Sarcopenia and physical frailty: two sides of the same coin.

Abstract

Since the last decade, geriatrics and geron-tology researchers have been devoting anincreasing amount of efforts in the attemptof designing, developing, and implement-ing preventive interventions against con-ditions determining/driving the disablingcascade. The urgency of moving ahead inthe field is not merely dictated by scientificinterests; such need has indeed become afrequent and central item in the agendas ofpublic health authorities (Guralnik et al.,1996). In fact, there is a growing demandfor the identification of effective solutionsagainst the detrimental consequences thatage-related conditions (in particular, dis-abilities) exert on our healthcare systems.Specialattentionhasbeengiventosarcope-nia (Janssen et al., 2004) and frailty (Clegget al., 2013) because both are (1) highlyprevalent in the elderly, (2) associated withnegative health-related events, (3) poten-tially reversible, and (4) relatively easy toimplement in the clinical practice.The term “sarcopenia” was coined byRosenberg to indicate the loss of musclemass that accompanies aging. He clearlystated that “there is probably no decline instructureandfunctionmoredramaticthanthe decline in lean body mass or musclemass over the decades of life” (Rosenberg,1997). The muscle loss was therefore seenasameansof convenienceforexploringtheaging process and its consequences on anindividual’s health. Nevertheless, the skele-talmusclecannotbeisolatedbythehostingorganism. As such, it is still subject to theinfluence of all the positive and negativestressors to which the organism is exposed.In other words,the endogenous and exoge-nous phenomena capable of modifying theaging trajectory of the organism can also(more or less directly) influence the qualityand quantity of the muscle.Frailtyisthetermusedtoindicateageri-atric syndrome characterized by reducedhomeostatic reserves, which exposes theindividual at increased risk of negativehealth-related events (including falls, hos-pitalizations, worsening disability, institu-tionalization, and mortality) (Rodriguez-Manas et al., 2012; Clegg et al., 2013).Different operational definitions have beenproposed for capturing the frailty status,each one focusing on specific aspects of thesyndrome and detecting slightly differentrisk profiles (Theou et al., 2014). Never-theless, there is an overall agreement aboutthe key role that physical function (in par-ticular, mobility) plays in the determina-tion of the status of extreme vulnerability(Ferrucci et al., 2004; Daniels et al., 2008;Abellan van Kan et al., 2009).Since the beginning (roughly about 15–20years ago), sarcopenia and frailty havebeen studied in parallel. Being organ-specific, sarcopenia was more frequentlyobject of research in basic science, whereasthe concept of frailty tended to be moreeasily applied in the clinical setting (Bauerand Sieber, 2008). However, it was quiteinevitable that the two would have sooneror later started converging due to theirclose relationship with the aging process.Unfortunately, the definition of a clearframework within which sarcopenia andfrailty can be accommodated and stud-ied has yet to come. One major issue inthis context is the long-lasting, tiring, andpotentially pointless controversy about thecausal relationship existing between thetwo. Determining whether frailty is dueto sarcopenia, or sarcopenia is a clinicalmanifestation of frailty is consuming con-siderable efforts,and (from a very practicalviewpoint) rather resembles the problemof “the egg and the chicken.”We realize that the clarification of thispoint might have major consequences inthe field,determining different risk profilesto be detected and, consequently, redraw-ing outcomes as well as interventions to beadopted.Yet,theisolationof asinglepatho-physiological determinant responsible forthesecomplexconditions(aswellasforanyother age-related process) is quite unlikelyto be obtained, simply because aging isa complicated and still largely unknownphenomenon (Cesari et al., 2013).By stating this, we are not surrenderingto the current limitations of science. Weare instead soliciting the taking of morepragmatic decisions on this topic, waitingthat next-to-come scientific advancementsallow a better clarification and definitionof such urgent and pivotal matters. Fromthis perspective, deconstructing the innerfoundations of these“twin”conditions andtrying to focus on the shared and clinicalrelevant features of them might representa possible solution. By this way, we mighthave the opportunity to (1) define a uniquetarget for both sarcopenia and frailty, (2)simplify their operational definition, and(3)promotetheimplementationof thetwoconditions in both clinical and researchsettings.As shown in