Recent progress in chlorophyll fluorescence research is reviewed, with emphasis on separation of photochemical and non-photochemical quenching coefficients (qP and qN) by the 'saturation pulse method'. This is part of an introductory talk at the Wageningen Meeting on 'The use of chlorophyll fluorescence and other non-invasive techniques in plant stress physiology'. The sequence of events is investigated which leads to down-regulation of PS II quantum yield in vivo, expressed in formation of qN. The role of O2-dependent electron flow for ΔpH- and qN-formation is emphasized. Previous conclusions on the rate of 'pseudocyclic' transport are re-evaluated in view of high ascorbate peroxidase activity observed in intact chloroplasts. It is proposed that the combined Mehler-Peroxidase reaction is responsible for most of the qN developed when CO2-assimilation is limited. Dithiothreitol is shown to inhibit part of qN-formation as well as peroxidase-induced electron flow. As to the actual mechanism of non-photochemical quenching, it is demonstrated that quenching is favored by treatments which slow down reactions at the PS II donor side. The same treatments are shown to stimulate charge recombination, as measured via 50 μs luminescence. It is suggested that also in vivo internal thylakoid acidification leads to stimulation of charge recombination, although on a more rapid time scale. A unifying model is proposed, incorporating reaction center and antenna quenching, with primary control of ΔpH at the PS II reaction center, involving radical pair spin transition and charge recombination to the triplet state in a first quenching step. In a second step, triplet excitation is trapped by zeaxanthin (if present) which in its triplet excited state causes additional quenching of singlet excited chlorophyll.