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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Low Testosterone and Cardiac Dysfunction
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<blockquote data-quote="Jinzang" data-source="post: 135583" data-attributes="member: 12925"><p>It's been known that men with low testosterone levels are more likely to have caridac problems. However, it has not been clear if there is a causal relationship. Does low testosterone cause cardiac problems or is it only a marker for other health problems associated with cardiac problems, such as obesity? This <a href="https://www.physiology.org/doi/abs/10.1152/ajpheart.00471.2018" target="_blank">mouse study</a> establishes a mechanism by which low testosterone can cause diastolic dysfunction:</p><p></p><p>"The impact of long-term gonadectomy (GDX) on cardiac contractile function was explored in the setting of aging. Male mice had a bilateral GDX or sham-operation (4 weeks) and were investigated at 16-18 months. Ventricular myocytes were field stimulated (2 Hz; 37°C). Peak Ca2+ transients (fura-2) and contractions were similar in GDX and sham, although Ca2+ transients (50% decay time=45.2 ± 2.3 vs. 55.6 ± 3.1 ms; p<0.05) and contractions (tau=39.1 ± 3.2 vs. 69.5 ± 9.3 ms; p<0.05) were prolonged in GDX. Action potential duration was increased in GDX myocytes but this did not account for prolonged responses, as Ca2+ transient decay was slow even when GDX cells were voltage-clamped with simulated "sham" action potentials. Western blots of proteins involved in Ca2+ sequestration and efflux showed that Na+-Ca2+ exchanger and sarco-endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) protein levels were unaffected, while phospholamban was dramatically higher in aging GDX ventricles (0.24 ± 0.02 vs. 0.86 ± 0.13; p<0.05). Myofilament Ca2+ sensitivity at physiological Ca2+ was similar, but phosphorylation of essential myosin light chain (ELC/MLC-1) was reduced by ≈50% in aging GDX hearts. M-mode echocardiography showed no change in systolic function (<em>e.g.</em> ejection fraction). Critically, pulse wave Doppler echocardiography showed that GDX slowed isovolumic relaxation time (12.9 ± 0.9 vs. 16.9 ± 1.0 ms; p<0.05), indicative of diastolic dysfunction. Thus, dysregulation of intracellular Ca2+ and myofilament dysfunction contribute to deficits in contraction in aging hearts exposed to testosterone deficiency. This suggests that low testosterone helps promote diastolic dysfunction in the aging heart."</p></blockquote><p></p>
[QUOTE="Jinzang, post: 135583, member: 12925"] It's been known that men with low testosterone levels are more likely to have caridac problems. However, it has not been clear if there is a causal relationship. Does low testosterone cause cardiac problems or is it only a marker for other health problems associated with cardiac problems, such as obesity? This [URL='https://www.physiology.org/doi/abs/10.1152/ajpheart.00471.2018']mouse study[/URL] establishes a mechanism by which low testosterone can cause diastolic dysfunction: "The impact of long-term gonadectomy (GDX) on cardiac contractile function was explored in the setting of aging. Male mice had a bilateral GDX or sham-operation (4 weeks) and were investigated at 16-18 months. Ventricular myocytes were field stimulated (2 Hz; 37°C). Peak Ca2+ transients (fura-2) and contractions were similar in GDX and sham, although Ca2+ transients (50% decay time=45.2 ± 2.3 vs. 55.6 ± 3.1 ms; p<0.05) and contractions (tau=39.1 ± 3.2 vs. 69.5 ± 9.3 ms; p<0.05) were prolonged in GDX. Action potential duration was increased in GDX myocytes but this did not account for prolonged responses, as Ca2+ transient decay was slow even when GDX cells were voltage-clamped with simulated "sham" action potentials. Western blots of proteins involved in Ca2+ sequestration and efflux showed that Na+-Ca2+ exchanger and sarco-endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) protein levels were unaffected, while phospholamban was dramatically higher in aging GDX ventricles (0.24 ± 0.02 vs. 0.86 ± 0.13; p<0.05). Myofilament Ca2+ sensitivity at physiological Ca2+ was similar, but phosphorylation of essential myosin light chain (ELC/MLC-1) was reduced by ≈50% in aging GDX hearts. M-mode echocardiography showed no change in systolic function ([I]e.g.[/I] ejection fraction). Critically, pulse wave Doppler echocardiography showed that GDX slowed isovolumic relaxation time (12.9 ± 0.9 vs. 16.9 ± 1.0 ms; p<0.05), indicative of diastolic dysfunction. Thus, dysregulation of intracellular Ca2+ and myofilament dysfunction contribute to deficits in contraction in aging hearts exposed to testosterone deficiency. This suggests that low testosterone helps promote diastolic dysfunction in the aging heart." [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Low Testosterone and Cardiac Dysfunction
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