PURPOSE: We tested the hypothesis that a strictly-controlled program of aerobic conditioning would increase vagal and decrease sympathetic responses to Valsalva straining. METHODS: Eleven young men performed a maximal aerobic capacity test, controlled frequency breathing (0.25 Hz), and three Valsalva maneuvers before and after 4 wk of exercise training on a cycle ergometer (30 min at > or = 70% max heart rate, 3 sessions. week-1). During controlled breathing and Valsalva straining, we recorded the electrocardiogram, noninvasive beat-by-beat arterial pressure, and peroneal nerve muscle sympathetic traffic at the popliteal fossa (pre- and postexercise sympathetic recordings were obtainable in 7 of 11 subjects). Vagal-cardiac tone was estimated from R-R interval standard deviations during controlled frequency breathing. Cardiovagal baroreflex sensitivity was derived from increases of R-R intervals as functions of increases in systolic pressures with linear regression analysis during phase IV pressure increases, and sympathetic sensitivity was derived from the quotient of total muscle sympathetic nerve activity and diastolic pressure changes during phase II pressure reductions. RESULTS: Exercise training increased VO2 max (3.38 +/- 0.10 pre-, and 3.64 +/- 0.11 L. min-1 postexercise; mean +/- SE; P = 0.04), R-R interval standard deviations (75 +/- 0.12 pre- and 94 +/- 0.14 ms postexercise; mean +/- SE; P = 0.03), and cardiovagal baroreflex sensitivity (15.0 +/- 1.1 pre-, and 25.0 ms. mm Hg-1 +/- 4.0 postexercise; mean +/- SE; P = 0.03). Exercise training did not change baseline sympathetic traffic (P = 0.31) or sympathetic nerve responses to diastolic pressure reductions (P = 0.12). CONCLUSIONS: Exercise training affects vagal and sympathetic mechanisms differently: cardiovagal baroreflex sensitivity is increased, but sympathetic responses to arterial pressure decreases are unchanged.
PURPOSE: We tested the hypothesis that a strictly-controlled program of aerobic conditioning would increase vagal and decrease sympathetic responses to Valsalva straining. METHODS: Eleven young men performed a maximal aerobic capacity test, controlled frequency breathing (0.25 Hz), and three Valsalva maneuvers before and after 4 wk of exercise training on a cycle ergometer (30 min at > or = 70% max heart rate, 3 sessions. week-1). During controlled breathing and Valsalva straining, we recorded the electrocardiogram, noninvasive beat-by-beat arterial pressure, and peroneal nerve muscle sympathetic traffic at the popliteal fossa (pre- and postexercise sympathetic recordings were obtainable in 7 of 11 subjects). Vagal-cardiac tone was estimated from R-R interval standard deviations during controlled frequency breathing. Cardiovagal baroreflex sensitivity was derived from increases of R-R intervals as functions of increases in systolic pressures with linear regression analysis during phase IV pressure increases, and sympathetic sensitivity was derived from the quotient of total muscle sympathetic nerve activity and diastolic pressure changes during phase II pressure reductions. RESULTS: Exercise training increased VO2 max (3.38 +/- 0.10 pre-, and 3.64 +/- 0.11 L. min-1 postexercise; mean +/- SE; P = 0.04), R-R interval standard deviations (75 +/- 0.12 pre- and 94 +/- 0.14 ms postexercise; mean +/- SE; P = 0.03), and cardiovagal baroreflex sensitivity (15.0 +/- 1.1 pre-, and 25.0 ms. mm Hg-1 +/- 4.0 postexercise; mean +/- SE; P = 0.03). Exercise training did not change baseline sympathetic traffic (P = 0.31) or sympathetic nerve responses to diastolic pressure reductions (P = 0.12). CONCLUSIONS: Exercise training affects vagal and sympathetic mechanisms differently: cardiovagal baroreflex sensitivity is increased, but sympathetic responses to arterial pressure decreases are unchanged.
Authors: Myles W O'Brien; Jarrett A Johns; Tristan W Dorey; Ryan J Frayne; Jonathon R Fowles; Said Mekary; Derek S Kimmerly Journal: Clin Auton Res Date: 2019-10-12 Impact factor: 4.435