The primary aim of this thesis was to develop a better understanding of the physiological mechanisms that cause the slow rise in O2 uptake ([V.O2]) that occurs during heavy- and severe-intensity exercise. The slow rise in [V.O2] during heavy-intensity exercise is known as the slow component of O2 uptake kinetics. This thesis includes a series of three studies investigating the mechanisms underlying the elevated O2 cost observed during heavy-intensity constant-load cycling exercise. Eight recreational cyclists ([V.O2]peak: [55.6 plus or minus 1.3 ml per kg per minute]) participated in each of the three studies. Each study was designed to manipulate blood lactate concentration ([La-]) and/or blood pH, or type II motor unit recruitment to determine if a corresponding change would occur in the amplitude of the [V.O2] slow component. All studies used a similar research design with each trial involving 3 minutes of baseline cycling (25 W) prior to 8 minutes of heavy-intensity constant-load cycling at a power output equal to 50% of the difference between the power output achieved at the ventilatory threshold and peak aerobic power ([change of] 50% work rate). Surface electromyographic (EMG) activity from the vastus medialis and vastus lateralis was measured throughout each constant-load cycling trial. Integrated EMG activity was used as an index of total neural activity, while the mean power frequency of the EMG signal was used as an indication of motor unit recruitment pattern. Blood lactate, pH and bicarbonate concentrations were determined under resting conditions prior to the start of exercise, at the end of 3 minutes at 25 W, and after 1.5, 3, 4.5, 6 and 8 minutes of heavy-intensity constant-load exercise. O2 uptake, CO2 production ([V.CO2]), and minute ventilation ([V.E]) were measured breath-by-breath while heart rate was measured continually throughout each constant-load trial. [V.O2] kinetics were determined using a double-exponential model with independent time delays beyond the phase I component.