myofilament การใช้

• More recently, myofilament protein changes have been studied in humans in response to resistance training.
• Furthermore, cellular and myofilament-level adaptations are related to diminished whole muscle and whole body performance.
• This study provides evidence of the mechanisms for both immediate and delayed myofilament response to exercise at the molecular level.
• Phosphorylation of cTnT at Ser278 and Thr287 by ROCK-II was shown to decrease myosin ATPase activity and myofilament force development in skinned cardiac muscle.
• While the research on muscle fiber remodeling is on-going, there are generally accepted facts about the myofilament from the American College of Sports Medicine.
• Ryanodine receptors are located within the membrane of the sarcoplasmic reticulum and function to release Ca 2 + required for myofilament activation ( Guyton, 2006 ).
• While the exact mechanism of myofilament alteration in response to exercise is still being studied in mammals, some interesting clues have been revealed in Thoroughbred race horses.
• This destructive fragmentation removes a part of the middle region tropomyosin binding site 1, leading to attenuation of the myofilament force production by decreasing the myosin ATPase activity.
• This study concludes that there is no clear relationship between fiber-type composition and in vivo muscle tension, nor was there evidence of myofilament packing in the trained muscles.
• Recent studies suggest that these conditions are associated with altered single fiber performance due to decreased expression of myofilament proteins and / or changes in myosin-actin cross-bridge interactions.
• Phosphorylation of Thr206 alone was sufficient to reduce myofilament calcium sensitivity and force production . cTnT is also phosphorylated at Thr194 and Ser198 under stress conditions, leading to attenuated cardiomyocyte contractility.
• In cardiomyocytes treated with doxorubicin, a model of anthracycline-induced cardiomyopathy, CARP mRNA and protein levels were depleted, myofilament gene transcription was attenuated and sarcomeres showed significant disarray.
• Again, researchers are not completely clear about the molecular mechanisms of change, and an alteration of fiber-type composition in the myofilament may not be the answer many athletes have long assumed.
• These muscle contractions are caused by calcium's bonding to troponin and unmasking the binding sites covered by the troponin-tropomyosin complex on the actin myofilament and allowing the myosin cross-bridges to connect with the actin.
• Embryonic cTnT with more negative charge at the N-terminal region exerts higher calcium sensitivity of actomyosin ATPase activity and myofilament force production, compared with the adult cardiac TnT, as well as a higher tolerance to acidosis.
• Skinned trabeculae or cardiac myocytes obtained from human patients carrying a " MYBPC3 " mutation or from heterozygous and homozygous " Mybpc3 "-targeted knock-in mice exhibited higher myofilament Ca2 + sensitivity than controls.
• MLC-2v phosphorylation at Ser14 and Ser15 increases myosin lever arm stiffness and promotes myosin head diffusion, which altogether slow down myosin kinetics and prolong the duty cycle as a means to fine-tune myofilament Ca2 + sensitivity to force.
• Absence of cMyBP-C ( " Mybpc3 "-targeted knock-out mice ) results in severe cardiac hypertrophy, increased heart-weight-to-body-weight-ratios, enlargement of ventricles, increased myofilament Ca2 + sensitivity and depressed diastolic and systolic function.
• Additionally, in patients with ischemic cardiomyopathy, dilated cardiomyopathy and hypertrophic cardiomyopathy, ALC-1 protein expression is shown to be reactivated, and ALC-1 expression correlates with calcium sensitivity of myofilament proteins in skinned fiber preparations, as well as ventricular dP / dtmax and ejection fraction.
• In vitro studies showed that N-terminal truncated cTnT preserved the overall cardiac myofilament calcium sensitivity and cooperativity, but altered TnT s binding affinities for tropomyosin, TnI and TnC proteins, and lead to slightly decreased maximum myosin ATPase activity and myofilament force production, which forms the basis of the selective decrease in contractile velocity of ventricular muscle to increase stroke volume without significant increase in energy expenditure.