We have demonstrated that in dogs antigen sensitization results in alterations of contractile properties. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. We therefore developed an index of isotonic relaxation, t1/2,CE (half time for relaxation that is independent of muscle load and initial contractile element length), for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle than that in controls, studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by t1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 ± 0.92 vs. 7.78 ± 0.93 s, means ± SE); however, it was prolonged significantly in the sensitized muscle only stimulated for 1 s (12.74 ± 2.5 s, mean ± SE) compared with the control (6.98 ± 1.01 s). During the late phase of isotonic relaxation, both groups showed an unexpected spontaneous increase in zero-load shortening velocity, which is an index of cross-bridge cycling rate. We conclude that (i) both contraction and relaxation properties of early normally cycling cross bridges are altered after sensitization and these changes may account for the hyperresponsiveness observed in asthmatics and (ii) the cross-bridge cycling rate increases spontaneously during isotonic relaxation, probably as a result of reactivation of the contractile mechanism.Key words: smooth muscle relaxation, isotonic relaxation, spontaneous activation in late relaxation, mechanisms for airway hyperresponsiveness, new index of muscle relaxation.