Physiologic + G z Tolerance Responses Over ... - IngentaConnect

RESEARCH ARTICLE

Physiologic +Gz Tolerance Responses Over Successive +Gz Exposures in Simulated Air Combat Maneuvers Sophie Lalande and Fred Buick LALANDE S, BUICK F. Physiologic 1Gz tolerance responses over successive 1Gz exposures in simulated air combat maneuvers. Aviat Space Environ Med 2009; 80:1032–8. Introduction: Fighter aircraft pilots are exposed to repetitive headward acceleration (1Gz) during air combat maneuvering. The objective of this study was to compare physiologic responses and the calculated 1Gz tolerances of multiple successive 1Gz exposures with the responses of the first 1Gz exposure. Methods: There were 13 subjects who performed simulated air combat maneuvering (SACM) profiles composed of 10 rapid-onset rate 1Gz cycles with different combinations of short- or long-duration 1Gz plateaus (8 or 20 s) and 1Gz pauses (1 or 15 s). 1Gz plateaus were individually set at levels inducing strong physiologic responses while the 1Gz pause was set at 1.4 Gz. Head-level systolic pressure, ear opacity, and vision quality were measured. Results: The nadirs of head-level systolic pressure, ear opacity, and visual quality during each 1Gz plateau were higher in subsequent cycles compared to the first 1Gz cycle. There was an average increase in calculated 1Gz tolerance of 0.35 6 0.21 Gz following the first 1Gz cycle. SACMs with short 1Gz pauses produced greater increases in 1Gz tolerance than SACMs with long 1Gz pauses. Discussion: Cardiovascular and visual responses were improved over the course of successive 1Gz cycles, indicating that the risk of 1Gz-induced loss of consciousness was not increased beyond the first 1Gz cycle. The increase in 1Gz tolerance beginning with the second cycle is attributed to a carryover of compensatory responses, primarily vasoconstriction, with possible contribution from greater venous return and baroreflex enhancement. Keywords: hypergravity, centrifuge, human, baroreflex, blood pressure, visual field.

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HE HUMAN PHYSIOLOGICAL response to a single exposure of high head-ward acceleration (1Gz) is well known (26,28). However, much less is known about the ability to withstand 1Gz, or 1Gz tolerance, during short-term, repeated 1Gz exposures. As reported by Newman and Callister (14), the air combat maneuvering environment is characterized by frequent and repetitive excursions to high 1Gz levels over several minutes. A reduction in 1Gz tolerance during such a series of repetitive 1Gz exposures could increase the risk of 1Gzinduced loss of consciousness (G-LOC) (27). 1Gz exposure induces a rapid decrease in head-level blood pressure, which unloads the carotid baroreceptors, causing increases in heart rate and cardiac contractility as well as vasoconstriction and venoconstriction in trying to protect head-level blood pressure (8,19,21,28). From past centrifuge studies, the ability to withstand 1Gz during successive 1Gz exposures is unclear, with two reports suggesting reduced tolerance (9,22) and two demonstrating improved tolerance (10,12). The former would not be unexpected given that blood pressure 1032

overshoots during Gz deceleration would activate vagal responses and sympathetic withdrawal and decrease subsequent tolerance. However, Peterson et al. (19) proposed that the overshoot is an indication of vasoconstriction; therefore this, along with increased circulating catecholamines (5), would predict an increase in 1Gz tolerance. Indeed, increased vascular resistance explained the augmented cardiovascular response observed in acute, repetitive head-up tilting (2,3,23). Another possibility is that 1Gz tolerance depends on the features of the repetitive 1Gz excursions with the issue relating to the different time courses of the cardiovascular reflexes. The neural responses are rapid but the vasoconstrictive response to a decrease in blood pressure takes twice as long as the vasodilatory response to an increase in blood pressure (7). Thus the repetition rate in a series of 1Gz exposures could be a factor determining 1Gz tolerance. Since the effect of acute, repetitive 1Gz excursions on 1Gz tolerance cannot be definitively answered, it was the objective of this investigation to compare the cardiovascular and visual responses during repetitive 1Gz cycles to the responses from a single 1Gz exposure. As the time interval between 1Gz exposures can vary during air combat maneuvering (14) and may influence the physiological responses, four simulated air combat maneuvering (SACMs) profiles were designed and consisted of 10 1Gz cycles with short or long high 1Gz plateaus and low 1Gz pauses. 1Gz tolerance can be operationally defined in a variety of ways, but the ability to withstand 1Gz ultimately depends on adequate headlevel blood pressure, which assures some minimal visual field and avoidance of G-LOC. Therefore, the measurements used in this investigation were indicators of the sufficiency of head-level blood pressure: vision, ear

From the Individual Readiness Section, Defence Research and Development Canada - Toronto, Toronto, Ontario, Canada. This manuscript was received for review in February 2009. It was accepted for publication in September 2009. Address reprint requests to: Sophie Lalande, Ph.D., Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905; [email protected]. Reprint & Copyright © by the Aerospace Medical Association, Alexandria, VA. DOI: 10.3357/ASEM.2525.2009

Aviation, Space, and Environmental Medicine x Vol. 80, No. 12 x December 2009

IMPROVED 1GZ TOLERANCE—LALANDE & BUICK opacity, ear opacity pulse (17,26,28), and indirect blood pressure measurement (18,23). METHODS There were 13 healthy individuals (11 men) (height: 179 6 3 cm, weight: 74.2 6 3.7 kg, age: 27 6 2 yr) who participated in the study. Participants were asked to refrain from alcohol for 36 h prior to the study, heavy exercise on the day of the study, smoking, chocolate, and caffeine for 3 h prior to the study, and a meal in the last hour before the study. Participants first underwent familiarization sessions in the centrifuge over several days to ensure motion habituation, complete muscle relaxation, and reliable reporting of visual changes. The study protocol was approved in advance by the Human Research Ethics Committee of Defence Research and Development Canada - Toronto. Each subject provided written informed consent before participating. The study was conducted in a 20-ft arm, computercontrolled human centrifuge. 1Gz level was measured at the subject’s heart level by an accelerometer (Microtron, Endevco 7990, Capistrano, CA) mechanically calibrated to 10 Gz against centrifuge turn radius and angular velocity. The gondola of the centrifuge was equipped with two-way audio and a one-way video communication system to the control room. The back of the gondola seat was reclined 13° from vertical. Baseline 1Gz (1.4 Gz) was attained in 5 s and was the immediate start point for all subsequent 1Gz excursions within a profile. Subjects were exposed to three types of centrifuge profiles: 1) gradual-onset rate acceleration (GOR) (0.1 G z s21); 2) rapid-onset rate acceleration (ROR) in which the target 1Gz level was reached in a constant 2.5 s and maintained for 15 s before returning to 1 Gz; and 3) SACM, consisting of ROR 1Gz cycles. Each study day consisted of two successive GOR profiles, a series of incremental ROR profiles, one of four SACMs, and ended with another series of ROR (Fig. 1). SACM profiles were performed on different study days separated by at least 24 h and assigned to the partici-

Fig. 1. Diagram of a study day consisting of two GOR exposures, a series of incremental ROR, one of four SACMs (short 1Gz plateau and short 1Gz pause), and another series of ROR. The breaks in the diagram represent the 1.5-min rest at 1 Gz between profiles.

pants in random order. The GOR profiles were performed as “warm-ups” (E.H. Wood, personal communication; 1999) and were terminated when the subject reached central light loss or 5.0 Gz, whichever came first. The separate ROR profiles started with a 2.0 Gz plateau and increased in steps of 0.5 Gz until the subject’s 1Gz limit level or a maximum of 5.0 Gz was reached. 1Gz limit was defined as the ROR 1Gz plateau level at which the real-time ear opacity pulse signal disappeared for at least three heartbeats and/or central vision was reported to be very gray or have complete light loss. The SACMs consisted of 10 successive 1Gz cycles characterized by high 1Gz plateaus of short or long duration (8 or 20 s) separated by 9 1Gz pauses of short or long duration (1 or 15 s) at 1.4 Gz: 1) short 1Gz plateau and short 1Gz pause; 2) short 1Gz plateau and long 1Gz pause; 3) long 1Gz plateau and short 1Gz pause; and 4) long 1Gz plateau and long 1Gz pause. These 1Gz plateau and pause durations were selected to be relevant to air combat maneuvering and to assess the role of time spent under 1Gz as well as time between high 1 Gz excursions on the physiological response. The high 1Gz level for the 1Gz plateaus of the SACMs was set at the subject’s 1Gz limit obtained from the first series of ROR and maintained for all subsequent SACMs. Subjects were unprotected, i.e., muscles relaxed and not wearing a 1Gz suit. All centrifuge profiles were separated by a 1.5-min rest at 1 Gz. A second series of ROR was performed after the SACM to determine if 1Gz limit had changed following the SACM profile. Measurements Beat-by-beat blood pressure was measured with Portapres™ (Model 2.0, T.N.O., Netherlands) by fitting two pressure cuffs on the two longest fingers of the right hand. The right forearm and hand lay on an armrest and a heating pad surrounded the hand and pressure cuffs to prevent vasoconstriction in the fingers. Hydrostatic correction between the fingers and the target blood pressure sites allowed the measurements of heart-level blood pressure (aortic valve at third intercostal space) and head-level blood pressure (eye/superior ear level) (18). Because it is the most closely linked indicator of impending G-LOC (27,28), only head-level systolic blood pressure at its nadir level during the 1Gz plateau will be reported. Pulse pressure, an index of stroke volume, was calculated as the difference between systolic and diastolic pressure at heart-level (1). Heart rate was measured from the R-R interval of a 5-lead electrocardiogram (Marquette Medical Systems, Inc., Casew 8000 v 4.0, Milwaukee, WI). Subjects reported visual changes as observed against a light bar composed of a centrally located red lightemitting diode (LED) and two peripheral green LEDs positioned 25° from center and flashing at a frequency of 1 Hz. The distance between the subject and the light bar was 87 cm. The subject’s quality of visual field was recorded immediately after each centrifuge profile and after each 1Gz plateau of the SACMs. The worst level of visual field was reported separately for both peripheral


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IMPROVED 1GZ TOLERANCE—LALANDE & BUICK and central vision using one of six ratings made reliable with training: 1) clear: no visual impairment; 2) slight: perceived that the amount of normal vision lost was slight, approximately 1–9% of normal vision; 3) dim: approximately 10–49% of normal vision lost i.e., less than half; 4) gray: approximately 50–89% of normal vision lost; 5) very gray: approximately 90–99% of normal vision lost, i.e., more than half but not complete light loss; 6) peripheral light loss or central light loss: 100% of normal peripheral or central vision lost. Direct-sensing indicators of head-level circulation were obtained from records of ear opacity and ear opacity pulse (25,27) acquired using a light wavelength near the isosbestic point (the isosbestic point represents the wavelength at which oxyhemoglobin and deoxyhemoglobin have the same optical density). Ear opacity is a plethysmographic representation of local blood content while ear opacity pulse amplitude represents the change in local blood content produced by systole. The custommade ear opacity device consisted of an earpiece, LED, and photo-detector. The earpiece was secured at the level of the ear pinna by a clamp fastened to a fiberglass (Scotchcast™ Plus Casting Tape, 3M Health Care, St. Paul, MN) shell cap made for each subject (26). Thermogenic ointment (Finalgonw, Boehringer Ingelheim, Burlington, ON, Canada) applied to the ear pinna promoted local vasodilation for the duration of the experiment so that cooling and vasoconstriction would not interfere with the responsiveness of ear opacity to headlevel blood pressure changes. Data Analysis Data from biomedical sensors (heart rate, ear opacity, blood pressure) were acquired at a sampling frequency of 100 Hz (Centrifuge Data Display and Acquisition System, Engineering Services Inc., Toronto, ON) and waveforms were analyzed without preprocessing using commercially available software (AcqKnowledge v. 3.5, Biopac, Santa Barbara, CA). The physiological values at 1 Gz were the average of 10 consecutive heartbeats taken at the start of the 30-s period preceding each SACM. So that the results from the four different variables could be expressed in common measurement units and that the overall findings could be described in practical terms, any changes in the physiological responses to each 1Gz cycle are reported by means of a calculated change in 1Gz tolerance. Increasing 1Gz levels cause progressively more severe changes in certain head-level cardiovascular variables and subjective symptoms (27,28). Therefore, linear regressions between 1Gz level and the nadir of head-level systolic pressure were determined for each participant from both series of ROR of a given day (Fig. 2). Both series of ROR were used in the calculation as the 1Gz limit was the same in the first and second series of ROR. Using these linear regressions, the “effective” 1Gz level for each 1Gz cycle of the SACM was calculated using the nadir of head-level systolic pressure for that particular cycle. For example, the linear regression shown in Fig. 2 is y 5 20.03733 1 4.70, where “y” is 1Gz level, “x” is the nadir 1034

Fig. 2. One subject’s linear regression as determined from the nadir of head-level blood pressure from both series of ROR on a given study day. Black squares: first series of ROR, black circles: second series of ROR.

of head-level systolic pressure, and the 1Gz limit was 4.0 Gz. If the nadir of head-level systolic pressure during a 1Gz cycle of a SACM was 30 mmHg, the calculated “effective” 1Gz level would be 3.6 Gz. Since the actual SACM 1Gz plateau level was 4.0 Gz, physiologically it is as if the subject was only at 3.6 Gz. Therefore, 1Gz tolerance had improved by 0.4 Gz. No change in 1Gz tolerance would be evident if “effective” 1Gz and SACM 1Gz plateau level were the same. Similar regressions and calculations were performed for each participant using data from ear opacity, ear opacity pulse, and visual ratings. A three-way analysis of variance was used to test for the main effects of the number of the 1Gz cycle, the duration of the 1Gz plateau, and the duration of the 1Gz pause. Follow-up post hoc analyses were performed using a Tukey HSD test. A P-value below 0.05 was considered significant and all results are presented as mean 6 SEM. RESULTS The SACM 1Gz plateaus were 2.5 Gz (one subject), 3.0 Gz (five subjects), 3.5 Gz (six subjects), and 5.0 Gz (one subject). No subject could withstand a 1Gz plateau level over 5.0 Gz. For comparisons across different SACMs and different subjects, physiological variables are presented as a percentage of their value at 1 Gz. The average values at 1 Gz for head-level systolic pressure and heart rate were 112 6 4 mmHg and 80 6 4 bpm, respectively. The nadir of head-level systolic pressure of the first 1Gz cycle was significantly lower than the nadirs of head-level systolic pressure for all successive 1Gz cycles except for cycles 8 to 10 for the SACMs with long 1Gz pauses (Fig. 3). The nadirs of head-level blood pressure for all 1Gz cycles of the SACMs with long 1Gz pauses, except 1Gz cycle 5 and 6, were lower than the nadirs of head-level blood pressure of the SACMs with short 1Gz pauses (Fig. 3). Pulse pressure of the first 1Gz cycle was significantly lower than the subsequent 1Gz cycles for SACMs with short pauses (58 6 3 vs. 71 6 4%). For SACMs with long 1Gz pauses, pulse pressure of the first


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Fig. 3. Nadir of head-level blood pressure and visual rating for SACMs with short versus long 1Gz pauses. Black circles: SACMs with short 1Gz pauses. White triangles: SACMs with long 1Gz pauses. * Significantly different from the first 1Gz cycle. † Significantly different from the SACMs with short 1Gz pauses.

1Gz cycle was significantly lower than the pulse pressures of 1Gz cycles 2 to 4 only (63 6 2 vs. 65 6 3%). For the SACMs with long 1Gz pauses, the greatest headlevel systolic pressure during the 1Gz pause was observed after 9 6 2 s and the highest head-level systolic pressure during the 1Gz pause was significantly greater for 1Gz cycles 1 and 2 when compared to 1Gz cycles 3 to 10 (112 6 4 vs. 103 6 3%). The highest heart rate during the 1Gz plateau significantly decreased after the first 1Gz cycle (141 6 5 vs. 132 6 5%). The highest heart rate was greater in SACMs with long 1Gz plateaus than in those with short 1Gz plateaus (136 6 5 vs. 129 6 5%). The visual ratings of the first 1Gz cycle were consistently very gray to complete light loss and improved toward clear vision over the successive 1Gz cycles of all SACMs (Fig. 3). The improvement in vision over successive 1Gz cycles was greater for the SACM with short 1Gz pauses when compared to SACM with long 1Gz pauses (Fig. 3). Changes in 1Gz Tolerance 1Gz tolerance determined from visual ratings increased by an average of 0.48 6 0.08 Gz over 1Gz cycles 2-10 for all SACMs. The increase in 1Gz tolerance was greater for the SACMs with short 1Gz pauses when compared to the SACMs with long 1Gz pauses (0.62 6 0.07 vs. 0.34 6 0.06 Gz). Similarly, the increase in 1Gz tolerance determined from head-level systolic pressure was greater for SACMs with short 1Gz pauses when compared to SACMs with long 1Gz pauses (0.45 6 0.15 vs. 0.18 6 0.10 Gz). The average increase in 1Gz tolerance determined by head-level blood pressure for all SACMs was 0.31 6 0.13 Gz. The average increase in 1Gz tolerance from ear opacity pulse obtained at the nadir of head-level blood pressure for all SACMs was 0.26 6 0.30 Gz. Since the ear opacity nadir occurred approximately 2-3 s after the nadir of head-level blood pressure, both 1Gz plateau duration conditions were not compared as the time needed to reach ear opacity nadir exceeded the short 1Gz plateau duration. The average increase in

1Gz tolerance determined from ear opacity nadir for the SACMs with long 1Gz plateaus was 0.31 6 0.29 Gz. In a summary format in which vision, head-level blood pressure, ear opacity, and ear opacity pulse are given equal weighting, the mean change in 1Gz tolerance over all SACMs was 0.35 6 0.21 Gz. The changes in 1Gz tolerance for each SACM as determined from all physiological variables are presented in Fig. 4. DISCUSSION Acute repetitive 1Gz exposures resulted in a smaller decrease in head-level blood pressure and an improvement in vision, translating into an increase in 1Gz tolerance. These findings were influenced by the duration of the 1Gz pauses in the SACMs as the improvement in 1Gz tolerance was greater for the 1-s 1Gz pauses in comparison to the 15-s 1Gz pauses. Consistent with our results, Meyer et al. (12) reported that a second 1Gz exposure following 30 s of recovery from a previous slowonset rate 1Gz exposure resulted in a 10% increase in 1Gz tolerance as determined by visual ratings. Hallenbeck (10) studied vision loss over six 1Gz exposures of 10 s at 4.2 Gz with different intervals between 1Gz exposures. Similar to our results, the observed severe visual symptoms improved over the successive 1Gz exposures and the improvements were greater and more consistent for the 4.7- and 9.4-s intervals versus the longer intervals of 19.4 and 29.1 s. In contrast, an increase in 1Gz tolerance with multiple 1Gz exposures was not reported by Erickson et al. (9), who observed that during simulated air combat maneuvering, rhesus monkeys had reduced cardiovascular compensation as evidenced by progressively greater decreases in blood pressure. Moreover, a subsequent gradual-onset rate 1Gz exposure reduced 1Gz tolerance by 1 Gz (9). Finally, performing a gradualonset rate 1Gz exposure to complete light loss 14 s after a 1-min 1Gz exposure to 7 Gz resulted in a reduction of 1Gz tolerance by almost 1 Gz (22). Of all the physiologic mechanisms defending headlevel blood pressure during 1Gz loading, vasoconstric-


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Fig. 4. Left panel: Mean changes in 1Gz tolerance determined by all physiological variables for each type of SACM. Black circles: short 1Gz plateau and short 1Gz pause. White diamonds: long 1Gz plateau and short 1Gz pause. Black squares: short 1Gz plateau and long 1Gz pause. White triangles: long 1Gz plateau and long 1Gz pause. Right panel: Mean changes in 1Gz tolerance across all SACMs as measured by each physiological variable. White diamonds: head-level systolic blood pressure. White triangles: ear opacity pulse. Black circles: vision. Black squares: ear opacity.

tion and the resulting increase in total peripheral resistance is considered the most effective (28). Indeed, an increase in vascular resistance is needed to increase systemic driving pressure in order to counteract the extended hydrostatic pressure gradient and maintain cerebral perfusion (28). Following a decrease in head-level blood pressure, the carotid and aortic baroreceptors stimulate an increase in peripheral resistance through vasoconstriction, with maximal vasoconstriction reached approximately 20 s into the 1Gz exposure (19). Because time for full vasomotor response is allowed, average 1Gz tolerance measured by gradual-onset rate 1Gz exposures is 5.6 Gz compared to only 3.7 Gz during rapidrate 1Gz onset (8,19). Centrifuge riders receiving beta-adrenergic blockade before moderate 1Gz exposure had a significant reduction in heart rate, but were able to maintain blood pressure through an enhanced vasoconstriction that further increased vascular resistance (4). Thus, vasoconstriction plays a key role in the maintenance of head-level blood pressure during 1Gz loading. Other investigators hypothesized that a delayed or inappropriate vascular response to large rapid changes in carotid sinus pressure could potentially lead to further hypotension during rapid changes in 1Gz acceleration (7). In anesthesized open-chest dogs, inducing rapid increases and decreases in carotid pressure in pulses of 10 s or less resulted in attenuation of the vasoconstriction and the vascular beds remained almost maximally vasodilated. Reflex vasodilation occurred significantly faster than vasoconstriction as an increase in carotid pressure lasting as little as 5 s was enough to elicit maximal vasodilation (7). In accordance with these results, we and others (10) have found that 1Gz tolerance was affected by the cycle characteristics of the SACMs or the durations of the rapid increases and decreases in carotid pressure. However, rather than extra hypotension, we observed that head-level systolic pressure decreased less during 1Gz over the successive cycles and that 1Gz 1036

tolerance was increased regardless of the 1Gz plateau duration and that it was greater in the SACMs with the short 1Gz pauses. Therefore, we believe that residual vasoconstriction from the previous 1Gz cycle led to the increased 1Gz tolerance, especially in SACMs with 1-s 1Gz pauses since this duration is too short to elicit any effective vasodilation. Increased peripheral vascular resistance was also suggested to explain elevated diastolic pressure over 10 cycles of head-up tilt using 20-s or 2-min head-up durations (2,23). This acute adaptation provided a stronger cardiovascular response to a subsequent orthostatic challenge induced by a squat-stand test (3). The reduced fall in the nadir of head-level blood pressure could also be linked to a more effective unloading of the carotid baroreceptors with successive 1Gz exposures. The neural components of the baroreflex are already rapid and it is plausible that the vascular innervation site or the smooth muscle itself remain primed from the previous 1Gz cycle (11,13), possibly related to the release and breakdown of local and circulating sympathetic transmitters. There is also the possibility that resetting of the baroreflex (20) results in a greater compensatory reaction that better protects head-level blood pressure during 1Gz cycles. Indeed, an enhanced sensitivity of the arterial baroreflex has been suggested to be the underlying mechanisms for the improved blood pressure regulation following sustained 1Gz exposures (6,15,16). Salzman et al. (21) observed that the ability to maintain head-level blood pressure was correlated to the magnitude of venoconstriction in dogs exposed to 1Gz levels, supporting the importance for the role of contraction of the venous reservoir in the support of cardiac output during 1Gz exposure. We did not measure stroke volume, but, when arterial capacitance is assumed to be constant, pulse pressure is directly related to stroke volume (1). Therefore, the observed increase in pulse pressure over successive 1Gz cycles suggest an increase


IMPROVED 1GZ TOLERANCE—LALANDE & BUICK in stroke volume which was greater for the SACMs with short 1Gz pauses. At the end of a 1Gz exposure, restoring the normal heart-head hydrostatic pressure gradient results in increased systemic venous return, which increases left ventricular volume and, through the Frank-Starling mechanism, stroke volume (1,24). The increase in stroke volume leads to an overshoot in blood pressure, which has been observed to be directly related to the magnitude of the previous 1Gz exposure (19). We also observed an overshoot in head-level blood pressure in the SACMs with long 1Gz pauses, with the greatest headlevel blood pressure being observed approximately 9 s after the end of the 1Gz plateau. The greatest overshoot in blood pressure was observed after the first 1Gz cycle (reaching 114% of head-level blood pressure at 1 Gz) and progressively declined to values toward normal levels with repetitive 1Gz cycles. One explanation for the decline in the blood pressure overshoot is a possible progressive easing of vasoconstriction or a progressive reduction in venous return (21). The overshoot in headlevel blood pressure during 1Gz unloading could itself induce additional physiological responses. One possibility is that the overshoot activates a vagal response on heart rate and reduces sympathetic drive to decrease peripheral resistance and blood pressure, a situation that makes the cardiovascular system ill prepared for a subsequent 1Gz exposure. This could partly explain why the SACMs with long 1Gz pauses had a smaller increase in 1Gz tolerance. Alternatively, 1Gz onset taking place during the blood pressure overshoot could reduce the fall in head-level blood pressure, which could reduce the severity of 1Gz-induced symptoms for the centrifuge rider. The present results indicate that the second and subsequent 1Gz cycles were physiologically less stressful than the first 1Gz cycle. Since 1Gz plateau level during the 1Gz cycles was constant, the increases in head-level blood pressure nadir, ear opacity, ear opacity pulse, and vision ratings after the first 1Gz cycle gave the impression that 1Gz tolerance had improved or that 1Gz cycles were being performed at a lower 1Gz level. Depending on the physiological variable and SACM, the calculated increase in 1Gz tolerance ranged from approximately 0.2 to 0.6 Gz. Given that the physiological variables were measured by different sensing procedures, the uniformity of the results indicates a valid assessment of the 1Gz tolerance changes. Of the two SACM characteristics, only 1Gz pause duration significantly influenced the physiological responses, with the cardiovascular response to the 1Gz exposures better for the short 1Gz pause compared to the long 1Gz pause SACMs. Interestingly, both SACMs with the greatest sustained acceleration, i.e., with a long 1Gz plateau, showed a tendency for a decrease in 1Gz tolerance throughout the SACM (Fig. 4). Erickson and Ritzman (9) previously reported that repeated exposure to sustained acceleration resulted in cardiovascular fatigue in rhesus monkeys, as demonstrated by greater decrements in blood pressure. Similarly, Burton (5) reported that repeated high 1Gz SACM resulted in progressive cardio-

vascular fatigue as observed through increases in heart rate responses. However, subjects were required to perform anti-Gz straining maneuvers, which could have accelerated the development of fatigue. Therefore, it is possible that cardiovascular fatigue plays a role in the tendency toward decreased 1Gz tolerance in the SACMs with long 1Gz plateaus and that longer sustained acceleration could result in further decline in 1Gz tolerance. Whether the physiological responses remain the same at higher 1Gz levels or how straining maneuvers affect these responses requires further investigation. 1Gz tolerance increases and is maintained over successive 1Gz exposures and is attributed to carryover of the compensatory responses, primarily vasoconstriction, with possible contributions from increased venous return and enhancement of the baroreflex. The finding of an increased 1Gz tolerance, as observed through a smaller decrease in head-level blood pressure and an improvement in vision, over successive 1Gz exposures suggests that aerial combat maneuvering does not lead to cardiovascular deterioration that would increase the risk of G-LOC. ACKNOWLEDGMENTS This study was conducted with financial support from the U.S. Office of Naval Research through Award N-00014-01-1-0044. Authors and afﬁliations: Sophie Lalande, Ph.D., Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN, and Fred Buick, Ph.D., Individual Readiness Section, Defence Research and Development Canada - Toronto, Toronto, Ontario, Canada. REFERENCES 1. Berne RM, Levy MN. Cardiovascular physiology, 4th ed. St Louis, Toronto, London: The C.V. Mosby Company; 1981. 2. Berry NM, Rickards CA, Newman DG. Acute cardiovascular adaptation to 10 consecutive episodes of head-up tilt. Aviat Space Environ Med 2006; 77:494–9. 3. Berry NM, Rickards CA, Newman DG. Squat-stand test response following 10 consecutive episodes of head-up tilt. Aviat Space Environ Med 2006; 77:1125–30. 4. Bjurstedt H, Rosenhamer G, Tyden G. Acceleration stress and effects of propranolol on cardiovascular responses. Acta Physiol Scand 1974; 90:491–500. 5. Burton RR. Human responses to repeated high G stimulated aerial combat maneuvers. Aviat Space Environ Med 1980; 51:1185–92. 6. Convertino VA. High sustained 1Gz acceleration: physiological adaptation to high-G tolerance. J Gravit Physiol 1998; 5:P51–4. 7. Doe CP, Self DA, Drinkhill MJ, McMahon N, Myers DS, Hainsworth R. Reflex vascular responses in the anesthetized dog to large rapid changes in carotid sinus pressure. Am J Physiol 1998; 275(4, Pt. 2):H1169–77. 8. Edelberg R, Henry JP, Maciolek JA, Salzman EW, Zuidema GD. Comparison of human tolerance to acceleration of slow and rapid onset. J Aviat Med 1956; 27:482–9. 9. Erickson HH, Ritzman JR. Instrumentation for the rhesus monkey as a cardiovascular analog for man during air-combat maneuvering acceleration. Aviat Space Environ Med 1976; 47:1153–8. 10. Hallenbeck GA. Effects on man of repetitive exposure to centrifugal force. Fed Proc 1945; 4:29–30. 11. Ikeda Y, Kawada T, Sugimachi M, Kawaguchi O, Shishido T, et al. Neural arc of baroreflex optimizes dynamic pressure regulation in achieving both stability and quickness. Am J Physiol 1996; 271(3, Pt. 2):H882–90. 12. Meyer JF, Brown WK. The effect of recovery time on 1Gz tolerance. Annual Scientific Meeting of Aerospace Medical Association; May 6-9, 1968; Bal Harbor, FL. Alexandria, VA: Aerospace Medical Association; 1968:97–98. 13. Mills FJ. The endocrinology of stress. Aviat Space Environ Med 1985; 56:642–50.


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