The three <i>ryanodine receptor 1</i> gene variants (<i>NN</i>: homozygous normal, <i>Nn</i>: heterozygous, <i>nn</i>: homozygous defective) and the degree of Hampshire origin (0 %, 25 %, 50 %) serve as model for the investigation of the <i>in vivo</i> glycogen muscle metabolism in 27 pigs. The pigs originate from 4 different cross-breeding lines with an age varying between 41 and 58 days and a body weight between 7.3 and 19 kg. <sup>13</sup>C nuclear magnetic resonance spectroscopy was applied non-invasively <i>in vivo</i> and in a few pigs also <i>post mortem</i> to study the metabolic processes in the biceps femoris muscle after halothane exposure. In contrast to no visible effects of the halothane challenge test, the heterozygous defective allele carriers showed a drastic reduction in the level of glycogen (57 %) coupled with an increase in body temperature (1.36 °C). Overall, these changes were intermediate compared to the dramatic response in the homozygous nn genotype and to the very slow processes in <i>NN</i>, considering that the drastic glycogen depletion in the heterozygous genotype occurred after a rather long time of halothane exposure ( >20 min). In addition, pigs with the highest degree of Hampshire origin (50% → <i>RN</i><sup>–</sup> allele frequency: ~31.5 %) showed the slowest glycogen depletion compared to pigs with a lower degree of Hampshire origin (0 or 25 %).