Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms

Heart ◽  
2011 ◽  
Vol 98 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Georgina M Ellison ◽  
Cheryl D Waring ◽  
Carla Vicinanza ◽  
Daniele Torella
2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 888-888
Author(s):  
Ted Graber ◽  
Chris Byrd ◽  
Emily Seguin ◽  
Anna Seguin ◽  
Alyssa Fennel ◽  
...  

Abstract With age, we experience a progressive loss of physical function. Exercise is a promising therapy to preserve muscle health and functional aptitude. Animal models are needed to examine the underlying molecular mechanisms at the intersection of aging, exercise, and functional decline. In this study, we compare the efficacy of two types of individualized endurance exercise training in older C57BL/6 mice (26-months old at completion): HIIT (high intensity interval training on a treadmill, n=10) and VWR (voluntary wheel running, n=8). We hypothesized that while both exercises would improve function, HIIT would promote more extensive adaptation. For four months the VWR mice ran 4 days/week and the HIIT group ran 3x/week. We determined function pre/post-training by utilizing our composite scoring system, the Comprehensive Functional Assessment Battery (CFAB). CFAB consists of the following: treadmill running (endurance), rotarod (overall motor function), wheel running (volitional exercise rate/activity), grip strength (fore-limb strength), and inverted cling (overall strength/endurance). EchoMRI determined body composition. After training, we found significant CFAB improvement (repeated measures t-test, p<0.05) in both exercise groups, specifically including: rotarod (+37%, HIIT and VWR); treadmill (+61% VWR; +58% HIIT), grip strength (+20% VWR), body mass (-17% VWR, -10% HIIT), and fat percentage (-44% VWR, -20% HIIT). Contrary to our hypothesis, HIIT did not improve function more than VWR, though we suspect increasing training intensity would improve response. Thus, future studies will need to address defining HIIT dose response and optimal training volume for older mice. We conclude that our models will be useful for future mechanistic investigations.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Louise Y. Takeshita ◽  
Peter K. Davidsen ◽  
John M. Herbert ◽  
Philipp Antczak ◽  
Matthijs K. C. Hesselink ◽  
...  

AbstractDespite good adherence to supervised endurance exercise training (EET), some individuals experience no or little improvement in peripheral insulin sensitivity. The genetic and molecular mechanisms underlying this phenomenon are currently not understood. By investigating genome-wide variants associated with baseline and exercise-induced changes (∆) in insulin sensitivity index (Si) in healthy volunteers, we have identified novel candidate genes whose mouse knockouts phenotypes were consistent with a causative effect on Si. An integrative analysis of functional genomic and transcriptomic profiles suggests genetic variants have an aggregate effect on baseline Si and ∆Si, focused around cholinergic signalling, including downstream calcium and chemokine signalling. The identification of calcium regulated MEF2A transcription factor as the most statistically significant candidate driving the transcriptional signature associated to ∆Si further strengthens the relevance of calcium signalling in EET mediated Si response.


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.


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 ◽  
...  

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.


2012 ◽  
Vol 113 (11) ◽  
pp. 1772-1783 ◽  
Author(s):  
Ingrid M. Bonilla ◽  
Andriy E. Belevych ◽  
Arun Sridhar ◽  
Yoshinori Nishijima ◽  
Hsiang-Ting Ho ◽  
...  

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.


2009 ◽  
Vol 41 (7) ◽  
pp. 1444-1451 ◽  
Author(s):  
MAN-GYOON LEE ◽  
DARLENE A. SEDLOCK ◽  
MICHAEL G. FLYNN ◽  
GARY H. KAMIMORI

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

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