We compared the response of the accessory pathway (AP), the atrial myocardium, the His-Purkinje system (HPS) and the ventricular myocardium during steady state (constant cycle length) and following an abrupt alteration in cycle length in 23 patients with Wolff-Parkinson-White syndrome. The durations of the anterograde and retrograde refractory periods were measured during constant drive cycle lengths of 600 and 400 ms (Method I) and during an abrupt change in cycle length of either short-to-long (400 to 600 ms) (Method II) or long-to-short (600 to 400 ms) (Method III) just before the extra stimulus. The mean durations of the anterograde effective refractory periods of the APs were 295 +/- 43, 243 +/- 39 and 273 +/- 37 ms at 600, 400 and 400 to 600 ms cycle lengths, respectively. For the atrial effective refractory periods at the three cycles, they were 238 +/- 18, 217 +/- 11 and 241 +/- 17 ms, respectively. During ventricular stimulation, the mean durations of the retrograde effective refractory periods of the APs were 263 +/- 25, 245 +/- 19 and 253 +/- 21 ms at cycle lengths of 600, 400 and 400 to 600 ms, respectively. For the relative refractory periods of the HPS, they were 335 +/- 29, 239 +/- 23 and 367 +/- 38 ms, respectively and, for the effective refractory periods of the ventricular myocardium, they were 227 +/- 17, 206 +/- 15 and 215 +/- 18 ms, respectively. The retrograde effective refractory period of the HPS could be measured in only five patients at the three cycles (600, 400 and 400 to 600 ms) and the mean values were 265 +/- 57, 225 +/- 14 and 305 +/- 27 ms, respectively. With Method III, AP and ventricular myocardium responded in a cumulative manner while HPS demonstrated paradoxical effect. Compared to Method I, changes with Methods II and III were statistically significant for all variables measured. During all three cycles, the retrograde effective refractory period of the HPS exceeded the effective refractory period of the AP; and the HPS demonstrated progressive conduction delay while the AP responded to no or minimal delays when the V1V2 intervals were similar. An abrupt cycle length change of the short-to-long type facilitated the induction of orthodromic tachycardia during ventricular pacing.(ABSTRACT TRUNCATED AT 400 WORDS)