We are investigating the material properties of Drosophila body wall muscle and are particularly interested in contributions from giant sarcomere associated proteins (gSAPs) such as the titin ortholog, sallimus. Our tethering hypothesis suggests that gSAPs contribute substantially to work loop hysteresis after motor neuronal activity. We used two techniques to test this: (1) the previously described RNAi knockdown of the sallimus gene in D. mel, (2) the myosin inhibitor para-amino blebbistatin to interrupt actomyosin cycling. Stress was measured in response to cyclical length change (strain) under three physiologic conditions: (1) passive muscle [epoch 1], (2) five seconds of 15 pps motor activation [epoch 2], and (3) 15 seconds following the cessation of stimulation [epoch 3]. Much work remains, but initial results show that variation in stress recorded during epoch 2 increased in animals with reduced sls expression (RNAi), which is consistent with the tethering hypothesis of gSAP action. Moreover, variation in the decay of stress after muscle activation was greatest in sls RNAi animals. We continue to investigate the tethering hypothesis using the myosin inhibitor, para-amino blebbistatin and predict that it’s application will not eliminate the increased variability of stress associated with sls knockdown. Such findings would be consistent with the hypothesis that sls can continue to modulate stress after cessation of stimulation or perhaps in the absence of actomyosin cycling.