Cardiovascular effects of cadence and workload

Increases in cadence may augment SV during submaximal cycling (> 65% V̇O_2max) via effects of increased muscle pump activity on preload. At lower workloads (45-65% V̇O_2max), SV tends to plateau, suggesting that effects of increases in cadence on pump activity have little influence on SV. We hypothesized that cadence-induced increases in CO at submaximal workloads, where SV tends to plateau, are due to elevations in HR and/or O₂ extraction. SV, CO, HR, V̇O₂, and Δa-vO₂ were assessed at 80 and 100 rpm during workloads of 50% (LO) or 65% (HI) of V̇O_2max in 11 male cyclists. No changes in SV were seen. CO was higher at 100 rpm in 10 of 11 subjects at LO (18.1 ± 2.7 vs. 17.2 ± 2.6 L/min). V̇O₂ at both workloads was greater at 100 than 80 rpm as was HR (LO: 129 ± 11 vs. 121 ± 10 beats/min; HI: 146 ± 13 vs. 139 ± 14 beats/min) (p < 0.05). Δa-vO₂ was greater at HI compared to LO at 80 (15.1 ± 1.6 vs. 13.6 ± 1.3 ml) and 100 rpm (16.0 ± 1.7 vs. 15.1 ± 1.6 ml) (p < 0.05). Results suggest that increases in O₂ demand during low submaximal cycling (50% V̇O_2max) at high cadences are met by HR-induced increases in CO. At higher workloads (65% V̇O _2max), inability of higher cadences to increase CO and O₂ delivery is offset by greater O₂ extraction.