Effects of endurance exercise-training on single-fiber contractile properties of insulin-treated streptozotocin-induced diabetic rats

2005 ◽  
Vol 99 (2) ◽  
pp. 472-478 ◽  
Author(s):  
Otto A. Sanchez ◽  
LeAnn M. Snow ◽  
Dawn A. Lowe ◽  
Robert C. Serfass ◽  
LaDora V. Thompson
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Extensor Digitorum Longus ◽  
Diabetic Rats ◽  
Contractile Properties ◽  
Extensor Digitorum ◽  
Single Fiber ◽  
Moderate Intensity ◽  
Specific Tension ◽  
Endurance Exercise Training

The purpose of this study was to characterize the contractile properties of individual skinned muscle fibers from insulin-treated streptozotocin-induced diabetic rats after an endurance exercise training program. We hypothesized that single-fiber contractile function would decrease in the diabetic sedentary rats and that endurance exercise would preserve the function. In the study, 28 rats were assigned to either a nondiabetic sedentary, a nondiabetic exercise, a diabetic sedentary, or a diabetic exercise group. Rats in the diabetic groups received subcutaneous intermediate-lasting insulin daily. The exercise-trained rats ran on a treadmill at a moderate intensity for 60 min, five times per week. After 12 wk, the extensor digitorum longus and soleus muscles were dissected. Single-fiber diameter, Ca2+-activated peak force, specific tension, activation threshold, and pCa50 as well as the myosin heavy chain isoform expression (MHC) were determined. We found that in MHC type II fibers from extensor digitorum longus muscle, diameters were significantly smaller from diabetic sedentary rats compared with nondiabetic sedentary rats ( P < 0.001). Among the nondiabetic rats, fiber diameters were smaller with exercise ( P = 0.038). The absolute force-generating capacity of single fibers was lower in muscles from diabetic rats. There was greater specific tension (force normalized to cross-sectional area) by fibers from the rats that followed an endurance exercise program compared with sedentary. From the results, we conclude that alterations in the properties of contractile proteins are not implicated in the decrease in strength associated with diabetes and that endurance-exercise training does not prevent or increase muscle weakness in diabetic rats.

scholarly journals The effect of exercise training on leptin levels in obese males

1998 ◽  
Vol 274 (2) ◽  
pp. E280-E286 ◽  
Author(s):  
W. J. Pasman ◽  
M. S. Westerterp-Plantenga ◽  
W. H. M. Saris
Keyword(s):  
Exercise Training ◽  
Body Fat ◽  
Endurance Exercise ◽  
Exercise Program ◽  
Moderate Intensity ◽  
Body Fat Percentage ◽  
Fat Percentage ◽  
Insulin Levels ◽  
Endurance Exercise Training ◽  
Plasma Leptin

The effect of endurance training on plasma leptin levels was investigated in 15 obese male subjects (age 37.3 ± 5.2 yr, body weight 96.5 ± 13.6 kg, and body mass index 29.8 ± 3.0 kg/m2) in a weight loss and exercise program. After 4 mo of treatment consisting of a very low energy diet (VLED) and endurance exercise training (3–4 times weekly, 1 h sessions, moderate intensity), two groups were formed. One group continued the exercise sessions (trained subjects, n = 7) and the other group stopped with the exercise program (control, n= 8). Measurements of anthropometry, aerobic power, and fasted blood samples were executed at fixed time points (0, 2, 4, 10, and 16 mo). With partial regression analysis, keeping the changes in insulin and body fat percentage constant, it was shown that the number of hours of exercise training was significantly correlated with changes in leptin levels, during the 16-mo period ( r = 0.56, P < 0.05). Changes in insulin levels were significantly related to the changes in leptin levels ( r = 0.47, P < 0.05), which were less for changes in body fat percentage ( r = 0.42, P = 0.07). During the VLED, the change in insulin concentration affected leptin levels significantly ( r = 0.79) but changes in body fat percentage were not noted. It is concluded that endurance exercise training decreased plasma leptin levels independently of changes in plasma insulin levels and body fat percentage.

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.

Resting Metabolic Rate after Endurance Exercise Training

2009 ◽  
Vol 41 (7) ◽  
pp. 1444-1451 ◽  
Author(s):  
MAN-GYOON LEE ◽  
DARLENE A. SEDLOCK ◽  
MICHAEL G. FLYNN ◽  
GARY H. KAMIMORI
Keyword(s):  
Exercise Training ◽  
Metabolic Rate ◽  
Endurance Exercise ◽  
Resting Metabolic Rate ◽  
Endurance Exercise Training

THE EFFECTS OF ENDURANCE EXERCISE TRAINING ON INTRAMUSCULAR SUBSTRATE USE DURING PROLONGED SUBMAXIMAL EXERCISE

1985 ◽  
Vol 17 (2) ◽  
pp. 259-260 ◽  
Author(s):  
B. F. Hurley ◽  
P. M. Nemeth ◽  
W. H. Martin ◽  
G. P. Dalaky ◽  
J. M. Hagberg ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Submaximal Exercise ◽  
Substrate Use ◽  
Endurance Exercise Training
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