Why the study?
Does chronic endurance training attenuate age-related shifts in cardiac myosin isozyme composition in Fischer 344 rats?
Does chronic endurance training attenuate age-related shifts in cardiac myosin isozyme composition in Fischer 344 rats?
Chronic endurance training does not prevent the age-related shift in cardiac myosin isozyme composition in rats.
Endurance training does not blunt age-related cardiac myosin shifts in rats; leaves open translation to human cardiac aging.
The effects of aging and exercise on isoforms of cardiac myosin and Ca2+-activated actomyosin adenosinetriphosphatase (ATPase) activity were examined in Fischer 344 rats. Rats were divided into running (R) and age-matched sedentary (S) groups. The groups initiated their exercise program at either 3, 4, or 18 mo of age. Rats were killed at 10, 12, 24, or 27 mo of age. ATPase activity decreased 25% in the S group and 28% in the R group from 12 to 27 mo of age. The myosin isozyme patterns shifted in both S and R groups from a predominantly V1 isozyme form (63.8%) at 10 mo of age to a more equal distribution of isozyme forms at 24 mo (V1, V2, and V3 comprising 40.0, 27.8, and 31.9%, respectively). Age-related shifts in myosin composition occurred despite chronic endurance training at an intensity of approximately 75% maximum O2 consumption. Improvement of cardiac performance through training during aging is not accompanied by attenuating shifts in myosin isozyme composition.
No takes yet. Share an insight, caveat, or question.
Farrar et al. (1988) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: