Voluntary Exercise and Heligmosomoides bakeri Parasitic Infection Change Body Composition and Blood Physiology of the Laboratory Mouse (Mus musculus) Host

Hookworm infection in humans causes substantial morbidity; however, the relationship between infection and host exercise has not been quantified experimentally for these types of parasites. Human immune response to hookworms is often modeled using laboratory mice (Mus musculus) infected with the intestinal nematode Heligmosomoides bakeri. I used this model to test (1) if voluntary exercise prior to infection would affect susceptibility of mice to H. bakeri, (2) if H. bakeri infection would change voluntary exercise of mice during the early (acute) and late (chronic) stages of infection, (3) if H. bakeri infection or voluntary exercise would alter energy acquisition/allocation of mice, and (4) if blood physiology had a relationship to either voluntary exercise or H. bakeri infection. I found no effects of voluntary exercise on infection susceptibility, as measured by systemic levels of H. bakeri specific immunoglobulin G1 (IgG1), infection intensity, parasite sex ratio, and parasite reproduction. I found no effects of H. bakeri infection on voluntary exercise, as measured by wheel running parameters and home cage activity. Voluntary exercise decreased apparent dry matter digestibility (DMD), but increased food intake, resulting in increased total body mass. H. bakeri infection increased DMD, but had no effect on food intake, and increased total body mass by the end of the experiment. Actual energy assimilated (after accounting for food intake and digestibility) increased with voluntary exercise, but did not change with H. bakeri infection. H. bakeri infection caused an increase in the small intestine mass per length, small intestine length and spleen mass, but a decrease in stomach, liver, and heart masses, while exercise increased cecum and liver masses. Overall, the data suggest that infection and exercise placed different demands, and in response the mice adjusted their energy acquisition and body composition accordingly. Additionally, I found blood physiology changed for both voluntary exercise and H. bakeri infection, again in very different ways. Non-exercised mice had decreased hematocrit on Day 14 post-infection (PI), while exercised mice had increased hematocrit on Day 6 PI and then levels returned to baseline on Day 14 PI. Hematocrit levels for infected mice increased on Day 6 PI and then decreased below baseline on Day 14 PI. Also, infected mice had 8% lower hemoglobin levels than uninfected mice on Day 14 PI. Blood physiology varied among exercised and infected mice, but because these changes were only tested on certain days of the experiment they did not show a clear effect of either treatment. Taken together, my data showed that voluntary exercise and H. bakeri infection separately and distinctly affected how the mouse acquired energy, where the mouse invested that energy (in terms of organ masses and fat/lean tissues), and how blood components changed.