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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Cerebral hemodynamics and resistance exercise.
PURPOSE: Repetitive resistance exercise with large muscle mass causes rapid fluctuations in mean arterial blood pressure (MAP). We sought to determine the effect of these fluctuations on the cerebrovasculature response determined by mean flow velocity (Vmean) of the middle cerebral artery.
METHODS: Nine subjects performed 10-repetition maximum leg press exercise. MAP was estimated by finger photoplethysmography, Vmean by Doppler ultrasound, and end-tidal CO2 (PETCO2) by mass spectrometry.
RESULTS: Vmean fluctuated with MAP with each repetition however averaged over the 10 repetitions, Vmean was unchanged from resting baseline values (66.9 +/- 10.8 vs 67.7 +/- 12.3 cm.s-1, baseline vs exercise, P > 0.05) despite an increased MAP (89.5 +/- 8.4 vs 105.0 +/- 4.9 Torr, P < 0.05). PETCO2 also remained unchanged from rest to exercise (37.7 +/- 2.8 vs 36.6 +/- 2.7 Torr, P > 0.05). Vmean decreased below resting levels for the first 5 s of recovery (59.8 +/- 9.1 cm.s-1, P < 0.05) as MAP returned rapidly to slightly below baseline (83.3 +/- 6.1, P > 0.05). MAP/Vmean, an index of cerebrovascular resistance, was elevated during exercise and returned to baseline after exercise. An increase in Vmean at 30 s post exercise (78.4 +/- 10.6 cm.s-1, P < 0.05) corresponded with elevated PETCO2 (43.0 +/- 4.8 Torr, P > 0.05).
CONCLUSION: The results suggest that fluctuations in MAP with individual muscle contractions during resistance exercise appear to be too rapid to be countered by cerebrovascular autoregulation. However, the progressive increase in MAP over a number of contractions was effectively countered to maintain Vmean near baseline values before a decrease in Vmean immediately after exercise.
METHODS: Nine subjects performed 10-repetition maximum leg press exercise. MAP was estimated by finger photoplethysmography, Vmean by Doppler ultrasound, and end-tidal CO2 (PETCO2) by mass spectrometry.
RESULTS: Vmean fluctuated with MAP with each repetition however averaged over the 10 repetitions, Vmean was unchanged from resting baseline values (66.9 +/- 10.8 vs 67.7 +/- 12.3 cm.s-1, baseline vs exercise, P > 0.05) despite an increased MAP (89.5 +/- 8.4 vs 105.0 +/- 4.9 Torr, P < 0.05). PETCO2 also remained unchanged from rest to exercise (37.7 +/- 2.8 vs 36.6 +/- 2.7 Torr, P > 0.05). Vmean decreased below resting levels for the first 5 s of recovery (59.8 +/- 9.1 cm.s-1, P < 0.05) as MAP returned rapidly to slightly below baseline (83.3 +/- 6.1, P > 0.05). MAP/Vmean, an index of cerebrovascular resistance, was elevated during exercise and returned to baseline after exercise. An increase in Vmean at 30 s post exercise (78.4 +/- 10.6 cm.s-1, P < 0.05) corresponded with elevated PETCO2 (43.0 +/- 4.8 Torr, P > 0.05).
CONCLUSION: The results suggest that fluctuations in MAP with individual muscle contractions during resistance exercise appear to be too rapid to be countered by cerebrovascular autoregulation. However, the progressive increase in MAP over a number of contractions was effectively countered to maintain Vmean near baseline values before a decrease in Vmean immediately after exercise.
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