Effects of Ischemic Preconditioning on Maximal Exercise and Metaboreflex Activation

Ischemic preconditioning is a manipulation that uses short bouts of ischemia in order to “condition” the tissue and protect from future damage related to a lack of blood and oxygen delivery. While it is known that IPC has benefits in medical settings such as cardiothoracic surgery, its application to exercise as an ergogenic aid is newer and rapidly evolving. The relative hypoxic environment of skeletal muscle during high‐intensity exercise may be similar to that of ischemic conditions, which IPC can be used to protect against. Here, we tested the hypothesis that IPC improves maximal cycle exercise performance (maximum watts) and increases maximal aerobic capacity (VO 2 max, oxygen consumption) in healthy, young subjects. Given the relationship between exercise capacity and metaboreflex activation, we also tested the hypothesis that IPC attenuates muscle metaboreflex activation. Healthy, young, men and women (n=8, 22.5 ± 5.5 yrs) participated in counterbalanced experimental visits, each consisting of two protocols: one to test the effects of IPC on the metaboreflex, and one that investigated the effects of IPC on maximal cycle exercise. First, subjects underwent a 40‐minute IPC session (4 × 5 min thigh cuff inflation on each leg at a pressure of 200 mmHg). On the sham visit, cuffs were inflated to 10mmHg so that leg blood flow was not affected by the intervention. Next, in order to test IPC’s effects on the metaboreflex, subjects performed 2 minutes of continuous static handgrip exercise, at 40% of their max contraction weight. Ten seconds prior to exercise cessation, a standard blood pressure cuff was rapidly inflated to 200mmHg on the exercising arm in order to trap metabolites, stimulate afferent nerves, and trigger the metaboreflex. Systemic hemodynamics including heart rate (ECG) and non‐invasive beat‐to‐beat pressure (Finometer) were monitored throughout. Compared to the sham conditions, IPC attenuated the increase in MAP (mean ± s.d) from rest to static contraction (Δ2.8 ± 2.2 mmHg vs. Δ1.6 ± 1.5 mmHg; p=0.03) and from rest to the final minute of post‐exercise occlusion (Δ2.6 ± 2.5 mmHg vs Δ1.1 ± 2.5 mmHg; p=0.017). In order to test IPC’s effect on maximal‐effort exercise, subjects performed a maximal exercise test on an electronically‐braked ergometer (Velotron) and indirect calorimetry was performed to collect breath‐by‐breath metabolic measurements (True One 2400, Parvo). IPC did not significantly affect exercise performance as measured by max wattage output (260 ± 49W vs 258 ± 49W; p=0.68), or VO 2 max (41.6 ± 10.2 mL/Kg/min vs 43.5 ± 10.5 mL/Kg/min; p=0.53). While IPC did not impact maximal exercise, the finding that IPC can attenuate the body’s metaboreflex is of interest. Given we tested a young, healthy population, it is possible that the metaboreflex was not limiting exercise performance. Therefore, it may be of interest to investigate the potential benefit of IPC in diseased populations where an exaggerated metaboreflex activation can contribute to limitations in exercise capacity. Support or Funding Information American Physiological Society, UGSRF (SAL) University of Dayton University Honors Program (SAL)