Abstract
Introduction: Testosterone therapy and resistance training have been demonstrated to improve muscle mass and strength in patients with testosterone deficiency. However the effects on cardiac mass and contractility of these interventions have not been identified in prospective placebo-controlled trials. The hypothesis of this trial was that resistance training and testosterone replacement would improve cardiac mass and contractility in male COPD patients with low testosterone levels. Methods: We conducted a 10 week trial in a 2 by 2 factorial design, randomizing 53 patients to replacement doses of testosterone enanthate (100 mg weekly) or placebo, as well as to a program of lower extremity resistance training or no exercise. We performed rest and exercise cardiac computed tomography (CCT) studies before and after 10 weeks of therapy to evaluate right and left heart function. Patients were injected with 40-50 ml of non-ionic, iodinated contrast and cine CCT images were obtained at rest. Patients were exercised to 60% of their maximal work rate on a semi-supine ergometer, then re-injected with another bolus of 40-50 ml of contrast and re-imaged. We evaluated cardiac output and left ventricular (LV) and right ventricular (RV) mass, LV and RV stroke volume, ejection fractions and end-diastolic volumes at rest and exercise, before and after therapy. Results: 42 men with COPD (mean FEV1=40%pred. pre-bronchodilator) and low testosterone levels (mean=320ng/dl) completed the 10 week protocol. Factorial analysis demonstrated that testosterone, but not resistance training increased LV and RV mass (by 4.9% and 8.3%, respectively). Resistance training, but not testosterone, was associated with increased LV ejection fraction at rest and during exercise (by 5.5% and 4.4%, respectively). In the entire study group, increases in both left and right ventricular mass were correlated with increases in lean body mass (assessed by DEXA) (r=0.49 and r=0.65, respectively). Conclusions: In men with COPD, testosterone replacement and strength training are associated with distinct alterations in cardiac structure and function. Specifically, resistance training improved ejection fraction, while testosterone increased lean body mass and LV mass.
Highlights
Testosterone therapy and resistance training have been demonstrated to improve muscle mass and strength in patients with testosterone deficiency
We hypothesized that resistance training and/or testosterone supplementation would result in significant improvements in cardiac mass and/or ejection fraction assessed by cardiac CT
In the entire study group, increases in both left and right ventricular mass were correlated with increases in lean body mass (r=0.49 and r=0.65, respectively)
Summary
Testosterone therapy and resistance training have been demonstrated to improve muscle mass and strength in patients with testosterone deficiency. The effects on cardiac mass and contractility of these interventions have not been identified in prospective placebo-controlled trials. The hypothesis of this trial was that resistance training and testosterone replacement would improve cardiac mass and contractility in male COPD patients with low testosterone levels. Men with COPD have been shown to have low testosterone levels which may further contribute to low muscle mass and muscle weakness. The hypothesis of the present study was that resistance training and testosterone replacement would increase cardiac mass and function while improving muscle mass and strength of the muscles of ambulation in a cohort of men with COPD whose circulating testosterone level was low. We hypothesized that resistance training and/or testosterone supplementation would result in significant improvements in cardiac mass and/or ejection fraction assessed by cardiac CT
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