Key result
Resistance exercise induces complex hemodynamic and shear rate changes that require evaluation during rather than solely after exercise to fully understand its effects on endothelial function.
This editorial emphasizes the need to evaluate shear rate profiles and hemodynamic changes during, rather than just after, resistance exercise to fully understand its impact on endothelial function.
Aerobic exercise enhances flow-mediated dilatation (FMD), an index of endothelial function, but this favourable effect is abolished when it mechanically attenuates shear rate (SR) (Tinken et al., 2009). These findings suggest that an exercise-induced increase in SR rather than systemic cardiovascular changes is a crucial stimulus for the improvement of endothelial function (Green, Hopman, Padilla, Laughlin, & Thijssen, 2017). In contrast, resistance exercise, an important component of health-promoting exercise programmes, decreases FMD in both active (Gonzales, Thompson, Thistlethwaite, & Scheuermann, 2011) and inactive limbs (Morishima, Tsuchiya, Iemitsu, & Ochi, 2018). The mechanism responsible for the acute attenuation of FMD after resistance exercise remains unclear, but changes in the SR profile and in the haemodynamic parameters during resistance exercise are speculated to provide key information that can help in elucidating these mechanisms. In this regard, in this issue of Experimental Physiology Thomas and colleagues (2020) tested the acute effect of resistance exercise on the SR profile in active and inactive limbs in young adults. Thomas et al. (2020) explored the acute effects of resistance exercise (three sets of 10 isotonic repetitions of bicep curls or knee extensions, with ∼5 min rest between sets) on the blood flow (BF) and SR in the brachial and superficial femoral arteries. Doppler and blood pressure (BP) measurements were performed before and for 3 min after each set. Systolic and diastolic BPs increased to a similar extent after the upper limb (UL) and lower limb (LL) exercises (systolic BP, +36–38 mmHg; diastolic BP, +23–24 mmHg). In the active limb, anterograde SR was increased but retrograde SR was abolished after UL and LL exercises. In contrast, in the inactive limb, anterograde SR was observed to increase, with no significant change in retrograde SR, after both exercises. Collectively, Thomas et al. (2020) concluded that resistance exercises, regardless of whether they involve the UL or LL, do not appear to result in detrimental SR profiles in the active and inactive limbs, at least after the exercises. Regarding the context of their interesting study, three important questions for discussion arise. First, can the effects of resistance exercise on endothelial function be evaluated by the postexercise SR profile? Second, should we consider that different types of resistance exercises cause large differences in SR profile in addition to haemodynamic parameters? Third, are physiological implications of retrograde SR during resistance exercise different from that of dynamic exercise? First, the study by Thomas and colleagues (2020) assessed the SR profile after participation in resistance exercise, but it remains unclear to what extent the response during exercise can be evaluated by the data obtained after exercise. Indeed, enhanced brachial anterograde SR was significantly blunted (25–50% reduction) and retrograde SR was abolished immediately after leg cycling (Atkinson et al., 2015), suggesting that the postexercise SR profile does not fully represent changes in SR during aerobic exercise. Given that the SR during exercise is the key stimulus for vascular adaptation (Tinken et al., 2009), most studies have investigated SR during aerobic exercise. In contrast, BPs change drastically during heavy resistance exercise. There is an elevation of BP up to fourfold during concentric contraction, and it decreases rapidly during eccentric contraction (MacDougall, Tuxen, Sale, Moroz, & Sutton, 1985). These haemodynamic changes during resistance exercise might greatly influence the SR profiles in the active and inactive limbs. Thus, resistance exercise might enlarge the differences in SR profile and haemodynamic parameters during exercise and postexercise compared with that of aerobic exercise. Despite the technical difficulties, previous work has examined the SR in the active limb during resistance exercise (Gonzales et al., 2011). The differences in the SR pattern between the active and inactive limbs might be emphasized during exercise compared with those after exercise; therefore, further studies that evaluate the SR profile during resistance exercise are needed in order to understand the resistance exercise-specific vascular changes. Second, different exercise modes (i.e. isometric or dynamic, speed, intensity, range of muscle contraction, the ratio of contraction and relaxation time, etc.) also affect SR and haemodynamic changes during resistance exercise. For example, sustained isometric contraction elevates intramuscular pressure with increasing exercise intensity and impedes or even occludes BF (Sadamoto, Bonde-Petersen, & Suzuki, 1983). In contrast, during dynamic resistance exercise, BF is restricted during the contraction phase, but postcontraction hyperaemia occurs during the relaxation phase (Gonzales et al., 2011). However, even during dynamic resistance exercise, a slower contraction speed can cause a sustained increase in intramuscular pressure with greater production of muscle metabolites in comparison to that of faster contractions. In this regard, brachial anterograde and retrograde SR were higher during fast contraction than slow contraction during the handgrip exercise (Gonzales et al., 2011). Moreover, high-intensity resistance exercise causes an extreme elevation in BP, attributable, in part, to the increased intrathoracic pressure caused by the Valsalva manoeuvre (MacDougall et al., 1985). Considering the large differences in haemodynamic parameters and SR profiles between different types of resistance exercise, the findings of Thomas et al. (2020) cannot be extrapolated directly to other exercises, such as isometric or higher-intensity resistance exercises. Third, it has been reported that retrograde SR has pro-atherogenic effects on the endothelium (Green et al., 2017), and in the study by Thomas et al. (2020), the change in retrograde SR was minimal after resistance exercise. Thus, they presumed that resistance exercises were not associated with detrimental SR profiles. However, given the deleterious influence of retrograde SR on the endothelium, it seems paradoxical that acute aerobic exercise increases retrograde SR in the inactive limb despite favourable adaptations to chronic exercise training (i.e. improvement in FMD; Green et al., 2017). Brachial retrograde SR is enhanced at the onset of leg cycling but gradually returns towards baseline levels owing to thermoregulatory cutaneous vasodilatation (Green et al., 2017), indicating that the increase in retrograde SR is transient during dynamic exercise. In addition, Tinken et al. (2009) revealed that cycling and handgrip exercise increased both anterograde and retrograde SR but induced similar levels of improvement in FMD, suggesting that an increase in anterograde SR might prevent the detrimental effects of retrograde SR during exercise. More importantly, Holder et al. (2019) recently reported that fluctuations in SR induced by intermittent negative pressure acutely improved brachial FMD even with an unaltered mean SR. Intermittent negative pressure-increased anterograde SR followed by a pressure release mediates increased retrograde SR. Similar to this, external counterpulsation (sequential inflation and deflation of compressible cuffs) increases anterograde and retrograde SR, resulting in an enhanced FMD (Gurovich & Braith, 2013). These findings indicate that SR fluctuation itself might have positive effects on the endothelium and that the contraction-induced increase in retrograde SR during resistance exercise might have different physiological implications from the continuous increase in retrograde SR, as seen in ageing and sympathetic activation. Interestingly, recent studies have presumed that a higher pressor response during resistance exercise rather than changes in SR is responsible for the acute decrease in FMD (Gonzales et al., 2011; Morishima et al., 2018). Thus, the physiological implications of retrograde SR during resistance exercise might be different from that of dynamic exercise. Collectively, evaluating the relationship between the SR profile and the haemodynamic changes during resistance exercise and postexercise FMD might be useful in identifying effective resistance exercise programmes for the improvement of endothelial function or muscular fitness, without a decline in vascular function. However, these important unresolved questions still need to be investigated. None declared. Both authors contributed to the drafting and revision of the manuscript. Both authors approved the final version of the manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed.
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Iwamoto et al. (2020) reported an editorial. Resistance exercise was evaluated. Resistance exercise induces complex hemodynamic and shear rate changes that require evaluation during rather than solely after exercise to fully understand its effects on endothelial function.
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