scholarly journals Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

2010 ◽  
Vol 12 (4) ◽  
pp. 323-330 ◽  
Author(s):  
Ching-Yi Chen ◽  
Hsiu-Ching Hsu ◽  
Bai-Chin Lee ◽  
Hung-Ju Lin ◽  
Ying-Hsien Chen ◽  
...  
2008 ◽  
Vol 295 (2) ◽  
pp. H842-H850 ◽  
Author(s):  
Pablo F. Soto ◽  
Pilar Herrero ◽  
Kenneth B. Schechtman ◽  
Alan D. Waggoner ◽  
Jeffrey M. Baumstark ◽  
...  

Aging is associated with decreases in aerobic capacity, cardiac function, and insulin sensitivity as well as alterations in myocardial substrate metabolism. Endurance exercise training (EET) improves cardiac function in a gender-specific manner, and EET has been shown to improve whole body glucose tolerance, but its effects on myocardial metabolism are unclear. Accordingly, we studied the effect of EET on myocardial substrate metabolism in older men and women. Twelve healthy older individuals (age: 60–75 yr; 6 men and 6 women) underwent PET with [15O]water, [11C]acetate, [11C]glucose, and [11C]palmitate for the assessment of myocardial blood flow (MBF), myocardial O2 consumption (MV̇o2), myocardial glucose utilization (MGU), and myocardial fatty acid utilization (MFAU), respectively, at rest and during dobutamine infusion (10 μg·kg−1·min−1). Measurements were repeated after 11 mo of EET. Maximal O2 uptake (V̇o2max) increased ( P = 0.005) after EET. MBF was unaffected by training, as was resting MV̇o2; however, posttraining dobutamine MV̇o2 was significantly higher ( P = 0.05), as was MGU ( P < 0.04). Although overall dobutamine MFAU was unchanged, posttraining dobutamine MFAU increased in women ( P = 0.01) but decreased in men ( P = 0.03). Thus, EET in older individuals improves the catecholamine response of myocardial glucose metabolism. Moreover, gender differences exist in the myocardial fatty acid metabolic response to training. These findings suggest a role for altered myocardial substrate metabolism in modulating the cardiovascular benefits of EET in older individuals.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 731-P
Author(s):  
MICHAEL W. SCHLEH ◽  
BENJAMIN J. RYAN ◽  
JENNA B. GILLEN ◽  
PALLAVI VARSHNEY ◽  
KATIE FOUG ◽  
...  

2009 ◽  
Vol 297 (2) ◽  
pp. H576-H582 ◽  
Author(s):  
Qibin Jiao ◽  
Yunzhe Bai ◽  
Toru Akaike ◽  
Hiroshi Takeshima ◽  
Yoshihiro Ishikawa ◽  
...  

Sarcalumenin (SAR), a Ca2+-binding protein located in the longitudinal sarcoplasmic reticulum (SR), regulates Ca2+ reuptake into the SR by interacting with cardiac sarco(endo)plasmic reticulum Ca2+-ATPase 2a (SERCA2a). We have previously demonstrated that SAR deficiency induced progressive heart failure in response to pressure overload, despite mild cardiac dysfunction in sham-operated SAR knockout (SARKO) mice ( 26 ). Since responses to physiological stresses often differ from those to pathological stresses, we examined the effects of endurance exercise on cardiac function in SARKO mice. Wild-type (WT) and SARKO mice were subjected to endurance treadmill exercise training (∼65% of maximal exercise ability for 60 min/day) for 12 wk. After exercise training, maximal exercise ability was significantly increased by 5% in WT mice ( n = 6), whereas it was significantly decreased by 37% in SARKO mice ( n = 5). Cardiac function assessed by echocardiographic examination was significantly decreased in accordance with upregulation of biomarkers of cardiac stress in SARKO mice after training. After training, expression levels of SERCA2a protein were significantly downregulated by 30% in SARKO hearts, whereas they were significantly upregulated by 59% in WT hearts. Consequently, SERCA2 activity was significantly decreased in SARKO hearts after training. Furthermore, the expression levels of other Ca2+-handling proteins, including phospholamban, ryanodine receptor 2, calsequestrin 2, and sodium/calcium exchanger 1, were significantly decreased in SARKO hearts after training. These results indicate that SAR plays a critical role in maintaining cardiac function under physiological stresses, such as endurance exercise, by regulating Ca2+ transport activity into the SR. SAR may be a primary target for exercise-related adaptation of the Ca2+ storage system in the SR to preserve cardiac function.


Diabetologia ◽  
2006 ◽  
Vol 50 (2) ◽  
pp. 404-413 ◽  
Author(s):  
F. Shojaee-Moradie ◽  
K. C. R. Baynes ◽  
C. Pentecost ◽  
J. D. Bell ◽  
E. L. Thomas ◽  
...  

1998 ◽  
Vol 76 (9) ◽  
pp. 891-894 ◽  
Author(s):  
P D Chilibeck ◽  
G J Bell ◽  
R P Farrar ◽  
T P Martin

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.


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