International Journal of Cardiology 184 (2015) 519–520

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Letter to the Editor

About the article: Effect of combined aerobic and resistance training versus aerobic training on arterial stiffness Amanda Veiga Sardeli a,b,⁎, Arthur Fernandes Gáspari a, Mara Patrícia Traina Chacon-Mikahil a,b a b

Laboratory of Exercise Physiology — FISEX, Faculty of Physical Education, University of Campinas– UNICAMP, Campinas, SP, Brazil Department of Gerontology — Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil

a r t i c l e

i n f o

Article history: Received 20 January 2015 Accepted 2 March 2015 Available online 3 March 2015 Keywords: Arterial stiffness Combined exercise training Aerobic exercise training

Dear Editor, The well conducted meta-analysis written by Montero and his colleagues [1], encouraged us to discuss a critical point of view about arterial stiffness and exercise that have been left out (adding a deserved complementary discussion to such interesting results). Many important researchers have committed a misunderstanding worrying, mixing analyses from central and peripheral arterial stiffness. Fortunately, looking at the current meta-analysis [1], we could indicate some consequences of this misunderstanding. We can find in some human physiology book, central and peripheral arteries differ structurally and functionally, implying in different physiological and pathological adaptations along lifespan. For instance, we will describe what happen with arteries from different regions during exercise. The peripheral arteries of exercised muscles suffer vasodilation while the peripheral arteries of non-exercised muscles suffer vasoconstriction. Aerobic exercise is the main representative of dynamic exercise type which usually induces whole body vasodilation, as it exercises the major muscle groups at a continuous fashion. In the other hand, resistance exercise – with high static component rather than dynamic – will induce peripheral vasoconstriction or vasodilation depending on the exercised muscles. The arterial vasodilation during exercise sessions, is broadly related to increase in local shear stress and nitric oxide bioavailability, ⁎ Corresponding author at: Laboratory of Exercise Physiology — FISEX, Faculty of Physical Education, University of Campinas– UNICAMP, Campinas, SP, Brazil. E-mail address: [email protected] (A.V. Sardeli).

http://dx.doi.org/10.1016/j.ijcard.2015.03.019 0167-5273/© 2015 Published by Elsevier Ireland Ltd.

which can improve arterial function in such specific regions [2,3]. In this way, both types of exercise are able to stimulate acute reductions in peripheral arterial stiffness and also improve arterial function after a period of training, nevertheless it seems to depend on proportion of exercised muscle mass and intensity of exercise [4]. However, regarding central arterial stiffness (aorta and carotid arteries), aerobic and resistance trainings may stimulated different adaptations. During aerobic exercise the moderate and continuous muscle contractions on whole body keep the central blood pressure a little elevated [5] which are expected to dilate slightly and continuously the central arteries. During resistance exercise the intense and intermittent muscle contractions on specific regions increase too much the central blood pressure [5] which are expected to dilate largely and intermittently the central arteries. The result of such difference is: aerobic training leads to reduction [1] while resistance training leads to increase in central arterial stiffness [6]. Thus, when researchers discuss the adaptation of arteries from different regions mixed, they are ignoring the existence of huge differences such as those. Returning to the findings of Montero et al. [1], only combined training (aerobic plus resistance) has caused different adaptations in arterial stiffness. Looking carefully to their Table 1, the original articles showing reduction in arterial stiffness were just the ones applying brachial–ankle PWV, which embraces central and peripheral arteries adaptation. Complementing this finding, the difference between aerobic (reduction of arterial stiffness) and combined training (maintenance of arterial stiffness), was seen just in trials applying carotid–femoral PWV (index of arterial stiffness just central). These findings perfectly fit to the current knowledge in this area, especially if we ponder the peculiarities of each type of exercise training. The combined training is composed by aerobic and resistance exercises. Thus, the stimulus to increase central arterial stiffness by resistance exercise may oppose the stimulus to reduce central arterial stiffness by aerobic exercise, resulting in the maintenance seen on carotid–femoral PWV with combined training. In contrast, as brachial–ankle PWV embraces central and peripheral arteries, in the studies which combined training reduced arterial stiffness, perhaps the reduction in the stiffness of some specific arteries overlap the increase in others. The physiological mechanisms able to explain the different adaptations between aerobic and resistance training on arterial stiffness are not well elucidated. But the different cardiovascular changes during exercise (described previously in 2nd paragraph), may alter the vessels' sympathetic tone, the vasoactive factors, or the elastic components of the arterial walls not in the same fashion to each type of exercise,

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which in turn will influence the diverse arterial stiffness adaptations founded. The main physiological mechanism currently pointed by researchers has been the intense and intermittent elevations in blood pressure during resistance exercise [7], surpassing the elastic limits of the central arterials walls, and consequently damaging their structure and load-bearing properties [8]; unlike the benefic effects from softly and continuous increases in blood pressure, seen during aerobic exercise, that might keep central arterial wall accustomed to stretching. Despite, we have put a little light in this controversial point regarding arterial stiffness and exercise training, research about the physiological mechanisms surrounding this phenomenon still crawling in the wide world of the physical exercise science. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] D. Montero, A. Vinet, C.K. Roberts, Effect of combined aerobic and resistance training versus aerobic training on arterial stiffness, Int. J. Cardiol. 178 (2015) 69–76.

[2] C. Goto, Y. Higashi, M. Kimura, K. Noma, K. Hara, K. Nakagawa, M. Kawamura, K. Chayama, M. Yoshizumi, I. Nara, Effect of different intensities of exercise on endothelium-dependent vasodilation in humans role of endothelium-dependent nitric oxide and oxidative stress, Circulation 108 (2003) 530–535. [3] R. Hambrecht, V. Adams, S. Erbs, A. Linke, N. Kränkel, Y. Shu, Y. Baither, S. Gielen, H. Thiele, J.F. Gummert, F.W. Mohr, G. Schuler, Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase, Circulation 107 (2003) 3152–3158. [4] D.H.J. Thijssen, A.J. Maiorana, G. O’Driscoll, N.T. Cable, M.T.E. Hopman, D.J. Green, Impact of inactivity and exercise on the vasculature in humans, Eur. J. Appl. Physiol. 108 (2010) 845–875. [5] L.B. Rowell, Human Circulation: Regulation During Physical Stress, Oxford University Press, 1986. [6] S.R. Collier, J.A. Kanaley, R. Carhart Jr., V. Frechette, M.M. Tobin, A.K. Hall, A.N. Luckenbaugh, B. Fernhall, Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives, J. Hum. Hypertens. 22 (2008) 678–686. [7] J.D. MacDougall, D. Tuxen, D.G. Sale, J.R. Moroz, J.R. Sutton, Arterial blood pressure response to heavy resistance exercise, J. Appl. Physiol. 58 (3) (Mar 1985) 785–790. [8] P.B. Dobrin, Mechanical factors associated with the development of intimal and medial thickening in vein grafts subjected to arterial pressure: a model of arteries exposed to hypertension, Hypertension 26 (1995) 38–43.

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