Trypanosoma brucei thwarts the host immune response by replacing its variant surface glycoprotein (VSG). The actively transcribed VSG is located in one of approximately 20 telomeric expression sites (ES). Antigenic variation can occur by transcriptional switching, reciprocal translocations, or duplicative gene conversion events among ES or with the large repertoire of telomeric and non-telomeric VSG. In recently isolated strains, duplicative gene conversion occurs at a high frequency and predominates, but the switching frequency decreases dramatically upon laboratory-adaptation. Uniquely, T. brucei telomeres grow--apparently indefinitely--at a steady rate of 6-12 base pairs (bp) per population doubling (PD), but the telomere adjacent to an active ES undergoes frequent truncations. Using two-dimensional gel electrophoresis, we demonstrate that all of the chromosome classes of fast-switching and minimally propagated T. brucei have shorter telomeres than extensively propagated Lister 427 clones, suggesting a link between laboratory adaptation, telomere growth, and VSG switching rates.