scholarly journals Gender differences in insulin action after a single bout of exercise

2004 ◽  
Vol 97 (3) ◽  
pp. 1013-1021 ◽  
Author(s):  
Leigh Perreault ◽  
Jennifer M. Lavely ◽  
Bryan C. Bergman ◽  
Tracy J. Horton

Effects of a single exercise bout on insulin action were compared in men ( n = 10) and women ( n = 10). On an exercise day, subjects cycled for 90 min at 85% lactate threshold, whereas on a rest (control) day, they remained semirecumbent. The period of exercise, or rest, was followed by a 3-h hyperinsulinemic-euglycemic clamp (30 mU·m−2·min−1) and indirect calorimetry. Glucose kinetics were measured isotopically by using an infusion of [6,6-2H2]glucose. Glucose infusion rate (GIR) during the clamp on the rest day was not different between the genders. However, GIR on the exercise day was significantly lower in men compared with women ( P = 0.01). This was mainly due to a significantly lower glucose rate of disappearance in men compared with women ( P = 0.05), whereas no differences were observed in the endogenous glucose rate of appearance. Nonprotein respiratory quotient (NPRQ) increased significantly during the clamp from preclamp measurements in men and women on the rest day ( P < 0.01). Exercise abolished the increase in NPRQ seen during the clamp on the rest day and tended to decrease NPRQ in men. Our results indicate the following: 1) exercise abolishes the usual increase in NPRQ observed during a hyperinsulinemic-euglycemic clamp in both genders, 2) men exhibit relatively lower whole body insulin action in the 3–4 h after exercise compared with women, and 3) gender differences in insulin action may be explained by a lower glucose rate of disappearance in the men after acute exercise. Together, these data imply gender differences in insulin action postexercise exist in peripheral tissues and not in liver.

2014 ◽  
Vol 117 (3) ◽  
pp. 289-296 ◽  
Author(s):  
M. H. Vendelbo ◽  
A. B. Møller ◽  
J. T. Treebak ◽  
L. C. Gormsen ◽  
L. J. Goodyear ◽  
...  

Background: phosphorylation of AS160 and TBC1D1 plays an important role for GLUT4 mobilization to the cell surface. The phosphorylation of AS160 and TBC1D1 in humans in response to acute exercise is not fully characterized. Objective: to study AS160 and TBC1D1 phosphorylation in human skeletal muscle after aerobic exercise followed by a hyperinsulinemic euglycemic clamp. Design: eight healthy men were studied on two occasions: 1) in the resting state and 2) in the hours after a 1-h bout of ergometer cycling. A hyperinsulinemic euglycemic clamp was initiated 240 min after exercise and in a time-matched nonexercised control condition. We obtained muscle biopsies 30 min after exercise and in a time-matched nonexercised control condition ( t = 30) and after 30 min of insulin stimulation ( t = 270) and investigated site-specific phosphorylation of AS160 and TBC1D1. Results: phosphorylation on AS160 and TBC1D1 was increased 30 min after the exercise bout, whereas phosphorylation of the putative upstream kinases, Akt and AMPK, was unchanged compared with resting control condition. Exercise augmented insulin-stimulated phosphorylation on AS160 at Ser341and Ser704270 min after exercise. No additional exercise effects were observed on insulin-stimulated phosphorylation of Thr642and Ser588on AS160 or Ser237and Thr596on TBC1D1. Conclusions: AS160 and TBC1D1 phosphorylations were evident 30 min after exercise without simultaneously increased Akt and AMPK phosphorylation. Unlike TBC1D1, insulin-stimulated site-specific AS160 phosphorylation is modified by prior exercise, but these sites do not include Thr642and Ser588. Together, these data provide new insights into phosphorylation of key regulators of glucose transport in human skeletal muscle.


1999 ◽  
Vol 276 (1) ◽  
pp. E118-E124 ◽  
Author(s):  
S. M. Phillips ◽  
K. D. Tipton ◽  
A. A. Ferrando ◽  
R. R. Wolfe

We examined the effect of resistance training on the response of mixed muscle protein fractional synthesis (FSR) and breakdown rates (FBR) by use of primed constant infusions of [2H5]phenylalanine and [15N]phenylalanine, respectively, to an isolated bout of pleiometric resistance exercise. Trained subjects, who were performing regular resistance exercise (trained, T; n = 6), were compared with sedentary, untrained controls (untrained, UT; n = 6). The exercise test consisted of 10 sets (8 repetitions per set) of single-leg knee flexion (i.e., pleiometric muscle contraction during lowering) at 120% of the subjects’ predetermined single-leg 1 repetition maximum. Subjects exercised one leg while their contralateral leg acted as a nonexercised (resting) control. Exercise resulted in an increase, above resting, in mixed muscle FSR in both groups (UT: rest, 0.036 ± 0.002; exercise, 0.0802 ± 0.01; T: rest, 0.045 ± 0.004; exercise, 0.067 ± 0.01; all values in %/h; P< 0.01). In addition, exercise resulted in an increase in mixed muscle FBR of 37 ± 5% (rest, 0.076 ± 0.005; exercise, 0.105 ± 0.01; all values in %/h; P < 0.01) in the UT group but did not significantly affect FBR in the T group. The resulting muscle net balance (FSR − FBR) was negative throughout the protocol ( P < 0.05) but was increased in the exercised leg in both groups ( P < 0.05). We conclude that pleiometric muscle contractions induce an increase in mixed muscle protein synthetic rate within 4 h of completion of an exercise bout but that resistance training attenuates this increase. A single bout of pleiometric muscle contractions also increased the FBR of mixed muscle protein in UT but not in T subjects.


2009 ◽  
Vol 296 (4) ◽  
pp. E787-E795 ◽  
Author(s):  
Christian Frøsig ◽  
Carsten Roepstorff ◽  
Nina Brandt ◽  
Stine J. Maarbjerg ◽  
Jesper B. Birk ◽  
...  

This study evaluated whether improved insulin-stimulated glucose uptake in recovery from acute exercise coincides with reduced malonyl-CoA (MCoA) content in human muscle. Furthermore, we investigated whether a high-fat diet [65 energy-% (Fat)] would alter the content of MCoA and insulin action compared with a high-carbohydrate diet [65 energy-% (CHO)]. After 4 days of isocaloric diet on two occasions (Fat/CHO), 12 male subjects performed 1 h of one-legged knee extensor exercise (∼80% peak workload). Four hours after exercise, insulin-stimulated glucose uptake was determined in both legs during a euglycemic-hyperinsulinemic clamp. Muscle biopsies were obtained in both legs before and after the clamp. Four hours after exercise, insulin-stimulated glucose uptake was improved (∼70%, P < 0.001) independent of diet composition and despite normal insulin-stimulated regulation of insulin receptor substrate-1-associated phosphatidylinositol 3-kinase, Akt, GSK-3, and glycogen synthase. Interestingly, exercise resulted in a sustained reduction (∼20%, P < 0.05) in MCoA content 4 h after exercise that correlated ( r = 0.65, P < 0.001) with improved insulin-stimulated glucose uptake. Four days of Fat diet resulted in an increased content of intramyocellular triacylglycerol ( P < 0.01) but did not influence muscle MCoA content or whole body insulin-stimulated glucose uptake. However, at the muscular level proximal insulin signaling and insulin-stimulated glucose uptake appeared to be compromised, although to a minor extent, by the Fat diet. Collectively, this study indicates that reduced muscle MCoA content in recovery from exercise may be part of the adaptive response leading to improved insulin action on glucose uptake after exercise in human muscle.


Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4216-4226 ◽  
Author(s):  
Yun Dai ◽  
Shanthie Thamotharan ◽  
Meena Garg ◽  
Bo-Chul Shin ◽  
Sherin U. Devaskar

Intrauterine growth restriction (IUGR) results in dysregulated glucose homeostasis and adiposity in the adult. We hypothesized that with aging, these perturbations will wane, and superimposition of postnatal growth restriction (PNGR) on IUGR [intrauterine and postnatal growth restriction (IPGR)] will reverse the residual IUGR phenotype. We therefore undertook hyperinsulinemic-euglycemic clamp, energy balance, and physical activity studies during fed, fasted, and refed states, in light and dark cycles, on postweaned chow diet-fed more than 17-month aging male IUGR, PNGR, and IPGR vs. control (CON) rat offspring. Hyperinsulinemic-euglycemic clamp revealed similar whole-body insulin sensitivity and physical activity in the nonobese IUGR vs. CON, despite reduced heat production and energy expenditure. Compared with CON and IUGR, IPGR mimicking PNGR was lean and growth restricted with increased physical activity, O2 consumption (VO2), energy intake, and expenditure. Although insulin sensitivity was no different in IPGR and PNGR, skeletal muscle insulin-induced glucose uptake was enhanced. This presentation proved protective against the chronologically earlier (5.5 months) development of obesity and dysregulated energy homeostasis after 19 wk on a postweaned high-fat diet. This protective role of PNGR on the metabolic IUGR phenotype needs future fine tuning aimed at minimizing unintended consequences.


1992 ◽  
Vol 24 (Supplement) ◽  
pp. S89
Author(s):  
J. Oao ◽  
U. M. Sherman ◽  
S. HcCune ◽  
K. Osat

Diabetes ◽  
2020 ◽  
Vol 69 (4) ◽  
pp. 578-590 ◽  
Author(s):  
Dorte E. Steenberg ◽  
Janne R. Hingst ◽  
Jesper B. Birk ◽  
Anette Thorup ◽  
Jonas M. Kristensen ◽  
...  

2005 ◽  
Vol 33 (2) ◽  
pp. 354-357 ◽  
Author(s):  
M. Björnholm ◽  
J.R. Zierath

Type II diabetes is characterized by defects in insulin action on peripheral tissues, such as skeletal muscle, adipose tissue and liver and pancreatic β-cell defects. Since the skeletal muscle accounts for approx. 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Thus identifying defective steps in this process may reveal attractive targets for drug development to combat insulin resistance and Type II diabetes. This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Evidence for impaired activation of the insulin receptor signalling cascade and defective glucose transporter 4 translocation in the skeletal muscle from Type II diabetic patients will be presented. Through the identification of the intracellular defects in insulin action that control glucose homoeostasis, a better understanding of the disease pathogenesis can be gained and strategies for intervention may be developed.


2002 ◽  
Vol 80 (8) ◽  
pp. 811-818 ◽  
Author(s):  
Maria A.G Reid ◽  
Martin G Latour ◽  
Dallas J Legare ◽  
Na Rong ◽  
W Wayne Lautt

The objective was to compare the ability of the rapid insulin sensitivity test (RIST), the hyperinsulinemic euglycemic clamp (HIEC), and the insulin tolerance test (ITT) to detect hepatic insulin sensitizing substance (HISS) dependent insulin action. HISS action was augmented by feeding and inhibited by fasting, blockade of hepatic nitric oxide synthase, or blockade of hepatic muscarinic cholinergic receptors. A significant correlation was found between the RIST index and ITT nadir (r2 = 0.84) but not between the glucose infusion rate of the HIEC and RIST index. There was, however, a relationship between the RIST index and the initial response during the HIEC. Use of the HIEC resulted in HISS-dependent insulin resistance in both conscious and anesthetized animals. We concluded that since the RIST and ITT were comparable in quantifying both HISS-dependent and HISS-independent insulin action, the RIST was validated against this standard. The observation that the HIEC is capable of detecting HISS action in the first rising slope of the test but not at the end of the test and that HISS release is fully blocked after the conclusion of the HIEC raises concerns about the use of the commonly used HIEC.Key words: HISS, insulin resistance, insulin sensitivity tests.


PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0188421 ◽  
Author(s):  
Adam J. Trewin ◽  
Itamar Levinger ◽  
Lewan Parker ◽  
Christopher S. Shaw ◽  
Fabio R. Serpiello ◽  
...  

2020 ◽  
Author(s):  
Karsten Koehler ◽  
Safiya E Beckford ◽  
Elise Thayer ◽  
Alexandra R Martin ◽  
Julie B Boron ◽  
...  

Although exercise modulates appetite regulation and food intake, it remains poorly understood how exercise impacts decision making about food. The purpose of the present study was to assess the impact of an acute exercise bout on hypothetical choices related to the amount and timing of food intake. Forty-one healthy participants (22.0 ± 2.6 years; 23.7 ± 2.5 kg/m2, 56% female) completed 45 minutes of aerobic exercise and a resting control condition in randomized order. Food amount preferences and intertemporal food preferences (preference for immediate vs. delayed consumption) were assessed using electronic questionnaires with visual food. Compared to rest, exercise resulted in a greater increase in the food amount selected, both immediately post exercise (+25.8 ± 11.0 vs. +7.8 ± 11.0 kcal/item, p = 0.02) and 30 min post exercise (+47.3 ± 12.4 vs. +21.3 ± 12.4 kcal/item, p = 0.005). Exercise further resulted in a greater increase in the preference for immediate consumption immediately post exercise (+0.23 ± 0.10 vs. +0.06 ± 0.10; p = 0.03) and 30 min post exercise (+0.30 ± 0.12 vs. +0.08 ± 0.12; p = 0.01). Our findings demonstrate that a single bout of aerobic exercise shifts hypothetical food choices towards greater amounts and more immediate consumption, highlighting the importance of the timing of food choices made in the exercise context.


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