The Effects of Growth Hormone Administration and Endurance Exercise Training on Insulin Resistance in Sprague-Dawley Rat

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S488
Author(s):  
Su-Ryun Jung ◽  
Mi-Jung Park ◽  
Hye-Eun Kwak ◽  
Hyun-Lyung Jung ◽  
Geuy-Laik Lee ◽  
...  
1998 ◽  
Vol 275 (5) ◽  
pp. R1468-R1477 ◽  
Author(s):  
Scott K. Powers ◽  
Haydar A. Demirel ◽  
Heather K. Vincent ◽  
Jeff S. Coombes ◽  
Hisashi Naito ◽  
...  

Experimental studies examining the effects of regular exercise on cardiac responses to ischemia and reperfusion (I/R) are limited. Therefore, these experiments examined the effects of endurance exercise training on myocardial biochemical and physiological responses during in vivo I/R. Female Sprague-Dawley rats (4 mo old) were randomly assigned to either a sedentary control group or to an exercise training group. After a 10-wk endurance exercise training program, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 20 min, followed by a 10-min period of reperfusion. Compared with untrained, exercise-trained animals maintained higher ( P < 0.05) peak systolic blood pressure throughout I/R. Training resulted in a significant ( P < 0.05) increase in ventricular nonprotein thiols, heat shock protein (HSP) 72, and the activities of superoxide dismutase (SOD), phosphofructokinase (PFK), and lactate dehydrogenase. Furthermore, compared with untrained controls, left ventricles from trained animals exhibited lower levels ( P < 0.05) of lipid peroxidation after I/R. These data demonstrate that endurance exercise training improves myocardial contractile performance and reduces lipid peroxidation during I/R in the rat in vivo. It appears likely that the improvement in the myocardial responses to I/R was related to training-induced increases in nonprotein thiols, HSP72, and the activities of SOD and PFK in the myocardium.


2003 ◽  
Vol 95 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Gary M. Diffee ◽  
Daniel F. Nagle

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. A number of studies have shown that the characteristics of cardiac myocytes vary across the width of the ventricular wall. We have previously shown that endurance exercise training alters the Ca2+ sensitivity of tension as well as contractile protein isoform expression in rat cardiac myocytes. We tested the hypothesis that these effects of training are not uniform across the ventricular wall but are more pronounced in the subendocardial (Endo) region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from the Endo region of the myocardium and from the subepicardial (Epi) region of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in T cells compared with C cells, but this difference was larger in the Endo cells than in the Epi cells. In addition, we found a training-induced increase in atrial myosin light chain 1 (aMLC1) expression that was larger in the Endo compared with Epi samples. We conclude that effects of exercise training on myocyte contractile and biochemical properties are greater in myocytes from the Endo region of the myocardium than those from the Epi region. In addition, these results provide evidence that the increase in aMLC1 expression may be responsible for some of the training-induced increase in myocyte Ca2+ sensitivity of tension.


2021 ◽  
Vol 22 (15) ◽  
pp. 8203
Author(s):  
Suryun Jung ◽  
Youjeong Kim ◽  
Mingyu Kim ◽  
Minjae Seo ◽  
Suji Kim ◽  
...  

Physical exercise reduces the extent, duration, and frequency of drug use in drug addicts during the drug initiation phase, as well as during prolonged addiction, withdrawal, and recurrence. However, information about exercise-induced neurobiological changes is limited. This study aimed to investigate the effects of forced moderate endurance exercise training on methamphetamine (METH)-induced behavior and the associated neurobiological changes. Male Sprague Dawley rats were subjected to the administration of METH (1 mg/kg/day, i.p.) and/or forced moderate endurance exercise (treadmill running, 21 m/min, 60 min/day) for 2 weeks. Over the two weeks, endurance exercise training significantly reduced METH-induced hyperactivity. METH and/or exercise treatment increased striatal dopamine (DA) levels, decreased p(Thr308)-Akt expression, and increased p(Tyr216)-GSK-3β expression. However, the phosphorylation levels of Ser9-GSK-3β were significantly increased in the exercise group. METH administration significantly increased the expression of NMDAr1, CaMKK2, MAPKs, and PP1 in the striatum, and exercise treatment significantly decreased the expression of these molecules. Therefore, it is apparent that endurance exercise inhibited the METH-induced hyperactivity due to the decrease in GSK-3β activation by the regulation of the striatal glutamate signaling pathway.


Metabolism ◽  
2009 ◽  
Vol 58 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Vitoon Saengsirisuwan ◽  
Somrudee Pongseeda ◽  
Mujalin Prasannarong ◽  
Kanokwan Vichaiwong ◽  
Chaivat Toskulkao

2017 ◽  
Vol 10 (4) ◽  
pp. 1651-1659 ◽  
Author(s):  
Hyung Lyung Jung ◽  
Jong Sik Ryu ◽  
Sang Yeong Kim ◽  
Young Taek Doo ◽  
Ho Youl Kang

2018 ◽  
Vol 314 (6) ◽  
pp. R892-R901 ◽  
Author(s):  
Noriaki Kawanishi ◽  
Kana Takagi ◽  
Hyeon-Cheol Lee ◽  
Daiki Nakano ◽  
Toshiaki Okuno ◽  
...  

Insulin resistance of peripheral muscle is implicated in the etiology of metabolic syndrome in obesity. Although accumulation of glycerolipids, such as triacylglycerol and diacylglycerol (DAG), in muscle contributes to insulin resistance in obese individuals, endurance-trained athletes also have higher glycerolipid levels but normal insulin sensitivity. We hypothesized that the difference in insulin sensitivity of skeletal muscle between athletes and obese individuals stems from changes in fatty acid composition of accumulated lipids. Here, we evaluated the effects of intense endurance exercise and high-fat diet (HFD) on the accumulation and composition of lipid molecular species in rat skeletal muscle using a lipidomic approach. Sprague-Dawley female rats were randomly assigned to three groups and received either normal diet (ND) in sedentary conditions, ND plus endurance exercise training, or HFD in sedentary conditions. Rats were fed ND or HFD between 4 and 12 wk of age. Rats in the exercise group ran on a treadmill for 120 min/day, 5 days/wk, for 8 wk. Soleus muscle lipidomic profiles were obtained using liquid chromatography/tandem mass spectrometry. Total DAG levels, particularly those of palmitoleate-containing species, were increased in muscle by exercise training. However, whereas the total DAG level in the muscle was also increased by HFD, the levels of DAG molecular species containing palmitoleate were decreased by HFD. The concentration of phosphatidylethanolamine molecular species containing palmitoleate was increased by exercise but decreased by HFD. Our results indicate that although DAG accumulation was similar levels in trained and sedentary obese rats, specific changes in molecular species containing palmitoleate were opposite.


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 ◽  
...  

2012 ◽  
Vol 112 (3) ◽  
pp. 501-510 ◽  
Author(s):  
Ashley J. Smuder ◽  
Kisuk Min ◽  
Matthew B. Hudson ◽  
Andreas N. Kavazis ◽  
Oh-Sung Kwon ◽  
...  

Controlled mechanical ventilation (MV) is a life-saving measure for patients in respiratory failure. However, MV renders the diaphragm inactive leading to diaphragm weakness due to both atrophy and contractile dysfunction. It is now established that oxidative stress is a requirement for MV-induced diaphragmatic proteolysis, atrophy, and contractile dysfunction to occur. Given that endurance exercise can elevate diaphragmatic antioxidant capacity and the levels of the cellular stress protein heat shock protein 72 (HSP72), we hypothesized that endurance exercise training before MV would protect the diaphragm against MV-induced oxidative stress, atrophy, and contractile dysfunction in female Sprague-Dawley rats. Our results confirm that endurance exercise training before MV increased both HSP72 and the antioxidant capacity in the diaphragm. Importantly, compared with sedentary animals, exercise training before MV protected the diaphragm against MV-induced oxidative damage, protease activation, myofiber atrophy, and contractile dysfunction. Further, exercise protected diaphragm mitochondria against MV-induced oxidative damage and uncoupling of oxidative phosphorylation. These results provide the first evidence that exercise can provide protection against MV-induced diaphragm weakness. These findings are important and establish the need for future experiments to determine the mechanism(s) responsible for exercise-induced diaphragm protection.


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