When administered alone, preinfection exercise training and
benznidazole-based
chemotherapy induce cardioprotection in
Chagas disease. However, the effect of concomitant exercise and
benznidazole treatment is unknown. We investigated whether exercise and specific
chemotherapy could interact to modulate
parasitemia,
inflammation, redox status and heart damage in a murine model of T. cruzi
infection. Wistar rats were randomized into an uninfected control group (CNT) and four groups infected with T. cruzi: sedentary untreated (SUN) and treated (STR), and trained untreated (TUN) and treated (TTR). Running training was administered 5 days/week for 4 weeks. Treated animals concomitantly received 100 mg/kg/day
benznidazole. Heart
inflammation and reactive damage were not detected in CNT animals. Compared to SUN, TUN animals presented increased levels of
parasitemia,
myocarditis,
nitric oxide,
hydrogen peroxide,
protein carbonyl,
malondialdehyde,
cytokines (IFN-γ, TNF-α, IL-4, IL-6, IL-10 and IL-17),
catalase,
superoxide dismutase and
glutathione reductase activity, as well as reduced heart non-
protein antioxidant levels (P < 0.05). TTR animals exhibited higher levels of
parasitemia,
myocarditis,
hydrogen peroxide,
malondialdehyde, IFN-γ, TNF-α and
IL-6 than STR animals (P < 0.05), which showed the lowest levels of all analyzed parameters compared to the other groups (P < 0.05). Our findings indicate that exercise aggravates acute
infection. When concomitantly administered with
benznidazole, exercise training impaired parasitic control and
chemotherapy-induced cardioprotection in T. cruzi-infected rats. Considering that exercise training and T. cruzi
infection constitute independent metabolic challenges, the negative effects of concomitant treatment are potentially related to the overlapping oxidative and immunoinflammatory demands of exercise and the
infection itself.