L S Goodman1, R D Banks, J D Grissett, P L Saunders. 1. Defence and Civil Institute of Environmental Medicine, Aerospace Life Support Section, Toronto, Ontario, Canada. len.goodman@dciem.dnd.ca
Abstract
BACKGROUND: The push-pull effect has been defined previously as decreased +Gz tolerance caused by previous baseline zero or -Gz exposure. Earlier work indicates that the delay in BP (BP) recovery during +Gz is a function of time at -G7, and is due to the lengthened time-course of sympathetically mediated peripheral vasoconstriction. HYPOTHESIS: The purpose of this study was to retrospectively determine whether heart rate (HR) varies with BP as duration at preceding -Gz increased. METHODS: Continuous ECG R-R interval data from 15 s of +2.25Gz after preceding 2, 5, 10, or 15 s at 2Gz obtained from previous experiments were analyzed and compared with the previously reported BP data. Repeated measures ANOVA and regression analyses were used to compare +2.25Gz HR responses after the four -Gz conditions and one control +2.25Gz condition. RESULTS: An initial rapid rise in HR was observed for all conditions with a consistent steady-state plateau achieved after the first 7 s of +2.25Gz. However, there were significant differences in mean HR attained during the +2.25Gz plateau for preceding 15 s -2.0 Gz vs. the control, 2, 5, and 10s -Gz conditions (109+/-1.1 vs. 102+/-1.8, 100+/-2.0, 97+/-1.1 and 101+/-1.1, bpm, respectively; p<0.05). CONCLUSIONS: HR, unlike BP, increases briskly across all preceding -Gz time conditions, adapting within the initial baroreflex-compensatory time frame typically expected for +Gz exposures. These results suggest there may be a threshold effect for HR response. Consequently, vasoconstrictor response is a critical adaptive mechanism during +Gz when preceded by long (>10 s) -Gz exposures.
BACKGROUND: The push-pull effect has been defined previously as decreased +Gz tolerance caused by previous baseline zero or -Gz exposure. Earlier work indicates that the delay in BP (BP) recovery during +Gz is a function of time at -G7, and is due to the lengthened time-course of sympathetically mediated peripheral vasoconstriction. HYPOTHESIS: The purpose of this study was to retrospectively determine whether heart rate (HR) varies with BP as duration at preceding -Gz increased. METHODS: Continuous ECG R-R interval data from 15 s of +2.25Gz after preceding 2, 5, 10, or 15 s at 2Gz obtained from previous experiments were analyzed and compared with the previously reported BP data. Repeated measures ANOVA and regression analyses were used to compare +2.25Gz HR responses after the four -Gz conditions and one control +2.25Gz condition. RESULTS: An initial rapid rise in HR was observed for all conditions with a consistent steady-state plateau achieved after the first 7 s of +2.25Gz. However, there were significant differences in mean HR attained during the +2.25Gz plateau for preceding 15 s -2.0 Gz vs. the control, 2, 5, and 10s -Gz conditions (109+/-1.1 vs. 102+/-1.8, 100+/-2.0, 97+/-1.1 and 101+/-1.1, bpm, respectively; p<0.05). CONCLUSIONS: HR, unlike BP, increases briskly across all preceding -Gz time conditions, adapting within the initial baroreflex-compensatory time frame typically expected for +Gz exposures. These results suggest there may be a threshold effect for HR response. Consequently, vasoconstrictor response is a critical adaptive mechanism during +Gz when preceded by long (>10 s) -Gz exposures.