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J Appl Physiol 101: 1531, 2006. First published August 10, 2006; doi:10.1152/japplphysiol.00830.2006
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POINT-COUNTERPOINT COMMENTS

Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis

Don D. Sheriff

Department of Exercise Science
The University of Iowa
Iowa City, Iowa

Robert A. Augustyniak1 and Donal S. O'Leary2

1Departments of Medicine and Physiology
2Department of Physiology
Wayne State University School of Medicine
Detroit, Michigan
e-mail: don-sheriff{at}uiowa.edu

The following letter is in response to the Point:Counterpoint "Active venoconstriction is/is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis" that appeared in the October issue.

To the Editor: Hainsworth and Drinkhill (4) argue against the importance of active venoconstriction in raising right atrial pressure (RAP) during exercise based in part on a low reserve of blood volume that can be mobilized by baroreflex-induced increases in sympathetic activity. Because the arterial baroreflex is largely a resistance-raising reflex and not a flow-raising reflex (1, 2), the low reserve is perhaps not surprising. In sharp contrast, the pressor response to muscle ischemia (termed the muscle chemoreflex or muscle metaboreflex) during dynamic exercise is produced almost entirely by an increase in cardiac output, the maintenance of which likely requires substantial venoconstriction (5, 6). Accordingly, we have demonstrated that the muscle chemoreflex is threefold more potent in raising right atrial pressure (5) than are the arterial baroreflexes (1). Moreover, when arterial pressure is maintained constant by ventricular pacing, strong activation of the muscle chemoreflex can reflexly raise RAP by 8 mmHg (5), a substantial fraction of which is likely due to extrasplenic venoconstriction (3). Therefore, it appears that the reserve capacity for central blood volume mobilization in conscious dogs during exercise is much greater than suggested by Hainsworth and Drinkhill (4). However, the extent to which the muscle chemoreflex is active during normal exercise remains a pressing issue.

REFERENCES

  1. Bennett TD, Wyss CR, and Scher AM. Changes in vascular capacity in awake dogs in response to carotid occlusion and administration of catecholamines. Circ Res 55: 440–453, 1984.[Abstract/Free Full Text]
  2. Collins HL, Augustyniak RA, Ansorge EJ, and O'Leary DS. Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction. Am J Physiol Heart Circ Physiol 280: H642–H648, 2001.[Abstract/Free Full Text]
  3. Rothe CF. Point: Active venoconstriction is important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. 101: 1262–1264, 2006.[Abstract/Free Full Text]
  4. Hainsworth R and Drinkhill M. Counterpoint: Active venoconstriction is not important in maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. 101: 1264–1265, 2006.[Free Full Text]
  5. Sheriff DD, Augustyniak RA, and O'Leary DS. Muscle chemoreflex induced increases in right atrial pressure. Am J Physiol Heart Circ Physiol 275: H767–H775, 1998.[Abstract/Free Full Text]
  6. Sheriff DD, Zhou XP, Scher AM, and Rowell LB. Dependence of cardiac filling pressure on cardiac output during rest and dynamic exercise in dogs. Am J Physiol Heart Circ Physiol 265: H316–H322, 1993.[Abstract/Free Full Text]




This Article
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101/5/1531    most recent
00830.2006v1
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Right arrow Articles by O'Leary, D. S.

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