The Effect of Exercise and Fasting on the Myocardial Protein and Lipid Metabolism in Experimental Bacterial Myocarditis

Abstract

A generally nonlethal Salmonella typhimurium infection in weanling rats produced bacterial myocarditis and myocardial hyperplasia. Myocardial lesions were characterized by focal infiltrates of inflammatory cells (predominantly mononuclear). segmental myocyte necrosis, and incipient fibrosis. Although bacterial infections are infrequently associated with myocarditis, the S. typhimurium infection in young rats produced a new experimental model of diffuse myocardial inflammatory foci. Biochemical changes in the myocardium included great increases in total myocardial contents of protein (23%), RNA (39%) and DNA (43%) and several lipid fractions (35–55%) as well as in tissue activities of acid hydrolases, such as cathepsin D (124%) and β‐glucuronidase (135%), all of which contrasted with the relatively limited areas of histologic involvement (1.5%). To study the effects of additional stress in this model infection, some rats were exercised by forced running in wheels for 2 hours and others were fasted for 24 hours before samples were obtained. The short period of forced exercise in this infection caused an additional increase of myocardial protein content (47%) but with no additional change in histology. The expected fasting‐induced degradation of protein as well as an infection‐associated increase in myocardial lipids were each prevented when rats were fasted during ongoing acute infection. Protein degradation, as reflected by heightened acid hydrolase activities, seemed to occur at a similar rate regardless of other stresses, whereas the rate of myocardial protein synthesis appeared to be alterable.

Carboxyl terminus of Hsp70‐interacting protein (CHIP) is required to modulate cardiac hypertrophy and attenuate autophagy during exercise

“…To examine this, we used voluntary unloaded wheel running, an established model of physiologic cardiac hypertrophy, [23][24][25] to determine whether cardiac Atg could be induced as it is in other muscles in response to exercise. [26][27][28] We found that hearts from CHIPÀ/À mice respond to voluntary exercise with an enhanced autophagic response that is associated with an exaggerated hypertrophic phenotype. We further determined that CHIP plays a role in regulating Akt signalling in cardiomyocytes.…”

“…It is already well documented that the ubiquitin ligase CHIP plays a critical role in maintaining cardiac structure and function during times of stress, prompting us to examine whether CHIP is involved in autophagic protein degradation in the heart. To examine this, we used voluntary unloaded wheel running, an established model of physiologic cardiac hypertrophy, to determine whether cardiac Atg could be induced as it is in other muscles in response to exercise . We found that hearts from CHIP−/− mice respond to voluntary exercise with an enhanced autophagic response that is associated with an exaggerated hypertrophic phenotype.…”

Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

“…Impairment in both formation and downstream lysosomal degradation of autophagosomes triggers mitochondrial and lysosomal pro‐apoptotic pathways, and therefore culminates in cardiomyocyte death 15,17. There is increasing evidence showing that exercise activates autophagy in muscle 19–21. Resistance exercise causes a significant increase in protein degradation activities, such as lysosomal hydrolyase and Vps34,19,20 and increases the content of myocardial protein synthesis,20,21 thus stimulating protein turnover.…”

“…There is increasing evidence to show that exercise up‐regulates autophagy, and increases the protein turnover rate;19–21 however, it is unknown whether exercise has the same effect on the failing heart. In the present study, we investigated the effect of exercise training on cardiac function in an infarcted rabbit model explored the possible mechanisms of this effect, by analysing biomarkers of oxidative stress, antioxidant capacity, autophagy, apoptosis, and fatty acid utilization.…”

Interactions Among Infections, Nutrients and Xenobiotics

“…In several infections the accumulation of fat occurs in infected tissues, often accompanied by tissue necrosis: when arteries are the targets of the microorganisms, arteriosclerotic changes may ensue (Ilback et al, 1984c;Ilback et al, 1990;Nystrom-Rosander et al, 2003). Inflammatory fluid seems to accelerate the uptake of lipoproteins in resident macrophages (Raymond et al, 1985) and the increased uptake of lipids in the heart in coxsackievirus myocarditis is histologically localized to "macrophage dense" areas (Ilback et al, 1990).…”