scholarly journals Effect of Endurance Exercise Training on Kinesin - 5 and Dynein Motor Proteins in Sciatic Nerves of Male Wistar Rats with Diabetic Neuropathy

2018 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Shiva Jahani Golbar ◽  
Reza Gharekhanlu ◽  
Mohammad Reza Kordi ◽  
Ali Khazani
Keyword(s):  
Exercise Training ◽  
Diabetic Neuropathy ◽  
Endurance Exercise ◽  
Wistar Rats ◽  
Motor Proteins ◽  
Endurance Exercise Training ◽  
Dynein Motor ◽  
Male Wistar Rats ◽  
Sciatic Nerves

scholarly journals High-volume endurance exercise training stimulates hematopoiesis by increasing ACE NH2-terminal activity

2021 ◽  
Author(s):  
Flávio de Castro Magalhães ◽  
Tiago Fernandes ◽  
Vinícius Bassaneze ◽  
Katt Coelho Mattos ◽  
Isolmar Schettert ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Wistar Rats ◽  
High Volume ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem ◽  
Endurance Exercise Training ◽  
First Time ◽  
Captopril Treatment

One of the health benefits of endurance exercise training (ET) is the stimulation of hematopoiesis. However, the mechanisms underlying ET-induced hematopoietic adaptations are understudied. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits proliferation of early hematopoietic progenitor cells. The angiotensin-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP. Here we demonstrate for the first time the role of ACE NH2-terminal in ET-induced hematopoietic adaptations. Wistar rats were subjected to 10 weeks of moderate-(T1) and high-(T2) volume swimming-training. Although both protocols induced classical ET-associated adaptations, only T2 increased plasma ACE NH2-domain activity (by 40%, p=0.0003) and reduced Ac-SDKP levels (by 50%, p<0.0001). T2 increased the number of hematopoietic stem cells (~200%, p=0.0008), early erythroid progenitor colonies (~300%, p<0.0001) and reticulocytes (~500%, p=0.0007), and reduced erythrocyte lifespan (~50%, p=0.022). Following, Wistar rats were subjected to T2 or T2 combined with ACE NH2-terminal inhibition (captopril treatment: 10 mg.kg-1.d-1). T2 combined with ACE NH2-terminal inhibition prevented Ac-SDKP decrease and attenuated ET-induced hematopoietic adaptations. Altogether, our findings show that ET-induced hematopoiesis was at least partially associated to increased ACE NH2-terminal activity and reduction of the hematopoietic inhibitor Ac-SDKP.

Effects of resveratrol supplementation in male Wistar rats undergoing an endurance exercise and acute exercise training

2019 ◽  
Vol 27 (4) ◽  
pp. 257-264 ◽  
Author(s):  
Reza Vafaee ◽  
Hamid Soori ◽  
Mehdi Hedayati ◽  
Elaheh Ainy ◽  
Hamidreza Hatamabadi
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Wistar Rats ◽  
Acute Exercise ◽  
Male Wistar Rats

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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