Abstract
Nine males with mean maximal oxygen consumption ( \(\dot V_{O_2 \max } \) ) =63.0 ml· kg−1 · min−1, SD 5.7 and mean body fat = 10.6%, SD 3.1 each completed nine counterbalanced treatments comprising 20, 50 and 80 min of treadmill exercise at 30, 50 and 70% \(\dot V_{O_2 \max } \) . The OZ deficit, 8 h excess post-exercise oxygen consumption (EPOC) and EPOC:O2 deficit ratio were calculated for all subjects relative to mean values obtained from 2 control days each lasting 9.3 h. The O2 deficit, which was essentially independent of exercise duration, increased significantly (P<0.05) with intensity such that the overall mean values for the three 30%, 50% and 70% \(\dot V_{O_2 \max } \) workloads were 0.83, 1.89 and 3.09 l, respectively. While there were no significant differences (P>0.05) between the three EPOCs after walking at 30% \(\dot V_{O_2 \max } \) for 20 (1.01 l), 50 (1.43 l) and 80 min (1.041), respectively, the EPOC thereafter increased (P<0.05) with both intensity and duration such that the increments were much greater for the three 70% \(\dot V_{O_2 \max } \) workloads (EPOC: 20 min=5.68 l; 50 min=10.04 l; 80 min= 14.59 l) than for the three 50% \(\dot V_{O_2 \max } \) workload (EPOC: 20 min =3.14 l; 50 min=5.19 l; 80 min= 6.10 l). An analysis of variance indicated that exercise intensity was the major determinant of the EPOC since it explained five times more of the EPOC variance than either exercise duration or the intensity times duration interaction. The mean EPOC:O2 deficit ratio ranged from 0.8 to 4.5 and generally increased with both exercise intensity and duration. These data imply that the EPOC is more than mere repayment of the O2 deficit because metabolism is increasingly disturbed from resting levels as exercise intensity and duration increase due to other physiological factors occurring after the steady-state has been attained.