Swimming causes myosin adaptations in the rat cardiac isograft.

Abstract:

:To investigate the contributions of humoral and hemodynamic factors to cardiac adaptations associated with chronic exercise, female Fischer 344 rats were subjected to chronic swimming, infrarenal cardiac transplantation, or both. Swimming resulted in hypertrophy (11-12%) of the in situ hearts in both the unoperated and operated animals compared with the matched sedentary controls. The cardiac isograft exhibited atrophy (32-35%), which was not attenuated by swimming. The cardiac isograft was also associated with a decrease in the percent of V1 myosin isoenzyme, which was attenuated by swimming (45 +/- 5% versus 66 +/- 6%). Swimming also increased the percent of this isomyosin in the in situ hearts of operated rats. These data suggest that hemodynamic load and/or neural innervation are necessary for hypertrophy associated with chronic conditioning by swimming, whereas myosin isoenzyme control is significantly mediated by humoral factors.

journal_name

Circ Res

journal_title

Circulation research

authors

Advani SV,Geenen D,Malhotra A,Factor SM,Scheuer J

doi

10.1161/01.res.67.3.780

subject

Has Abstract

pub_date

1990-09-01 00:00:00

pages

780-3

issue

3

eissn

0009-7330

issn

1524-4571

journal_volume

67

pub_type

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