The AV node filters atrial impulses. Underlying rate-dependent refractory properties are assessed with the effective (ERPN, longest non-conducted atrial cycle length) and functional (FRPN, shortest His bundle cycle) refractory period determined with premature protocols at different basic rates. Fast rates prolong ERPN, and shorten FRPN but these effects vary with subjects, age, and species. We propose that these opposite and variable effects reflect the net sum of concurrent cumulative and non-cumulative effects associated to basic (BCL) and pretest cycle length (PTCL), respectively. To test this hypothesis, selective and combined effects of 5 BCL (S₁S₁) and 6 PTCL (S₁S₂) on ERPN, FRPN, and their subintervals (ERPN= A₂H₂+H₂A₃; FRPN=H₂A₃+A₃H₃; A, atrium; H, His bundle) were assessed with S₁S₂S₃ protocols in 6 rabbit heart preparations. At control BCL, PTCL shortenings prolonged ERPN (113±12 ms vs. 101±14 ms, p<0.01) as a net result of prolonged A₂H₂ and curtailed H₂A₃. At control PTCL, BCL shortenings increased ERPN (127±20 ms vs. 101±14 ms, p<0.01) by prolonging A₂H₂. FRPN did not vary with BCL but decreased (163±6 ms vs. 175±10 ms, p<0.01) with PTCL that curtailed H₂A₃. Equal BCL and PTCL shortenings as in standard protocols prolonged ERPN but left FRPN unchanged. Notably, ERPN and FRPN significantly correlated through their H₂A₃ subinterval. In conclusion, BCL and PTCL are both important determinants of AV nodal refractoriness and together account for rate-induced changes in ERPN and FRPN observed during standard premature protocols. ERPN and FRPN are related variables. Similar functional rules may govern nodal refractory behavior during supraventricular tachyarrhythmias.