Albumin in Athletes: What Low Levels on Your Blood Test Really Mean
Table of Contents
Introduction
In my clinical work, I often notice that many patients — and even athletes — associate albumin primarily with urine testing, particularly in the context of kidney health. Far fewer have a clear understanding of what albumin actually does in the bloodstream. Outside of specific clinical situations such as renal or systemic disease, I find that serum albumin is measured relatively infrequently and often receives little attention in otherwise healthy individuals.
At the same time, albumin is a protein whose concentration, synthesis rate, and redox state shift simultaneously in response to training load, nutritional adequacy, and systemic inflammation. In athletes, this makes albumin a uniquely context-dependent marker — one that I believe cannot be interpreted meaningfully using standard population-based reference ranges alone.
In this article, I explain the physiology of albumin in athletes, why standard reference ranges can be misleading, how to interpret a low result in the athletic context, and which interventions are most likely to influence it.
What Albumin Actually Does — and Why It Matters for Athletes
Albumin is the most abundant circulating protein found in plasma, representing half of the plasma’s total protein content (3.5 g/dL to 5 g/dL) in healthy human patients [1]. Liver hepatocytes synthesise albumin and rapidly excrete it into the bloodstream at about 10 g to 15 g per day [1]. Its functions span three interrelated domains directly relevant to athletic performance.
The first is oncotic pressure and plasma volume regulation. Albumin is the dominant determinant of colloid osmotic pressure in blood, attracting and retaining water within the intravascular compartment. This function sits at the heart of training adaptation: exercise-induced plasma volume expansion is mechanistically linked to albumin. After a single bout of intense intermittent exercise (eight 4-min bouts at 85% maximal O₂ uptake with 5-min recovery periods), plasma albumin content was elevated by 0.17 ± 0.04 g/kg body weight at 1 hour of recovery, accounting for the entire increase in total plasma protein content [2]. At 24 hours of recovery, plasma volume was expanded by 4.5 ± 0.7 ml/kg body weight (10 ± 1%), and plasma albumin content was increased by 0.19 ± 0.05 g/kg body weight. If 1 g of albumin holds 18 ml of water, this increase in plasma albumin content can account for a 3.4-ml/kg body weight expansion of the plasma volume [2]. This mechanism is directly related to the dilutional pseudoanemia that is commonly observed in endurance-trained athletes.
In my clinical work, the importance of albumin becomes particularly evident in patients with kidney disease and those with ascites. In these settings, reduced albumin levels contribute to a loss of colloid oncotic pressure, allowing fluid to move from the intravascular space into the interstitial tissues and body cavities, such as the peritoneal cavity.
In patients with ascites, this often becomes clinically apparent as visible abdominal distension. More broadly, this shift in fluid balance can present as progressive oedema or fluid accumulation. In more severe cases, albumin replacement may be considered as part of the overall management strategy, particularly when intravascular volume balance is compromised.
The second function is transport. Albumin carries free fatty acids, bilirubin, ions, and many drugs through the circulation [1]. During sustained aerobic exercise, free fatty acid mobilisation from adipose tissue relies substantially on albumin as the plasma carrier.
The third function — and perhaps least appreciated in sports contexts — is antioxidant defence. Human serum albumin (HSA) contains a single free cysteine residue at position 34 (Cys34), which constitutes the most abundant thiol of plasma. This redox thiol group, in connection with the high concentration of HSA in the circulation, accounts for 80% of thiols in plasma, constituting the major extracellular source of reactive free thiol [3]. Working as a free radical scavenger, the Cys34 residue is able to trap multiple reactive oxygen and nitrogen species, such as hydrogen peroxide (H₂O₂), peroxynitrite (ONOO⁻), superoxide, or hypochlorous acid (HOCl) [3]. For athletes generating substantial oxidative stress during heavy training blocks, this function is not trivial.
From a clinical perspective, albumin is often most familiar in the context of urine testing rather than serum measurements. In everyday practice, clinically significant hypoalbuminaemia is relatively uncommon in otherwise healthy individuals. In my experience, it is only in more advanced disease states that low serum albumin becomes clearly clinically relevant. This is most often seen in patients with significant kidney disease or in those with ascites, where reduced albumin contributes to fluid shifts and becomes part of the overall clinical picture.
Why Albumin in Athletes Looks Different on a Blood Test
The standard clinical reference range for albumin (35–50 g/L) was established in largely sedentary or non-athletic populations. Contextualising albumin levels, traditionally defined for sedentary or non-athlete populations, for athletes training or competing is important for interpreting the implications of either decreased or elevated plasma albumin [4].
The central complication is plasma volume expansion. Endurance exercise stimulates mainly the synthesis of albumin and globulins produced by the liver, resulting in an expansion of the plasma volume [5]. In a study of 49 sedentary subjects and 40 endurance athletes (long- and middle-distance runners, cyclists), the plasma volume in sedentary subjects was 42.7 (35.8–51.7) ml/kg body weight as compared to 54.6 (46.7–65.9) ml/kg body weight in athletes, while total protein concentrations were 71.0 (66.5–77.1) g/L in sedentary subjects and 69.0 (64.8–75.2) g/L in athletes [5]. The total intravascular mass of proteins was 22% higher in athletes despite the lower concentration — a direct consequence of dilution into an expanded plasma compartment [5].
This is the same physiological mechanism that drives dilutional pseudoanemia in endurance sport: plasma expands faster than the cellular and protein fractions, depressing concentration-based values without any true deficit. A well-trained endurance runner with an albumin of 38 g/L may therefore carry an entirely adequate — or even increased — total intravascular albumin mass, despite a value that a non-sports clinician might flag as borderline low.
The timing of the blood draw adds another layer. Dehydration results in a reduction of the circulating plasma volume (PV), which may lead to artificially high values of some blood parameters [6]. Conversely, a sample drawn immediately post-exercise reflects haemoconcentration rather than true baseline albumin status. For detailed guidance on preparing blood tests correctly as an athlete, including fasting, hydration, and timing relative to training, this matters considerably. For meaningful albumin interpretation, athletes should be sampled fasted, well-hydrated, and in a rested state.
However, it is worth noting that, in athletes, changes in serum albumin are rarely clinically significant in isolation. In most cases, they are better understood as contextual findings rather than markers of pathology. In practical terms, these fluctuations are often little more than clinical curiosities and do not, in themselves, usually lead to specific therapeutic interventions.
More broadly, in routine clinical practice, serum albumin is not measured particularly frequently outside specific indications. It is most often assessed in the context of proteinuria, unexplained oedema, or suspected systemic disease, typically within internal medicine or nephrology settings. In primary care, it may still be encountered in patients with advanced chronic conditions, such as long-standing diabetes or chronic kidney disease.
The Causes of Low Albumin in Athletes
It is also worth remembering that there is no athlete-specific indication for measuring serum albumin. In my clinical practice, the reasons for testing do not differ from those in the general population.
However, when albumin is measured in an athlete and a genuinely low value is confirmed under standardised sampling conditions, I approach it in the same structured way as in any otherwise healthy individual. In these cases, three main mechanisms warrant consideration.
Inadequate protein intake. Protein deficiency decreases blood proteins, especially albumin, and low protein intake seems to decrease the rate of albumin synthesis [4]. In the absence of disease, low blood protein, low albumin, and elevated urea nitrogen may be indicative of insufficient protein intake in athletes [4]. A habitual protein intake of 1.5 g/kg of body mass (BM)⁻¹·day⁻¹ is typical in male and female endurance athletes; however, contemporary protein requirement studies suggest a daily protein intake of approximately 1.8 g·kgBM⁻¹·day⁻¹ should be advocated for endurance athletes, with the caveat that requirements may be further elevated in excess of 2.0 g·kgBM⁻¹·day⁻¹ during periods of carbohydrate-restricted training [7]. Athletes pursuing weight-category sports, plant-based diets without careful planning, or aggressive caloric restriction during competition preparation are particularly vulnerable. This pattern also overlaps substantially with RED-S and the female athlete triad, where low energy availability drives multiple concurrent blood test changes.
A similar physiological pattern can be observed in states of overt malnutrition, where insufficient dietary protein limits albumin synthesis. In severe cases, this may contribute to the development of oedema or ascites despite an otherwise cachectic body composition. In practice, however, this is something I encounter only rarely. In high-income settings, such presentations are uncommon, but they remain well recognised in more extreme conditions such as famine or advanced malnutrition.
Systemic inflammation. Albumin is a negative acute-phase reactant, and its reduction accompanies inflammatory processes [8]. Elevated inflammatory cytokines — including interleukin-6 — suppress albumin gene expression in hepatocytes while stimulating the production of positive acute-phase proteins such as C-reactive protein and serum amyloid A [8]. In the context of high training loads or inadequate recovery, sustained elevation of these inflammatory signals may contribute to gradual albumin decline. Notably, the same IL-6-driven response that suppresses albumin is also responsible for the hepcidin spike that impairs iron absorption in the hours following training. Albumin should therefore be interpreted alongside CRP and inflammatory markers and training load records — a low albumin in athletes with concurrent elevated CRP in an underperforming individual warrants careful evaluation.
In my clinical experience, however, inflammation-related changes in albumin are rarely clinically significant on their own or lead to specific interventions. More pronounced and clinically relevant reductions are typically seen in pathological states such as nephritis or nephrotic syndrome, where renal protein loss becomes a dominant mechanism.
Other contributors. Additional causes — including gastrointestinal protein loss, liver dysfunction, and renal protein wasting — should enter the differential if nutritional and training-related explanations are insufficient. These mechanisms are not specific to athletes, although they may of course occur in athletic populations.
In my clinical practice, the investigation of these conditions follows standard medical protocols. Athlete status does not meaningfully alter the diagnostic approach, and evaluation proceeds according to established clinical pathways, including appropriate liver and renal function testing.
Conclusion
In my clinical work, albumin is a marker that rarely draws attention in isolation — and in athletes, this is especially true. Most changes in serum albumin reflect underlying physiology rather than pathology, particularly the combined effects of plasma volume expansion, training load, nutritional status, and low-grade inflammation.
For this reason, albumin should not be interpreted as a standalone value in athletic populations. A low-normal result in a well-trained endurance athlete is often a consequence of training adaptation rather than deficiency, while transient fluctuations may simply reflect recent training or hydration status rather than any clinically meaningful process.
At the same time, when a genuinely low albumin is identified under appropriate conditions, the approach should remain firmly grounded in general clinical medicine. In my practice, I do not treat athletes differently in this regard — the same core mechanisms apply: inadequate protein or energy intake, systemic inflammation, or less commonly, underlying pathology affecting the liver, kidneys, or gastrointestinal system.
Ultimately, albumin is best understood as a contextual marker. Its value lies not in the number itself, but in how it fits within the broader clinical picture — including training history, nutritional intake, inflammatory markers, and overall performance status. When interpreted in this way, it can provide useful supporting information. When taken out of context, it is far more likely to mislead than to inform.
Bibliography
[1] https://www.ncbi.nlm.nih.gov/books/NBK459198/
[2] https://doi.org/10.1152/jappl.1991.71.5.1914
[3] https://doi.org/10.1186/2110-5820-3-4
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC5640004/
[5] https://pubmed.ncbi.nlm.nih.gov/1001317/
[6] https://doi.org/10.1002/dta.2571
