Maintaining muscle mass: what your biomarkers reveal about muscle health

Declining testosterone and anabolic hormones

Testosterone is the most well-studied hormonal driver of muscle mass. It directly stimulates muscle protein synthesis, supports the growth and proliferation of satellite cells (the stem cells that repair and grow muscle tissue), and has anti-catabolic and anti-inflammatory effects on muscle. Research shows testosterone levels decline at approximately 1% per year in total testosterone and 2% per year in free testosterone from the mid-to-late twenties onwards. By their seventies, 40 to 70% of men are likely to have clinically low testosterone levels. This progressive anabolic decline creates an imbalance where the rate of muscle breakdown begins to outpace the rate of repair and synthesis. In women, the hormonal picture is more complex but equally relevant: declining androgens, including testosterone and DHEA, contribute to age-related muscle loss at twice the rate in women compared with men, when adjusted for initial muscle mass.

Falling IGF-1 (insulin-like growth factor 1)

IGF-1 is the principal downstream mediator of growth hormone's effects on muscle tissue. It directly stimulates muscle protein building and repair, and lower IGF-1 is strongly linked to reduced protein synthesis, slower recovery from training, and higher sarcopenia risk. Research shows that the rate of myosin heavy chain synthesis, a key contractile protein in muscle, begins declining at age 50, and that this decline correlates with falling levels of IGF-1 and DHEAS. IGF-1 occupies the somatotropic axis of the anabolic hormone system alongside growth hormone, meaning that interventions supporting sleep quality and resistance training, both of which stimulate natural growth hormone release, also influence IGF-1 levels over time.

Chronic systemic inflammation

Sarcopenia, the age-related loss of skeletal muscle mass and strength, is now understood as having a significant inflammatory component. Chronically elevated inflammatory markers, including CRP and interleukin-6, create a catabolic environment that tilts muscle protein metabolism toward breakdown rather than synthesis. This is sometimes called "inflammaging," the low-grade inflammatory state that accelerates tissue loss with age. Elevated CRP in the context of muscle loss is not just a marker of inflammation but an active driver of it. Tracking CRP over time, alongside interventions including resistance training, dietary changes, and gut health optimisation, gives an objective picture of whether the inflammatory burden is shifting in the right direction.

Vitamin D and muscle receptor function

Skeletal muscle tissue contains vitamin D receptors, and the evidence for vitamin D's role in maintaining muscle function is compelling. Deficiency is associated with reduced muscle fibre size, impaired muscle cell differentiation, and lower muscle strength across age groups. Vitamin D also stimulates IGF-1 production, creating a mechanistic link between a widely prevalent deficiency and two of the most important drivers of muscle mass. In people over 50, subclinical vitamin D insufficiency is extremely common and is rarely investigated in the context of unexplained muscle weakness or slower than expected training response.

Protein status and albumin

Albumin is the primary protein circulating in blood and reflects overall protein nutritional status and systemic inflammation. Low albumin, or low-normal albumin, indicates that the body may not have the protein reserves required to support muscle synthesis and repair. This is most relevant in people who are dieting, under-eating protein, or experiencing significant physiological stress. Research involving sarcopenia biomarkers consistently identifies low albumin as associated with accelerated muscle loss and reduced physical performance. The relationship is bidirectional: insufficient protein drives low albumin, and low albumin reflects a state in which muscle maintenance is compromised.

Gut microbiome and muscle metabolism

The connection between gut health and muscle mass is increasingly well evidenced. The gut microbiome produces short-chain fatty acids that support muscle protein synthesis through IGF-1 and insulin signalling pathways. Gut dysbiosis is associated with elevated systemic inflammation, which directly drives catabolic muscle metabolism. Additionally, impaired gut integrity reduces the absorption efficiency of protein, amino acids, zinc, and other nutrients that the muscle maintenance system depends on. In people experiencing muscle loss alongside digestive symptoms or poor food tolerance, gut microbiome testing alongside a blood biomarker panel can reveal whether gut health is a primary contributor.

DNA and genetic predisposition

DNA methylation testing can reveal genetic variants that affect muscle metabolism, including variants in the ACTN3 gene (which governs muscle fibre type composition), genes involved in testosterone and DHEA metabolism, and methylation patterns that affect the efficiency of protein synthesis pathways. Understanding genetic predisposition helps personalise the nutrition and training strategy for muscle maintenance rather than applying population-average guidance to an individual biology.

Standard GP testing is unlikely to assess any of the biomarkers most relevant to muscle maintenance. Testosterone may be measured in men reporting symptoms, but IGF-1, inflammation markers, vitamin D, and nutritional status are rarely assessed together in this context.

A comprehensive testing approach for muscle health should include:

Testosterone (total and free) measures the primary anabolic hormone driving muscle protein synthesis and satellite cell activity. Low testosterone is one of the most common and most treatable contributors to accelerated muscle loss.

IGF-1 reflects anabolic drive from the growth hormone axis. Lower levels are associated with reduced protein synthesis and higher sarcopenia risk, and can be influenced by sleep quality, resistance training, and dietary protein.

Vitamin D is consistently linked to muscle fibre quality, muscle strength, and IGF-1 production. Deficiency is common and directly affects the biological machinery of muscle maintenance.

CRP reveals the degree of systemic inflammation creating a catabolic environment. Tracking CRP over time maps the trajectory of the inflammatory driver of muscle loss.

Vitamin B12 and ferritin support the energy metabolism and oxygen delivery that muscle tissue requires for synthesis and repair. Deficiency in either contributes to fatigue and reduced training capacity that compounds muscle loss.

HbA1c reflects metabolic status. Insulin resistance and elevated average blood glucose are associated with accelerated sarcopenia, as insulin is an anabolic signal for muscle protein synthesis.

Home biomarker testing is most useful for people over 35 who are noticing a reduced training response or unexplained muscle loss, and for anyone wanting to build a baseline picture of their muscle health that can be tracked and compared at six-month intervals.

Resistance training as a non-negotiable foundation

Resistance training is the single most effective intervention for maintaining muscle mass at any age. It stimulates muscle protein synthesis, drives IGF-1 release, and creates the mechanical stimulus that signals the body to maintain and rebuild muscle tissue. Research consistently shows that two to three sessions per week of progressive resistance training is sufficient to maintain and increase muscle mass in adults of all ages, including those over 70. The key variable is progressive overload: gradually increasing the challenge over time. Tracking biomarkers including IGF-1 and testosterone gives an objective measure of whether the training stimulus is producing the expected anabolic hormonal response.

Protein intake and timing

Adequate protein is the nutritional foundation of muscle maintenance. Research suggests that older adults require 1.0 to 1.2 grams per kilogram of body weight per day to maintain muscle mass, with some evidence suggesting higher intakes of up to 1.6 grams per kilogram in those actively trying to build or preserve muscle. Protein timing matters: distributing intake across three to four meals, with each meal containing 25 to 30 grams of protein, creates a more sustained anabolic environment than concentrating intake in one or two large meals. Leucine, an amino acid particularly abundant in animal proteins, dairy, and certain plant sources including legumes and soy, is the primary trigger for muscle protein synthesis at the cellular level.

Addressing vitamin D and inflammation together

Vitamin D insufficiency and chronic inflammation frequently co-occur and compound each other's effect on muscle loss. Correcting vitamin D through testing-informed supplementation, and reducing systemic inflammation through dietary changes, improved sleep, and gut health support, addresses both drivers simultaneously. Tracking CRP and vitamin D at six-month intervals gives a clear picture of whether these interventions are producing measurable biological change rather than simply feeling better subjectively.

Sleep quality and hormone optimisation

Testosterone and growth hormone are predominantly secreted during deep sleep. Consistently poor or insufficient sleep directly suppresses the anabolic hormone environment that muscle maintenance depends on. The relationship between sleep and IGF-1 is well established: even one or two nights of reduced sleep quality produce measurable reductions in circulating growth hormone and its downstream effects. Optimising sleep quality and sleep timing, alongside testing the hormonal markers that reflect anabolic status, gives both the intervention and the objective measure of its effect.