Stretch activation (SA) is a delayed increase in force that enables high power and efficiency from a cyclically contracting muscle. SA exists in various degrees in almost all muscle types. In Drosophila, the indirect flight muscle (IFM) displays exceptionally high SA force production (F_SA), whereas the jump muscle produces only minimal F_SA. We previously found that expressing an embryonic (EMB) myosin heavy chain (MHC) isoform in the jump muscle transforms it into a moderately SA muscle type and enables positive cyclical power generation. To investigate if variation in MHC isoforms is sufficient to produce even higher F_SA, we substituted the IFM MHC isoform (IFI) into the jump muscle. Surprisingly, we found that IFI only caused a 1.7-fold increase in F_SA, less than half the increase previously observed with EMB, and only at a high Pi concentration, 16 mM. This IFI induced F_SA is much less than what occurs in IFM, relative to isometric tension, and did not enable positive cyclical power generation by the jump muscle. Both isometric tension and F_SA of control fibers decreased with increasing Pi concentration. However, for IFI expressing fibers, only isometric tension decreased. The rate of F_SA generation was about 1.5-fold faster for IFI fibers than control fibers, and both rates were Pi dependent. We conclude that MHC isoforms can alter FSA and hence cyclical power generation, but that isoforms can only endow a muscle type with moderate F_SA. Highly SA muscle types, such as IFM, likely use a different or additional mechanism.