The impact of remote ischemic preconditioning on cardiac biomarker and functional response to endurance exercise.

Remote ischemic preconditioning (RIPC; repeated short reversible periods of ischemia) protects the heart against subsequent ischemic injury. We explored whether RIPC can attenuate post-exercise changes in cardiac troponin T (cTnT) and cardiac function in healthy individuals. In a randomized, crossover design, 14 participants completed 1-h cycling time trials (TT) on two separate visits; preceded by RIPC (arms/legs, 4 × 5-min 220 mmHg), or SHAM-RIPC (20 mmHg). Venous blood was sampled before and 0-, 1-, and 3-h post-exercise to assess high sensitivity (hs-)cTnT and brain natriuretic peptide (NT-proBNP). Echocardiograms were performed at the same time points to assess left and right ventricular systolic (ejection fraction; EF and right ventricular fractional area change; RVFAC, respectively) and diastolic (early transmitral flow velocities; E) function. Baseline hs-cTnT was not different between RIPC and SHAM. Post-exercise hs-cTnT levels were consistently lower following RIPC (18 ± 3 vs 21 ± 3; 19 ± 3 vs 23 ± 3; and 20 ± 2 vs 25 ± 2 ng/L at 0, 1 and 3-h post-exercise, respectively; P < 0.05). There was no main effect of time, trial, or interaction for NT-proBNP and left ventricular EF or RVFAC (all P < 0.05). A main effect of time was evident for E which transiently declined immediately after exercise to a similar level in both trials (0.85 ± 0.04 vs 0.74 ± 0.04 m/s, respectively; P < 0.05). In summary, RIPC was associated with lower hs-cTnT levels after exercise but there was no independent effect of RIPC for NT-proBNP or LV systolic and diastolic function. The lower hs-cTnT levels after RIPC suggests that further research should evaluate the role of ischemia in exercise-induced elevation in hs-cTnT.