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Postexercise hypotension due to resistance exercise is not mediated by autonomic control: A systematic review and meta-analysis

      Highlights

      • Acute resistance exercise induces changes in blood pressure and autonomic control.
      • Greater sympathetic and lower vagal activity occurred with postexercise hypotension.
      • Autonomic changes after resistance exercise counteract blood pressure reduction.
      • Acute hypotension after resistance exercise is not mediated by autonomic control.

      Abstract

      Changes in autonomic control have been suggested to mediate postexercise hypotension (PEH). We investigated through meta-analysis the after-effects of acute resistance exercise (RE) on blood pressure (BP) and autonomic activity in individuals with normal and elevated BP. Electronic databases were searched for trials including: adults; exclusive RE interventions; and BP and autonomic outcomes measured pre- and postintervention for at least 30 min. Analyses incorporated random-effects assumptions. Thirty trials yielded 62 interventions (N = 480). Subjects were young (33.6 ± 15.6 yr), with systolic BP (SBP)/diastolic BP (DBP) of 124.2 ± 8.9/71.5 ± 6.6 mm Hg. Overall, RE moderately reduced SBP (normal BP: ~1 to 4 mm Hg, p < 0.01; elevated BP: ~1 to 12 mm Hg, p < 0.01) and DBP (normal BP: ~1 to 4 mm Hg, p < 0.03; elevated BP: ~0.5 to 7 mm Hg, p < 0.01), which was in general parallel to sympathetic increase (normal BP: g = 0.49 to 0.51, p < 0.01; elevated BP: g = 0.41 to 0.63, p < 0.01) and parasympathetic decrease (normal BP: g = −0.52 to −0.53, p < 0.01; elevated BP: g = −0.46 to −0.71, p < 0.01). The meta-regression showed inverse associations between the effect sizes of BP vs. sympathetic (SBP: slope − 0.19 to −3.45, p < 0.01; DBP: slope − 0.30 to −1.60, p < 0.01), and direct associations vs. parasympathetic outcomes (SBP: slope 0.17 to 2.59, p < 0.01; DBP: slope 0.21 to 1.38, p < 0.01). In conclusion, changes in BP were concomitant to sympathetic increase and parasympathetic decrease, which questions the role of autonomic fluctuations as potential mechanisms of PEH after RE.

      Keywords

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