Ramzi A Al-Horani, Mukhallad A Mohammad, Saja Haifawi, Mohammed Ihsan
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引用次数: 1
Abstract
This study investigated the changes in myocardial myosin heavy chain (MHC) isoforms, MHC-α and MHC-β composition in young healthy rodents following endurance training, with and without post-exercise cold-water immersion (CWI). Male rats were either trained on a treadmill for 10 weeks with (CWI) or without (Ex) regular CWI after each running session, or left sedentary (CON). Left ventricular mRNA of MHC-α, MHC-β, thyroid receptor α1 (TR-α1) and β (TR-β) were analyzed using rt-PCR and semiquantitative PCR analysis. MHC isoform protein composition was determined using SDS-PAGE electrophoresis. MHC-α isoform protein was predominant in all groups. The relative expression of MHC-β (%MHC-β) protein was not different between groups (CWI 34.7 ± 6.9%; Ex 32 ± 5.3%; CON 35.5 ± 10%; P = 0.7). MHC-β mRNA was reduced in Ex (0.7 ± 0.3-fold) compared to CWI (1.3 ± 0.2-fold; P < 0.001) and CON (1.01 ± 0.2-fold; P = 0.03). TRα1 mRNA was lower in CWI (0.4 ± 0.05-fold) than Ex (1.02 ± 0.3-fold) and CON (1.01 ± 0.2-fold) (P < 0.001 for both). CWI exhibited greater %MHC-β mRNA (56.8 ± 4.1%) than Ex (44.4 ± 7.7%; P = 0.001) and CON (48.5 ± 7.8%; P = 0.03). Neither exercise nor post-exercise CWI demonstrated a distinct effect on myocardial MHC protein isoform composition. However, CWI increased the relative expression of MHC-β mRNA compared with Ex and CON. Although this implicates a potential negative long-term impact of post-exercise CWI, future studies should include measures of cardiac function to better understand the effect of such isoform mRNA shifts following regular use of CWI.
期刊介绍:
The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.