulate insulin secretion and action. Leptin was administered here to insulin-resistant rats to determine its effects on secretagogue-stimulated insulin release, whole body glucose disposal, and insulin-stimulated skeletal muscle glucose uptake and transport. Male Wistar rats were fed either a normal (Con) or a high-fat (HF) diet for 3 or 6 mo. HF rats were then treated with either vehicle (HF), leptin (HF-Lep, 10 mg · kg−1 · day−1 sc), or food restriction (HF-FR) for 12–15 days. Glucose tolerance and skeletal muscle glucose uptake and transport were significantly impaired in HF compared with Con. Whole body glucose tolerance and rates of insulin-stimulated skeletal muscle glucose uptake and transport in HF-Lep were similar to those of Con and greater than those of HF and HF-FR. The insulin secretory response to either glucose or tolbutamide (a pancreatic β-cell secretagogue) was not significantly diminished in HF-Lep. Total and plasma membrane skeletal muscle GLUT-4 protein concentrations were similar in Con and HF-Lep and greater than those in HF and HF-FR. The findings suggest that chronic leptin administration reversed a high-fat diet-induced insulin-resistant state, without compromising insulin secretion.

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Variation at the Beta-1Adrenoceptor Gene Locus is Associated with Left Ventricular Mass in Endurance Athletes

Medicine & Science in Sports & Exercise ◽

10.1097/00005768-200405001-00473 ◽

2004 ◽

Vol 36 (Supplement) ◽

pp. S100

Author(s):

Bernd M. Wolfarth ◽

Johannes Scherr ◽

Helga Duerr ◽

Susanne Muehlbauer

Keyword(s):

Left Ventricular Mass ◽

Gene Locus ◽

Left Ventricular ◽

Endurance Athletes ◽

Ventricular Mass

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Variation at the Beta-1Adrenoceptor Gene Locus is Associated with Left Ventricular Mass in Endurance Athletes

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-200405001-00473 ◽

2004 ◽

Vol 36 (Supplement) ◽

pp. S100

Author(s):

Bernd M. Wolfarth ◽

Johannes Scherr ◽

Helga Duerr ◽

Susanne Muehlbauer

Keyword(s):

Left Ventricular Mass ◽

Gene Locus ◽

Left Ventricular ◽

Endurance Athletes ◽

Ventricular Mass

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Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humans

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.6.e769 ◽

1988 ◽

Vol 255 (6) ◽

pp. E769-E774 ◽

Cited By ~ 114

Author(s):

A. D. Baron ◽

G. Brechtel ◽

P. Wallace ◽

S. V. Edelman

Keyword(s):

Skeletal Muscle ◽

Glucose Uptake ◽

Serum Glucose ◽

Whole Body ◽

Healthy Men ◽

Catheter Technique ◽

Muscle Tissues ◽

Skeletal Muscle Glucose Uptake ◽

The Difference

In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Although the principal tissue sites for IMGU are skeletal muscle, the tissue sites for NIMGU at a given serum glucose concentration are not known. To examine this issue, rates of whole body glucose uptake (Rd) were measured at basal and during glucose clamp studies performed at euglycemia (approximately 90 mg/dl) and hyperglycemia (approximately 220 mg/dl) in six lean healthy men. Studies were performed during hyperinsulinemia (approximately 70 microU/ml) and during somatostatin-induced insulinopenia to measure IMGU and NIMGU, respectively. During each study, leg glucose balance (arteriovenous catheter technique) was also measured. With this approach, rates of whole body skeletal muscle IMGU and NIMGU can be estimated, and the difference between overall Rd and skeletal muscle glucose uptake represents non-skeletal muscle Rd. The results indicate that approximately 20% of basal Rd is into skeletal muscle. During insulinopenia approximately 86% of body NIMGU occurs in non-skeletal muscle tissues at euglycemia. When hyperglycemia was created, whole body NIMGU increased from 128 +/- 6 to 213 +/- 18 mg/min (P less than 0.01); NIMGU into non-skeletal muscle tissues was 134 +/- 11 and 111 +/- 6 mg/min at hyperglycemia and euglycemia, respectively, P = NS. Therefore, virtually all the hyperglycemia induced increment in NIMGU occurred in skeletal muscle. During hyperinsulinemia, IMGU in skeletal muscle represented 75 and 95% of body Rd, at euglycemia and hyperglycemia, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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Left Ventricular Mass in Elite Olympic Weight Lifters

The American Journal of Cardiology ◽

10.1016/j.amjcard.2007.05.036 ◽

2007 ◽

Vol 100 (7) ◽

pp. 1177-1180 ◽

Cited By ~ 13

Author(s):

Sophie Lalande ◽

James Christopher Baldi

Keyword(s):

Left Ventricular Mass ◽

Left Ventricular ◽

Ventricular Mass ◽

Weight Lifters

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Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes

The American Journal of Cardiology ◽

10.1016/0002-9149(88)90228-7 ◽

1988 ◽

Vol 62 (4) ◽

pp. 301-305 ◽

Cited By ~ 65

Author(s):

Martin C. Milliken ◽

James Stray-Gundersen ◽

Ronald M. Peshock ◽

Jose Katz ◽

Jere H. Mitchell

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Left Ventricular Mass ◽

Left Ventricular ◽

Endurance Athletes ◽

Resonance Imaging ◽

Ventricular Mass

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Effect of perfusion rate on the time course of insulin-mediated skeletal muscle glucose uptake

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1996.271.6.e1067 ◽

1996 ◽

Vol 271 (6) ◽

pp. E1067-E1072 ◽

Cited By ~ 15

Author(s):

A. D. Baron ◽

G. Brechtel-Hook ◽

A. Johnson ◽

J. Cronin ◽

R. Leaming ◽

...

Keyword(s):

Skeletal Muscle ◽

Glucose Uptake ◽

Time Course ◽

Specific Inhibitor ◽

Time Dependent ◽

Whole Body ◽

Glucose Disposal ◽

Dependent Manner ◽

Skeletal Muscle Glucose Uptake ◽

Oxide Synthase

To better define the time course of skeletal muscle glucose uptake and its modulation by changes in perfusion, we performed systemic euglycemic-hyperinsulinemic clamps (40 mU.m-2.min-1) for a 90-min period in a group of lean, insulin-sensitive subjects (n = 9) on two occasions (approximately 4 wk apart) with insulin-mediated vasodilation intact or inhibited. Insulin-mediated vasodilation was inhibited by an intrafemoral artery infusion of NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthase. During the study, leg blood flow (LBF) and arteriovenous glucose difference (AVG delta) were measured every 10 min; leg glucose uptake (LGU) was calculated as LGU = LBF x AVG delta. The systemic insulin infusion caused a time-dependent increase in LBF from 0.194 +/- 0.024 to 0.349 +/- 0.046 l/min (P < 0.01). The intrafemoral artery infusion of L-NMMA completely inhibited this increase in LBF. AVG delta, LGU, and whole body glucose disposal rates increased in a time-dependent manner in both studies. The maximum AVG delta was lower with insulin-mediated vasodilation intact than when inhibited (25.9 +/- 2.5 vs. 35.0 +/- 1.6 mg/dl, P < 0.001). The time to achieve half-maximal (T1/2) AVG delta was somewhat longer with insulin-mediated vasodilation intact compared with inhibited (35.6 +/- 4.1 vs. 29.7 +/- 1.6 min, P < 0.01). Maximal LGU was 93.9 +/- 26.8 and 57.2 +/- 11.6 mg/min (P < 0.005), and the T1/2 LGU was 50.2 +/- 16.0 and 36.3 +/- 8.8 min (P = 0.1) during intact and inhibited insulin-mediated vasodilation, respectively. Thus insulin-mediated vasodilation has a modest effect in slowing the time course at which insulin stimulates glucose uptake but has a marked effect in augmenting the maximal rate of insulin-stimulated glucose uptake in skeletal muscle. Impaired insulin-mediated vasodilation, as observed in patients with essential hypertension, may explain, at least in part, the insulin resistance observed in these patients.

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