title: Resistance training improves hemodynamic function, collagen deposition and inflammatory profiles: experimental model of heart failure.
abstract: The role of resistance training on collagen deposition, the inflammatory profile and muscle weakness in heart failure remains unclear. Therefore, this study evaluated the influence of a resistance training program on hemodynamic function, maximum strength gain, collagen deposition and inflammatory profile in chronic heart failure rats. Thirty-two male Wistar rats submitted to myocardial infarction by coronary artery ligation or sham surgery were assigned into four groups: sedentary sham (S-Sham, n = 8); trained sham (T-Sham, n = 8); sedentary chronic heart failure (S-CHF, n = 8) and trained chronic heart failure (T-CHF, n = 8). The maximum strength capacity was evaluated by the one maximum repetition test. Trained groups were submitted to an 8-week resistance training program (4 days/week, 4 sets of 10-12 repetitions/session, at 65% to 75% of one maximum repetition). After 8 weeks of the resistance training program, the T-CHF group showed lower left ventricular end diastolic pressure (P<0.001), higher left ventricular systolic pressure (P<0.05), higher systolic blood pressure (P<0.05), an improvement in the maximal positive derivative of ventricular pressure (P<0.05) and maximal negative derivative of ventricular pressure (P<0.05) when compared to the S-CHF group; no differences were observed when compared to Sham groups. In addition, resistance training was able to reduce myocardial hypertrophy (P<0.05), left ventricular total collagen volume fraction (P<0.01), IL-6 (P<0.05), and TNF-α/IL-10 ratio (P<0.05), as well as increasing IL-10 (P<0.05) in chronic heart failure rats when compared to the S-CHF group. Eight weeks of resistance training promotes an improvement of cardiac function, strength gain, collagen deposition and inflammatory profile in chronic heart failure rats.
authors.affiliation: Laboratory of Physiology, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Jadson P
authors.initials: JP
authors.lastname: Alves
authors.affiliation: Laboratory of Physiology, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Ramiro B
authors.initials: RB
authors.lastname: Nunes
authors.affiliation: Laboratory of Physiology, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Giuseppe P
authors.initials: GP
authors.lastname: Stefani
authors.affiliation: Laboratory of Physiology, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Rio Grande do Sul, Brazil; Department of Physical Therapy, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Pedro
authors.initials: P
authors.lastname: Dal Lago
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D006332:Cardiomegaly / Q000097:blood / Q000150:complications / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism*; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D007249:Inflammation / Q000097:blood / Q000150:complications / Q000473:pathology; D008099:Liver / Q000473:pathology; D008168:Lung / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D017208:Rats, Wistar; D055070:Resistance Training; D016019:Survival Analysis
chemical_list: D016207:Cytokines; D003094:Collagen