Sympathetic outflow is modified during acute homeostatic stress through increased firing of low-threshold axons, recruitment of latent axons, and synaptic delay modifications. However, the role of central mechanisms versus peripheral-reflex control over sympathetic recruitment remains unknown. Here, we examined sympathetic discharge patterns during fatiguing static handgrip (SHG) exercise and post-exercise circulatory occlusion (PECO) to study the central versus peripheral-reflex elements of sympathetic neural coding. Muscle sympathetic nerve activity (MSNA; microneurography) was measured in six males (25±3 yrs) at baseline (3 minutes) and during 5 minutes of SHG exercise completed at 20% maximal voluntary contraction. Isolation of the peripheral metaboreflex component was achieved by PECO for 3 minutes. Action potential (AP) patterns were studied using wavelet-based methodology. Compared to baseline, total MSNA increased by minute three of SHG, remaining elevated throughout the duration of exercise and PECO (all P<0.05). The AP content per burst increased above baseline by minute four of SHG (4±2), remaining elevated at minute five (6±4) and PECO (4±4; all P<0.05). Similarly, total AP clusters increased by minute four of SHG (5±5), and remained elevated at minute five (6±3) and PECO (7±5; all P<0.01), indicating recruitment of latent sub-populations. Finally, the AP cluster size-latency profile was shifted downward during minute four (–32±22 ms) and five (–49±17 ms; both P<0.05) of SHG, but was not different than baseline during PECO (P>0.05). Our findings suggest that central perceptual factors play a specific role in the synaptic delay aspect of sympathetic discharge timing, whereas peripheral-reflex mechanisms affect recruitment of latent axons.