These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Endurance training in the rat. I. Myocardial mechanics and biochemistry.
    Author: Nutter DO, Priest RE, Fuller EO.
    Journal: J Appl Physiol Respir Environ Exerc Physiol; 1981 Oct; 51(4):934-40. PubMed ID: 6170621.
    Abstract:
    The effects of physical training and detraining on cardiac structure and myocardial mechanics were studied in young and adult male rats trained by graded treadmill running for 12 wk and compared with sedentary controls. Detraining was produced by training for 12 wk followed by 6 sedentary wk. A training effect was demonstrated by increased succinate dehydrogenase activity in skeletal muscle (trained 10.0 +/- 1.2 mumol . g-1 . min-1; sedentary 6.4 +/- 0.8 mumol . g-1 . min-1; P less than 0.05). Although heart weight-to-body weight ratios were increased in trained rats of both ages, left ventricular fiber diameters and myocardial RNA, DNA, and collagen content were unchanged by training. Active and passive mechanics (myocardial contractility and stiffness) were studied in left ventricular papillary muscles and did not differ significantly between groups, with the exception of depressed contractility observed in young trained rats [(e.g., papillary peak developed isometric tension at Lmax (length at peak tension)] was 2.64 +/- 0.24 g/mm2 in trained vs. 3.59 +/- 0.22 g/mm2 in sedentary (P less than 0.01). This difference was abolished by detraining. Papillary muscle contractile responses to calcium, norepinephrine, and hypoxia were not altered by training or detraining. In conclusion, moderate endurance training did not result in significant cardiac hypertrophy, altered myocardial stiffness, or consistent changes in myocardial contractility.
    [Abstract] [Full Text] [Related] [New Search]