Exercise induced augmentation of myocardial oxygen extraction in spite of normal coronary dilatory capacity in dogs

Restorff, W. v.; Holtz, J.; Bassenge, E.

doi:10.1007/bf00585334

Cited by 85 publications

(51 citation statements)

References 21 publications

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“…In dogs, the increase in coronary blood flow produced by treadmill exercise does not fully match the increased myocardial O 2 demand; thus, even during mild to moderate levels of exercise (Ͻ70% of maximum heart rate), an increase in O 2 extraction [3][4][5][6][7] and, hence, a decrease in cvPO 2 occur. 5,[7][8][9] In contrast, in humans, minimal changes in O 2 extraction occur at mild to moderate levels of exercise, [15][16][17][18][19][20] although an increase in O 2 extraction and a decrease in cvO 2 content have been reported in humans during heavy exercise (Ͼ85% of maximum heart rate).…”

Section: Myocardial O 2 Extraction During Treadmill Exercisementioning

confidence: 99%

“…Compared with swine, in dogs, horses, and sheep, O 2 delivery to the myocardium is facilitated by even more prominent increases in Hb concentration (20% to 50%) during exercise and by the resultant increase in the O 2 -carrying capacity of arterial blood. 3,4,[43][44][45] The increase in Hb concentration is virtually abolished after splenectomy, 43,44 indicating that exercise elicits splenic contraction that expresses erythrocyterich blood into the general circulation. In dogs, splenectomy also necessitated a greater increase in coronary blood flow at comparable levels of MV O 2 during norepinephrine infusion.…”

Section: ␣-Adrenoceptorsmentioning

confidence: 99%

“…The close coupling of coronary blood flow and myocardial O 2 demand has been proposed to depend primarily on messengers released from the myocardium and endothelium but is also modulated by the autononomic nervous system. 1,2 Thus, in dogs, the treadmill exercise-induced increases in coronary blood flow and, hence, O 2 delivery do not fully match the increase in myocardial O 2 demand, so that even at mild to moderate levels of exercise (Ͻ70% of maximum heart rate), myocardial O 2 extraction increases [3][4][5][6][7] and cvPO 2 decreases. 5,[7][8][9] The decrease in cvPO 2 may represent a metabolic error signal needed for a negative-feedback control mechanism 1,10 but is at least in part due to ␣-adrenergic vasoconstriction of coronary resistance vessels.…”

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Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Duncker

Stubenitsky

Verdouw

1998

Circulation Research

110

159

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Abstract-To date, no studies have investigated coronary vasomotor control of myocardial O 2 delivery (MDO 2 ) and its modulation by the autonomic nervous system in the porcine heart during treadmill exercise. We studied 8 chronically instrumented swine under resting conditions and during graded treadmill exercise. Exercise up to 85% to 90% of maximum heart rate produced an increase in myocardial O 2 consumption (MV O 2 ) from 163Ϯ16 mol/min (meanϮSE) at rest to 423Ϯ75 mol/min (PՅ0.05), which was paralleled by an increase in MDO 2 , so that myocardial O 2 extraction (79Ϯ1% at rest) and coronary venous O 2 tension (cvPO 2 , 23.7Ϯ1.0 mm Hg at rest) were maintained. ␤-Adrenoceptor blockade blunted the exercise-induced increase of MDO 2 out of proportion compared with the attenuation of the exercise-induced increase in MV O 2 , so that O 2 extraction rose from 78Ϯ1% at rest to 83Ϯ1% during exercise and cvPO 2 fell from 23.5Ϯ0.9 to 19.6Ϯ1.1 mm Hg (both PՅ0.05). In contrast, ␣-adrenoceptor blockade, either in the absence or presence of ␤-adrenoceptor blockade, had no effect on myocardial O 2 extraction or cvPO 2 at rest or during exercise. Muscarinic receptor blockade resulted in a decreased O 2 extraction and an increase in cvPO 2 at rest, an effect that waned during exercise. The vasodilation produced by muscarinic receptor blockade was likely due to an increased ␤-adrenoceptor activity, since combined muscarinic and ␤-adrenoceptor blockade produced similar changes in O 2 extraction and cvPO 2 , as did ␤-adrenoceptor blockade alone. In conclusion, in swine myocardium, MV O 2 and MDO 2 are matched during exercise, which is the result of feed-forward ␤-adrenergic vasodilation in conjunction with minimal ␣-adrenergic vasoconstriction. ␤-Adrenergic vasodilation is due to an increase in sympathetic activity but may also be supported by withdrawal of muscarinic receptor-mediated inhibition of ␤-adrenergic coronary vasodilation. The observation that cvPO 2 levels are maintained even during heavy exercise suggests that a decrease in cvPO 2 is not essential for coronary vasodilation during exercise. (Circ Res. 1998;82:1312-1322.)

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Section: Myocardial O 2 Extraction During Treadmill Exercisementioning

confidence: 99%

Section: ␣-Adrenoceptorsmentioning

confidence: 99%

mentioning

confidence: 99%

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Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Duncker

Stubenitsky

Verdouw

1998

Circulation Research

110

159

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“…4 -7 Additionally, oxygen extraction may also increase. 8 Cardiac output is maintained during pacing in the nonhypertrophied heart. 8 Thus, the nonhypertrophied myocardium tolerates chronotropic stress well.…”

Section: -2mentioning

confidence: 99%

“…8 Cardiac output is maintained during pacing in the nonhypertrophied heart. 8 Thus, the nonhypertrophied myocardium tolerates chronotropic stress well. Conversely, attenuated coronary blood flow response to exercise and pharmacologically stimulated tachycardia have been reported in experimental myocardial hypertrophy, although impaired coronary blood flow response has not always been observed.…”

Section: -2mentioning

confidence: 99%

Hypertension-induced cardiac hypertrophy. Oxygen supply and consumption with pacing.

Cimini¹,

Weiss²

1990

Hypertension

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The purpose of this study was to determine if hypertrophied myocardium was associated with diminished cardiac function, restricted oxygen supply, or oxygen consumption during tachycardia. Myocardial oxygen supply and oxygen consumption were determined during baseline and atrial pacing conditions 30 days after New Zealand White rabbits were prepared as one-kidney, one clip Goldblatt hypertensive or uninephrectomized sham control rabbits. Coronary blood flow and cardiac output, using radioactive microspheres, and small vessel oxygen saturations, using microspectrophotometry, were measured in hypertrophied and nonhypertrophied hearts. After 30 days, baseline blood pressure was significantly higher in the Goldblatt rabbits compared with sham controls, and hypertension was maintained during pacing. The myocardium was hypertrophied in the Goldblatt hypertensive rabbits compared with sham controls. Baseline heart rates were not different between animal groups (242 ±32 and 244±24 beats/min, respectively). Both groups were paced 35% above baseline heart rates; during pacing, cardiac output was similar to baseline values in the sham controls (304 ±99 versus 321±116 ml/min, respectively) but reduced in the hypertensive rabbits (248±43 versus 325±62 ml/min). Myocardial oxygen consumption increased twofold in both nonhypertrophied and hypertrophied ventricles during tachycardia. Oxygen extraction was significantly elevated, but coronary blood flow was not altered during pacing in either animal group. Therefore, at the pacing level chosen the diminished function in cardiac hypertrophy was not associated with reduced oxygen consumption. Conversely, reduced efficiency during pacing in the hypertrophied myocardium was suggested. (Hypertension 1990;16:35-42) S ystemic hypertension leads to myocardial hypertrophy, which is thought to be a beneficial, adaptive response. The oxygen supply in pressure-induced hypertrophied myocardium appears to be sufficient under baseline conditions. -2Resting myocardial oxygen consumption measured in hypertrophy may or may not be elevated. 12 However, coronary flow reserves are generally diminished in hypertension-induced cardiac hypertrophy compared with the nonhypertrophied myocardium, and minimal coronary vascular resistance is elevated.2 Clinical and experimental evidence suggest that the hypertension-induced hypertrophied myocardium is especially vulnerable to ischemia during stress.3 These observaFrom the Heart and Brain

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Peripheral Circulation

Laughlin

Davis

Secher

et al. 2012

Comprehensive Physiology

211

234

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Blood flow (BF) increases with increasing exercise intensity in skeletal, respiratory, and cardiac muscle. In humans during maximal exercise intensities, 85% to 90% of total cardiac output is distributed to skeletal and cardiac muscle. During exercise BF increases modestly and heterogeneously to brain and decreases in gastrointestinal, reproductive, and renal tissues and shows little to no change in skin. If the duration of exercise is sufficient to increase body/core temperature, skin BF is also increased in humans. Because blood pressure changes little during exercise, changes in distribution of BF with incremental exercise result from changes in vascular conductance. These changes in distribution of BF throughout the body contribute to decreases in mixed venous oxygen content, serve to supply adequate oxygen to the active skeletal muscles, and support metabolism of other tissues while maintaining homeostasis. This review discusses the response of the peripheral circulation of humans to acute and chronic dynamic exercise and mechanisms responsible for these responses. This is accomplished in the context of leading the reader on a tour through the peripheral circulation during dynamic exercise. During this tour, we consider what is known about how each vascular bed controls BF during exercise and how these control mechanisms are modified by chronic physical activity/exercise training. The tour ends by comparing responses of the systemic circulation to those of the pulmonary circulation relative to the effects of exercise on the regional distribution of BF and mechanisms responsible for control of resistance/conductance in the systemic and pulmonary circulations.

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Exercise induced augmentation of myocardial oxygen extraction in spite of normal coronary dilatory capacity in dogs

Cited by 85 publications

References 21 publications

Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Autonomic Control of Vasomotion in the Porcine Coronary Circulation During Treadmill Exercise

Hypertension-induced cardiac hypertrophy. Oxygen supply and consumption with pacing.

Peripheral Circulation

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