We measured respiratory ratio (RR), pulmonary ventilation (VE) and end-tidal carbon dioxide partial pressure (ETPCO2) at rest and during cycling aerobic workloads (20%, 40%, 60% of estimated maximal oxygen uptake). Measurements were taken after overnight fasting and after an oral glucose load. RR, VE and ETPCO2 increased with workload. Glucose load caused RR and VE increments at rest (0.75 ± 0.01 vs. 0.86 ± 0.02, p < 0.01, and 10.8 ± 0.43 vs. 12.1 ± 0.49 l/min, p < 0.01, respectively) and for each workload (20% estimated maximal oxygen uptake: 0.77 ± 0.01 vs. 0.855 ± 0.02, p < 0.01, and 16.2 ± 0.73 vs. 17.7 ± 0.8 l/min, p < 0.01; 40% estimated maximal oxygen uptake: 0.76 ± 0.02 vs. 0.82 ± 0.01, p < 0.01, and 25.9 ± 1.1 vs. 28.3 ± 1.3 l/min, p < 0.05; 60% estimated maximal oxygen uptake: 0.85 ± 0.02 vs. 0.91 ± 0.02, p < 0.01, and 37.4 ± 1.7 vs. 40.9 ± 1.9 l/min, p < 0.05) but ETPCO2 did not change. The differences in RR before and after glucose load became smaller as the workload increased. Linear regression analysis of VE and carbon dioxide output yielded virtually identical results for both fasting and glucose load conditions. We have concluded that: a) for the metabolic carbon dioxide load increment due to glucose-induced RR increment, the physiological response is an increase of VE at all workloads. This response modulates constant ETPCO2 values; b) on workload increment, skeletal muscle increasingly utilises more and more glycogen stores, regardless of the blood glucose availability. This reduces the usefulness of dietary manipulations decreasing carbon dioxide metabolic load during muscular work in respiratory failure; c) the absolute value of metabolic carbon dioxide load exerts a role in ventilation regulation at rest and during aerobic exercise.