Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 99: 775, 2005; doi:10.1152/japplphysiol.00603.2005
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POINT-COUNTERPOINT COMMENTS

Kinetics of restoration of arteriolar tone after exercise.

Thomas J Barstow, Barbara J Lutjemeier, and Leonardo F Ferreira

Kinesiology and Anatomy and Physiology
Kansas State University
Manhattan, Kansas
e-mail: tbarsto{at}ksu.edu

This letter is in response to the Point-Counterpoint series "The muscle pump is/is not an important determinant of muscle blood flow during exercise" that appeared in the July issue (vol. 99: 371–375, 2005; doi:10.1152/japplphysiol.00381; http://jap.physiology.org/content/vol99/issue1).

Letter to Editor: In response to the recent Point-Counterpoint, we make a couple of points.

First, the key issue to us is not whether there is a muscle pump effect, but rather under what conditions might it be evident? This has been summarized by Sheriff.

Second, we take exception to the dismissive conclusion by Clifford et al., that in our recent publication (4), "no consideration (was) given to the notion that vasodilation may ebb rapidly." First, we considered this (page 1581 of Ref. 4), but found no supporting evidence in the literature. Second, both blood flow and pressure were statistically similar across the first four cardiac cycles in recovery for all seven work rates tested, as noted in the paper, statistically validating our assumption. Moreover, direct observations of feed arteries/arterioles after cessation of contractions reveal a time delay or latency of 6–60 s before a reduction in diameter begins (2, 3). Our window of four cardiac cycles clearly fits within this latency period. Finally, the comment by Clifford et al. that "Because vasodilation can occur in the first cardiac beat after contraction... it may be reversed just as quickly" reveals a surprising naiveté regarding cardiovascular regulation during exercise transients. Tissue requirements (as VO2) for O2delivery (QO2) predict temporal asymmetry between exercise and recovery blood flow kinetics (1). Not only would a rapid reduction in arterial/arteriolar diameter (and flow) during recovery be counterproductive by compromising QO2/VO2, but if the loss of vasodilation were fast enough, this might require constant readjustment during rhythmic exercise.

REFERENCES

  1. Barstow TJ, Lamarra N, and Whipp BJ. Modulation of muscle and pulmonary O2 uptakes by circulatory dynamics during exercise. J Appl Physiol 68: 979–989, 1990.[Abstract/Free Full Text]
  2. Bearden SE, Payne GW, Chisty A, and Segal SS. Arteriolar network architecture and vasomotor function with ageing in mouse gluteus maximus muscle. J Physiol 561.2: 535–545, 2004.
  3. Gorczynski RJ and Duling BR. Role of oxygen in arteriolar functional vasodilation in hamster striated muscle. Am J Physiol Heart Circ Physiol 235: H505–H515, 1978.[Abstract/Free Full Text]
  4. Lutjemeier BJ, Miura A, Scheuermann BW, Koga S, Townsend DK, and Barstow TJ. Muscle contraction-blood flow interactions during upright knee extension exercise in humans. J Appl Physiol 98: 1575–1583, 2005.[Abstract/Free Full Text]




This Article
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