Dynamic Adjustment Of Beat-by-beat Cardiac Output And Vo2 Kinetics During Moderate Intensity Exercise Transitions

Abstract

The kinetic adjustment of oxygen utilization (VO2) to exercise transitions of higher metabolic demands is proposed to be affected by central and peripheral alterations within the O2 transport system and/or intracellular mechanisms of control. Although limitations in O2 availability within the microcirculation but not at the conduit artery level have been proposed, knowledge is limited in relation to the contribution of the dynamic adjustment of cardiac output (Q) to the VO2 kinetics response, and how training status might modify this response. PURPOSE: This study aimed to compare the adjustment of muscle VO2 (i.e., Phase II VO2) to that of central O2 delivery as examined by the adjustment of Q during step transitions to moderate intensity exercise. METHODS: Sixteen young healthy male participants (35 ± 6 yrs) performed 3 step transitions from 20W to moderate-intensity cycling on a cycle ergometer to determine the breath-by-breath VO2 and the beat-by-beat Q responses. Participants were separated into two groups: trained (n= 9, VO2max 4.54 ± 0.40 L/min) and untrained (n= 7, VO2max 3.49 ± 0.68 L/min). Phase II VO2 and Q were modeled with a monoexponential model. Paired and unpaired t-tests and Pearson product moment correlations were used to compare the time constants of VO2 (τVO2) and Q (τQ). Statistical significance was set at P<0.05. RESULTS: Mean τVO2 was faster in the trained (13.9 ± 2.7s) compared to untrained (24.4 ± 6.4 s). τQ was slower than τVO2 in the trained (18.5 ± 6.0 s) but not untrained (20.2 ± 9.2 s). No difference was found between τQ between groups. Overall mean data showed no difference between τVO2 (18.5 ± 7.1 s) and τQ (19.3 ± 7.3 s). No significant correlations were found between τVO2 and τQ in trained (r=0.34), untrained (r=0.47), or when considering the two conditions together (r=0.37). CONCLUSION: This study demonstrated the dynamic adjustment of Q to exercise transition within the moderate intensity domain does not differ amongst trained and untrained individuals, even in the presence of training induced speeding of the VO2 kinetics. These data support the notion that mechanisms other than central delivery of O2, such as improved blood flow redistribution within the active tissues and/or intracellular components are responsible for controlling the rate of adjustment of VO2.