AUTHOR=Lopes Thiago R. , Sabino-Carvalho Jeann L. , Ferreira Thiago H. N. , Succi José E. , Silva Antônio C. , Silva Bruno M. 

TITLE=Effect of Ischemic Preconditioning on the Recovery of Cardiac Autonomic Control From Repeated Sprint Exercise

JOURNAL=Frontiers in Physiology

VOLUME=9

YEAR=2018

URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2018.01465

DOI=10.3389/fphys.2018.01465

ISSN=1664-042X

ABSTRACT=<p>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 × 5 min at 220 mmHg) or control (CT; 3 × 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 180° 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 (<inline-formula><mml:math id="M1" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mover accent="true"><mml:mtext>V</mml:mtext><mml:mo>˙</mml:mo></mml:mover><mml:msub><mml:mtext>O</mml:mtext><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math></inline-formula>peak), peak carbon dioxide output (<inline-formula><mml:math id="M2" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mover accent="true"><mml:mtext>V</mml:mtext><mml:mo>˙</mml:mo></mml:mover><mml:msub><mml:mtext>O</mml:mtext><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math></inline-formula>peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of <inline-formula><mml:math id="M3" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mover accent="true"><mml:mtext>V</mml:mtext><mml:mo>˙</mml:mo></mml:mover><mml:msub><mml:mtext>O</mml:mtext><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:math></inline-formula> 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: <italic>P</italic> = 0.03; partial eta square (η<sup>2</sup><sub><italic>p</italic></sub>) = 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.</p>