Journal
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
Volume 40, Issue 5, Pages 864-870Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e3181666f08
Keywords
autonomic nervous system; heart rate variability; blood pressure variability; resistance exercise
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Purpose: To test the association between exercise mode and the recovery pattern of baroreflex sensitivity (BRS) after exercise. Methods: The study population included healthy male subjects (N = 12, age: 31 +/- 3 yr). Four different interventions were performed in a randomized order: 1) aerobic exercise session on a bicycle ergometer, 2) light resistance exercise session, 3) heavy resistance exercise session, and 4) control intervention with no exercise. All interventions lasted 40 min. R - R intervals and continuous blood pressure were measured before (10 min) and 30 - 180 min after the interventions. BRSLF was calculated by the transfer function method from the low-frequency band (LF, 0.04 - 0.15 Hz) of the R - R intervals and systolic blood pressure spectra. Results: BRSLF had blunted until 30 min after aerobic and light resistance exercise (11.1 +/- 4.3 and 10.0 +/- 3.6 vs 17.5 +/- 7.0 ms.mm Hg (- 1), P = 0.002 for both, compared with the control intervention, respectively). However, BRSLF was significantly blunted until 60 min after heavy resistance exercise (9.3 +/- 2.3 vs 15.1 +/- 4.7 ms.mm Hg (- 1), P = 0.005, compared with the control intervention). The high-frequency power of R - R intervals (0.15 - 0.4 Hz) was significantly reduced, and the LF power of systolic blood pressure oscillation was significantly augmented 30 min after heavy resistance exercise (P < 0.01 for both), whereas both indices were restored to the control level by 30 min after aerobic and light resistance exercise. Conclusion: BRS after acute exercise is associated with exercise intensity, showing relatively rapid recovery after aerobic and light resistance exercise and delayed recovery after heavy resistance exercise. The delayed BRS pattern after heavy resistance exercise is regulated by delicate interplay between the withdrawal of vagal outflow and the probably increased sympathetic vasomotor tone documented by measurements of heart rate and blood pressure variability.
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