Systolic Blood Pressure

When high

Confirm it is real first:

• Repeat over 5-7 days at the same time of day. Single readings are unreliable, and white-coat effect is common.
• Correct technique: seated, feet flat, back supported, arm at heart level, no caffeine or training in the preceding 30 minutes. A cuff that is too small for a large arm reads falsely high, which catches out many lifters.

Address the driver, not just the number:

• Check Haematocrit and Haemoglobin. Raised haematocrit thickens blood and drives pressure up. Treating that often fixes the blood pressure without any antihypertensive.
• Reduce or drop the offending compound where possible. Trenbolone and oral AAS are frequent causes, and the effect is usually reversible.
• Sodium and water balance. Aromatising compounds drive retention; managing oestradiol sensibly (not crashing it) helps. See Estradiol.
• Stimulants including clenbuterol and high-dose caffeine raise it acutely and are easy to overlook.

Lifestyle levers with real effect sizes:

• Regular steady-state cardio, 150 min/week, typically lowers systolic by 5-8 mmHg
• Sodium reduction toward 2g/day, 3-5 mmHg
• Weight loss where applicable, roughly 1 mmHg per kg
• Alcohol reduction, 3-4 mmHg in regular drinkers

Supplements:

• Citrulline malate -- 6-8g/day, modest reduction via nitric oxide
• Magnesium -- 300-400mg/day, small effect, larger if deficient
• Taurine -- 3g/day, some evidence in mild hypertension
• Omega-3 -- 2-3g/day EPA/DHA combined

Pharmacological options (physician-supervised):

• Telmisartan -- ARB, 40-80mg/day. Popular in this population because it does not blunt training adaptation, and its PPAR-gamma activity may modestly help lipids and insulin sensitivity. Monitor Potassium and Creatinine.
• Nebivolol -- beta-blocker with nitric-oxide-mediated vasodilation, 5-10mg/day. Less impact on lipids, glucose, and erectile function than older beta-blockers, though any beta-blocker can blunt maximal heart rate and perceived training capacity.
• Avoid non-selective beta-blockers and thiazides as first choice here, given their lipid and glucose effects on top of what AAS already do.

When it is urgent:

• Readings persistently above 180 systolic, or above 160 alongside headaches, visual changes, or chest symptoms, warrant same-day medical review rather than a supplement plan.

References:

• Whelton, P. K., Carey, R. M., Aronow, W. S., et al. (2018). 2017 ACC/AHA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Hypertension, 71(6), e13-e115. DOI: 10.1161/HYP.0000000000000065
• Achar, S., Rostamian, A., & Narayan, S. M. (2010). Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. American Journal of Cardiology, 106(6), 893-901. DOI: 10.1016/j.amjcard.2010.05.013
• Rasmussen, J. J., Schou, M., Madsen, P. L., et al. (2018). Increased blood pressure and aortic stiffness among abusers of anabolic androgenic steroids. Journal of Hypertension, 36(7), 1470-1477. DOI: 10.1097/HJH.0000000000001728

When low

Low systolic pressure (below 90 mmHg):

• Often benign in trained individuals with good cardiovascular fitness, particularly if you have no symptoms.
• Symptomatic low pressure (dizziness on standing, fainting, persistent fatigue) is worth investigating.

Common causes in this population:

• Aggressive diuretic use, especially before a show. This is genuinely dangerous and a common cause of collapse.
• Over-treatment with an antihypertensive after the underlying driver was already removed. If you dropped the compound that raised your pressure but stayed on the medication, the dose likely needs revisiting.
• Dehydration, or a very low sodium intake combined with heavy sweating.
• Adrenal insufficiency after prolonged corticosteroid use.

Action:

• Check Sodium and Potassium if diuretics are involved.
• Review any antihypertensive dose with the prescriber rather than stopping abruptly.