Effect of a single bout of exercise and chronic exercise training on insulin sensitivity in racing sled dogs

2014 ◽  
Vol 10 (3) ◽  
pp. 167-172 ◽  
Author(s):  
S.E. Pratt-Phillips ◽  
R.J. Geor ◽  
M. Buser ◽  
A. Zirkle ◽  
A. Moore ◽  
...  

Two experiments were designed to investigate the role of exercise on insulin sensitivity (IS) in Alaskan racing sled dogs. In both experiments, IS was quantified with an isoglycemic-hyperinsulinemic clamp (IHC), whereby IS was defined as the glucose infusion rate (GIR) divided by the mean insulin concentration during the clamp. In Experiment 1, IS was quantified in 12 racing sled dogs during three stages of exercise training: unexercised for 4 months over the summer (deconditioned), and after two and four months of exercise conditioning. At each stage IS was assessed in unexercised dogs (n=6) and 60 h following a standard exercise challenge (n=6) consisting of a 35.4 km run completed in 2.5 h. In Experiment 2, IS was assessed in deconditioned dogs (n=6) and in well-conditioned dogs that had either completed a 708 km race 5-days prior (n=3) or were unraced for the previous month (n=3). In Experiment 1, there were no significant differences (Pã0.05) in GIR or IS between the three levels of conditioning, nor were there any effects of the exercise bout 60 h prior to the IHC. In Experiment 2 there was no significant difference in IS between well-conditioned dogs and untrained dogs (Pã0.05). However, dogs that completed a 708 km race 5-days prior to the IHC had a significantly higher IS than dogs that were deconditioned and those that were conditioned but unraced. These results suggest that the workload of an exercise challenge is a factor in post-exercise changes in IS but that exercise conditioning has little impact on IS in Alaskan sled dogs.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Cesar Meza ◽  
Mario Garcia ◽  
Jerremy Serrano ◽  
Manuel Gomez ◽  
Manuel Amador ◽  
...  


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.



2017 ◽  
Vol 13 (4) ◽  
pp. 227-235
Author(s):  
P.M. Davitt ◽  
G.C. Henderson ◽  
A.J. Walker ◽  
S.M. Arent

Physiological changes with endurance exercise (EE) and resistance training (RT) are likely influenced by the metabolic and hormonal response to each exercise bout, but may be blunted in obese individuals. To compare acute effects of EE, RT, and a control upon hormonal changes in obese women, sedentary, obese women (n=12) participated in a randomised crossover-design study on 3 occasions. EE consisted of treadmill walking (65% VO2max for 1 h). A total-body RT workout consisted of 3 sets of 10 repetitions, 90 s rest for 8 exercises at 90-100% of 10RM. Blood samples were taken 30 min before exercise (0 min), 30 min post-exercise (120 min), and again at 200, 280, and 520 min to assess changes in growth hormone (GH), cortisol, and insulin throughout the postprandial period. A 20 kcal/kg fat-free mass (FFM) meal was given after post-exercise blood sample. There was a main effect of condition for GH ΔAUC (change in area under the curve), with both RT and EE significantly different from the control (RT = 463.0±138.2; EE = 243.2±131.6; Control = -90.4±157.6 ng/ml * 400 min, P<0.02, Control vs EE, effect size (ES) = 2.3; Control vs RT, ES=3.7; EE vs RT, ES=1.6). There were no condition effects for cortisol or insulin ΔAUC. There were no significant time-by-condition interactions for any variables. In obese women, circulating GH concentration is enhanced in the postprandial state following a single bout of either EE or RT, with the GH response being more robust than cortisol or insulin. As circulating GH has shown to be reduced in obesity, the present observations could be considered beneficial, particularly alongside the absence of enhanced cortisol level after exercise.



1999 ◽  
Vol 277 (6) ◽  
pp. E1055-E1060 ◽  
Author(s):  
Joseph A. Houmard ◽  
Christopher D. Shaw ◽  
Matthew S. Hickey ◽  
Charles J. Tanner

The purpose of this study was to determine if the improvement in insulin sensitivity with exercise training is associated with enhanced phosphatidylinositol 3-kinase (PI 3-kinase) activity. Nine sedentary men were studied before and after 7 days of exercise training (1 h/day, ≈75% maximal oxygen consumption). Insulin sensitivity was determined with a euglycemic-hyperinsulinemic glucose clamp in the sedentary state and 15–17 h after the final exercise bout. PI 3-kinase activity was determined from samples (vastus lateralis) obtained in the fasted condition and after 60 min of submaximal insulin stimulation during the clamp. After exercise, glucose infusion rate increased ( P < 0.05) significantly (means ± SE, 7.8 ± 0.5 vs. 9.8 ± 0.8 mg ⋅ kg−1 ⋅ min−1), indicating improved insulin sensitivity. Insulin-stimulated (insulin stimulated/fasting) phosphotyrosine immunoprecipitable PI 3-kinase activity also increased significantly ( P < 0.05) with exercise (3.1 ± 0.8-fold) compared with the sedentary condition (1.3 ± 0.1-fold). There was no change in fasting PI 3-kinase activity. These data suggest that an enhancement of insulin signal transduction in skeletal muscle may contribute to the improvement in insulin action with exercise.





Metabolism ◽  
2013 ◽  
Vol 62 (10) ◽  
pp. 1485-1494 ◽  
Author(s):  
Katharine E. Hall ◽  
Matthew W. McDonald ◽  
Kenneth N. Grisé ◽  
Oscar A. Campos ◽  
Earl G. Noble ◽  
...  


Author(s):  
Froukje Vanweert ◽  
Sebastiaan C. Boone ◽  
Bram Brouwers ◽  
Dennis O. Mook-Kanamori ◽  
Renée de Mutsert ◽  
...  

Abstract Aims To evaluate whether the association between plasma branched-chain amino acids (BCAA) and intrahepatic lipid (IHL) was affected by physical activity level. Furthermore, to investigate if a conventional exercise training program, a subcategory of physical activity, could lower plasma BCAA along with alterations in IHL content in patients with type 2 diabetes (T2DM) and people with nonalcoholic fatty liver (NAFL). Methods To investigate the effect of physical activity on the association between plasma BCAA and IHL content, linear regression analyses were performed in 1983 individuals from the Netherlands Epidemiology of Obesity (NEO) stratified by physical activity frequency. Furthermore, the effect of a 12-week supervised combined aerobic resistance-exercise program on plasma BCAA, insulin sensitivity (hyperinsulinemic–euglycemic clamp), and IHL (proton-magnetic resonance spectroscopy (1H-MRS)) was investigated in seven patients with T2DM, seven individuals with NAFL and seven BMI-matched control participants (CON). Results We observed positive associations between plasma valine, isoleucine and leucine level, and IHL content (1.29 (95% CI: 1.21, 1.38), 1.52 (95% CI: 1.43, 1.61), and 1.54 (95% CI: 1.44, 1.64) times IHL, respectively, per standard deviation of plasma amino acid level). Similar associations were observed in less active versus more active individuals. Exercise training did not change plasma BCAA levels among groups, but reduced IHL content in NAFL (from 11.6 ± 3.0% pre-exercise to 8.1 ± 2.0% post exercise, p < 0.05) and CON (from 2.4 ± 0.6% pre-exercise to 1.6 ± 1.4% post exercise, p < 0.05), and improved peripheral insulin sensitivity in NAFL as well by ~23% (p < 0.05). Conclusions The association between plasma BCAA levels and IHL is not affected by physical activity level. Exercise training reduced IHL without affecting plasma BCAA levels in individuals with NAFL and CON. We conclude that exercise training-induced reduction in IHL content is not related to changes in plasma BCAA levels. Trial registration Trial registry number: NCT01317576.



1991 ◽  
Vol 261 (4) ◽  
pp. E437-E443 ◽  
Author(s):  
J. A. Houmard ◽  
P. C. Egan ◽  
P. D. Neufer ◽  
J. E. Friedman ◽  
W. S. Wheeler ◽  
...  

Exercise training has been proposed to improve whole body insulin sensitivity through a postreceptor adaptation in skeletal muscle. This study examined if levels of the insulin-responsive muscle glucose transporter protein (GLUT-4) were associated with improved insulin sensitivity in trained vs. sedentary middle-aged individuals. Muscle GLUT-4 levels and oral glucose tolerance test (OGTT) responses were obtained in age-matched trained and sedentary men (n = 11). Plasma insulin levels during the OGTT were significantly lower (P less than 0.01) in the trained men, whereas no differences were seen in plasma glucose responses. GLUT-4 protein content was approximately twofold higher in the trained men (2.41 +/- 0.17 vs. 1.36 +/- 0.11 micrograms standard, P less than 0.001). OGTT responses and GLUT-4 levels were not altered 15-18 h after a standard exercise bout in six representative sedentary subjects. These data suggest that GLUT-4 levels are increased in conjunction with insulin sensitivity in chronically exercise-trained middle-aged men. This finding suggests a possible mechanism for the improved insulin sensitivity observed with exercise training in humans.



2011 ◽  
Vol 301 (5) ◽  
pp. R1501-R1509 ◽  
Author(s):  
Tobias Nørresø Haase ◽  
Stine Ringholm ◽  
Lotte Leick ◽  
Rasmus Sjørup Biensø ◽  
Kristian Kiilerich ◽  
...  

The transcriptional coactivator peroxisome proliferator-activated receptor (PPAR)-γ coactivator (PGC)-1α plays a role in regulation of several metabolic pathways. By use of whole body PGC-1α knockout (KO) mice, we investigated the role of PGC-1α in fasting, acute exercise and exercise training-induced regulation of key proteins in gluconeogenesis and metabolism in the liver. In both wild-type (WT) and PGC-1α KO mice liver, the mRNA content of the gluconeogenic proteins glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) was upregulated during fasting. Pyruvate carboxylase (PC) remained unchanged after fasting in WT mice, but it was upregulated in PGC-1α KO mice. In response to a single exercise bout, G6Pase mRNA was upregulated in both genotypes, whereas no significant changes were detected in PEPCK or PC mRNA. While G6Pase and PC protein remained unchanged, liver PEPCK protein content was higher in trained than untrained mice of both genotypes. The mRNA content of the mitochondrial proteins cytochrome c (Cyt c) and cytochrome oxidase (COX) subunit I was unchanged in response to fasting. The mRNA and protein content of Cyt c and COXI increased in the liver in response to a single exercise bout and prolonged exercise training, respectively, in WT mice, but not in PGC-1α KO mice. Neither fasting nor exercise affected the mRNA expression of antioxidant enzymes in the liver, and knockout of PGC-1α had no effect. In conclusion, these results suggest that PGC-1α plays a pivotal role in regulation of Cyt c and COXI expression in the liver in response to a single exercise bout and prolonged exercise training, which implies that exercise training-induced improvements in oxidative capacity of the liver is regulated by PGC-1α.



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