IGF-1 in Athletes: What Your Blood Test Is Really Telling You
Table of Contents
Key Takeaways: IGF-1 in Athletes
- IGF-1 in athletes is biologically interesting, but it should not be treated as a routine performance marker or optimization target.
- Athletic status alone is not a medical indication to measure IGF-1. In ordinary clinical practice, IGF-1 is mainly relevant when there is a specific endocrine question, such as suspected pituitary disease, acromegaly, gigantism, or growth-related pathology.
- IGF-1 is linked to anabolic physiology, including muscle protein signaling, tissue repair pathways, bone metabolism, nutrition, and energy availability — but biological relevance does not automatically mean clinical usefulness.
- Acute exercise can affect total IGF-1, but the direction of change is not predictable enough to interpret it as a simple “training response” marker.
- Resistance training may increase IGF-1 in some study settings, but the evidence is heterogeneous and does not establish a universal athlete-specific rule.
- A modestly higher IGF-1 value in strength-trained athletes compared with sedentary controls should not be overinterpreted as clinically meaningful.
- Protein intake may influence free IGF-1 acutely, but this does not establish chronic protein thresholds for “optimizing” IGF-1.
- Sustained low energy availability during competition preparation may be more clinically relevant, because it has been associated with reductions in IGF-1 and IGFBP-3 in physique athletes.
- IGF-1 misuse in doping should be kept separate from normal medical interpretation. Pharmacological manipulation is not the same as ordinary training adaptation.
- The practical message is simple: IGF-1 can help explain physiology, but it is not a shortcut for measuring recovery, muscle growth, or athletic performance.
Introduction: IGF-1 in Athletes
IGF-1 — insulin-like growth factor-1 — is a clinically measurable hormone biologically linked to muscle protein signaling, bone metabolism, sleep-related endocrine physiology, and energy availability. In athletes, this makes IGF-1 an interesting marker, but not a routine performance marker. It is not part of standard laboratory panels, and athletic status alone is not a medical indication to measure it.
In everyday clinical practice, IGF-1 is usually considered only in more specific endocrine contexts. From my perspective as a physician, this is an important distinction: an athlete being highly trained, tired, plateaued, or interested in optimization does not by itself make IGF-1 testing medically indicated. The test becomes more relevant when there is a genuine suspicion of endocrine disease.
One example is suspected pituitary disease. Excess IGF-1 production can be seen in conditions such as acromegaly, and in younger patients before epiphyseal closure, gigantism. These are not typical “sports performance” findings, but endocrine diagnoses where IGF-1 has a clearer clinical role.
In the athletic world, IGF-1 may also come up in discussions around performance-enhancing drug use. In my view, this is a separate issue from ordinary athlete blood work. There are situations where IGF-1 or related anabolic pathways may be discussed in the context of steroid or hormone-related doping, but this should not be confused with using IGF-1 as a routine performance-monitoring test. In that sense, IGF-1 is best understood as a clinically specific endocrine marker, not a general performance metric.
What IGF-1 in Athletes Actually Measures: The GH–IGF-1 Axis
Insulin-like growth factor-1 is a peptide hormone primarily produced by the liver in response to growth hormone (GH) stimulation. This GH–IGF-1 axis is an important anabolic pathway involved in skeletal muscle protein synthesis, tissue remodeling, and growth-related physiology.
At the cellular level in skeletal muscle, the mechanism is well characterized. Insulin-like growth factor-1 (IGF-1) increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. [1] These downstream nodes are involved in translating anabolic signals into protein production. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. [1] In other words, IGF-1 signaling simultaneously supports protein synthesis and reduces some protein-degradation pathways — a dual role relevant to both muscle development and the preservation of lean mass during physiological stress.
IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. [1] This review-level evidence comes primarily from cellular and animal models; direct extrapolation to athlete-specific outcomes requires additional evidence beyond what is established by the mechanistic literature.
Beyond muscle, IGF-1 is associated with bone metabolism. A Mendelian randomization study using genetic instruments for IGF-1 selected at genome-wide significance level from a study of 358,072 individuals found that for a 1-SD increase in IGF-1, the change of estimated bone mineral density (eBMD) levels was 0.04 g/cm² (95% CI, 0.01–0.07; P = .011) and the odds ratio of fracture was 0.94 (95% CI, 0.91–0.98; P = .003). [2] The authors concluded that the present study supports a role for IGF-1 in preventing fracture, possibly and partly mediated by greater bone mineral density. [2] This was a general population study using genetic associations, not an athlete-specific intervention trial, and Mendelian randomization establishes genetic association rather than direct clinical intervention effects.
Although IGF-1 is biologically important in muscle physiology, its clinical role in athletes is much more limited than many people might assume. From a sports physiology perspective, it is easy to see why IGF-1 attracts interest: it is connected to anabolic signaling, growth hormone physiology, muscle protein pathways, and tissue repair. But in everyday clinical medicine, athletic status alone rarely creates a specific reason to measure IGF-1.
In practice, the situations where IGF-1 is medically evaluated are usually endocrine rather than performance-related. The most relevant examples are suspected pituitary disorders, such as acromegaly, or selected growth-related disorders where the GH–IGF-1 axis is part of the clinical question. These are not ordinary athlete optimization scenarios. They are medical situations where the result may help answer a specific diagnostic question.
There is also a separate and less positive context: doping. In sport, IGF-1 may appear in discussions around performance-enhancing drug use because of its relationship to insulin-like and growth-hormone-related anabolic pathways. In my view, this should be kept clearly separate from normal medical blood work. The fact that a hormone can be misused in doping does not make it a useful routine performance marker for athletes.
As a physician, and especially from a general medical perspective, IGF-1 is not a hormone I would expect to encounter often in routine athlete care. It belongs mainly to selected endocrine evaluations. For most athletes, IGF-1 does not have a special clinical function simply because they train hard, build muscle, or compete. It may be biologically interesting, but clinically it remains a specific endocrine marker rather than a general sports performance test.
How Training Modulates IGF-1 in Athletes: Acute vs. Chronic Responses
Available studies suggest that IGF-1 responses differ between acute and chronic exercise contexts, and both matter for how a blood result should be interpreted.
Acute responses. A systematic review and meta-analysis of 21 studies found that there was an effect of endurance exercise on total IGF-1 (P = .01), but not on free IGF-1 (P = .36). Resistance exercise similarly affected total IGF-1 (P = .003), but not free IGF-1 (P = .37). The effect size indicated that total IGF-1 was more affected by endurance exercise (ES = 0.81) than by resistance exercise (ES = 0.46). [3] However, this does not mean that acute exercise reliably raises or lowers IGF-1 in a predictable direction. The authors noted that serum IGF-1 changes occur under conditions that are not well defined, and the broader literature includes reports of increases, decreases, and no change after exercise. [3] The safest interpretation is that acute exercise can alter total IGF-1 more consistently than free IGF-1, but the direction and practical meaning of that change depend on the study context. For longitudinal comparisons, blood-draw timing relative to recent training should therefore be standardized.
Chronic adaptations. With consistent resistance training, the picture shifts. A systematic review and meta-analysis of 33 randomized controlled trials found that the pooled estimate demonstrated a significant increase in IGF-1 (WMD: 10.34 ng/ml, 95% CI: 4.93, 15.74, p = 0.000, I² = 90.3%) after resistance training compared with the control group. [4] Subgroup analyses demonstrated that the increase in IGF-1 levels following resistance training was only statistically significant in treatment duration ≤16 weeks (WMD: 8.04 ng/ml), participants aged more than 60 years old (WMD: 9.84 ng/ml), and in women (WMD: 17.27 ng/ml). [4] The high heterogeneity (I² = 90.3%) across included trials reflects the broad range of populations studied (ages 22.7–82 years), and the results should not be assumed to apply uniformly across all athlete groups.
It is important to keep this in perspective. Although exercise can shape IGF-1 values in both the short and long term, this does not automatically create a meaningful clinical use for the marker in everyday athlete care. From a practical medical standpoint, the exercise-related movement of IGF-1 is usually more of a physiological curiosity than something that changes routine clinical decision-making.
In my clinical view, this is where the distinction between physiology and medicine matters. A marker can be biologically interesting without being clinically useful in ordinary practice. For most athletes, the fact that IGF-1 may change after training does not mean that the value needs to be measured, optimized, or interpreted as a performance signal.
So while the training-related behavior of IGF-1 is worth understanding intellectually, it should not be overmedicalized. In normal clinical medicine, there is usually no need to draw conclusions from exercise-induced IGF-1 fluctuations unless there is a separate endocrine reason to investigate the GH–IGF-1 axis.
IGF-1 in Athletes vs. Sedentary Controls: Why Reference Ranges Need Context
Many clinical IGF-1 reference intervals are age- and sex-adjusted; athlete-specific reference intervals are not established by the cited evidence. A cross-sectional study recruiting 28 male collegiate athletes performing strength training and 29 age-matched normal controls found that the IGF-1 concentration was higher in the athlete group (324 ± 80 vs. 263 ± 134 ng/ml). [9] This single study of male strength-training collegiate athletes cannot establish reference ranges for all athlete populations, but it illustrates that trained individuals may present with IGF-1 values above population norms, and that context matters when interpreting a result.
A single IGF-1 value within the general population reference range may still require contextual interpretation in a trained athlete, particularly if prior personal values are available for trend comparison. The same principle applies across the hormonal panel more broadly. For further discussion of how testosterone in athletes and SHBG in athletes follow analogous interpretive patterns, see the dedicated guides. Note that IGF-1 bioavailability is regulated by IGF-binding proteins — a separate regulatory system from SHBG, which specifically governs sex steroid binding.
Another point worth keeping in perspective is the size of the difference. It is interesting that IGF-1 may be higher in some athletic populations than in sedentary controls, but the difference reported in this type of study is still relatively modest. For example, the study discussed above found roughly a 23% higher IGF-1 concentration in male collegiate strength-training athletes compared with age-matched controls. [9]
From a clinical point of view, that is very different from the kind of IGF-1 abnormality that may be seen in true endocrine pathology. In disorders of the GH–IGF-1 axis, the values may be clearly outside the expected range and sometimes in a completely different clinical category. A modest group-level difference between trained and untrained young men should therefore not be overinterpreted as a diagnostic or performance signal.
In my view, this is another example of the gap between physiology and clinical medicine. The finding is interesting as a research observation, but in ordinary clinical practice, a difference of this size does not usually change medical decision-making by itself. It is better understood as a physiological curiosity that helps us interpret the literature, not as a reason to start measuring or optimizing IGF-1 in otherwise healthy athletes.
Nutrition and IGF-1 in Athletes: The Protein–IGF-1 Relationship
Acute protein intake is one dietary factor associated with IGF-1 physiology. A crossover study in 24 participants (11 females, mean age 24.9 ± 4.6 years) examined the acute effects of a high-protein meal (42 g), exercise, or combined exercise plus protein on plasma free IGF-1. In the protein condition, the 24h free IGF-1 was 17.5% higher (p=0.02) than baseline. [8] In this acute study, combining exercise with protein did not produce an additive increase in free IGF-1. [8] This was a single acute crossover study, not a longitudinal diet trial, and does not establish specific chronic protein intake thresholds for IGF-1 optimization.
The key practical point is that protein intake is one dietary factor associated with IGF-1 physiology, but it should not be overinterpreted as a stand-alone explanation for IGF-1 changes in athletes. [8] In an acute crossover study, a single high-protein meal increased 24h free IGF-1, but this does not establish chronic protein intake thresholds for IGF-1 optimization. Separately, in physique athletes, sustained low energy availability during competition preparation was associated with significant reductions in IGF-1 and IGFBP-3. [5] The contribution of protein intake specifically should therefore be interpreted separately from the broader energy deficit and overall anabolic environment.
This is also a useful reminder that “anabolic” does not automatically mean “directly increases IGF-1 in a simple measurable way.” Exercise, especially resistance training, is commonly thought of as anabolic because it stimulates muscle adaptation, but that does not mean every anabolic pathway rises neatly in the blood after training. In the acute crossover study discussed here, exercise did not appear to amplify the free IGF-1 response to protein intake. The clearer short-term signal came from nutrition rather than exercise itself.
From a clinical perspective, this distinction matters. Training can be anabolic at the tissue level without making IGF-1 a straightforward performance marker in blood work. That is one reason I would be cautious about interpreting IGF-1 as something athletes should try to “optimize” through routine testing. The physiology is interesting, but the clinical value in ordinary athlete care remains limited.
There is, however, a separate and less healthy context: doping. Because IGF-1 is connected to growth hormone, insulin-like signaling, and anabolic pathways, some athletes may try to bypass normal physiological regulation by using IGF-1 or related compounds as performance-enhancing drugs. That should be kept clearly separate from normal medical interpretation. The misuse of IGF-1 in doping does not make it a routine clinical performance marker; if anything, it highlights how different pharmacological manipulation is from ordinary training adaptation.
Conclusion: IGF-1 in Athletes as a Physiological Signal, Not a Performance Target
IGF-1 is an important hormone in human physiology, and in athletes it sits at an interesting intersection between growth hormone signaling, muscle protein pathways, bone metabolism, nutrition, and energy availability. That makes it scientifically relevant, but not automatically clinically useful as a routine performance marker. This distinction is important. A hormone can be central to muscle biology without becoming a useful blood test for everyday athlete monitoring.
The evidence discussed in this article shows why IGF-1 needs careful interpretation. Acute exercise can affect total IGF-1, but the direction of change is not predictable enough to treat it as a simple training-response marker. Resistance training may increase IGF-1 in some study settings, but the findings are heterogeneous and do not establish a universal athlete-specific rule. Protein intake may influence free IGF-1 acutely, but this does not create a chronic protein threshold for “optimizing” IGF-1. In physique athletes, sustained low energy availability during competition preparation appears more clinically relevant, because it has been associated with reductions in IGF-1 and IGFBP-3 — but even there, IGF-1 should be interpreted as part of the broader physiological picture, not in isolation.
From my perspective as a physician, the most useful lesson is the gap between physiology and clinical medicine. IGF-1 is biologically interesting, but for most athletes it is not a number that needs to be routinely measured, chased, or optimized. Athletic status alone is not a medical indication for IGF-1 testing. In ordinary clinical practice, IGF-1 remains mainly a specific endocrine marker, most relevant when there is a genuine question about the GH–IGF-1 axis, such as suspected pituitary disease, acromegaly, growth-related disorders, or other endocrine pathology.
This also helps prevent overmedicalization. A modest difference between athletes and sedentary controls, or a short-term change after training or nutrition, should not be mistaken for a clinically meaningful abnormality. These findings are useful for understanding the physiology, but they rarely change day-to-day medical decision-making by themselves. IGF-1 may help explain part of the anabolic environment, but it is not a shortcut to measuring recovery, muscle growth, or performance.
For athletes and coaches, the practical message is simple: do not confuse biological relevance with clinical usefulness. Training, nutrition, sleep, and energy availability all matter for adaptation, but IGF-1 is not the main tool for managing those variables in routine practice. When IGF-1 is measured, it should be interpreted cautiously, in context, and usually for a clear endocrine reason. In that sense, IGF-1 in athletes is best understood as a meaningful physiological signal — not a general performance target.
Bibliography
[1] https://doi.org/10.3390/cells9091970
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC7993594/
[3] https://pubmed.ncbi.nlm.nih.gov/32259791/
[4] https://pubmed.ncbi.nlm.nih.gov/32444042
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC11829922/
