title: Living high training low induces physiological cardiac hypertrophy accompanied by down-regulation and redistribution of the renin-angiotensin system.
abstract: OBJECTIVE
  Living high training low" (LHTL) is an exercise-training protocol that refers living in hypoxia stress and training at normal level of O2. In this study, we investigated whether LHTL caused physiological heart hypertrophy accompanied by changes of biomarkers in renin-angiotensin system in rats.
  
  
  METHODS
  Adult male SD rats were randomly assigned into 4 groups, and trained on living low-sedentary (LLS, control), living low-training low (LLTL), living high-sedentary (LHS) and living high-training low (LHTL) protocols, respectively, for 4 weeks. Hematological parameters, hemodynamic measurement, heart hypertrophy and plasma angiotensin II (Ang II) level of the rats were measured. The gene and protein expression of angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II receptor I (AT1) in heart tissue was assessed using RT-PCR and immunohistochemistry, respectively.
  
  
  RESULTS
  LLTL, LHS and LHTL significantly improved cardiac function, increased hemoglobin concentration and RBC. At the molecular level, LLTL, LHS and LHTL significantly decreased the expression of ACE, AGT and AT1 genes, but increased the expression of ACE and AT1 proteins in heart tissue. Moreover, ACE and AT1 protein expression was significantly increased in the endocardium, but unchanged in the epicardium.
  
  
  CONCLUSIONS
  LHTL training protocol suppresses ACE, AGT and AT1 gene expression in heart tissue, but increases ACE and AT1 protein expression specifically in the endocardium, suggesting that the physiological heart hypertrophy induced by LHTL is regulated by region-specific expression of renin-angiotensin system components.
authors: Laboratory of Neuroscience and Brain Development, School of Life Science, Beijing Normal University, Beijing 100875, China. shiweiphd@gmail.com
authors: Wei
authors: W
authors: Shi
authors: J Gary
authors: JG
authors: Meszaros
authors: Shao-ju
authors: SJ
authors: Zeng
authors: Ying-yu
authors: YY
authors: Sun
authors: Ming-xue
authors: MX
authors: Zuo
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics / Q000502:physiology; D000804:Angiotensin II / Q000097:blood / Q000235:genetics; D000818:Animals; D059267:Cardiomegaly, Exercise-Induced / Q000235:genetics* / Q000502:physiology*; D015536:Down-Regulation; D004699:Endocardium / Q000378:metabolism / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology; D000860:Hypoxia / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000096:biosynthesis / Q000235:genetics; D010496:Pericardium / Q000378:metabolism / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D011945:Receptors, Angiotensin / Q000096:biosynthesis / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics* / Q000502:physiology*
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A
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