ATP-sensitive K+ Channel Contribution to Skeletal Muscle Vascular Control in Rats During High Speed Running

Authors

Clark Holdsworth¹ , Scott Ferguson¹ , Trenton Colburn¹ , Sue Hageman¹ , David Poole¹ , Timothy Musch¹

1. Kansas State University

Conference / event

American College of Sports Medicine Annual Meeting, May 2015 (San Diego, CA, United States)

Poster summary

The ATP-sensitive K+ (KATP) channel is a class of inward rectifier K+ channels that can link local O2 availability to vasomotor tone across exercise-induced metabolic transients. Thus, the KATP channel contribution to vascular control is expected to be related to the magnitude of metabolic demand during exercise in vivo. The aim of this investigation was to test the hypothesis that KATP channel blockade via glibenclamide (GLI) would decrease exercising hindlimb skeletal muscle blood flow (BF) and vascular conductance (VC) in a speed-dependent manner during treadmill exercise at 40 and 60 m·min-1. In 13 adult male Sprague Dawley rats mean arterial pressure (MAP), blood [lactate], and hindlimb muscle BF (radiolabelled microspheres) was determined during treadmill exercise (5% incline) at 40 (n = 6) or 60 m·min-1 (n = 7) under control (CON) and GLI conditions (2.5 mg·kg-1, i.a). KATP channel function does not differentially alter total hindlimb skeletal muscle BF and VC at 40 and 60 m·min-1 in rats. However, the magnitude of the decrease in VC (24% and 33%, respectively) is greater than that previously demonstrated at 20 m·min-1 (20%) and the fiber-type dependent effects persisted despite the presumably increased recruitment of type IIb/dx fibers at higher speeds.

Keywords

exercise hyperemia, vascular control, metabolic coupling

Research areas

Anatomy and Physiology

References

No data provided

Funding

No data provided

Supplemental files

No data provided

Additional information

Competing interests

No competing interests were disclosed.

Data availability statement

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

Creative Commons license

Copyright © 2022 Holdsworth et al. This is an open access work distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.