Endurance exercise training increases APPL1 expression and improves insulin signaling in the hepatic tissue of diet-induced obese mice, independently of weight loss

2012 ◽  
Vol 227 (7) ◽  
pp. 2917-2926 ◽  
Author(s):  
R. Marinho ◽  
E.R. Ropelle ◽  
D.E. Cintra ◽  
C.T. De Souza ◽  
A.S.R. Da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Insulin Signaling ◽  
Hepatic Tissue ◽  
Obese Mice ◽  
Endurance Exercise Training

Physiological adaptations to a weight-loss dietary regimen and exercise programs in women

1997 ◽  
Vol 83 (1) ◽  
pp. 270-279 ◽  
Author(s):  
William J. Kraemer ◽  
Jeff S. Volek ◽  
Kristine L. Clark ◽  
Scott E. Gordon ◽  
Thomas Incledon ◽  
...  
Keyword(s):  
Weight Loss ◽  
Exercise Training ◽  
Body Mass ◽  
Endurance Exercise ◽  
Density Lipoprotein ◽  
Training Group ◽  
Lipoprotein Cholesterol ◽  
Exercise Programs ◽  
Dietary Regimen ◽  
Endurance Exercise Training

Kraemer, William J., Jeff S. Volek, Kristine L. Clark, Scott E. Gordon, Thomas Incledon, Susan M. Puhl, N. Travis Triplett-McBride, Jeffrey M. McBride, Margot Putukian, and Wayne J. Sebastianelli.Physiological adaptations to a weight-loss dietary regimen and exercise programs in women. J. Appl. Physiol. 83(1): 270–279, 1997.—Thirty-one women (mean age 35.4 ± 8.5 yr) who were overweight were matched and randomly placed into either a control group (Con; n = 6), a diet-only group (D; n = 8), a diet+aerobic endurance exercise training group (DE; n = 9), or a diet+aerobic endurance exercise training+strength training group (DES; n = 8). After 12 wk, the three dietary groups demonstrated a significant ( P ≤ 0.05) reduction in body mass, %body fat, and fat mass. No differences were observed in the magnitude of loss among groups, in fat-free mass, or in resting metabolic rate. The DE and DES groups increased maximal oxygen consumption, and the DES group demonstrated increases in maximal strength. Weight loss resulted in a similar reduction in total serum cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol among dietary groups. These data indicate that weight loss during moderate caloric restriction is not altered by inclusion of aerobic or aerobic+resistance exercise, but diet in conjunction with training can induce remarkable adaptations in aerobic capacity and muscular strength despite significant reductions in body mass.

Endurance exercise training ameliorates insulin resistance and reticulum stress in adipose and hepatic tissue in obese rats

2011 ◽  
Vol 111 (9) ◽  
pp. 2015-2023 ◽  
Author(s):  
Gabrielle da Luz ◽  
Marisa J. S. Frederico ◽  
Sabrina da Silva ◽  
Marcelo F. Vitto ◽  
Patricia A. Cesconetto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Hepatic Tissue ◽  
Endurance Exercise Training ◽  
Obese Rats

Effects of Endurance Exercise Training on Insulin Signaling in Human Skeletal Muscle

Diabetes ◽  
2007 ◽  
Vol 56 (8) ◽  
pp. 2093-2102 ◽  
Author(s):  
Christian Frøsig ◽  
Adam J. Rose ◽  
Jonas T. Treebak ◽  
Bente Kiens ◽  
Erik A. Richter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Insulin Signaling ◽  
Human Skeletal Muscle ◽  
Endurance Exercise Training

Coimmunoprecipitation of FAT/CD36 and CPT I in skeletal muscle increases proportionally with fat oxidation after endurance exercise training

2006 ◽  
Vol 291 (2) ◽  
pp. E254-E260 ◽  
Author(s):  
Simon Schenk ◽  
Jeffrey F. Horowitz
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Fatty Acid ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Dietary Intervention ◽  
Fat Oxidation ◽  
Acid Oxidation ◽  
Endurance Exercise Training ◽  
Cpt I

Although the increase in fatty acid oxidation after endurance exercise training has been linked with improvements in insulin sensitivity and overall metabolic health, the mechanisms responsible for increasing fatty acid oxidation after exercise training are not completely understood. The primary aim of this study was to determine the effect of adding endurance exercise training to a weight loss program on fat oxidation and the colocalization of the fatty acid translocase FAT/CD36 with carnitine palmitoyltransferase I (CPT I) in human skeletal muscle. We measured postabsorptive fat oxidation and acquired a muscle sample from abdominally obese women before and after 12% body weight loss through either dietary intervention with endurance exercise training (EX + DIET) or dietary intervention without endurance exercise training (DIET). Immunoprecipitation techniques were used on these muscle samples to determine whether the association between FAT/CD36 and CPT I is altered after DIET and/or EX + DIET. FAT/CD36 was found to coimmunoprecipitate with CPT I, and the amount of FAT/CD36 that coimmunoprecipitated with CPT I increased by ∼25% after EX + DIET ( P < 0.005) but was unchanged after DIET. In addition, the increase in the amount of FAT/CD36 that coimmunoprecipitated with CPT I in EX + DIET was strongly correlated with the increase in whole body fat oxidation ( R2 = 0.857, P < 0.003). In conclusion, the findings from this study indicate that exercise training alters the localization of FAT/CD36 and increases its association with CPT I, which may help augment fat oxidation.

Higher mitochondrial fatty acid oxidation following intermittent versus continuous endurance exercise training

1998 ◽  
Vol 76 (9) ◽  
pp. 891-894 ◽  
Author(s):  
P D Chilibeck ◽  
G J Bell ◽  
R P Farrar ◽  
T P Martin
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Endurance Exercise ◽  
High Intensity ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Interval Exercise ◽  
Endurance Exercise Training ◽  
Mitochondrial Fatty Acid

It has been well documented that skeletal muscle fatty acid oxidation can be elevated by continuous endurance exercise training. However, it remains questionable whether similar adaptations can be induced with intermittent interval exercise training. This study was undertaken to directly compare the rates of fatty acid oxidation in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria following these different exercise training regimes. Mitochondria were isolated from the gastrocnemius-plantaris muscles of male Sprague-Dawley rats following exercise training 6 days per week for 12 weeks. Exercise training consisted of either continuous, submaximal, endurance treadmill running (n = 10) or intermittent, high intensity, interval running (n = 10). Both modes of training enhanced the oxidation of palmityl-carnitine-malate in both mitochondrial populations (p < 0.05). However, the increase associated with the intermittent, high intensity exercise training was significantly greater than that achieved with the continuous exercise training (p < 0.05). Also, the increases associated with the IMF mitochondria were greater than the SS mitochondria (p < 0.05). These data suggest that high intensity, intermittent interval exercise training is more effective for stimulation of fatty acid oxidation than continuous submaximal exercise training and that this adaptation occurs preferentially within IMF mitochondria.Key words: muscle, subsarcolemmal mitochondria, intermyofibrillar mitochondria.

Endurance exercise training increases insulin responsiveness in isolated adipocytes through IRS/PI3-kinase/Akt pathway

2005 ◽  
Vol 98 (3) ◽  
pp. 1037-1043 ◽  
Author(s):  
Sidney B. Peres ◽  
Solange M. Franzói de Moraes ◽  
Cecilia E. M. Costa ◽  
Luciana C. Brito ◽  
Julie Takada ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Insulin Receptor ◽  
Endurance Exercise ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Β Subunit ◽  
Endurance Exercise Training ◽  
Isolated Adipocytes

Endurance exercise training promotes important metabolic adaptations, and the adipose tissue is particularly affected. The aim of this study was to investigate how endurance exercise training modulates some aspects of insulin action in isolated adipocytes and in intact adipose tissue. Male Wistar rats were submitted to daily treadmill running (1 h/day) for 7 wk. Sedentary age-matched rats were used as controls. Final body weight, body weight gain, and epididymal fat pad weight did not show any statistical differences between groups. Adipocytes from trained rats were smaller than those from sedentary rats (205 ± 16.8 vs. 286 ± 26.4 pl; P < 0.05). Trained rats showed decreased plasma glucose (4.9 ± 0.13 vs. 5.3 ± 0.07 mM; P < 0.05) and insulin levels (0.24 ± 0.012 vs. 0.41 ± 0.049 mM; P < 0.05) and increased insulin-stimulated glucose uptake (23.1 ± 3.1 vs. 12.1 ± 2.9 pmol/cm2; P < 0.05) compared with sedentary rats. The number of insulin receptors and the insulin-induced tyrosine phosphorylation of insulin receptor-β subunit did not change between groups. Insulin-induced tyrosine phosphorylation insulin receptor substrates (IRS)-1 and -2 increased significantly (1.57- and 2.38-fold, respectively) in trained rats. Insulin-induced IRS-1/phosphatidylinositol 3 (PI3)-kinase (but not IRS-2/PI3-kinase) association and serine Akt phosphorylation also increased (2.06- and 3.15-fold, respectively) after training. The protein content of insulin receptor-β subunit, IRS-1 and -2, did not differ between groups. Taken together, these data support the hypothesis that the increased adipocyte responsiveness to insulin observed after endurance exercise training is modulated by IRS/PI3-kinase/Akt pathway.

scholarly journals Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death

2012 ◽  
Vol 113 (11) ◽  
pp. 1772-1783 ◽  
Author(s):  
Ingrid M. Bonilla ◽  
Andriy E. Belevych ◽  
Arun Sridhar ◽  
Yoshinori Nishijima ◽  
Hsiang-Ting Ho ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Cardiac Death ◽  
Outward Current ◽  
Calcium Handling ◽  
Transient Outward Current ◽  
Cellular Electrophysiology ◽  
Endurance Exercise Training

The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171–H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period ( n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization ( P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group ( P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K+ current, which was restored by exercise training ( P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training ( P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.

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