Pseudoathletic appearance is a medical sign meaning to have the false appearance of a well-trained athlete due to pathologic causes (disease or injury) instead of true athleticism.

For instance, some individuals with Duchenne and Becker muscular dystrophy may start with true muscle hypertrophy, but later develop into pseudohypertrophy.

[4] In healthy individuals, resistance training and heavy manual labour creates muscle hypertrophy through signalling from mechanical stimulation (mechanotransduction) and from sensing available energy reserves (such as AMP through AMP-activated protein kinase); however, in the absence of a sports or vocational explanation for muscle hypertrophy, especially with accompanying muscle symptoms (such as myalgia, cramping, or exercise intolerance), then a neuromuscular disorder should be suspected.

[5][6] In lipodystrophy, an abnormal deficit of subcutaneous fat accentuates the appearance of the muscles, though in some forms the muscles are quantifiably hypertrophic (possibly due to a metabolic abnormality).

[24][25] (types A2, A4, B1, B2, B5, B6, C2, C3, C4, C5, C7, C8, C9, C12, C14) (formerly Emery–Dreifuss muscular dystrophy 6, X-linked) (formerly, LGMD1B) /extensor digitorum brevis muscles (MYOT gene, Ser55Phe missense mutation phenotype) (formerly, LGMD1A) (PYROXD1 gene) (20s-70s) (formerly, LGMD2W) (delayed muscle relaxation) (Chloride channelopathy, CLCN1 gene) /general[44][45] (Sodium channelopathy, SCN4A gene) /general[44][45] (formerly, Brody myopathy) (RMD2 formerly, LGMD1C) /general[48][49] (Köbberling–Dunnigan syndrome) /general[50][7] (Berardinelli–Seip syndrome) (spasticity or rigidity) (pinched nerve) (formerly, LGMD2V) (30s) (gene ISCU) (As of 2017 was excluded from LGMD, but not yet assigned new nomenclature)[25] (teens-50s) (poor diet, malabsorption diseases, or drug side effect such as lipase inhibitor Orlistat)[77] (also known as osteomalacic myopathy) (no rickets) Congenital myopathy 1 A & B, Malignant hyperthermia susceptibility (RYR1 gene) Types 1, 2, & 6 Childhood- to adult-onset (formerly, nemaline myopathy 11, autosomal recessive) (genes STIM1, ORAI1) (gene MYH7) (Myopathy, distal, 1; MPD1) (Congenital myopathy 7A, myosin storage; CMYP7A) /general (chronic denervation hypertrophy secondary to primary disease) (gene STIM1) (excessive teeth grinding or clenching) (cyst or cavity within spinal cord) /calf muscle[104] (Neuromyotonia, Morvan syndrome, Benign fasciculation syndrome, Cramp fasciculation syndrome) /calf muscle[104] (Episodic ataxia with myokymia; EAM) (Potassium channelopathy, gene KCNA1) (Muscle hypertrophy syndrome, myalgic[10]) (Latin for true muscle hypertrophy) /masseter muscle[111][112] (early 20s) (Metabolic crises, recurrent, with rhabdomyolysis, cardiac arrhythmias, and neurodegeneration; MECRCN) Adolescence- or early adult-onset Post-thrombotic syndrome Neuromuscular disease centre, Washington University - Large or prominent muscles National Center for Biotechnology Information (NCBI) - Skeletal muscle hypertrophy, generalized muscle hypertrophy, calf muscle hypertrophy, thigh hypertrophy