Partial persistence of exercise-induced myocardial angiogenesis following 4-week detraining in the rat

Abstract

Enhanced angiogenesis, or capillary growth, has a prominent role among the various beneWcial eVects of exercise training on the myocardium. The aim of the present study is to assess if training-induced increases in capillarity and vascularization persist after 4 weeks of detraining. Adult male rats were trained to run on a treadmill for 10 weeks at »60% VO 2max , which did not induce cardiac hypertrophy, but increased (P < 0.05) the soleus/ body weight ratio, left ventricle capillarity and von Willebrand-positive cell density (n = 6). In another group of animals (n = 6) subjected to training followed by 4-week detraining, the soleus/body weight ratio returned to normal, with only partial reversal of left ventricle capillarity and von Willebrand-positive cell density. Markers of angiogenesis (VEGF, KDR/VEGF-R2 and HIF-1 mRNA, studied by real-time RT-PCR) were upregulated at the end of training, and returned to baseline value after detraining. Electron microscopy highlighted some morphological features in trained hearts (endothelial cell sprouting and bridges and pericyte detachment), suggestive of endothelial cell proliferation and capillary growth that were absent in untrained and detrained hearts. We conclude that the training-induced increase in cardiac capillarity and vascularization are retained for some time upon cessation of the training program even in the absence of angiogenic stimuli.

Exercise training-induced enhancement in myocardial mechanics is lost after 2 weeks of detraining in rats

“…Our work showed complete regression of the analyzed data after just 2 weeks of detraining, contrasting with other studies (Craig et al 1991) which showed that the cardiac mass in rats regressed to baseline only after around 21 days of physical inactivity. Furthermore, a recent report (Marini et al 2008) found reversal to baseline values of LV capillarity and cell density, as well as upregulation of angiogenesis markers after 4 weeks of detraining. The higher tension in the T group indicates an enhancement of contractility, which can be attributed to several mechanisms, including increases on the activity of the Na + / Ca 2+ exchanger (Tibbits et al 1989), Ca 2+ ATPase of sarcolemma and sarcoplasmic reticulum (Pierce et al 1989;WisløV et al 2001), and sensitivity of the Ca 2+ myoWlaments (WisløV et al 2001).…”

Myocardial tolerance to ischemia–reperfusion injury, training intensity and cessation

“…Although angiogenesis may not develop in Eur J Appl Physiol (2011) 111:859-868 865 short-term exercise , it may become critical in long-term training (Brown 2003;Laughlin et al 1998). In a previous work using a different set of animals, we reported that long-term low-intensity training increases capillary density and the number of von Willebrandt factorpositive cells, as well as gene expression of VEGF and its receptor KDR, but not of bFGF (Marini et al 2008). In HIGH-DET animals gene changes were reverted, while capillary density and the number of von Willebrandt factorpositive cells tended to return to basal (UNT) level (Marini et al 2008).…”

“…In a previous work using a different set of animals, we reported that long-term low-intensity training increases capillary density and the number of von Willebrandt factorpositive cells, as well as gene expression of VEGF and its receptor KDR, but not of bFGF (Marini et al 2008). In HIGH-DET animals gene changes were reverted, while capillary density and the number of von Willebrandt factorpositive cells tended to return to basal (UNT) level (Marini et al 2008). In principle, the lack of VEGF protein expression changes in the present study may stem from protein instability 24 h after the last training session, or it may reflect failure of training to accelerate angiogenesis.…”

“…Our group showed moderate exercise-dependent changes in proteins involved with antioxidant defense (Marini et al 2007), vascular endothelial growth factors (VEGF) mRNA (Marini et al 2008), and HSP70 (inducible form) expression (Tarricone et al 2008). However, to our knowledge, no studies investigated training intensity as a potential factor affecting myocardial ischemia tolerance induced by exercise.…”

State-of-the-art technologies, current opinions and developments, and novel findings: news from the field of histochemistry and cell biology

“…Morphological methods were applied in numerous recent original papers to address a wide variety of topics in development, function and disease of the cardiovascular system (e.g., Schroeter et al 2007;Zaman et al 2007;Borisov et al 2008;Marini et al 2008). In an excellent review, Taatjes and colleagues highlighted the use and beneWts of microscopy imaging systems in conjunction with histochemical techniques in studies aimed at elucidating mechanisms underlying cardiovascular diseases at the cell and molecular level ("Imaging aspects of cardiovascular disease at the cell and molecular level"; Taatjes et al 2008a, b).…”