Reduction in Circulating Testosterone Relates to Exercise Capacity in Men With Chronic Heart Failure |
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| Authors: | Ewa A. Jankowska Gerasimos Filippatos Beata Ponikowska Ludmila Borodulin-Nadzieja Stefan D. Anker Waldemar Banasiak Philip A. Poole-Wilson Piotr Ponikowski |
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| Affiliation: | 1. Staten Island University Hospital, Staten Island, NY, USA;2. University of Arkansas for Medical Sciences, Little Rock, AR, USA;3. Detroit Medical Center, Detroit, MI, USA;1. Heart Diseases Biomedical Research Group, Program of Research in Inflammatory and Cardiovascular Disorders, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain;2. Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain;3. Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands;4. Center for Heart Diseases, Military Hospital, Wroclaw, Poland;5. Department of Heart Diseases, Wroclaw Medical University, Poland;6. Laboratory for Applied Research on Cardiovascular System, Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland;1. Department for Heart Diseases, Wroclaw Medical University, Wroclaw, Poland;2. Cardiology Department, Centre for Heart Diseases, Military Hospital, Wroclaw, Poland;1. Department of Cardiology, Gulhane Medical Academy, Ankara, Turkey;2. Department of Pulmonary Medicine, Gulhane Medical Academy, Ankara, Turkey;3. Department of Internal Medicine, Gulhane Medical Academy, Ankara, Turkey;4. Gulhane Medical Academy, Department of Clinical Chemistry, Ankara, Turkey |
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| Abstract: | BackgroundWe investigated whether anabolic deficiency was linked to exercise intolerance in men with chronic heart failure (CHF). Anabolic hormones (testosterone, dehydroepiandrosterone sulfate, insulin-like growth factor 1 [IGF1]) contribute to exercise capacity in healthy men. This issue remains unclear in CHF.Methods and ResultsWe studied 205 men with CHF (age 60 ± 11 years, New York Heart Association [NYHA] Class I/II/III/IV: 37/95/65/8; LVEF [left ventricular ejection fraction]: 31 ± 8%). Exercise capacity was expressed as peak oxygen consumption (peak VO2), peak O2 pulse, and ventilatory response to exercise (VE-VCO2 slope). In multivariable models, reduced peak VO2 (and reduced peak O2 pulse) was associated with diminished serum total testosterone (TT) (P < .01) and free testosterone (eFT; estimated from TT and sex hormone globulin levels) (P < .01), which was independent of NYHA Class, plasma N-terminal pro-brain natriuretic peptide, and age. These associations remained significant even after adjustment for an amount of leg lean tissue. In multivariable models, high VE-VCO2 slope was related to reduced serum IGF1 (P < .05), advanced NYHA Class (P < .05), increased plasma NT-proBNP (P < .0001), and borderline low LVEF (P = .07). In 44 men, reassessed after 2.3 ± 0.4 years, a reduction in peak VO2 (and peak O2 pulse) was accompanied by a decrease in TT (P < .01) and eFT (P ≤ .01). Increase in VE-VCO2 slope was related only to an increase in plasma NT-proBNP (P < .05).ConclusionsIn men with CHF, low circulating testosterone independently relates to exercise intolerance. The greater the reduction of serum TT in the course of disease, the more severe the progression of exercise intolerance. Whether testosterone supplementation would improve exercise capacity in hypogonadal men with CHF requires further studies. |
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