Two experiments were conducted to test if manipulations of the Arginine-Nitric oxide pathway during the earlylife of rainbow trout would act on its early myogenic process. In experiment 1, trout embryos were immersed at72° days post-fertilization (°dpf) or 104°dpf in water alone (control treatment, C) or containing 2 mM/L L-Arg(treatment A) or 1 mM/L of L-NAME, a NOS inhibitor (treatment N). We observed the beginning of expression ofmyf5 and fmhc genes at 72°dpf and 96°dpf, respectively. “A” treatment doubled the free Arg content of eggs butdid not affect either the pattern of expression of myf5 and fmhc, nor white muscle cross-sectional area andnumber of white muscle fibres at hatching, nor embryo survival and fry growth. “N” treatment also did not affectthese markers. In experiment 2, trout fry were fed from first feeding onwards and during 20 days either a controldiet (C) or the same diet supplemented with L-NAME (0.1 g/100 g diet, N-diet). In C-fed fry, distribution of asingle meal after overnight fasting induced changes in pcna, myod1, myog, fmhc, inos, nnos and ctsd geneexpressions. N-feeding decreased fry growth but did not change their growth trajectory or survival. Twenty daysof N-feeding led, compared to C-feeding, to changes in kinetics of transcription of pcna, myod1, myog, fmhc,inos, nnos, ctsd genes and to decreased white muscle cross-sectional area, total number of white muscle fibres,and number of large muscle fibres. L-NAME feeding thus decreased fry muscle growth by altering both hyperplasiaand hypertrophy.