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Journal of Diabetes Research
Volume 2015 (2015), Article ID 654204, 11 pages
http://dx.doi.org/10.1155/2015/654204
Review Article

Cardiovascular Control during Exercise in Type 2 Diabetes Mellitus

1School of Science and Health, University of Western Sydney, Sydney, NSW 2751, Australia
2Neuroscience Research Australia, Sydney, NSW 2751, Australia
3Department of Physiology, School of Medicine, Trinity College Dublin, Dublin 1, Ireland
4Department of Medicine, University of Otago, Dunedin, Otago 9054, New Zealand
5Department of Physiology-HeartOtago, University of Otago, Dunedin, Otago 9054, New Zealand
6Division of General Internal Medicine, Center for Women’s Health Research, Department of Medicine, School of Medicine, University of Colorado, Denver, CO 80210, USA

Received 22 January 2015; Accepted 17 March 2015

Academic Editor: Raffaele Marfella

Copyright © 2015 Simon Green et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Controlled studies of male and female subjects with type 2 diabetes mellitus (DM) of short duration (~3–5 years) show that DM reduces peak (L·min−1 and mL·kg−1·min−1) by an average of 12–15% and induces a greater slowing of the dynamic response of pulmonary during submaximal exercise. These effects occur in individuals less than 60 years of age but are reduced or absent in older males and are consistently associated with significant increases in the exercise pressor response despite normal resting blood pressure. This exaggerated pressor response, evidence of exertional hypertension in DM, is manifest during moderate submaximal exercise and coincides with a more constrained vasodilation in contracting muscles. Maximum vasodilation during contractions involving single muscle groups is reduced by DM, and the dynamic response of vasodilation during submaximal contractions is slowed. Such vascular constraint most likely contributes to exertional hypertension, impairs dynamic and peak responses, and reduces exercise tolerance. There is a need to establish the effect of DM on dynamic aspects of vascular control in skeletal muscle during whole-body exercise and to clarify contributions of altered cardiovascular control and increased arterial stiffness to exertional hypertension.