Exaggerated cardiovascular responses to treadmill running in rats with peripheral arterial insufficiency

J. Matthew Kuczmarski, Kellee Unrath, Gail Thomas

Research output: Contribution to journalArticle

Abstract

Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by <60%. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [μMAP: =10 ± 1 (SE) vs. =18 ± 3 mmHg and μHR: =94 ± 12 vs. =148 ± 15 beats/min, P ± 0.05] and female rats (μMAP: =16 ± 3 vs. =30 ± 5 mmHg and μHR: =128 ± 20 vs. =178 ± 19 beats/min, P ± 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article’s corresponding podcast at http://ajpheart.pod-bean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/.

Original languageEnglish (US)
Pages (from-to)H114-H121
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume314
Issue number1
DOIs
StatePublished - Jan 1 2018

Fingerprint

Running
Peripheral Arterial Disease
Arterial Pressure
Femoral Artery
Heart Rate
Exercise
Muscles
Ligation
Webcasts
Hindlimb
Walking
Sprague Dawley Rats
Equipment and Supplies

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{fded1557b6d641b09a93af6ed11f81b2,
title = "Exaggerated cardiovascular responses to treadmill running in rats with peripheral arterial insufficiency",
abstract = "Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by <60{\%}. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [μMAP: =10 ± 1 (SE) vs. =18 ± 3 mmHg and μHR: =94 ± 12 vs. =148 ± 15 beats/min, P ± 0.05] and female rats (μMAP: =16 ± 3 vs. =30 ± 5 mmHg and μHR: =128 ± 20 vs. =178 ± 19 beats/min, P ± 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article’s corresponding podcast at http://ajpheart.pod-bean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/.",
author = "Kuczmarski, {J. Matthew} and Kellee Unrath and Gail Thomas",
year = "2018",
month = "1",
day = "1",
doi = "10.1152/ajpheart.00401.2017",
language = "English (US)",
volume = "314",
pages = "H114--H121",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "1",

}

Exaggerated cardiovascular responses to treadmill running in rats with peripheral arterial insufficiency. / Kuczmarski, J. Matthew; Unrath, Kellee; Thomas, Gail.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 314, No. 1, 01.01.2018, p. H114-H121.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Exaggerated cardiovascular responses to treadmill running in rats with peripheral arterial insufficiency

AU - Kuczmarski, J. Matthew

AU - Unrath, Kellee

AU - Thomas, Gail

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by <60%. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [μMAP: =10 ± 1 (SE) vs. =18 ± 3 mmHg and μHR: =94 ± 12 vs. =148 ± 15 beats/min, P ± 0.05] and female rats (μMAP: =16 ± 3 vs. =30 ± 5 mmHg and μHR: =128 ± 20 vs. =178 ± 19 beats/min, P ± 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article’s corresponding podcast at http://ajpheart.pod-bean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/.

AB - Patients with atherosclerotic peripheral artery disease have an augmented pressor response to treadmill walking, but the underlying mechanisms remain poorly understood and difficult to isolate because of the confounding presence of numerous cardiovascular risk factors. In the present study, we tested the hypothesis that a chronic deficit in muscle blood flow capacity would be sufficient to trigger an exaggerated pressor response to dynamic exercise. Sprague-Dawley rats (5 male and 5 female) were instrumented with radiotelemetry devices to measure the cardiovascular responses to treadmill running before and after bilateral femoral artery ligation, which has been previously shown to reduce the blood flow capacity of distal hindlimb muscles by <60%. Treadmill running evoked reproducible increases in mean arterial pressure (MAP) and heart rate (HR), which were significantly augmented 3 days after femoral artery ligation in both male rats [μMAP: =10 ± 1 (SE) vs. =18 ± 3 mmHg and μHR: =94 ± 12 vs. =148 ± 15 beats/min, P ± 0.05] and female rats (μMAP: =16 ± 3 vs. =30 ± 5 mmHg and μHR: =128 ± 20 vs. =178 ± 19 beats/min, P ± 0.05). Similar exaggerated MAP and HR responses were observed at repeated intervals between 3 and 65 days postligation. These findings indicate that a chronic deficit in muscle blood flow capacity is an important, persistent cause of the abnormal pressor and cardioaccelerator responses to dynamic exercise in both male and female rats with peripheral arterial insufficiency. NEW & NOTEWORTHY Using radiotelemetry to assess cardiovascular effects of exercise, we showed that femoral artery obstruction in male and female rats is an important, persistent cause of exaggerated pressor and cardioaccelerator responses to treadmill running. This translational model reproduces the abnormal cardiovascular response to exercise seen in patients with peripheral artery disease. Listen to this article’s corresponding podcast at http://ajpheart.pod-bean.com/e/treadmill-bp-in-simulated-peripheral-artery-disease/.

UR - http://www.scopus.com/inward/record.url?scp=85043463685&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85043463685&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.00401.2017

DO - 10.1152/ajpheart.00401.2017

M3 - Article

VL - 314

SP - H114-H121

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 1

ER -