Key result
Ischemic preconditioning increased short-term heart rate recovery at 60 seconds by 12.8% after repeated sprint exercise compared to control, without changing long-term recovery or energy metabolism.
Why the study?
Does ischemic preconditioning improve recovery of cardiac autonomic control from repeated sprint exercise in healthy men?
RCT (n=15)
Single-blind
Randomized
No
Does ischemic preconditioning improve recovery of cardiac autonomic control from repeated sprint exercise in healthy men?
Effect estimate: 12.8% change (95% CI 5.8-19.7)
p-value: p=0.03
Ischemic preconditioning accelerates short-term heart rate recovery after repeated sprint exercise in healthy men, without altering energy metabolism.
Supports IPC for faster autonomic recovery after repeated sprints in healthy men; extends prior findings to this exercise protocol.
Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i.e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 x 5 min at 220 mmHg) or control (CT; 3 x 5 min at 20 mmHg) 48 h, 24 h and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180º change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake (V̇O2peak), peak carbon dioxide output (V̇CO2peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of V̇O2 decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: P = 0.03; partial eta square (η2p) = 0.27, i.e. large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.
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Lopes et al. (2018) conducted an RCT in Healthy team-sport practitioners (n=15). Ischemic preconditioning vs. Control (3 x 5 min at 20 mmHg) was evaluated on Heart rate recovery at 60 seconds (HRR60s) (12.8% change, 95% CI 5.8-19.7, p=0.03). Ischemic preconditioning increased short-term heart rate recovery at 60 seconds by 12.8% after repeated sprint exercise compared to control, without changing long-term recovery or energy metabolism.
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