Aldosterone in Athletes: What Your Blood Test Is Actually Telling You
Table of Contents
Introduction: Why Aldosterone in Athletes Is Frequently Misinterpreted
Aldosterone is a clinically important hormone. Many medications that affect blood pressure also influence aldosterone physiology, and aldosterone sits behind several key mechanisms in fluid balance, electrolyte regulation, and cardiovascular control. In routine clinical practice, however, aldosterone itself is not measured very often as a standalone marker. It is more commonly assessed in specific contexts, such as endocrinology or nephrology evaluations, particularly when investigating conditions like primary aldosteronism or other disorders of mineralocorticoid regulation.
In athletes, this interpretation becomes even more nuanced. Aldosterone can behave differently from the sedentary reference population on which many laboratory ranges are based. Recent exertion, training history, hydration status, posture, dietary sodium intake, medications, and other pre-analytical conditions can all influence aldosterone and the aldosterone-to-renin ratio (ARR). Interpreting an ARR without this context risks turning a physiological training-related finding into a suspected diagnosis — or, conversely, overlooking a genuinely abnormal result.
In this article, I will explain what aldosterone and the aldosterone-to-renin ratio (ARR) actually mean in an athletic context. I will cover how acute exercise can raise these markers dramatically, how chronic training may reshape the renin-angiotensin-aldosterone system (RAAS) over time, why the ARR is so vulnerable to pre-analytical variables, and how I would approach an abnormal result on a sports blood panel in practice. For a broader overview of which hormonal and metabolic markers belong on an athlete’s panel in the first place, see the guide to which blood tests do athletes actually need.
What Is Aldosterone and How Does the RAAS Work?
Aldosterone is a mineralocorticoid hormone produced by the adrenal cortex. Its primary role is to regulate sodium and potassium balance: it promotes renal sodium retention and potassium excretion, thereby supporting extracellular fluid volume and blood pressure regulation [1]. Understanding sodium in athletes and potassium in athletes requires understanding aldosterone first — it is the hormonal driver behind both.
Renin is released from the kidney in response to decreased renal perfusion pressure, sympathetic activation, and reduced sodium delivery to the macula densa. Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II; angiotensin II stimulates aldosterone secretion from the adrenal cortex [4].
The aldosterone-to-renin ratio (ARR) compares aldosterone output against renin drive. In a healthy system, aldosterone rises and falls proportionally with renin. In primary aldosteronism (PA), aldosterone production is at least partly autonomous of normal RAAS regulation, with suppressed renin and aldosterone that is inappropriately high relative to renin, producing an elevated ARR. This is the pattern ARR is designed to screen for [1].
In clinical practice, I see aldosterone as a hormone that sits very close to everyday blood pressure management. Many commonly used medications influence aldosterone physiology, especially blood pressure medications such as ACE inhibitors and angiotensin receptor blockers. These drugs affect aldosterone indirectly through the renin-angiotensin-aldosterone system, and in many situations they can lower aldosterone activity.
I also encounter aldosterone physiology when using direct aldosterone antagonists such as spironolactone. These medications affect blood pressure and electrolyte balance by blocking aldosterone’s action. Spironolactone itself can be a somewhat tricky medication in clinical use because it may have a strong effect on electrolytes, especially potassium levels. For that reason, careful electrolyte monitoring is needed. This is also why spironolactone is usually not a first-line medication for routine hypertension, even though it can be very useful in specific indications.
From an athlete’s perspective, this matters because aldosterone is not just an abstract hormone on a lab report. It is connected to blood pressure medication, sodium and potassium balance, hydration, and even anti-doping considerations. Spironolactone, for example, has hormonal effects and is also relevant in sport because it is prohibited as a diuretic and masking agent.
Acute Exercise: The Dramatic Short-Term Rise of Aldosterone in Athletes
The single most important concept for interpreting aldosterone in athletes is the magnitude of exercise-induced RAAS activation. The effect is not modest.
In a study of four male athletes who performed three 300-metre running bouts, plasma renin activity increased 108% (range 27–230%, p < 0.05), plasma renin concentration increased 490% (range 240–800%, p < 0.01), plasma angiotensin II increased 830% (range 400–1,970%, p < 0.025), and plasma aldosterone increased 1,600% (range 160–3,920%, p < 0.02) — all measured 30 minutes post-exercise [2]. Urinary aldosterone excretion increased 120% (range 42–180%, p < 0.025) [2].
In treadmill exercise studies comparing sedentary men with moderately trained runners (15–25 miles/week) and highly trained runners (>45 miles/week), acute exercise was associated with elevations in plasma aldosterone, renin activity, potassium, and ACTH in all three groups at exercise intensities of 70 and 90% VO2max [3]. The only training-related difference was a blunted response of plasma renin activity at 90% VO2max in highly trained athletes [3].
Acute changes in aldosterone during exercise are part of normal physiology. In most athletes, these short-term changes do not have direct clinical significance on their own. More broadly, aldosterone is not commonly measured as a standalone marker in routine clinical practice. It is usually assessed in more specific settings, such as endocrine or nephrological evaluation, especially when investigating disorders like primary aldosteronism.
For that reason, acute exercise-related aldosterone changes are often more relevant as physiology than as an everyday clinical problem. In many cases, they are closer to a research-level curiosity than something that directly changes patient care. The clinical relevance appears mainly when aldosterone or the aldosterone-to-renin ratio has actually been measured, and the result is being interpreted without considering recent exercise, posture, sodium intake, medications, or other pre-analytical factors.
However, if aldosterone or the aldosterone-to-renin ratio is measured shortly after exercise, the result should be interpreted with considerable caution. A post-exercise abnormality should not be treated as diagnostic on its own. Instead, it should usually prompt repeat testing under rested, standardised conditions before any clinical conclusions are drawn. Clinicians who interpret post-marathon blood work encounter this regularly across multiple markers — aldosterone is among the most volatile.
Chronic Training and Aldosterone in Athletes: A Different Resting RAAS Phenotype
What chronic training does to aldosterone at rest is more nuanced than the acute response.
A 2023 meta-analysis of 18 randomised controlled trials comprising 803 participants found that after exercise training, plasma aldosterone was reduced (SMD −0.37; 95% CI −0.65 to −0.09; p = 0.009; n = 8 trials), plasma angiotensin-II was reduced (SMD −0.71; 95% CI −1.24 to −0.19; p = 0.008; n = 9 trials), and norepinephrine was reduced — however, plasma renin activity remained unchanged in this analysis (SMD −0.16; p = 0.585; n = 7 trials) [4]. Systolic BP was reduced (MD −6.2 mmHg; 95% CI −9.9 to −2.6; p = 0.001) and diastolic BP was also reduced (MD −4.5 mmHg; 95% CI −6.9 to −2.1; p < 0.001) [4].
A separate systematic review and meta-analysis found that plasma renin activity was reduced after exercise training across seven randomised controlled trials (SMD −0.25; 95% CL −0.5 to −0.001; p = 0.049), and noted that cross-sectional studies have reported lower plasma renin activity in athletes than in untrained subjects [5]. The evidence is therefore mixed on resting PRA: the 2023 analysis showed no change across 7 RCTs [4] while the 2015 analysis showed a reduction across a different set of 7 RCTs [5]. Claims about resting PRA in trained athletes should be made with this uncertainty in mind.
What the evidence does support is that lower renin can raise ARR arithmetically, so a borderline ratio in an athlete with normal aldosterone and no hypertension should prompt repeat testing under standardised conditions rather than immediate diagnostic escalation.
In parallel, exercise and heat acclimation alter how peripheral tissues respond to aldosterone. During 10 days of exercise and heat acclimation, the concentration and total content of sodium in sweat as well as plasma aldosterone were significantly decreased from day 1 to day 10 [6]. The study found increased sweat sodium reabsorption relative to plasma aldosterone after acclimation, which the authors interpreted as suggesting augmented eccrine gland responsiveness to aldosterone [6].
This adaptation parallels what is seen with other adrenal hormones in trained athletes. Chronic training reshapes the entire HPA and adrenal axis, not just aldosterone — the cortisol in athletes article covers the parallel story for glucocorticoids, and cortisol and overtraining addresses what happens when cumulative training stress begins to dysregulate adrenal output.
In clinical practice, I also see aldosterone as part of the broader physiology behind the blood volume changes seen in athletes. Although aldosterone itself is not commonly measured directly in routine clinical practice, its physiological effects can still be clinically relevant. Aldosterone influences sodium and water balance, and these mechanisms are closely connected to plasma volume regulation.
Endurance training can expand plasma volume, which may make haemoglobin concentration and haematocrit appear relatively low even when the athlete is not truly anaemic. This is clinically relevant because a low-normal haemoglobin or haematocrit in an endurance athlete may reflect dilution from increased plasma volume rather than reduced red blood cell mass.
Aldosterone belongs in this discussion because it regulates sodium and water retention. However, I would be careful not to say that lower aldosterone activity itself causes the increase in blood volume. More accurately, training-related plasma volume expansion changes the hormonal environment, and aldosterone may decrease as part of the body’s adjustment to a larger circulating volume.
The same physiology also helps explain why aldosterone antagonists such as spironolactone are relevant in sport. Spironolactone blocks aldosterone’s effect at the mineralocorticoid receptor, promoting sodium and water excretion while reducing potassium loss. This diuretic effect can be misused for rapid weight loss before a weigh-in, for cosmetic fluid reduction in bodybuilding, or as a masking agent in anti-doping contexts. For example, fluid manipulation can complicate the interpretation of haemoglobin and haematocrit when blood manipulation or erythropoietin use is being investigated.
For this reason, spironolactone is prohibited in sport as a diuretic and masking agent, not because it is a classic anabolic performance-enhancing drug. WADA classifies diuretics and masking agents as prohibited at all times, and USADA specifically lists spironolactone as prohibited at all times under this category [7].
Conclusion: Aldosterone in Athletes Requires Context
Aldosterone is not a hormone that is routinely measured in most athletic or general clinical blood panels, but its physiological effects are still highly relevant. It sits at the intersection of blood pressure regulation, sodium and potassium balance, plasma volume, medication effects, and anti-doping considerations. In athletes, this makes interpretation especially dependent on context.
The key point is that aldosterone should not be interpreted as an isolated number. Acute exercise can markedly activate the RAAS, while chronic training may reshape resting aldosterone and renin physiology over time. At the same time, posture, sodium intake, hydration status, recent training, medications, and menstrual cycle factors can all influence the aldosterone-to-renin ratio. A single abnormal result from a non-standardised situation should therefore be interpreted cautiously rather than treated as a diagnosis.
Clinically, aldosterone becomes most important when it has actually been measured, when ARR is being used to screen for primary aldosteronism, or when medications such as ACE inhibitors, angiotensin receptor blockers, or spironolactone are part of the picture. In athletes, it also helps explain why blood markers such as haemoglobin and haematocrit may need to be interpreted in light of plasma volume adaptation rather than judged purely against sedentary reference expectations.
My practical conclusion is simple: aldosterone in athletes is usually more about physiology and context than pathology. But when the value is abnormal, the next step should be careful interpretation, review of pre-analytical conditions, and repeat testing under standardised conditions when needed. Athletic physiology does not rule out endocrine disease, but it does demand a higher standard of interpretation before lab results are turned into diagnoses.
References
[1] https://academic.oup.com/jcem/article/110/9/2453/8196671
[2] https://pubmed.ncbi.nlm.nih.gov/972128/
[3] https://pubmed.ncbi.nlm.nih.gov/2851526/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC10844078/
[5] https://www.nature.com/articles/hr2015100
[6] https://pubmed.ncbi.nlm.nih.gov/3759782/
[7] https://www.wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf
