Key result
Endurance training boosts creatine kinase but fails to reverse most myocardial abnormalities in BDNF-deficient rats.
Why the study?
To determine whether heterozygous BDNF-deficient rats exhibit pathological myocardial changes and whether a 5-week moderate-intensity endurance training program can reverse adverse changes in the heart muscle.
Does a 5-week moderate-intensity endurance training program reverse adverse changes in the heart muscle of heterozygous BDNF-deficient rats?
Does a 5-week moderate-intensity endurance training program reverse adverse changes in the heart muscle of heterozygous BDNF-deficient rats?
In a rat model of BDNF deficiency, moderate endurance training increased myocardial creatine kinase activity but failed to reverse most underlying metabolic and enzymatic abnormalities in the heart.
Answers are grounded in this paper and cite their sources.
Moderate endurance training fails to reverse most cardiac abnormalities in BDNF-deficient rats; leaves open optimal regimens in this model.
Introduction: The study aimed to determine whether heterozygous BDNF-deficient (BDNF-knockout, SD-BDNF) rats exhibit pathological changes in the myocardium and to assess whether a 5-week moderate-intensity endurance training program can reverse adverse changes in the heart muscle. Methods: Experiments were conducted on four groups of rats: control wild-type, control BDNF knockout, trained wild-type and trained BDNF knockout. Knockout rats were selected due to the presence of symptoms resembling metabolic syndrome in serum and liver while 5-week moderate endurance training was used as an intervention targeted at restoring heart function. Measurements of BDNF/Trk-B concentrations and molecules levels and activities, such as cardiac specific enzymes like creatine kinase and creatine kinase myocardial band, lipids as total cholesterol, low-density lipoprotein and triglycerides, metabolic enzymes including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase and lactate dehydrogenase and interleukin-1 were carried out in myocardium homogenates. Results: In BDNF-deficient rats, the myocardium showed significantly reduced lipid concentrations, decreased metabolic and cardiac enzyme activity, and elevated Trk-B levels, all of which are indicative of myocardial ischemia or hypoxia. These changes in critical biomarkers were consistent with those earlier observed in the livers of BDNF-deficient rats, suggesting a link between the liver and cardiac function. Moderate endurance training led to an increase in creatine kinase activity in the myocardium of trained rats, suggesting increased production and utilization of energy required for myocardial contraction in trained wild-type and knockout populations of rats. Discussion: BDNF-deficient rats exhibited numerous myocardial abnormalities, most of which were not reversible after moderate-intensity endurance training. These findings provide a basis for a deeper understanding of the mechanisms underlying myocardial disorders in BDNF-deficient rats, which appear to be a suitable model for studying various aspects of metabolic disorders.
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Grzelak et al. (2024) studied Myocardial disorders in BDNF deficiency (n=41). Moderate-intensity endurance training vs. Sedentary control was evaluated on Myocardial biomarker levels (BDNF, Trk-B, CK, CK-MB, lipids, metabolic enzymes). Moderate-intensity endurance training increased myocardial creatine kinase activity but did not reverse most of the myocardial abnormalities, such as reduced lipid and enzyme levels, in BDNF-deficient rats.
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