In 2008, Clark and Manini published a seminal paper calling attention to the importance of age-associated loss of skeletal muscle strength (which they named dynapenia), proposing that this loss should not be considered a direct result of muscle wasting (usually named sarcopenia) [1]. All consensus definitions published in the immediate years supported their view on the relevance of muscle function, defining sarcopenia as the loss of muscle mass and function [2]. All but one of these definitions used the term sarcopenia as an inclusive word that comprised both low muscle mass and low muscle function. Even when the concept was there, the word dynapenia was never widely adopted.

However, the term sarcopenia is still widely used in the literature to describe reduced muscle mass (also named muscle wasting) without any measure of muscle function. This has occurred especially in fields where the role of skeletal muscle in the prognosis of different comorbidities is of emerging importance and occurs in individuals of any age [3,4,5,6,7]. The fact that sarcopenia is used with two different meanings (low muscle mass, or low muscle mass plus low muscle function) is causing confusion to researchers and clinicians, and hindering advances in this important area of medicine, nutrition, and other healthcare fields.

It may be argued that we may well move back to the suggestion of using sarcopenia to describe isolated low muscle mass and dynapenia to refer to low muscle strength. However, muscle function measures go well beyond muscle strength [8], and all modern definitions of sarcopenia agree in using this term to refer to the complex syndrome of losing both skeletal muscle mass and function associated with aging. Although contentious, there are even suggestions to drop muscle mass assessments [9,10,11]. The comprehensive approach to define sarcopenia as a combined presence of low muscle mass and function makes sense, as even when the term sarcopenia was first proposed in 1989, the strong association between the decline in ‘lean body mass’ (which includes muscle mass, a compartment now termed lean mass) and physical behaviour, including mobility, ambulation, and independence, was clearly noted [12]. The first sarcopenia workshop in 1995 also stressed the importance of muscle function [13]. In fact, the term sarcopenia has become much wider than what its direct translation from Greek would suggest—sarx for flesh and penia for loss—in a very similar way as happened with other familiar terms such as delirium or diabetes mellitus, whose concepts go well beyond the etymology of the word [14, 15]. Likewise, the first consensus definition of sarcopenic obesity has included a measure of muscle function, not only of muscle mass, although recognizing the need to further explore this definition in clinical settings, where muscle mass has been mostly used to explore the condition [16].

Low muscle mass goes beyond sarcopenia, as skeletal muscle has different functional and metabolic functions [17]. Its importance is recognized in the Global Leadership Initiative on Malnutrition (GLIM), which includes low muscle mass as one of the five parameters to define malnutrition [18, 19]. This definition focuses on the role of skeletal muscle as a relevant nutrition (protein)-regulating and endocrine organ. As such, GLIM acknowledges the importance of low muscle mass or its related compartments (appendicular lean soft tissue, lean mass, and fat-free mass) in the diagnosis of malnutrition, and its independent association with patient outcomes across a variety of clinical conditions, in individuals of any age.

The most widely used definitions of cachexia also include an assessment of low muscle mass, but in this case as a consequence of the catabolic state associated with severe chronic disease, usually with a high degree of inflammation, and a normal or reduced fat mass [20,21,22,23]. Following these definitions, a patient with cancer who has low muscle mass may well have cachexia, malnutrition or sarcopenia, or a blend of two or three of these problems. Unravelling which of them are present is key to management, as different interventions may be needed for each condition. In this way, defining such a patient as sarcopenic because a low muscle mass is present would be too simplistic.

Another critical issue to discuss is the assessment of muscle mass. The relationship between muscle function and functional outcomes depends on muscle mass and its composition. Most of the studies on sarcopenia evaluated muscle mass by dual-energy X-ray absorptiometry (DXA). DXA allows indirect measurement of muscle mass through appendicular lean soft tissue (ALST), usually named appendicular skeletal muscle mass. ALST is composed of muscle, but also of water, fibrotic and connective tissue, which may confound the true assessment of muscle mass. Furthermore, muscle is ALST’s major component in young individuals; however, the percentage of muscle in ALST is decreased in older subjects, impairing muscle mass estimation [24]. In addition to the indirect measurement of muscle mass, DXA does not assess muscle composition, an essential element to understand the relationship between muscle and function. These facts may explain the lack of association between muscle mass and functional outcomes shown by many sarcopenia studies, where surrogate assessments of muscle mass were used [11]. Emerging findings from D3 creatine dilution studies, a method of muscle assessment encompassing its “functional component”, showed a better association between its muscle assessment and functional outcomes, although it is currently under discussion [25,26,27]. Conversely, muscle mass assessed by computed tomography (CT) is independently associated with clinical outcomes in most clinical studies. CT provides a better assessment of muscle mass and an estimation of muscle composition through muscle radiodensity, both overall strong predictors of clinical outcomes.

Given what was discussed above, sarcopenia defined as low muscle mass and function can be conceived as an age-related condition, which begins around the fourth decade of life with an accelerated loss as age increases, especially in very old age. Its consequences are related to muscles considered a locomotor organ affecting functional outcomes and disability. Conversely, low muscle mass can occur at any age, and in the context of chronic or acute conditions. It is associated with metabolic stress and related to muscle as a metabolic organ and its dysfunction (e.g. immune response, tissues/organ structure and functioning) (Fig. 1).

Fig. 1
figure 1

Main differences between causes, dysfunctions, and outcomes associated with sarcopenia and low muscle mass

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In conclusion, we argue (Box 1) that sarcopenia ≠ low muscle mass. We suggest that low skeletal muscle (lean) mass should be considered a sign (and named low muscle mass or muscle wasting), and the term sarcopenia should be reserved to name a complex geriatric syndrome of low muscle mass and low muscle function diagnosed by a validated definition. The ongoing Global Leadership Initiative on Sarcopenia (GLIS) [17, 28] will further clarify the role of muscle mass within the definition.