Ischemic preconditioning does not alter muscle sympathetic responses to static handgrip and metaboreflex activation in young healthy men

Ischemic preconditioning (IPC) has been hypothesized to elicit ergogenic effects by reducing feedback from metabolically sensitive group III/IV muscle afferents during exercise. If so, reflex efferent neural outflow should be attenuated. We investigated the effects of IPC on muscle sympathetic nerve activity (MSNA) during static handgrip (SHG) and used post-exercise circulatory occlusion (PECO) to isolate for the muscle metaboreflex. Thirty-seven healthy men (age: 24 +/- 5years [mean +/- SD]) were randomized to receive sham (n=16) or IPC (n=21) interventions. Blood pressure, heart rate, and MSNA (microneurography; sham n=11 and IPC n=18) were collected at rest and during 2min of SHG (30% maximal voluntary contraction) and 3min of PECO before (PRE) and after (POST) sham or IPC treatment (3x5min 20mmHg or 200mmHg unilateral upper arm cuff inflation). Resting mean arterial pressure was higher following sham (79 +/- 7 vs. 83 +/- 6mmHg, P<0.01) but not IPC (81 +/- 6 vs. 82 +/- 6mmHg, P>0.05), while resting MSNA burst frequency was unchanged (P>0.05) with sham (18 +/- 7 vs. 19 +/- 9 bursts/min) or IPC (17 +/- 7 vs. 19 +/- 7 bursts/min). Mean arterial pressure, heart rate, stroke volume, cardiac output, and total vascular conductance responses during SHG and PECO were comparable PRE and POST following sham and IPC (All P>0.05). Similarly, MSNA burst frequency, burst incidence, and total MSNA responses during SHG and PECO were comparable PRE and POST with sham and IPC (All P>0.05). These findings demonstrate that IPC does not reduce hemodynamic responses or central sympathetic outflow directed toward the skeletal muscle during activation of the muscle metaboreflex using static exercise or subsequent PECO.