Reply to “Letter to the editor: ‘Deconstructing the dogma of sympathetic restraint and its role in the cardiovascular response to exercise’”

: We thank Dr. Tschakovsky (3) for his interest andenthusiasm regarding our recent study (1) dealing with sym-pathetic control of blood ow in different tissues of the leg inhumans at rest and during exercise. Dr. Tschakovsky impor-tantly emphasises that exercise-evoked vasodilation cannotdirectly spread from the active quadriceps muscle group to theinactive hamstring muscles. This was not what we literallymeant, and although according to our understanding ascendingvasodilatation and its spread to inactive tissues could be con-tributing to some marginal extent, his concern in this regardwas apparently mainly raised from our integration of ourndings with those of Moore and colleagues (2), togethersuggesting that -adrenergic-mediated sympathetic constraintis important for optimization of blood ow and oxygen extrac-tion to the most metabolically active tissues of the limb. Wealso fully agree with Dr. Tschakovsky that investigating bloodow in active versus inactive muscle groups is not the samething as investigating blood ow around active versus inactivemuscle bers within an exercising muscle. We tried to empha-sise this notion already in the introduction of our paper (1).Regarding the ndings from -adrenergic blockade duringexercise, we indeed could not document any change in bloodow in the exercising muscle. Increased blood ow occurred ininactive muscles and other tissues, indeed very much challeng-ing the common belief that there is sympathetic constraint inthe vasculature of active muscles during exercise, as pointedout by Dr. Tschakovsky (3). Moreover, to the best of ourknowledge, previous research in this area has relied on ratherindirect assessments and estimations. Our study is one of therst to directly and quantitatively address this topic in humans.However, as also discussed in the original report (1), we madeour observations during fairly low-intensity exercise, whenalso an only fairly small mass of active muscle was exercising.Thus, even if methodologically quite challenging, it still re-mains to be tested whether the ndings are similar at higherexercise intensities and particularly when performing wholebody exercise. In those conditions, it might well be that somesympathetic restraint is needed also in active muscle vascula-ture. At this moment, there is little human experimental evi-dence to support this idea, despite some indirect estimations. Inall, we think that the insightful comments of Dr. Tschakovskywill help vascular and exercise physiologists to better under-stand sympathetic regulation of cardiovascular function duringexercise in humans.