There is no evidence of interaction between anti-G cardiovascular reflexes and heat-induced volume shifts. The pattern differs for dehydration. Taliaferro et al.
Heat and acute dehydration effects on acceleration response in man SARAH A. NUNNELEY AND RICHARD F. STRIBLEY Crew Protection Branch, US Air Force School of Aerospace Brooks Air Force Base, Texas 78235
NUNNELEY, SARAH A., AND RICHARD F. STRIBLEY. Heat and acute dehydration effects on acceleration response in man. J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47(l): 19’7-200, 1979.-Though heat and dehydration each impair acceleration tolerance, interactions among these stresses have not previously been studied. Seven men were dehydrated in heat by 0, 1, and 3% of body weight before a series of +G,, gradual-onset centrifuge runs with the capsule first 38”C, then 20°C. Heat alone raised heart rate by 6.5 beats/min independent of other stresses. Dehydration and acceleration appeared to act synergistically in raising HR. Heat lowered relaxed G tolerance by 0.3 G; dehydration tended to lower G tolerance and increased the variability of response to heat. A high-tolerance subgroup (n = 4) could normally sustain +7 G, for 60 s with anti-G suit and straining, but 3% dehydration reduced mean time to 35 s. Dehydration was associated with a decrease in the loss of plasma volume at 7 G. Heat-induced tolerance loss appears similar for both gradual- and rapid-onset centrifuge profiles. In contrast, dehydration effects are greater in rapidonset runs, evidence that normal anti-G protective mechanisms can partly counteract the effect of fluid deficit. The results are relevant for crew members of high-performance aircraft, where unexpected diminution of their normally high G tolerance can have disastrous consequences. combined
stress; plasma volume;
acceleration
tolerance
LIMITED ABILITY to withstand +G, (head-to-foot) acceleration is a recurring problem in aerospace physiology and has assumed growing importance with the advent of the latest high-performance aircraft, which can sustain acceleration beyond the crew’s tolerance. In this case human physiology becomes a critical determinant of performance for the entire man-machine system. The situation is complicated because acceleration tolerance is affected by various other stresses in the flight environment. Cockpits of high-performance aircraft are often uncomfortably hot, and losses of l-3% of body weight occur during fighter sorties in hot weather (4, 11). Furthermore, crew members may arrive at the aircraft with a fluid deficit due to subclinical illness, stressful leisure activities, or inadequate recovery from a previous flight. Several early studies with human centrifuges indicated that high ambient temperatures decreased the grayout threshold of relaxed subjects (5, 7, 15), and later experiments showed that core and skin heating each play significant roles (1). The effect of acute heat-induced dehydration on acceleration response is the topic of only two studies (9, 19). Possible interactions among heat,
MAN'S
OlSl-7567/79/oooO-0000$01.25
Copyright
0 1979 the American
Physiological
Medicine,
dehydration, and acceleration tolerance have remained unexplored, and this study was designed to help fill the gap. Subjects were dehydrated, then underwent +G, acceleration in a centrifuge capsule that was first heated and then cooled. MATERIALS
AND METHODS
Subjects were seven male volunteers aged 22-39 yr with the following characteristics (mean t SD): height 173 t 6 cm, weight 74.8 t 3.4 kg, and body fat by underwater volumetry (2) 22.0 t 3.7%. Each man learned to ride the centrifuge in two different ways: 1) relaxed, avoiding all voluntary muscle contraction, and 2) using the Valsalva-like M-l straining maneuver to maximize G tolerance. Training continued for at least 4 different days and until the subject could reliably reproduce his tolerance limit, i.e., peripheral light loss and/or central dimming. He was then studied once at each dehydration level, 0; I, and 3% body weight loss (termed Do, D1 and DS, respectively). Experiments were separated by 1 wk, with order balanced by design. The subjects were instructed to avoid strenuous activity, alcohol, and extremes of fluid intake for 24 h preceding each experiment. Dehydration. Dehydration was scheduled for completion at noon. Nude weight (bladder empty) was measured t 10 g on a bench scale (Detecto). The subject was instrumented with ECG leads and thermistors (Yellow Springs Instrument 700 series) to record temperature in the auditory canal (T,,) and rectum (T,,). Dehydration was produced by passive heating: T,, was kept at 38.038.5OC by alternate immersion in a bath at 415°C and exposure to air at 40°C. The T,, and heart rate (HR) were monitored for safety purposes. When the required weight loss had been achieved, the subject moved to a comfortable room (22 t 2°C) and rested until vital signs returned to base line. The subject voided before final nude weighing, and any excess weight loss was exactly replaced with cool fluids; a further 30-60 min rest allowed stabilization of plasma volume. For control (Do) studies, the subject reported for weighing and rest 60 min before dressing for the centrifuge. Acceleration. The acceleration runs were performed between 1 and 4 P.M. A fixed sequence of runs (hot before cool) was selected for its resemblance to aircraft operation (hot ground operations and low-level flight followed by cooling at higher altitudes). Past experience indicated that the initial set of four relaxed runs in a warm capsule Society
197
198
S. A. NUNNELEY
did not significantly alter responses to the later runs in a cool capsule. The subject was instrumented with ECG leads and skin thermistors (12 sites), then dressed in summer flight clothing and an anti-G suit. The centrifuge capsule was preheated to 38°C and the subject sat in an aircraft seat (tilted 13” back from the vertical) for a 20min equilibration period. A series of three relaxed runs followed: 2 G for 1 min, 3 G for 1 min, and then the rise to their tolerance limit. The rate of acceleration was 1 G/15 s and each run was separated by 5min rest periods. The subject remained seated while the capsule cooled to 20°C (30 min), and the three relaxed runs were then repeated. For the final run, 7 G for 1 min, the anti-G suit was activated and the subject strained as needed to maintain vision. Four subjects could normally tolerate the 60-s plateau; they constituted the high-tolerance (HT) group. Three other subjects had reproducible limits of less than 60 s; they comprised the low-tolerance (LT) group. There was no significant difference between the two groups in age, height, weight, body composition, or apparent motivation; the variability of tolerance for high G is a normal finding among any group of volunteer centrifuge riders. Blood sampling. Blood measurements were performed on six of the subjects. Samples were drawn without stasis from the antecubital vein with the subject seated: I) before dehydration (control), 2) after dehydration, 30-60 min following fluid replacement, 3) 2 min after the 7-G run, and 4) 15 min after the run. Hemoglobin concentration (Hb) was measured in triplicate by the cyanomethemoglobin technique with Hycel’s standards. Hematocrit (Hct) was determined in triplicate with a microcapillary centrifuge; no correction was applied for trapped plasma. Heart rate. HR was counted from a l&beat segment of the ECG at the end of each run. Mean skin temperature (Tsk) was calculated from 12 sites (10). Changes in plasma volume (APV, o/o)were estimated using the following equation (8) APV(%) = 100 ([HbB/HbA][(l
- HctA)/(l
AND
R. F. STRIBLEY
Heart rates for all the relaxed steady-state runs are presented in Fig. 1. Heat raised HR by a mean of 6.5 beats/min under all conditions (P < O.Ol), showing no significant interaction with dehydration or G level. Resting (1 G) HR was raised by dehydration by 6.1 beats/ min (Dl) and 14.0 beats/min (Ds) (NS). Dehydration also appeared to enhance the effect of G on HR, the interaction approaching significance (P = 0.07) (Fig. 1). The HR at relaxed grayout threshold increased slightly with both heat and dehydration and mean HR’s for the 7-G runs were 162, 165, and 169 beats/min for Do, D1, and Da, respectively, but these trends did not reach statistical significance. Relaxed acceleration tolerances appear in Fig. 2. The change from hot to cool conditions caused a significant rise in mean relaxed acceleration tolerance of 0.4 G. Dehydration tended to lower tolerance, though the trend was not statistically significant; under cool conditions, three subjects reached 5.5-5.7 G for Do, whereas only one exceeded 5.0 G for D3. A retrospective comparison of relaxed grayout threshold for the HT and LT groups gave mean levels of 5.3 and 4.5 G, respectively. Time tolerated at 7 G (Fig. 3) decreased with fluid deficit; the change was significant even though the distribution was truncated by the arbitrary 60-s limit. Subjects noted a persistent loss of ability to sense the color TABLE
1. Temperatures aboard centrifuge Hot
Cool
37.9 t 1.1 35.8 t 0.6 37.0 t, 0.2
Tdb
Rk TO,
20.6 t 1.4 34.0 t 0.8 36.3 t 0.4
Values are means k SD, in “C. Tdt,, dry bulb temperature; skin temperature; T,,, oral temperature.
Tsk, mean
130
- HctB)] -1)
where B is before and A after stress. All data are means t SD. Statistical analyses were done by appropriate forms of analysis of variance (ANOVA) and the null hypothesis was rejected when P < 0.05. RESULTS
During the dehydration phase the subjects lost weight at a rate of 1.2 t 0.3 kg/h. In only one case did T,, reach the 39OC cutoff, at the end of the necessary heat exposure. Excess weight lossesthat required fluid replacement were 752 t 288 g for D1 and 374 t 108 g for Da. Comparison of control blood values with those just before the subjects transferred to the centrifuge showed that PV decreased by 5.0 t 2.9 and 11.7 t 2.4% for D1 and D3, respectively. Temperatures aboard the centrifuge appear in Table 1. Subjects reported feeling warm and mildly sweaty during the hot phase and comfortable on cooling. Weight loss during the 3 h on board was 217 t 112 g and & was 35.8 t 0.6”C, confnming a mild degree of heat stress in the capsule.
T
120 .-F E > w : aE
/
110
100
2 k a iii
90
80
70
ACCEL.
(G):
DEHYD.
(‘ol:
I
I
1 -1
1
2
3
0
1
2 1
3 1
2
3
3
FIG. 1. Mean heart rate vs. condition. Abscissa indicates acceleration plateau (G units) and dehydration (% body wt). SymboZs: 0, hot environment; l , cool environment; bars, t 1 SE.
HEAT,
DEHYDRATION,
AND
ACCELERATION
0
1 DEHYDRATION
ENVIRON.
C H
CH
C
DEHYD. (%): 0 1 3 FIG. 2. Relaxed acceleration tolerance vs. condition. Abscissa indicates environment (H, hot; C, cool; see text) and dehydration (‘95 body wt). Symbols: light lines connect individual values; heavy lines show means. 60
00 0
FIG.
values
3. Tolerance times for same individual.
1
2
DEHYDRATION
(%)
at +7 G, vs. dehydration.
3
Lines
connect
of peripheral lights at 7 G, and had to strain harder to maintain vision at all. Runs were terminated early due to physical exhaustion and/or impending blackout. The HT group suffered the greatest effect, 3% dehydration reducing their mean time at 7 G to 35 s (range 25-45 s), whereas the LT group showed no meaningful change (Fig. 3). Changes in PV following the 7-G run appear in Fig. 4. For Do there was a loss of 12.5% at 2 min postrun, with a residue of 4.0% at 15 min. Dehydration was associated with much smaller G-induced shifts (P < O.Ol), which were independent of time at 7 G. Loss of PV seemed to approach a ceiling of 18-20% (Fig. 4). DISCUSSION
Upright man at 1 G is protected from syncope in part by baroreceptor-mediated cardiovascular reflexes (3). The importance of these reflexes at higher G levels is shown by comparing rapid-onset acceleration with grad-
3
(%)
4. Mean change in plasma volume vs. dehydration. l ,preacceleration; A,2~pOStSCCSlSrStiOn;O,15m~pOS~CCSlerStiOn. Bars indicate f 1 SD. FIG.
--I : H
2
Symbols:
t&-onset profiles; the latter produce significantly higher relaxed grayout thresholds (18). Heat and dehydration resemble acceleration in reducing central blood volume and therefore may also interact with the normal anti-G reflexes. Our gradual-onset results can be compared with two other studies of heat and acceleration which used rapid-onset rtms (1, 5). Control tolerance differed as expected, being 3.2 & 0.4 G for (1) compared to 5.0 f 0.8 G here. Nevertheless, tolerance losses due to heat were similar in all of the studies, averaging 0.4 G (here), 0.3 G (l), and 0.2 G (5). There is no evidence of interaction between anti-G cardiovascular reflexes and heat-induced volume shifts. The pattern differs for dehydration. Taliaferro et al. (19) used heat to dehydrate four men by 2.5-3.5% before rapid-onset centrifuge runs, producing tolerance losses of 0.7-1.2 G. Since these changes were much larger than seen in our gradual-onset profiles, compensatory reflexes may help protect man from the combined effects of G and fluid depletion. Both studies showed great variability of dehydration effects. If 2-3% of normal body weight constitutes an internal reserve of “free water” whose depletion has little effect beyond a slight rise in HR (14), then both studies brought subjects to the threshold for major dehydration effects, and this might explain much of the variation in response. The decrease in PV with acceleration in our experiments agrees with other evidence that the G-induced APV diminishes with preexisting fluid deficit (6, 20). In a series of high-G rims with tilt-back seat, mean maximum loss of PV was 16.5% with a curvilinear recovery pattern that is similar to Do results here (6). No data are available for higher levels of dehydration. Long-term compensatory capacity can be judged by comparing acute and chronic dehydration, notably from studies simulating the very slow onset of acceleration on return from space flight (9,20). Slow fluid depletion over a 48-h period produced the same changes in G tolerance as did acute dehydration (9). Mild hypovolemia induced over a 5-day period resulted in significant but highly variable decreases of tolerance for both slow- and rapidonset acceleration (17). Other experiments indicate that chronic hypovolemia in ambulatory subjects causes little change in acceleration tolerance (20). The most striking change with dehydration was the decreased ability of the HT group to sustain 7 G. As
200 noted above, the HT/LT dichotomy of G tolerance is normal to any group of volunteer centrifuge riders. Crew members of high-performance aircraft resemble the HT subjects in their ability to maintain vision under stress. Such persons appear to have above-average reflex protection against pooling, as well as superior ability to mobilize reserves through voluntary straining. Withstanding 7 G for 1 min requires great physical effort, and under these conditions even small losses of PV may become critical. For LT subjects other factors seem to intervene, making PV less important. The findings reported here are particularly relevant to aircrews in high-performance aircraft, where unexpected diminution of G tolerance can have serious consequences. Recent advances in instrumentation now allow recording of cockpit conditions in flight, and it is increasingly clear that heat stress is a common problem (11). The clearest dehydration effect involved the HT group during the 7-
S. A. NUNNELEY
AND
R. F. STRIBLEY
G run, the condition which most resembled actual flight. Queries to pilots show that during hot-weather sorties a substantial number experience tunnel vision at lowerthan-normal G levels, sometimes forcing premature break off of maneuvers (unpublished data). Improved knowledge of the underlying physiology may justify future changes in design of aircraft cooling systems and flight procedures. The authors thank Antonio Sustaita, Sr., and the staffs of E Chamber and the Human Centrifuge for their assistance. We also gratefully acknowledge the time and forbearance contributed by the volunteer subjects. Expert consultation on biometrics was provided by Ken
StevensandBob Fuchs.
The voluntary informed consent of the subjects participating in this study was obtained in accordance with AFR 80-33. The research was conducted by personnel of the Crew Technology Division, USAF School of Aerospace Medicine, Brooks AFB, TX. Received
8 November
1978; accepted
in final
form
20 February
1979.
REFERENCES 1. ALLAN, J. R., AND R. J. CROSSLEY. Effect of controlled elevation of body temperature on human tolerance to +G, acceleration. J. AppZ. Physiol. 33: 418-420, 1972. 2. ALLEN, T. H. Measurement of human body fat: a quantitative method suitable for use by aviation medical officers. Aerospace Med. 34: 907-909, 1963. 3. BEISER, G. D., R. ZELIS, S. E. EPSTEIN, D. T. MASON, AND E. BRAUNWALD. Role of skin and muscle resistance vessels in reflexes mediated by the baroreceptor system. J. CZin. Inuest. 49: 225-231, 1970. 4. BOLLINGER, R. R., AND G. R. CARWELL. Biomedical cost of lowlevel flight in a hot environment. Aviat. Space Environ. Med. 46: 1221-1226, 1975. 5. BURGESS, B. F. The Effect of Temperature on ToZerance to Positive AcceZeration. Naval Air Development Center, NADC-MA-5905, 1959. 6. BURTON, R. R. Physiologic response to repeated high-G simulated aerial combat maneuvers. Aerosp. Med. Assoc. Preprints p. 84-85, 1977. 7. CODE, C. F., E. J. BALDES, E. H. WOOD, AND E. H. LAMBERT. The effect of environmental temperature upon man’s G-tolerance (Abstract). Federation Proc. 18: 5, 1946. 8. DILL, D. B., AND D. L. COSTILL. Calculation of percentage change in volumes of blood, plasma, and red cells in dehydration. J. AppZ. Physiol. 37: 247-248, 1974. 9. GREENLEAF, J. E., M. MATTER, JR., L. G. DOUGLAS, S. A. RAYMOND, J. S. Bosco, E. G. AVERKIN, AND R. H. ST. JOHN, JR. Effects of acute and chronic hypohydration on tolerance to +G, acceleration in man. I. Physiological results. NASA Tech. Memo. X-1285, 1966. 10. HARDY, J. D., AND E. F. DUBOIS. The technique of measuring
radiation and convection. J. Nutr. 15: 461-475, 1938. 11. HARRISON, M. H., C. HIGENBOTTAM, AND R. J. RIGBY. Relationship between ambient, cockpit, and pilot temperatures during routine air operations. Aviat. Space Environ. Med. 49: 5-13, 1978. 12. HENRY, J. P., AND 0. H. GAUER. Influence of temperature upon venous pressure in the foot. J. CZin. Inuest. 29: 855-861, 1950. 13. KEATINGE, W. R., AND P. HOWARD. Effect of local cooling of the legs on tolerance to positive acceleration. J. AppZ. Physiol. 31: 819822, 1971. 14. LADELL, W. S. S. Effects of water and salt intake upon the performance of men working in hot, humid environments. J. Physiol. London 127: 11-46, 1955. 15. MARTIN, E. E., AND J. P. HENRY. The effect of time and temperature upon tolerance to positive acceleration. Auiat. Med. 22: 382390, 1951. 16. ROWELL, L. B. Competition between skin and muscle for blood flow during exercise. In: ProbZems with Temperature Regulation during Exercise, edited by E. R. Nadel. New York: Academic, 1977, p. 49-76. 17. SHUBROOKS, S. J., JR. Relationship of sodium deprivation to +G, acceleration tolerance. Aerosp. Med. 43: 954-956, 1972. 18. STOLL, A. M. Human tolerance to positive G as determined by the physiological end points. Aviat. Med. 27: 356-367, 1956. 19. TALIAFERRO, E. H., R. R. WEMPEN, AND W. J. WHITE. Effects of minimal dehydration upon human tolerance to positive acceleration. Aerosp. Med. 36: 922-926, 1965. 20. VAN BEAUMONT, W., J. E. GREENLEAF, H. L. YOUNG, AND L. JUHOS. Plasma volume and blood constituent shifts during +G, acceleration after bedrest with exercise conditioning. Aerosp. Med. 45: 425-430, 1974.
