Journal of Applied Physiology AJP: Renal Physiology
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J Appl Physiol 105: 772, 2008; doi:10.1152/japplphysiol.90362.2008
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LETTER TO THE EDITOR

Commentary on Viewpoint: Exercise and cardiovascular risk reduction: Time to update the rationale for exercise?

TO THE EDITOR: That exercise training improves clinical symptoms and slows the progression of cardiovascular disease (CVD) is not in question (5). To date, however, the prognostic importance of endothelial function in conferring protection from CVD has been largely confined to a role as "best supporting actor." The commentary by Green and coworkers (4) serves as a timely reminder that the endothelium has become a major target for therapeutic interventions and, more importantly, that exercise training can directly improve endothelial function independently of modification of traditional risk factors (via a direct effect on the vascular wall). But, as usual, there is a sting in the tail. Low and moderate [25–50% of maximal oxygen uptake (VO2max)] intensity endurance training decrease oxidative stress and improve endothelium-dependent vasodilation in healthy subjects, but high (75% of VO2max) intensity training increases oxidative stress and impairs endothelial function (3). Sustained intense exercise is associated with an increase in free radical formation (2) and a decrease in circulating antioxidants (1), the net effect being a reduction in nitric oxide bioavailability and consequently endothelial dysfunction. It would appear that the impact of any exercise intervention on endothelial function is likely to depend on a fine balance between free radical production, antioxidant defenses, and their combined impact on nitric oxide production and subsequent bioavailability. Future studies of the effect of different exercise modes and intensities on CVD and associated risk factors should incorporate direct markers of endothelial function as independent outcome measures.

FOOTNOTES


Address for reprint requests and other correspondence: J. A. Hawley, School of Medical Sciences, RMIT Univ., PO Box 71, Bundoora, Victoria 3083, Australia (e-mail: john.hawley{at}rmit.edu.au)

REFERENCES

  1. Bergholm R, Mäkimattila S, Valkonen M, Liu ML, Lahdenperä S, Taskinen MR, Sovijärvi A, Malmberg P, Yki-Järvinen H. Intense physical training decreases circulating antioxidants and endothelium-dependent vasodilatation in vivo. Atherosclerosis 145: 341–349, 1999.[CrossRef][Web of Science][Medline]
  2. Davies KJ, Quintanilha AT, Brooks GA, Packer L. Free radicals and tissue damage produced by exercise. Biochem Biophys Res Commun 107: 1198–1205, 1982.[CrossRef][Web of Science][Medline]
  3. Goto C, Higashi Y, Kimura M, Noma K, Hara K, Nakagawa K, Kawamura M, Chayama K, Yoshizumi M, Nara I. Effect of different intensities of exercise on endothelium-dependent vasodilation in humans: role of endothelium-dependent nitric oxide and oxidative stress. Circulation 108: 530–535, 2003.[Abstract/Free Full Text]
  4. Green DJ, O'Driscoll G, Joyner MJ, Cable NT. Viewpoint: Exercise and cardiovascular risk reduction: time to update the rationale for exercise? J Appl Physiol; doi:10.1152/japplphysiol.01028.2007.[Free Full Text]
  5. Walther C, Gielen S, Hambrecht R. The effect of exercise training on endothelial function in cardiovascular disease in humans. Exerc Sport Sci Rev 32: 129–134, 2004.[CrossRef][Web of Science][Medline]

Julianne J. Reid
John A. Hawley
 School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia





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