These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Cardiovascular effects of cadence and workload.
    Author: Moore JL, Shaffrath JD, Casazza GA, Stebbins CL.
    Journal: Int J Sports Med; 2008 Feb; 29(2):116-9. PubMed ID: 17960509.
    Abstract:
    Increases in cadence may augment SV during submaximal cycling (> 65 % VO2max) via effects of increased muscle pump activity on preload. At lower workloads (45 - 65 % VO2max), 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, VO2, and delta a - vO2 were assessed at 80 and 100 rpm during workloads of 50 % (LO) or 65 % (HI) of VO2max 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). VO2 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). delta a - 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 % VO2max) at high cadences are met by HR-induced increases in CO. At higher workloads (65 % VO2max), inability of higher cadences to increase CO and O2 delivery is offset by greater O2 extraction.
    [Abstract] [Full Text] [Related] [New Search]