It is well established that the basis for flagellar movement is an ATP-dependent sliding between doublet microtubules.  However, mechanism how this sliding converts into flagellar bending remains to be answered.  To answer this question, mammalian spermatozoa are extremely suitable specimens because of variations in their flagellar movement.  The hyperactivated motility is characterized by large bending at the proximal midpiece and low beat frequency.  The biochemical analyses of this movement using demembranated spermatozoa defined the factors introducing these features; namely, large asymmetrical flagellar movement observed in the early stage of the hyperactivation was induced with a high Ca²⁺ concentration and large symmetrical flagellar movement in the late stage of the hyperactivation was generated with low Ca²⁺ and high cAMP concentrations.  Under these conditions, the microtubule sliding of bull sperm flagella, from which the plasma membrane and the mitochondria had been extracted, was investigated by disintegrating the sperm flagella with MgATP^2-.  For investigating the microtubule sliding of sperm flagella, mammalian spermatozoa are also ideal because elastase or trypsin is not necessary to induce microtubule sliding; thus, certain regulatory mechanisms responsible for the control of interdoublet sliding are retained.  A long thick fiber of the doublet microtubules was extruded and formed a loop at the midpiece at a high Ca²⁺ concentration.  This loop became reduced in size with decreasing Ca²⁺ concentration.  These results demonstrated that the large asymmetrical flagellar movement was caused by a long sliding displacement of a fiber of the doublet microtubules.  In contrast, more than two short, thin fibers of the doublet microtubules were separated and made many small loops at the midpiece at high cAMP and low Ca²⁺ concentrations.  A large amount of microtubule sliding by many doublet microtubules certainly produces the large symmetrical flagellar movement of the hyperactivated spermatozoa.