Abstract
We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels (~106 ± 4 μm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was ~25, 40, and 60% of KCl-induced preconstriction after the longterm, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside- evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by ~70 and ~160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 433-442 |
| Number of pages | 10 |
| Journal | Journal of Applied Physiology |
| Volume | 88 |
| Issue number | 2 |
| State | Published - Feb 2000 |
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Keywords
- Acetylcholine
- Coronary resistance arteries
- Coronary vascular function
- Endothelin-1
- Endothelium
- Myocardial function
- Sodium nitroprusside
- Thromboxane A
- U-46619
- Vascular smooth muscle
ASJC Scopus subject areas
- Physiology
- Endocrinology
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation
Cite this
Microvascular and myocardial contractile responses to ischemia : Influence of exercise training. / Symons, J. David; Rendig, Stephen V.; Stebbins, Charles L; Longhurst, John C.
In: Journal of Applied Physiology, Vol. 88, No. 2, 02.2000, p. 433-442.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Microvascular and myocardial contractile responses to ischemia
T2 - Influence of exercise training
AU - Symons, J. David
AU - Rendig, Stephen V.
AU - Stebbins, Charles L
AU - Longhurst, John C.
PY - 2000/2
Y1 - 2000/2
N2 - We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels (~106 ± 4 μm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was ~25, 40, and 60% of KCl-induced preconstriction after the longterm, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside- evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by ~70 and ~160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
AB - We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels (~106 ± 4 μm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was ~25, 40, and 60% of KCl-induced preconstriction after the longterm, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside- evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by ~70 and ~160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
KW - Acetylcholine
KW - Coronary resistance arteries
KW - Coronary vascular function
KW - Endothelin-1
KW - Endothelium
KW - Myocardial function
KW - Sodium nitroprusside
KW - Thromboxane A
KW - U-46619
KW - Vascular smooth muscle
UR - http://www.scopus.com/inward/record.url?scp=0033974486&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033974486&partnerID=8YFLogxK
M3 - Article
C2 - 10658008
AN - SCOPUS:0033974486
VL - 88
SP - 433
EP - 442
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 2
ER -