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Physical training improves cardiac structure and function, antioxidant capacity, and exercise tolerance in spontaneously hypertensive rats
Author(s) -
Okoshi Marina Politi,
Pagan Luana,
Damatto Ricardo,
Cezar Marcelo,
Campos Dijon,
Lima Aline,
Damatto Felipe,
Gomes Mariana,
Caldonazo Tulio,
Okoshi Katashi
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.838.6
Subject(s) - medicine , cardiology , cardiac function curve , sed , vo2 max , diastole , blood pressure , treadmill , ex vivo , hemodynamics , oxidative stress , heart rate , heart failure , chemistry , biochemistry , in vitro
Chronic hemodynamic overload such as hypertension induces genetic, molecular, cellular, and interstitial alterations which clinically manifest as changes in heart size, shape, and function, a process known as cardiac remodeling. Pressure overload caused by hypertension may produce imbalance between reactive oxygen species (ROS) production and antioxidant capacity. Exercise plays an important role in mitigating cardiovascular risk factors such as hypertension. The aim of this study was to evaluate the influence of physical training on cardiac structures and function, physical capacity, and myocardial oxidative stress in spontaneously hypertensive rats (SHR). Methods Thirteen month old SHR were divided into two groups: sedentary (SED, n=18) and exercised (EX, n=22). Physical training was performed 5 times per week for 16 weeks on a treadmill. Physical performance was assessed by exercise test on a treadmill with a gradual speed increase. Systolic arterial pressure (SAP) was measured by tail cuff method. Echocardiogram (Echo) was performed to evaluate in vivo cardiac structures and left ventricular (LV) function. In vitro myocardial function was analyzed in LV papillary muscle preparations. Cardiomyocyte size was measured in LV histological sections. Myocardial antioxidant enzyme activity was quantified by spectrophotometry. NADPH oxidase activity was analyzed by the lucigenin reduction method. Statistics: Student's t test (p<0.05). Results Physical capacity was higher in EX. SAP did not differ between groups at the end of the experiment (SED 194 ± 22 vs. EX 188 ± 12 mmHg). Echo showed reduced diastolic posterior wall thickness (SED 1.63 ± 0.10 vs. EX 1.53 ± 0.08 mm), left atrium diameter (SED 6.57 ± 0.51 vs. EX 6.18 ± 0.49 mm), left atrium diameter‐to‐aorta diameter ratio (SED 1.49 ± 0.11 vs. EX 1.42 ± 0.13), and LV relative wall thickness (SED 0.43 ± 0.05 vs. EX 0.40 ± 0.04) in EX group. The in vitro myocardial functional study showed better performance in EX (positive derivative of tension developed: SED 52.2 ± 12.4 vs. EX 63.4 ± 9.49 g/mm 2 /s). Cardiomyocyte size and NADPH oxidase activity did not differ between groups. Antioxidant enzymes superoxide dismutase and catalase activity was higher in EX. Conclusion Physical training improves exercise capacity and induces beneficial effects on cardiac structures and function and myocardial antioxidant capacity in spontaneously hypertensive rats. Support or Funding Information Support: FAPESP, CNPq, and CAPES