Resistance exercise and appropriate nutrition to counteract muscle wasting and promote muscle hypertrophy.

The main purpose of this review is to examine thestrategies that are available to counteract atrophy result-ingfromgeneralmuscledisuse.Disuseofskeletalmusclearisesduetoanumberofrelevantclinicalconditionssuchasbedrest,immobilizationduetofracture(forreviewsee[1]), and abrupt sedentarism [2] due, for example, toillness. There are also nonclinical conditions such asspaceflight in which the gravitational loading that nor-mallypreservesourmusclemassislost[1].Inanumberofpathological conditions muscle wasting occurs in whichdisuse is certainly playing a role; however, these patho-logicalconditionssuchasAIDS[3–5],sepsis[6,7],cancercachexia [6,7], uremia [8], and burns [3] are also associ-ated with a marked inflammatory condition and largeelevations in inflammatory cytokines and cortisol [3–5]which are not characteristics of uncomplicated muscleatrophy [9–11], in fact to generate hypercortisolemiaduring prolonged bed rest exogenous source of glucocor-ticoids have to be administered [12]. Another importantconsequence of studying uncomplicated (i.e., nonpatho-logical) disuse-induced muscle atrophy is that the causalmechanisms for why muscle mass is lost are largelyopposite, or so it would seem, to those thought to occurin disease-induced wasting [13 ,14]. We view disuse-induced atrophy as being the consequence of a reductionin the basal [10,15,16,17 ,18,19 ] and feeding-inducedstimulationofmuscleproteinsynthesis(MPS) [17 ].Wehave reviewed the evidence that is both supportive andcounter to this thesis [13 ] and so will not discuss itfurther here. By contrast, a number of observations,mainly relying on data from small mammals in patho-logical conditions (sepsis, prolonged starvation, cancercachexia,anduremia),havepointedtoincreasedmarkersof proteolysis and muscle protein breakdown (MPB) asbeing the driving force underpinning atrophy duringdisuseandinpathologicalstates[6,20–22].Itisimportant