Impact of exercise training on ventricular properties in a canine model of congestive heart failure

Koji Todaka, J. I E Wang, Mathias Knecht, Richard Stennett, Milton Packer, Daniel Burkhoff

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHFEX, 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2, 540 ±440 vs. 1, 720 ±300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 ±5 vs. 19 ±4 mmHg, P < 0.05) in CHFEX compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 ±0.47 in CHFS, 1.77 ±0.38 in CHFEX, and 3.05 ±0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 ±3 in CHFs, 21 ±3 in CHFEx, 20 ±4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume41
Issue number3
StatePublished - 1997

Fingerprint

Canidae
Heart Failure
Exercise
Hemodynamics
Dogs
Blood Pressure
Pressure
Left Ventricular Function
In Vitro Techniques

Keywords

  • Collagen
  • Maximal elastance
  • Myocardial oxygen consumption
  • Pressure-volume relationship
  • Relaxation
  • Stiffness constant
  • Stress-strain analysis

ASJC Scopus subject areas

  • Physiology

Cite this

Impact of exercise training on ventricular properties in a canine model of congestive heart failure. / Todaka, Koji; Wang, J. I E; Knecht, Mathias; Stennett, Richard; Packer, Milton; Burkhoff, Daniel.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 41, No. 3, 1997.

Research output: Contribution to journalArticle

Todaka, Koji ; Wang, J. I E ; Knecht, Mathias ; Stennett, Richard ; Packer, Milton ; Burkhoff, Daniel. / Impact of exercise training on ventricular properties in a canine model of congestive heart failure. In: American Journal of Physiology - Heart and Circulatory Physiology. 1997 ; Vol. 41, No. 3.
@article{d33c8db5ef9b41d8af0a4d30e13ec819,
title = "Impact of exercise training on ventricular properties in a canine model of congestive heart failure",
abstract = "Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHFEX, 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2, 540 ±440 vs. 1, 720 ±300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 ±5 vs. 19 ±4 mmHg, P < 0.05) in CHFEX compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 ±0.47 in CHFS, 1.77 ±0.38 in CHFEX, and 3.05 ±0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 ±3 in CHFs, 21 ±3 in CHFEx, 20 ±4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.",
keywords = "Collagen, Maximal elastance, Myocardial oxygen consumption, Pressure-volume relationship, Relaxation, Stiffness constant, Stress-strain analysis",
author = "Koji Todaka and Wang, {J. I E} and Mathias Knecht and Richard Stennett and Milton Packer and Daniel Burkhoff",
year = "1997",
language = "English (US)",
volume = "41",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Impact of exercise training on ventricular properties in a canine model of congestive heart failure

AU - Todaka, Koji

AU - Wang, J. I E

AU - Knecht, Mathias

AU - Stennett, Richard

AU - Packer, Milton

AU - Burkhoff, Daniel

PY - 1997

Y1 - 1997

N2 - Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHFEX, 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2, 540 ±440 vs. 1, 720 ±300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 ±5 vs. 19 ±4 mmHg, P < 0.05) in CHFEX compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 ±0.47 in CHFS, 1.77 ±0.38 in CHFEX, and 3.05 ±0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 ±3 in CHFs, 21 ±3 in CHFEx, 20 ±4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.

AB - Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHFEX, 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2, 540 ±440 vs. 1, 720 ±300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 ±5 vs. 19 ±4 mmHg, P < 0.05) in CHFEX compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 ±0.47 in CHFS, 1.77 ±0.38 in CHFEX, and 3.05 ±0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 ±3 in CHFs, 21 ±3 in CHFEx, 20 ±4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.

KW - Collagen

KW - Maximal elastance

KW - Myocardial oxygen consumption

KW - Pressure-volume relationship

KW - Relaxation

KW - Stiffness constant

KW - Stress-strain analysis

UR - http://www.scopus.com/inward/record.url?scp=33751294563&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33751294563&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:33751294563

VL - 41

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 3

ER -