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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Hard Cardio while on AAS? Ally/Enemy/Indifferent?
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<blockquote data-quote="tareload" data-source="post: 230237"><p>Chronic HIIT + AAS a recipe for disaster?</p><p></p><p>[URL unfurl="true"]https://forums.t-nation.com/t/importance-of-cardio-for-heart-health/275825/7[/URL]</p><p></p><p>[URL unfurl="true"]https://www.acc.org/latest-in-cardiology/articles/2021/05/19/12/30/non-ischemic-myocardial-fibrosis-in-athletes[/URL]</p><p></p><p><em>Myocardial fibrosis or scar is characterized by the accumulation of collagen in the extracellular matrix as a result of myocardial damage from a range of pathologies. The patterns of fibrosis can be broadly classified as reactive or replacement fibrosis.1 Reactive fibrosis is characterized by the synthesis of collagen by myocytes in response to cardiac stress from aging, pressure or volume overload, reactive oxygen species, or the renin-angiotensin aldosterone system and beta-adrenergic system. In replacement fibrosis, myocytes damaged by ischemia or viral infection are replaced by collagen. Reactive fibrosis may progress to replacement fibrosis.1 Replacement fibrosis can be localized as in myocardial infarction or can be more diffuse following systemic conditions such as viral myocarditis.</em></p><p><em></em></p><p><em>Myocardial fibrosis reduces ventricular compliance, the downstream effects of which include heart failure with preserved or reduced ejection fraction, atrial enlargement, atrial fibrillation, and ventricular arrhythmias. Replacement myocardial fibrosis can be easily identified using magnetic resonance imaging (MRI) after the injection of gadolinium-based contrast agents (late gadolinium enhancement [LGE]). The presence of myocardial LGE is an emerging risk factor for future cardiac events and mortality in multiple pathologic states in the non-athletic population.2 Reactive fibrosis, on the other hand, is a more diffuse process and may not be easily detected using LGE. Recent developments in nonparametric cardiac MRI techniques such as T1 mapping (myocardial T1 and extracellular volume [ECV] measurements) allow for identification and quantification of diffuse reactive fibrosis. T1 relaxation time varies in relation to the composition of the myocardium and rises with any increase in fibrotic tissue. T1 maps can depict even relatively small variations of T1 within the heart to highlight tissue pathology. T1 mapping performed before and after the injection of a contrast agent allows measurement of ECV, which quantifies the relative expansion of extracellular matrix as a result of diffuse reactive fibrosis.3</em></p><p><em></em></p><p><em>Emerging data in athletes suggest that prolonged, high-intensity exercise may also cause cardiac damage and fibrosis even in the absence of predisposition to cardiac disease.4 One animal study looking at rats that were forced to run for 16 weeks (equivalent to 10 years of endurance exercise training in humans) demonstrated the development of eccentric cardiac hypertrophy, myocardial fibrosis and inducible ventricular tachycardia in 42% of the rats. Interestingly, the fibrotic changes were reversed after an 8-week exercise cessation.5 Not all studies, however, support this hypothesis.6,7 Athletes with LGE tend to be older than athletes without LGE. The prevalence of LGE also increases with years of competitive exercise training and the number of completed endurance events.8</em></p></blockquote><p></p>
[QUOTE="tareload, post: 230237"] Chronic HIIT + AAS a recipe for disaster? [URL unfurl="true"]https://forums.t-nation.com/t/importance-of-cardio-for-heart-health/275825/7[/URL] [URL unfurl="true"]https://www.acc.org/latest-in-cardiology/articles/2021/05/19/12/30/non-ischemic-myocardial-fibrosis-in-athletes[/URL] [I]Myocardial fibrosis or scar is characterized by the accumulation of collagen in the extracellular matrix as a result of myocardial damage from a range of pathologies. The patterns of fibrosis can be broadly classified as reactive or replacement fibrosis.1 Reactive fibrosis is characterized by the synthesis of collagen by myocytes in response to cardiac stress from aging, pressure or volume overload, reactive oxygen species, or the renin-angiotensin aldosterone system and beta-adrenergic system. In replacement fibrosis, myocytes damaged by ischemia or viral infection are replaced by collagen. Reactive fibrosis may progress to replacement fibrosis.1 Replacement fibrosis can be localized as in myocardial infarction or can be more diffuse following systemic conditions such as viral myocarditis. Myocardial fibrosis reduces ventricular compliance, the downstream effects of which include heart failure with preserved or reduced ejection fraction, atrial enlargement, atrial fibrillation, and ventricular arrhythmias. Replacement myocardial fibrosis can be easily identified using magnetic resonance imaging (MRI) after the injection of gadolinium-based contrast agents (late gadolinium enhancement [LGE]). The presence of myocardial LGE is an emerging risk factor for future cardiac events and mortality in multiple pathologic states in the non-athletic population.2 Reactive fibrosis, on the other hand, is a more diffuse process and may not be easily detected using LGE. Recent developments in nonparametric cardiac MRI techniques such as T1 mapping (myocardial T1 and extracellular volume [ECV] measurements) allow for identification and quantification of diffuse reactive fibrosis. T1 relaxation time varies in relation to the composition of the myocardium and rises with any increase in fibrotic tissue. T1 maps can depict even relatively small variations of T1 within the heart to highlight tissue pathology. T1 mapping performed before and after the injection of a contrast agent allows measurement of ECV, which quantifies the relative expansion of extracellular matrix as a result of diffuse reactive fibrosis.3 Emerging data in athletes suggest that prolonged, high-intensity exercise may also cause cardiac damage and fibrosis even in the absence of predisposition to cardiac disease.4 One animal study looking at rats that were forced to run for 16 weeks (equivalent to 10 years of endurance exercise training in humans) demonstrated the development of eccentric cardiac hypertrophy, myocardial fibrosis and inducible ventricular tachycardia in 42% of the rats. Interestingly, the fibrotic changes were reversed after an 8-week exercise cessation.5 Not all studies, however, support this hypothesis.6,7 Athletes with LGE tend to be older than athletes without LGE. The prevalence of LGE also increases with years of competitive exercise training and the number of completed endurance events.8[/I] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Hard Cardio while on AAS? Ally/Enemy/Indifferent?
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