[Truncated abstract] It is well established that fish, amphibians and reptiles recovering from physical activity of near maximal intensity can replenish completely their muscle glycogen stores in the absence of food. In contrast, the extent to which these stores are replenished under these conditions in humans has been reported in all but one study to be partial. This implies that a few consecutive bouts of intense exercise might eventually lead to the sustained depletion of the muscle glycogen stores in humans if food is unavailable, thus limiting their capacity to engage in fight or flight behaviors unless mechanisms exist to protect muscle glycogen against sustained depletion. The objective of Study 1 was to test this prediction. Eight participants performed three intense exercise bouts each separated by a recovery period of 75 minutes. Although only 53% of muscle glycogen was replenished after the first exercise bout (postexercise and post-recovery glycogen levels of 246 ± 25 and 320 ± 36 mmol.kg-1 dry mass, respectively), all the glycogen mobilised during the second and third bouts was completely replenished during the respective recovery periods, with glycogen reaching levels of 319 ± 29 mmol.kg-1 dry mass after recovery from the third bout. These findings show that humans are not different from other vertebrate species in that there are conditions where humans have the ability to completely replenish without food intake the muscle glycogen mobilised during exercise. The results of our first study raise the intriguing possibility that humans have pre-set muscle glycogen levels that are protected against sustained depletion, with the extent to which muscle glycogen stores are replenished after exercise being dependent on the amount of glycogen required to attain those protected levels. ... During recovery, glycogen levels in the NORM group increased by more than ~50% and reached levels close to those alleged to be protected (189 ± 21 mmol.kg-1 dry mass), whereas no glycogen was deposited in the HCHO group. The sustained post-exercise activation of glycogen synthase, the transient fall in whole body carbohydrate oxidation rate, the increased mobilisation of body proteins, and the prolonged elevation in NEFA levels most probably played important roles in enabling glycogen synthesis in the NORM group. In conclusion, this thesis shows for the first time that there are some conditions (e.g. low pre-exercise muscle glycogen levels) where humans recovering from intense exercise have the capacity, like other species, to replenish completely their muscle glycogen stores from endogenous carbon sources. This study also suggests that humans protect preset levels of muscle glycogen against sustained depletion and at levels high enough to support at least one maximal sprint effort to exhaustion. Evidence is also provided for the existence of a feedback mechanism whereby glycogen below their protected levels mediate the activation of glycogen synthase to restore the depleted muscle glycogen stores back to their protected levels. Our findings, however, leave us with a number of novel unanswered questions which clearly show that the regulation of glycogen metabolism is far from the simple process generally depicted in most textbooks of biochemistry.