We have recently shown that unloaded cardiac myocytes, from the remote non-infarcted, hypocontractile regions of remodeled rat hearts, contract normally. Since load is an important determinant of contractile response, we investigated the effects of viscous loading on the contractile function (video edge detection) of 268 myocytes isolated from the remodeled myocardium of infarcted (MI) rat hearts, (n = 7, 6 weeks Post-MI) and compared them with 288 cells from age matched sham operated hearts (Sham; n = 7). Viscosity of the myocyte suspension buffer was varied by adding inert methyl cellulose [4 mM Ca2+; 1, 15, 200 & 300 centipoise (cp)]. Buffer perfused MI hearts had significantly depressed global function (Langendorff LV developed pressure 46 Vs 113 mm Hg, p < 0.05).Basal % myocyte shortening (1 cp) was not significantly different between Sham and MI cells (p = 0.08). A viscosity-dependent decrease was seen in % shortening and velocity of shortening in Sham and MI (p < 0.001, ANOVA). There was no difference in the myocyte % shortening between Sham and MI at 15 cp & 200 cp (p = 0.37 & 0.96). At 300 cp, MI myocyte contractile response was greater than Sham cells (p < 0.01). While viscous loading significantly decreases myocyte shortening in both Sham & MI, it does not affect the MI cells more adversely. Therefore, the global LV dysfunction seen in the remodeled rat infarct model may not be explained by diminished contractile response of the individual myocytes from the remodeled myocardium.