In agreement with previous research, our results show that an acute RE bout causes central arterial stiffening with no change in distensibility in the peripheral arteries (8,9,11,16,22,32). Furthermore, the increase in central artery stiffness was associated with a decrease in TPR and an increase in vasodilatory capacity, without any significant changes in blood pressure. Mean arterial pressure was similar after both exercise modalities. Thus, changes in blood pressure per se cannot account for the differential changes in arterial stiffness after acute RE compared to AE. Several studies have suggested that because arterial stiffness was only observed in the central arteries and not in the peripheral arteries, the decrease in distensibility may only be a limited mechanical phenomenon or a transient result of acute RE (11,16,18). Also consistent with previous findings, we found that AD increases after an acute AE bout (9,11,16,18,22,32). However, we found that this increase in AD was not accompanied by an increase in vasodilatory capacity, nor was there a decrease in TPR or MAP after the aerobic bout. This implies that the changes in AD after AE may not be associated with vasodilatation of the microvascular beds.
To our knowledge, this is the first study to investigate the response of peripheral resistance arteries to RH after an acute bout of aerobic vs. resistance training. One study has shown that an acute bout of maximal AE did not change peak flow in response to RH (4), but overall blood flow was increased. This finding supports our observation that peak FBF did not increase in response to RH and thus cannot explain the decrease in arterial stiffness after AE. Additionally, contrary to the findings of Baynard et al., we did not observe an increase in the AUC for vasodilatory capacity after AE (4). This disparate finding may be related to the timing of the measurement and the intensity of the exercise, because they measured vasodilatory capacity immediately after a maximal exercise test. We measured vasodilatory capacity 60 minutes after an acute 30-minute submaximal AE bout; thus, it is possible that the residual effects of the exercise were no longer present, explaining the lack of a response in our study.
Because our subjects were all young and healthy, it is possible that our RE bout yielded a more intense physiologic stimulus compared to the aerobic bout, but it is very difficult if not impossible to equate exercise intensity between AE and RE. Certainly, the muscle stimulus may be greater during the type of resistance training employed in our study, but it is unclear if that would be associated with a greater stimulus for blood flow and increased shear stress. It is possible that the muscle ischemic response to RE may elicit a lingering effect that may have enhanced the RH response more so than what we observed for AE. Thus, an increase in relaxing factors from local contractions may explain the differences in flow response from the resistance compared to the aerobic bout (14).
A limitation to the interpretation of the results of this study is that matching the exercise intensity of the RE vs. AE is difficult at best. Therefore, our exercise and intensity choices were guided by guidelines from the American College of Sports Medicine Position Stand (2) and conducted as sessions commonly practiced.
There is a great need to compare exercise modes directly in current research, especially because acute bouts of exercise have divergent effects on the systemic physiology. The present study indicates that an acute bout of RE shows many favorable cardiovascular benefits and should therefore be considered as part of a daily exercise training program. Further, for the clinical end user, RE may offer greater benefits from the increases in blood flow to active muscles and could be implemented as companion to an aerobic training regimen.
This study was funded in part by a Michael Pollock Grant from Life Fitness (PI, Scott R. Collier). The author would like to express thanks to the subjects that participated in this study.
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