Research conducted in the 1920s and 1930s described the glycemic response to a variety of exercise conditions (20, 21, 27, 74). It was demonstrated that despite a marked increase in carbohydrate oxidation, glucose homeostasis was generally maintained during moderate-intensity exercise provided that carbo hydrate reserves were adequate (27). On the other hand, glucose levels were shown to increase during high-intensity exercise (20), and extreme hypogly cemia was shown to be a frequent occurrence at the latter stage of a marathon when the carbohydrate reserves were exhausted (74). Classic work from the Harvard Fatigue Laboratory illustrated the importance of circulating glucose as a fuel by showing that glucose ingestion during prolonged, glycogen-de pleting exercise increased endurance in dogs by more than threefold (21). Research in the area of glucose metabolism and exercise was further advanced by Swedish studies that used techniques for obtaining splanchnic and limb arteriovenous differences and muscle biopsies to characterize aspects of sub strate fluxes during muscular work (4, 7, 28, 122, 123). The next major step in understanding the regulation of glucose fluxes during exercise followed the development of sensitive hormone assay techniques. This allowed for the effects of exercise on known and putative glucoregulatory hormone levels in arterial blood, as well as those of the sympathetic neurotransmitter norepineph rine, to be comprehensively described (32), which paved the way for recent