Your blood pressure is one of the most direct windows into your cardiovascular readiness to perform. Even readings in the high-normal range quietly increase cardiac workload, reduce arterial compliance, and blunt the efficiency of oxygen delivery during exercise. A natural compound with a well-characterised mechanism and a consistent reduction of 6 to 10 mmHg across dozens of trials is worth understanding precisely.

Why Blood Pressure Quietly Limits Athletic Performance

Blood pressure is typically framed as a health concern for older adults managing cardiovascular disease. For active people and athletes, it rarely gets the same attention — and that gap is a mistake. Arterial stiffness and elevated blood pressure do not simply raise cardiovascular risk; they reduce the mechanical efficiency of the cardiovascular system in ways that directly affect performance. Every beat of the heart has to work harder against a stiffer system. The heart's output per contraction falls. Oxygen delivery to working muscle becomes less efficient. Recovery between hard efforts slows.

The problem is not confined to people with clinically diagnosed hypertension. High-normal blood pressure — readings between 120–129 mmHg systolic — is increasingly common in active adults who train intensely, especially during phases of high training load, poor sleep, or elevated life stress. In this range, the vascular system is less compliant than optimal, nitric oxide (NO) bioavailability is often reduced, and endothelial responsiveness to exercise is blunted. The athlete does not feel ill. But the physiology is not performing at its ceiling.

The two amino acids at the centre of this article — L-arginine and L-citrulline — address this problem through the most fundamental mechanism of vascular control: nitric oxide synthesis. The question is whether they do so reliably enough, and in the right populations, to be worth considering as part of a cardiovascular foundation strategy.

Two Amino Acids, One Pathway

L-arginine is a semi-essential amino acid and the sole substrate for endothelial nitric oxide synthase (eNOS), the enzyme that produces NO in vascular tissue. NO diffuses into the surrounding smooth muscle, triggering relaxation and vasodilation — the fundamental mechanism that lowers vascular resistance and blood pressure. L-citrulline is arginine's metabolic partner: a non-essential amino acid produced as a byproduct of NO synthesis and found in high concentrations in watermelon. What makes citrulline scientifically interesting is not where it comes from but how it behaves in the body. Unlike oral arginine, which is heavily degraded by arginase enzymes in the intestine and liver before reaching the bloodstream, citrulline bypasses this first-pass extraction almost entirely. It travels to the kidneys, where it is converted back into arginine — cleanly, efficiently, and without the metabolic losses that limit oral arginine's bioavailability.

The pharmacokinetic evidence for this advantage is strong. Schwedhelm et al. (2008) demonstrated in a double-blind crossover trial that oral L-citrulline at 3 g raised plasma arginine concentrations and improved the arginine-to-ADMA ratio more effectively than an equivalent dose of oral arginine. ADMA (asymmetric dimethylarginine) is a naturally occurring inhibitor of eNOS; raising the arginine-to-ADMA ratio restores the balance in favour of NO production. This is why combining both amino acids makes pharmacokinetic sense — arginine provides immediate substrate for eNOS while citrulline sustains systemic arginine availability over subsequent hours through renal conversion, extending the window of NO-pathway support.

How Arginine and Citrulline Lower Blood Pressure: Four Mechanisms

What the Clinical Research Shows

The evidence base for blood pressure effects of arginine and citrulline is substantially larger than for ergogenic performance outcomes, and the effect sizes are proportionally larger too. Meta-analytic data now span over 35 RCTs when arginine and citrulline studies are combined, with consistent directionality and clinically meaningful magnitudes. A reduction of 6 to 10 mmHg in systolic blood pressure is comparable to the effect of regular aerobic exercise, a dietary sodium reduction of approximately 2 g/day, or some first-line antihypertensive medications — making these findings noteworthy for athletes and active individuals, not just clinical populations.

It is worth being clear about the populations where this evidence is strongest: hypertensive adults, postmenopausal women, overweight individuals, and people with type 2 diabetes. These are populations with established endothelial dysfunction — reduced baseline NO bioavailability, elevated ADMA, and impaired vascular reactivity. In healthy young adults with normal blood pressure, the evidence for meaningful BP reduction is limited. That said, for the large and growing segment of active adults with borderline or elevated readings, the evidence is directly relevant.

What This Means for Active People and Athletes

A reduction of 6 mmHg in resting systolic blood pressure is not merely a number on a cuff. Research in large epidemiological cohorts consistently shows that a 5–6 mmHg reduction in SBP is associated with approximately a 15–20% reduction in stroke risk and a 10% reduction in coronary heart disease risk over time. For athletes whose cardiovascular system is under sustained demand, lower resting blood pressure also translates directly into reduced cardiac workload per beat, more compliant arteries that buffer the pulse wave more efficiently, and a cardiovascular system that has more reserve during intense effort. The impact at high-normal readings — not just clinical hypertension — is less studied but mechanistically plausible through the same NO pathway.

The timing and population specificity of the evidence are important to understand honestly. The strongest blood pressure effects are consistently found in populations with some degree of endothelial dysfunction: hypertensive adults, postmenopausal women, and overweight or diabetic individuals. Porto et al. (2025) found no hemodynamic effects with an acute 3 g arginine dose in healthy young men — reinforcing that a well-functioning vascular system with normal NO production at rest does not respond the same way. For athletes in this category, the cardiovascular rationale is less about acute blood pressure lowering and more about long-term vascular maintenance, especially during periods of high training stress when oxidative load is elevated and endothelial function can temporarily deteriorate. Whether this translates to measurable acute BP reduction in trained normotensive athletes has not been established.

The practical implication is a segmented view of who this evidence speaks most directly to: active adults with borderline-elevated readings, older athletes managing cardiovascular risk alongside performance goals, and individuals coming back from surgery or enforced rest where deconditioning may have shifted their vascular baseline. For this group, supplementing with arginine and citrulline in the context of regular exercise — as Hambrecht et al. (2000) demonstrated in heart failure patients, and Kang et al. (2022) showed in hypertensive postmenopausal women — may produce additive benefits beyond either intervention alone.

The Evidence-Based Protocol

What the Research Doesn’t Yet Tell Us

Three limitations stand out as particularly relevant for anyone using this evidence to inform their supplementation decisions. First, the dose-response ceiling and the attenuation at 24 days in the Shiraseb 2022 arginine data are unexplained and counterintuitive. The most credible hypothesis is compensatory upregulation of arginase — the enzyme that breaks down arginine — with chronic high-dose exposure, effectively restoring the baseline arginine-to-ADMA equilibrium and negating the initial vascular benefit. If confirmed, this would imply that cycling or periodising arginine supplementation may be more effective than continuous use, but no trial has tested this directly. Second, the blood pressure evidence for citrulline alone is still evolving. The Mirenayat 2018 null finding from only five trials was a legitimate scientific position at the time; the more recent Luo 2025 and Bahari 2026 analyses have shifted the balance considerably, but the evidence for citrulline alone on brachial blood pressure in mixed populations remains categorised as Moderate rather than High. Third, no study has tested the specific combination of 10 g L-arginine and 3 g L-citrulline twice daily as a protocol — the combined-supplementation subgroup analysis in Luo 2025 pooled heterogeneous trial designs.

A further caveat that no review can responsibly omit: virtually all of the positive blood pressure findings come from populations with some degree of baseline endothelial dysfunction. Porto et al. (2025) found no hemodynamic effect in healthy young men with an acute dose, and multiple studies in well-trained, normotensive individuals have shown null results. The research has not yet established whether arginine or citrulline meaningfully lowers blood pressure in healthy athletes with already-optimal vascular function — and it may be that the answer is it does not, at least acutely. That is an honest limitation, not a reason to dismiss the evidence for those who may benefit most.