Int J Sports Med 2013; 34(11): 1020
DOI: 10.1055/s-0033-1358670
Letter to the Editor
© Georg Thieme Verlag KG Stuttgart · New York

Letter to the Editor

A. Veiga Sardeli
A. F. Gáspari
Further Information

Publication History

Publication Date:
07 November 2013 (online)

Okamoto T , Masuhara M , Ikuta K . Low-Intensity Resistance Training after High-Intensity resistance training can prevent the increase of Central Arterial Stiffness . Int J Sports Med 2013 ; 34 : 385 – 390

Dear Editor

We have given some thought to the Okamoto’s group ideas about arterial stiffness. Although resistance training (RT) can increase central arterial stiffness (CAS) [4], it sometimes exhibits no change [2]. For this reason, Okamoto’s group has tried to explain the relation between several RT protocols and CAS.

In their recent publication [10], they concluded that the rise normally seen in CAS following high-intensity RT could be prevented by subsequent low-intensity RT. Looking carefully at these protocols, we are able to see only slight differences between them: the sessions of the protocol that they called BLRT were concluded with 3 high-intensity sets of 1 training item instead the 2 low-intensity sets seen in ALRT; BLRT and ALRT consisted of 30 and 25 sets of interposed intensity, respectively; BLRT always had 2-min rest interval following high-intensity sets and 30-s rest intervals following low-intensity sets, while ALRT had some of the high-intensity sets followed by a 30-s rest interval and some followed by a 2-min rest interval as well as low-intensity sets thereof. Thus, the groups performed the same exercises and intensities, but with small differences in sequence.

We reflected on the physiologic mechanisms able to justify the results obtained. We will not discredit the relation between CAS and chronic changes in autonomic modulation or in endothelial function, even though they are not always linked to CAS [6] [7]. However the total load of the protocols was strictly similar, and the small differences in the sequence of training intensity difficultly would justify these results through these mechanisms. Or is it possible that the last 2 low-intensity sets in ALRT have suppressed the acute sympathetic nervous activity in a different fashion than BLRT? Or should we perhaps believe that the maintenance of CAS was due to the enhanced production of vasodilators via hypoxia induced by low-intensity RT just in ALRT?

The known influence of vigorous and intermittent elevations in blood pressure (BP) during high-intensity RT on CAS is a mechanism that needs to be elucidated [5]. Higher elevations in BP and longer rest intervals possibly lead to more firing frequency from the arterial baroreceptors to the autonomic nervous system and add time to the baroreceptors reset until their next activation, offering an effective vasoconstrictive response [9]. On the other hand, small elevations in BP accompanied by short rest intervals may maintain the firing frequency from the baroreceptors, which in turn reduces the potential activation and generates less vasoconstrictive response, as is expected in excitable cells [1]. Anyway, in the Okamoto et al. [10] study, the only variation in the training protocols related to the baroreflex activation was the presence of a few long rest intervals preceded by different exercise intensities, which is unlikely to explain the differences found in CAS after 10 weeks of training.

Furthermore, no one could ensure that the results obtained by Okamoto et al. [10] are exactly the effects elicited for the ten weeks of the RT applied. The reason for this is that the time of measurement, i. e., the post-experimental period, was only 20 to 24 h after the last exercise bout. It is known that the effect of exercise over the endothelial function can last around 24 h [8]. This may be explained by the antioxidant imbalance caused by the last exercise bout, which consequently reduces the nitric oxide bioavailability (main contributor to the vasodilation). Likewise, we know the acute effect of the autonomic modulation recovery can last for this period [3], and might influence the vasodilation. Along these lines, one could regard the additional sets performed by the BLRT group as higher volume, which could provide more oxidative stress [8] or more autonomic imbalance [11], thereby interfering with CAS. Moreover, because the acute time recovery might vary inter-individually, the replicability of the Okamoto et al. [10] results cannot be guaranteed on a measurement taken after some days from the last training bout.

Finally, could the effects of the final exercise set change the effects of the entire session, supporting a chronic adaptation? Given that these results are largely unexplained by a physiological mechanism, we need more research to affirm that the low-intensity RT performed after high-intensity RT would prevent the increase in basal CAS.

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