Baroreflex Resetting of Sympathetic Action Potential Subpopulations During Fatiguing Isometric Handgrip and Post‐Exercise Circulatory Occlusion

Abstract

The arterial baroreflex exerts heterogeneous control over the varying‐sized action potential (AP) subpopulations active within human muscle sympathetic nerve activity (MSNA) under baseline conditions. How baroreflex control of sympathetic AP discharge becomes reset to facilitate sympathoexcitation during physical exercise remains to be investigated. Therefore, we quantified the baroreflex gain for each sympathetic AP cluster (i.e., reflecting different c‐fibres) within the MSNA filtered neurogram (microneurography and continuous wavelet transform) during baseline conditions (BSL), the last 2‐min of a 5‐min fatiguing isometric handgrip (20% of max; IHG), and during post‐exercise circulatory occlusion (PECO) in six healthy young participants (3 females, 23–31 years). Baroreflex gain was measured as the slope of the linear function between AP probability (%) versus diastolic blood pressure (DBP; Finometer). We classified AP clusters based on peak‐to‐peak amplitude using the following allocations: small (clusters 1–2), medium (clusters 3–8) and large (clusters 9–15). During BSL, medium AP clusters (e.g., cluster 3: −9.4 ± 2.7 %/mmHg) expressed the greatest baroreflex gains while small (e.g., cluster 1: −1.9 ± 0.4 %/mmHg) and large (e.g., cluster 9: −2.4 ± 0.9 %/mmHg) clusters expressed lesser gains (both P < 0.05 vs. cluster 3). Compared to BSL, baroreflex functions for most AP clusters during IHG and PECO were reset upwards to greater firing probabilities (both Condition‐by‐Cluster Interactions: P < 0.05) and rightwards to higher DBP (BSL: 69 ± 4, IHG: 81 ± 3, PECO: 79 ± 2 mmHg; both P < 0.05 vs. BSL). However, compared to BSL, the gains of the AP cluster baroreflex functions remained unchanged with IHG (e.g., cluster 1: −1.6 ± 0.4, cluster 3: −8.2 ± 2.9, cluster 9: −4.3 ± 1.8 %/mmHg, Main Effect: P > 0.05). Nonetheless, AP cluster gains were augmented above BSL during PECO (e.g., cluster 1: −2.6 ± 1.0, cluster 3: −16.0 ± 4.4, cluster 9: −5.5 ± 1.8 %/mmHg; Main Effect: P < 0.05). IHG (e.g., cluster 15: −1.6 ± 0.5 %/mmHg) and PECO (e.g., cluster 15: −0.6 ± 0.3 %/mmHg) recruited a subpopulation of previously silent larger and faster conducting APs that expressed weak baroreflex gains. These data suggest that during fatiguing isometric handgrip exercise the interaction between the central command feature and the skeletal muscle metaboreflex resets baroreflex control of discrete AP subpopulations to higher blood pressures and greater levels of discharge. In addition to resetting the baroreflex functions, independent activation of the muscle metaboreflex augments the strength of baroreflex control over subpopulations of previously active APs.Support or Funding InformationSupported by the Natural Sciences and Engineering Research Council (NSERC) of Canada.