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Am J Physiol Heart Circ Physiol 276: H1172-H1177, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 4, H1172-H1177, April 1999

Phospholamban deficiency does not compromise exercise capacity

Kavin H. Desai1, Eric Schauble1, Wusheng Luo2, Evangelia Kranias2, and Daniel Bernstein1

1 Department of Pediatrics, Stanford University, Stanford, California 94305; and 2 Department of Pharmacology and Cell Biophysics, University of Cincinnati, Cincinnati, Ohio 45267-0575

Deficiency of phospholamban (PLB) results in enhancement of basal murine cardiac function and an attenuated response to beta -adrenergic stimulation. To determine whether the absence of PLB also reduces the reserve capacity of the murine cardiovascular system to respond to stress, we evaluated the heart rate (HR), blood pressure, and metabolic responses of PLB-deficient (PLB-/-) mice to graded treadmill exercise (GTE). PLB-/- mice were hypertensive at rest (125 ± 19 vs. 109 ± 16 mmHg, P < 0.05) but had normal tachycardic and hypotensive responses to isoproterenol. The HR response to GTE was normal; however, the hypertension in PLB-/- mice normalized at peak exercise. Their exercise capacities, as measured by duration of exercise and peak oxygen consumption (VO2), were normal. The oxygen pulse (VO2/HR) curve was also normal in PLB-/- mice, suggesting an ability to appropriately increase stroke volume and oxygen extraction during GTE, despite an inability to increase beta -adrenergically stimulated cardiac contractility. Thus deficiency of PLB, although resulting in diminished beta -adrenergic inotropic reserve, does not compromise cardiac performance during exercise.

treadmill; oxygen pulse; oxygen consumption; contractility; adrenergic


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