Modifying effects of exercise on clinical course and biochemical response of the myocardium in influenza and tularemia in mice
| Autor: | Anthony J. Johnson, G Friman, William R. Beisel, N G Ilbäck, R F Berendt |
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| Rok vydání: | 1984 |
| Předmět: |
Male
Physical Exertion Immunology Muscle Proteins Cathepsin D Spleen Physical exercise Oxidative phosphorylation Microbiology Tularemia Mice Orthomyxoviridae Infections Nucleic Acids medicine Animals Glycolysis chemistry.chemical_classification biology Myocardium medicine.disease Infectious Diseases medicine.anatomical_structure Enzyme chemistry Catalase biology.protein Parasitology Research Article |
| Zdroj: | Infection and Immunity. 45:498-504 |
| ISSN: | 1098-5522 0019-9567 |
| Popis: | For a study of the interactions of strenuous physical exercise (daily swimming to exhaustion) and a viral as compared with a bacterial infection with regard to the clinical course and the biochemical response of the myocardium, influenza and tularemia of similar lethality were used in mice. In both infections, expected infection-induced catabolic alterations in the ventricular myocardium were evident 2 days before median lethality was achieved, with a more pronounced wasting in influenza than in tularemia. Exercise before inoculation (preconditioning) was beneficial in that the catabolic effects of both infections were limited and lethality in influenza was reduced. Thus, the myocardial protein-degrading effect of influenza did not occur with preconditioning, and oxidative tissue enzyme activities decreased less. In tularemia, cytochrome c oxidase activity was fully preserved with preconditioning, and activation of catalase was less pronounced. Exercise during ongoing infection counteracted the infection-induced decrease in the activities of glycolytic and oxidative enzymes in tularemia, but lethality and bacterial counts in the spleen were uninfluenced. Conversely, exhaustive exercise in influenza increased lethality and had no significant effect on cardiac enzymes. These exercise models caused no major alterations in activation of lysosomal enzymes (beta-glucuronidase and cathepsin D). |
| Databáze: | OpenAIRE |
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