Our results suggest that calcium toxicity in calcifugous bryophytes is caused by insufficient control over the balance of intracellular Ca2+ uptake/efflux. Cell-wall cation-exchange sites of living mosses remain unsaturated with Ca2+ even in calcareous solutions, contradicting the proposed inhibitory effect of Ca2+-oversaturation on cell-wall expansion and monovalent cation uptake. Growth and biomass accumulation of brown mosses was highest in alkaline fen waters, but they could also survive and germinate in poor-fen waters. Calcium-tolerant sphagna survived along the entire poor–rich gradient, but their growth was inhibited by calcium bicarbonate. The three most obviously expanding sphagna produced protonemata even under calcareous conditions. Flowing but not stagnant alkaline fen waters were toxic for calcifugous sphagna, the strongest competitors in poor-fen waters. Increased potassium availability facilitated the survival of calcifugous sphagna in alkaline fens, corroborating field observations that potassium facilitates sphagnum expansion. Surprisingly, the rare and declining moss Hamatocaulis vernicosus was supported by nitrogen and phosphorus more than its competitors. Our comparison of fundamental and realized niches suggests that the dominance of particular moss functional groups in fens is governed by a competitive hierarchy altered by different calcium levels. The expansion of calcium-tolerant sphagna into brown-moss fens therefore requires perturbation that weakens competition. Additionally, expansion of calcifugous sphagna to alkaline environments may be stimulated by potassium availability.