scholarly journals Absence of cardiac damage induced by long-term intensive endurance exercise training: a cardiac magnetic resonance and exercise echocardiography analysis in masters athletes.

2021 ◽  
pp. 100196
Author(s):  
Olivier Missenard ◽  
Charline Gabaudan ◽  
Helene Astier ◽  
Florian Desmots ◽  
Eric Garnotel ◽  
...  
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Exercise Echocardiography ◽  
Cardiac Damage ◽  
Endurance Exercise Training ◽  
Masters Athletes

P311Cardiac damage induced by long term and intensive endurance exercise training in senior athletes: a cardiac magnetic resonance and exercise echocardiography analysis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Missenard ◽  
P L Massoure ◽  
H Astier ◽  
C Gabaudan ◽  
F Desmots ◽  
...  
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Late Gadolinium Enhancement ◽  
Myocardial Fibrosis ◽  
Endurance Exercise ◽  
Cardiac Biomarkers ◽  
Gadolinium Enhancement ◽  
Procollagen Type ◽  
Endurance Exercise Training ◽  
Senior Athletes

Abstract Background Moderate intensity regular physical activity is a mainstay of cardiovascular prevention. However, it is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage. It has been proposed that long-term endurance exercise may be associated with myocardial fibrosis detected by late gadolinium-enhancement (LGE) cardiac magnetic resonance (CMR), and/or with right ventricle contractile dysfunction, creating a potential substrate for ventricular arrythmia, but these aspects are not constantly found across studies. Extracellular volume (ECV) determined by CMR, circulating cardiac biomarkers, and longitudinal global 2D strain (LGS) assessed by cardiac echography are relevant tools to explore these potential adverse effects of exercise in senior athletes. Purpose To assess the presence of myocardial fibrosis detected by CMR (LGE and ECV) and biomarkers, and to evaluate ventricles function with LGS, in endurance senior competitive athletes. Methods Thirty-three asymptomatic endurance senior athletes (47±6 years old, 9,6±1,7 h of training per week for 26±6 years), were compared to 18 sedentary controls (49±7 years old). They underwent a CMR protocol including morphological and late gadolinium-enhancement (LGE) analysis, T1 mapping and calculation of ECV using a 1.5 T MRI scanner. A maximal exercise transthoracic echography with LGS analysis was performed. Cardiac biomarkers (N terminal pro brain natriuretic peptide, high-sensitivity troponin T and plasma markers of collagen biosynthesis and degradation procollagen type I N terminal propeptide and procollagen type III NT propeptide) were also analysed. Results Athletes had higher left (84,0±20,8 vs 67,62±12,4 ml/m2; p=0,00593) and right (41,3±9,5 vs 32,9±6,0 ml/m2; p=0,00228) ventricular volumes, higher total biventricular mass (109,61±14,18 vs 98,66±16,25 g/m2; p=0,02038), and higher stroke volume (50,7±12,6 vs 40,1±9,2 ml/m2; p=0,00441) assessed by CMR versus controls. Native T1 (left ventricle: 938±21 vs 940±34 ms; p=0,8098 - right ventricle: 1027±53 vs 1026±114 ms; p=0,92983) and ECV (21,5±1,6 vs 22,0±2,2%; p=0,40868) were not significantly different in athletes compared with controls. LGE was not found in athletes. Peak exercise LGS values were higher in athletes for left (23,19±2,86 vs 20,82±2,05%; p=0,00335) and right (29,25±3,47 vs 26,48±3,22%; p=0,00777) ventricles, compared with control. The levels of cardiac biomarkers were normal in all subjects. Conclusion Athletes showed signs of physiological cardiac remodelling, consistent with previous descriptions of athlete's heart. Despite this important remodelling, there was no evidence of myocardial fibrosis or exercise left or right ventricular dysfunction in athletes. Our results are not supporting the hypothesis of deleterious cardiac effects induced by long term and intensive endurance exercise training.

scholarly journals Chronic cardiac damage in competitive master endurance athletes: A cardiac magnetic resonance and exercise echocardiography study

2018 ◽  
Vol 10 (1) ◽  
pp. 123
Author(s):  
P. Massoure ◽  
O. Camus ◽  
M. Chenilleau-Vidal ◽  
A. Boussuges ◽  
L. Fourcade
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Endurance Athletes ◽  
Exercise Echocardiography ◽  
Cardiac Damage

scholarly journals Monitoring exercise intensity during long‐term endurance exercise training in aging rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Marie Hoffman ◽  
Tiffany Akins ◽  
Gregory Barton ◽  
Susan McKiernan ◽  
Judd Aiken ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Exercise Intensity ◽  
Aging Rats ◽  
Endurance Exercise Training

The effects of intermittent exposure to hypoxia during endurance exercise training on the ventilatory responses to hypoxia and hypercapnia in humans

1998 ◽  
Vol 78 (3) ◽  
pp. 189-194 ◽  
Author(s):  
Keisho Katayama ◽  
Yasitake Sato ◽  
Koji Ishida ◽  
Shigeo Mori ◽  
Miharu Miyamura
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Ventilatory Responses ◽  
Endurance Exercise Training ◽  
Intermittent Exposure

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.

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