Hard Cardio while on AAS? Ally/Enemy/Indifferent?

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Also, not sure #1 went 5 days a week?

Experiment 1. The subjects started training after their˙VO2max and maximal accumulated oxygen deficit were measured. They exercised 5 d·wk-1 for 6 wk at an intensity that elicited 70% of each subject's ˙VO2max. The pedaling rate was 70 rpm, and the duration of the training was 60 min. As each subject's ˙VO2max increased during the training period, exercise intensity was increased from week to week as required to elicit 70% of the actual ˙VO2max. During the training, the maximal accumulated oxygen deficit was measured before, at 4 wk, and after the training. ˙VO2max was determined before and after the training and every week during the training period.

 

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Cholesterol Meds On Cycle To Keep LDL and HDL Good

Cardiac damage training. Mad props. I wonder what his blood work would show? Real life X-man.

forums.t-nation.com

 

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I just had to link this. This dude is an overachiever:

https://onlinelibrary.wiley.com/doi/10.1002/ehf2.12494

Case report​

A 53-year-old, otherwise healthy bodybuilder was seen in the emergency department with 3 months of progressive dyspnoea, palpitations, headache, and an episode of syncope. He admitted to a history of fatigue, decreased libido, and erectile dysfunction for which he had been prescribed topical androgen and sildenafil. He is employed as a firefighter, does not smoke tobacco, and uses <6 oz of alcohol per week. He is married with two children and denies any family history of cardiomyopathy. He enjoys 60–90 min of vigorous exercise daily, which predominantly involves heavy weightlifting.


Vital signs were remarkable for a regular heart rate of 90 b.p.m. and a blood pressure of 167/95 mmHg. The physical examination demonstrated a muscular man, elevated central venous pressure (12 cm H2O), normal symmetric pulses, a slightly enlarged and laterally displaced cardiac point of maximal impulse, a grade 3/6 holosystolic murmur at the apex, and a positive third heart sound. Chest X-ray revealed cardiomegaly, and a Doppler echocardiogram demonstrated a dilated left ventricle (6.9 cm) with severe global hypokinesis, left ventricular septal thickness in diastole (LVSthd) of 1.0 cm (normal < 1.2 cm), and a calculated left ventricular ejection fraction (LVEF) of 15% (Figure 1A). Colour Doppler images demonstrated severe mitral regurgitation (Figure 1B); myocardial speckle tracking showed a severely abnormal global longitudinal strain pattern (Figure 2). Of note, 3 years prior, his LVEF had been 57%.


The patient was admitted for diagnosis of new-onset heart failure, and subsequent evaluation revealed normal coronary angiogram, iron panel, and thyroid studies and negative blood viral panel (human immunodeficiency virus, Lyme disease, and hepatitis) and urine toxicology panel for illicit drugs. B-type natriuretic peptide was 303 pg/mL (normal < 100 pg/mL), and high-sensitivity troponin was 0.05 ng/mL (normal < 0.05 ng/mL) on initial presentation.


The patient was referred to the Advanced Heart Failure Therapy program at Aurora St. Luke's Hospital, Milwaukee, WI. Upon further questioning, the patient admitted to a 3 year history of routine intramuscular androgen administration for bodybuilding. A testosterone level was obtained and documented at 30 160.0 ng/dL (normal 280–1100 ng/dL). The patient was counselled extensively about the cardiovascular risks associated with AAS use. AAS use was discontinued, and he was started on guideline-directed medical therapy (GDMT) with comprehensive neurohormonal blockade with a focus on maximum tolerated doses of carvedilol; final doses of therapy were lisinopril 5 mg daily, spironolactone 25 mg daily, and carvedilol 25 mg twice daily. Subsequent outpatient care documented resolution of the patient's symptoms by 3 months. A repeat Doppler echocardiogram at 6 months indicated a normal LV dimension (4.5 cm) with improved cardiac function (LVEF of 53%) and LVSthd of 0.9 cm (normal < 1.2 cm), resolution of mitral regurgitation (Figure 3A,B), and improvement in, but not normalization of, the global longitudinal strain pattern (Figure 4). Subsequent clinical testing revealed testosterone level of 603.7 ng/dL and normalization of B-type natriuretic peptide (19 pg/mL).

Regardless of whether or not a testosterone level that high can directly cause heart failure, a "blood pressure of 167/95 mmHg," sustained for several years can. If I had to bet, it was his (likely) sustained hypertension that caused the heart failure. The testosterone likely caused or worsened his hypertension.