Key result
High-intensity muscle metaboreflex activation attenuated the muscle pump-induced inhibition of MSNA burst frequency during low-intensity leg cycling (-1% vs -39% with cycling alone).
Why the study?
Data were lacking on whether high-intensity muscle metaboreflex activation attenuates muscle pump-induced inhibition of muscle sympathetic nerve activity during leg cycling.
Does high-intensity muscle metaboreflex activation attenuate muscle pump-induced inhibition of MSNA during leg cycling?
Does high-intensity muscle metaboreflex activation attenuate muscle pump-induced inhibition of MSNA during leg cycling?
Absolute Event Rate: -1% vs -39%
p-value: p=0.845
Muscle metaboreflex activation attenuates the inhibition of muscle sympathetic nerve activity during low-intensity leg cycling in an intensity-dependent manner.
Muscle sympathetic nerve activity (MSNA) decreases during leg cycling at low intensity because of muscle pump-induced increases in venous return and loading of the cardiopulmonary baroreceptors. However, MSNA increases during leg cycling when exercise is above moderate intensity or for a long duration, suggesting that the sympathoinhibitory effect of the cardiopulmonary baroreflex can be overridden by a powerful sympathoexcitatory drive, such as the skeletal muscle metaboreflex. Therefore, we tested the hypothesis that high-intensity muscle metaboreflex activation attenuates muscle pump-induced inhibition of MSNA during leg cycling. MSNA (left radial nerve) was recorded during graded isolation of the muscle metaboreflex in the forearm with postexercise ischemia (PEI) after low (PEI-L)- and high (PEI-H)-intensity isometric handgrip exercise (20% and 40% maximum voluntary contraction, respectively). Leg cycling (15–20 W) was performed alone and during each PEI trial (PEI-L+Cycling, PEI-H+Cycling). Cycling alone induced a significant decrease in MSNA burst frequency (BF) and total activity (TA). MSNA BF and TA also decreased when cycling was performed during PEI-L. However, the magnitude of decrease in MSNA during PEI-L+Cycling [∆BF: –19 ± 2% ( P < 0.001), ∆TA: –25 ± 4% ( P < 0.001); mean ± SE] was less than that during cycling alone [∆BF: –39 ± 5% ( P = 0.003), ∆TA: –45 ± 5% ( P = 0.002)]. More importantly, MSNA did not decrease during cycling with PEI-H [∆BF: –1 ± 2% ( P = 0.845), ∆TA: +2 ± 3% ( P = 0.959)]. These results suggest that muscle pump-induced inhibition of sympathetic vasomotor outflow during low-intensity leg cycling is attenuated by muscle metaboreflex activation in an intensity-dependent manner. NEW & NOTEWORTHY There are no available data concerning the interaction between the sympathoinhibitory effect of muscle pump-induced cardiopulmonary baroreflex loading during leg cycling and the sympathoexcitatory influence of the muscle metaboreflex. In this study, muscle metaboreflex activation attenuated the inhibition of muscle sympathetic nerve activity (MSNA) during leg cycling. This may explain, in part, the response of MSNA to graded-intensity dynamic exercise in which low-intensity leg cycling inhibits MSNA whereas high-intensity exercise elicits graded sympathoexcitation.
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Katayama et al. (2019) studied this question. Leg cycling with concurrent postexercise ischemia (PEI) after high-intensity isometric handgrip exercise vs. Leg cycling alone was evaluated on Change in muscle sympathetic nerve activity (MSNA) burst frequency (BF) (p=0.845). High-intensity muscle metaboreflex activation attenuated the muscle pump-induced inhibition of MSNA burst frequency during low-intensity leg cycling (-1% vs -39% with cycling alone).
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