Ergogenic effect of ischemic preconditioning is not directly conferred to isolated skeletal muscle via blood.

PURPOSE: Ischemic preconditioning (IPC) in humans has been demonstrated to confer ergogenic benefit to aerobic exercise performance, with an improvement in the response rate when the IPC stimulus is combined with concurrent exercise. Despite potential performance improvements, the nature of the neuronal and humoral mechanisms of conferral and their respective contributions to ergogenic benefit remain unclear. We sought to examine the effects of the humoral component of ischemic preconditioning on skeletal muscle tissue using preconditioned human serum and isolated mouse soleus. METHODS: Isolated mouse soleus was electrically stimulated to contract while in human serum preconditioned with either traditional (IPC) or augmented (AUG) ischemic preconditioning compared to control (CON) and exercise (ERG) preconditioning. Force frequency (FF) curves, twitch responses, and a fatigue-recovery protocol were performed on muscles before and after the addition of serum. After preconditioning, human participants performed a 4 km cycling time trial in order to identify responders and non-responders to IPC. RESULTS: No differences in indices of contractile function, fatiguability, nor recovery were observed between conditions in mouse soleus muscles. Further, no human participants improved performance in a 4-km cycling time trial in response to traditional nor augmented ischemic preconditioning compared to control or exercise conditions (CON 407.7 ± 41.1 s, IPC 411.6 ± 41.9 s, ERG 408.8 ± 41.4 s, AUG 414.1 ± 41.9 s). CONCLUSIONS: Our findings do not support the conferral of ergogenic benefit via a humoral component of IPC at the intracellular level. Ischemic preconditioning may not manifest prominently at submaximal exercise intensities, and augmented ischemic preconditioning may have a hormetic relationship with performance improvements.

Cardiac autonomic recovery following traditional and augmented remote ischemic preconditioning.

PURPOSE: While the possible ergogenic benefits of remote ischemic preconditioning (RIPC) make it an attractive training modality, the mechanisms of action remain unclear. Alterations in neural tone have been demonstrated in conjunction with circulatory occlusion, yet investigation of the autonomic nervous system following RIPC treatment has received little attention. We sought to characterize alterations in autonomic balance to both RIPC and augmented RIPC (RIPCaug) performed while cycling, using acute and sustained autonomic indices. METHODS: Thirteen participants (8M:5F) recorded baseline waking heart rate variability (HRV) for 5 days prior to treatment. Participants then completed control exercise (CON), RIPC, and RIPCaug interventions in a randomized cross-over design. Cardiovascular measurements were recorded immediately before and after each intervention at rest, and during an orthostatic challenge. Waking HRV was repeated the morning after each intervention. RESULTS: RIPC resulted in acutely reduced resting heart rates (HR) (∆ - 4 ± 6 bpm, P = 0.02) and suppressed HR 30 s following the orthostatic challenge compared to CON (64 ± 10 vs 74 ± 9 bpm, P = 0.003). RIPCaug yielded elevated HRs compared to CON and RIPC prior to (P = 0.003) and during the orthostatic challenge (P = 0.002). RIPCaug reduced LnSDNN (Baseline 4.39 ± 0.27; CON 4.44 ± 0.39; RIPC 4.41 ± 0.34; RIPCaug 4.22 ± 0.29, P = 0.02) and LnHfa power (Baseline 7.82 ± 0.54; CON 7.73 ± 1.11; RIPC 7.89 ± 0.78; RIPCaug 7.23 ± 0.87, P = 0.04) the morning after treatment compared to all other conditions. CONCLUSIONS: Our data suggest that RIPC may influence HR acutely, possibly through a reduction in cardiac sympathetic activity, and that RIPCaug reduces HRV through cardiac vagal withdrawal or increased cardiac sympathetic modulation, with alterations persisting until the following morning. These findings imply a dose-response relationship with potential for optimization of performance.