Eur J Appl Physiol (1992) 65:485-491 Applied Journal of

Physiology and Occupational Physiology © Springer-Verlag 1992

Marathon running: physiological and chemical changes accompanying late-race functional deterioration Robert Cade, David Packer, Christian Zauner*, David Kaufmann, John Peterson, Donald Mars, Malcolm Privette, Norman Hommen, Melvin J. Fregly, and James Rogers**

Department of Medicine, The Center for Physical and Motor Fitness, and Department of Physiology, University of Florida, Gainesville, Florida 32 610-0204, USA

Accepted July 7, 1992

Summary. Twenty-one experienced runners were studied before, during and immediately after a marathon race to ascertain whether either depletion of energy substrate or rise in body temperature, or both, contribute to late- race slowing of running pace. Seven runners drank a glucose/electrolyte (GE) solution ad libitum (Na + 21 mmol 1-1, K + 2.5 mmol 1 -a, CI- 17 mmol 1-1, PO 2- 6 mmol 1-a, glucose 28 mmol l-a) throughout the race; 6 drank water and 8 drank the GE solution diluted 1 : 1 with water. Although average running speeds for the three groups were not significantly different during the first two-thirds (29 kin) of the race, rectal temperature was significantly higher (P< 0.05) and reduction of plas- ma volume was greater (P<0.05) in runners who re- placed sweat losses with water. During the last one-third of the race, the average running pace of the water- replacement group slowed by 37.2%; the pace slowed by 27.9% in the 8 runners who replaced their sweat loss with GE diluted 1 : 1 with water (1/2GE) and 18.2% in runners who replaced fluid loss with full-strength solu- tion (GE). Eleven runners (5 in the water group, 4 in the 1/2GE group and 2 in the GE group) lapsed into a walk/run/walk pace during the last 6 miles of the race. Ten of these had a rectal temperature of 39 ° C or greater after 29 km of running, and plasma volume in these run- ners was reduced by more than 10%. Only I runner among those who ran steadily throughout the race had such an elevation of temperature and reduction of plas- ma volume. A significant reduction in plasma glucose concentration (less than 3.3 mmol 1-1) was present in 5 of the 11 walk/run/walk subjects and in none of those who ran steadily. The results are consistent with the sug- gestion that assumption of the walk/run/walk pace re-

* Present address: Department of Physical Education, Oregon State University, Corvallis, Oregon 97331, USA ** Present address: Department of Psychology, Wheaton College, Wheaton, Illinois 60187, USA

Correspondence to: R. Cade, Departments of Medicine and Phys- iology, P.O. Box 100204, U of F Health Science Center, Gaines- ville, FL 32610, USA

sulted from high body temperature associated with either diminished plasma volume or low blood sugar.

Key words: Marathon running - Body temperature - Plasma volume - Blood pressure - Plasma glucose

Introduction

The sudden onset of extreme fatigue in the later stages of a marathon race is a frequent occurrence even among well-trained athletes. Levin et al. (1924) and Gordon et al. (1925) suggested that severe reduction of plasma glu- cose concentration was the major cause of their incapac- ity. Other investigators have implicated a reduction of plasma volume (Cade et al. 1971, 1972; Nose et al. 1988), dehydration (Cohen et al. 1969; Costill et al. 1970; Nadel et al. 1980; Wyndham and Strydom 1969; Syndham 1977), and hyperthermia (Cade et al. 1972; Costill et al. 1970) as causes of late-race morbidity. In support of the hyperthermia/volume-reduction hypothe- sis, it has long been recognized that endurance runners perform much better in moderately cold weather (8- 12°C) than when temperatures are higher (18-24°C; Anon 1974).

We have examined, the changes in body temperature, sweat loss and composition, plasma volume and compo- sition, blood pressure, plasma glucose concentration, and running speed in 21 runners during a competitive marathon run. Although studying athletes during com- petition imposes logistic problems, we think the urge to perform well during competitive racing, unlike what happens in the laboratory, ensures that athletes perform at their highest capacity.

Our study was performed to find how vascular vol- ume depletion and its consequent hyperthermia develop and how they and hypoglycemia relate to late-race im- pairment of performance and specifically to the severe impairment known to runners as "hitting the wall".

486

Table 1. Physiological profiles of subjects

Fluid a Age Number of previous D~O2max group (years) marathons run (ml kg -1)

Time to run last marathon (min)

Training Body fat Weight Height (km week- 1) (0/0)b (kg) (cm)

Water 28.5 5.2 62.8 182 (4.2) c (3.1) (3.2) (25)

1/2GE 26.6 4.6 60.9 189 (2.1) (3.5) (5.8) (20)

GE 31.6 4.3 61.6 189 (6.5) (2.3) (5.0) (22)

132 9.2 61.7 173.7 (14.5) (5.0) (5.0) (8.6)

129 12.3 70.5 176.9 (14.5) (2.6) (8.6) (3.8)

130 11.0 67.1 176.8 (13.7) (4.4) (10.0) (5.6)

a GE, glucose/electrolyte solution; 1/2GE, half-strength GE b From skin-fold thickness

c Standard deviation

Methods

Subjects. Eighteen men and three women, all experienced mara- thon runners, all members of the University of Florida Track Club, who trained regularly in Florida, volunteered for the study. A profile of the runners in each group is given in Table 1.

Runners were first divided into performance groupings accord- ing to times in their most recent marathons and considering their assessment of their training progress during the 3 months preced- ing the study. Seven performance groups were established with 3 matched runners in each group: group 1 was composed of 3 run- ners expected to finish the race in between 2 h 30 rain and 2 h 40 rain, group 2 of 3 runners expected to finish in between 2 h 40 rain and 2 h 50 min etc. through group 7, whose runners were expected to finish in between 3 h 30 rain and 3 h 40 rain. Each run- ner was asked to give two choices of the fluid he or she would drink throughout the race. Fifteen runners drank their first choice while 6 were assigned their second choice for fluid replacement. In this way, three matched fluid-replacement groups, i.e. water, full- strength glucose/electrolyte (GE) solution (Na ÷ 21 mmol 1-1, C1- 17mmol l -1 , p o 2- 6mmol1-1 , K ÷ 2.4 mmol1-1, glucose 28 mmol 1 - 1; osmotic pressure 310 mosmol kg - 1) and GE diluted 1:1 with water (1/2GE) were created. Each performance group had one athlete drinking water; one drinking 1/2GE, and one drinking GE. This structure held except for group 6, in which the runner assigned to water ingestion changed his mind on the day of the race and insisted that he be allowed to drink his first choice, which was 1/2GE. Thus, the water-treatment group had no repre- sentative in performance group six in which 1 runner drank GE and 2 drank 1/2GE.

All subjects ate a high-carbohydrate diet for 3-5 days before the race.

Measurements and sampling. Measurements were made on all run- ners before the race and after 14, 29 and 42.3 km of running. At each of the four study points, runners were weighed on a beam- balance scale; standing blood pressure and pulse rate were re- corded with a Dinamap 850 automatic blood-pressure measuring device within less than 1 rain after entering the study station; rec- tal temperature was measured with an electronic thermometer in- serted approximately 50 mm into the rectum and left until read- ings were constant. A 40-ml sample of blood was collected for chemical measurements. At the 14-, 29- and 43-kin stations, a plastic glove worn throughout the race for collection of sweat without evaporation was removed from the runner; the opposite hand wiped with a clean wet towel and another glove put on it so that sweat could be collected independently from alternate hands for each 14-km segment of the race. It is recognized that the use of this i~rocedure may result in values higher than those found by analysis of whole-body sweat (Sohar et al. 1965). However, of the methods available, this appeared to be the one most readily app- licable for use in a marathon run.

The time required in the 14-kin and 29-km study stations for collection of data averaged 102 s with a range from 81 s to 240 s. Blood pressure measurement and insertion of the rectal thermom- eter were accomplished immediately on arrival at the study sta- tion. Variability of the time required for collection of samples was due almost entirely to the ease or difficulty in collecting blood from volume-depleted subjects, many of whom were severely fati- gued. With only two exceptions, both of which occurred at the 29-kin study point, blood was collected without stasis. The time required for all determinations and collections after completion of the race varied between 128 s and 640 s and averaged 248 s.

Each runner was accompanied throughout the race by a bicy- clist who carried a 500-ml graduated squeeze-bottle filled with the replacement solution his runner would drink. Fluid was taken ad libitum throughout the race. At each study station, the exact amount of fluid in the squeeze-bottle was measured and the bottle refilled for the next segment of the race.

Analyses. Blood samples were either analyzed immediately or pre- pared (separated or chilled as appropriate) at the study station, for later analysis. Electrolytes in plasma and sweat, including sodium, potassium, chloride and protein (both albumin and globulin) were measured by methods previously reported (Cade et al. 1972). In- sulin was measured by a radioimmunoassay technique (Wide 1969). Sera were examined for isoenzymes of lactate dehydrogen- ase (Wyndham 1977) to help assess the degree of hemolysis that had occurred, and plasma was assayed for haptoglobin (Killings- worth and Savory 1972) for the same purpose.

The volume of sweat for each segment of the race was esti- mated using weight lost plus fluid ingested for that segment. No attempt was made to correct for respiratory water loss. Cumula- tive losses of sodium and potassium were estimated by multiplying the volume of sweat (estimated by weight loss) by the measured electrolyte concentration. Changes in plasma volume were calcu- lated as the percentage change using the change in albumin con- centration, globulin concentration, and total plasma protein con- centration independently, and averaging values from the three cal- culations. Calculations of change in plasma volume using hemo- globin and hematocrit (Dill and CostiU 1974) were also made, but only for data collected after 14 km because marked elevation of lactate dehydrogenase fraction 2, depression of the concentration of haptoglobin in the plasma and a marked fall in hemoglobin and hematocrit in 2 subjects in the 29- and 42-kin samples indicated that enough hemolysis had occurred for the results not to be relia- ble.

All subjects signed an informed consent form before accept- ance into the study. A two-way analysis of variance with three treatment groups and seven performance blocks was used to ana- lyze the data. A follow-up Newman-Keuls test was used to com- pare directly each pair of treatment groups (Dayton 1970; Garrett and Woodworter 1960).

The ambient temperature at the beginning of the race was 16.1 ° C; this rose to 18 ° C after 1 h and continued to rise slowly to

22.5°C after 3.5 h. The relative humidity was 80°70 at the begin- ning of the race; it decreased to 67°70 after 1 h and to 60070 after 2 h, where it remained until the end of the race. Wind velocity varied from 0 to 7 km h -~

Results

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487

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Changes in rectal temperature for the three groups are shown in Fig. 1. Body temperature increased in all run- ners during the first 14 km of racing. As there was no significant difference between running speed for the three groups (see Table 2) during the first 14 km of rac- 37.0

ing, and body mass and 12Ozmax of the three groups were similar; heat production should have been approxi- mately equal for the three groups. During the second 14- kin segment of the race, rectal temperatures continued to rise in all runners. Again, running speed was approxi- mately the same for the three fluid-treatment groups. However, during the third 13.3-km segment of the race, a decrease in rectal temperature of the water-treated group from 39.5°C to 39.0°C was associated with a slowing of pace as 5 runners adopted a walk/run/walk pace. Rectal temperature also declined slightly in the 1/

~- 4 2GE group as four runners went to a walk/run/walk pace. In the GE group during the last one-third of the race, the mean rectal temperature rose slightly to a high _ 3 of 38.8 ° C as 5 runners maintained their pace. At 14 km ...J

and 29 km, the rectal temperature of the group receiving GE differed significantly from that of the groups given z ~ 2 I /2GE (P<0.05) and water (P<O.O1). ~- <

I.U Figure 2 shows the cumulative intake of fluid, sweat

loss and the resultant estimated overall deficit of fluid co 1 for each of the three groups during each segment of the <~ race. When the data were analyzed with the subjects in ~-

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each treatment group blocked into performance groups, - as discussed in the statistical evaluation, a highly signifi- cant (P<0.01) effect of treatment was found, in which the group drinking GE ingested more fluid than the oth- er two groups.

When cumulative sweat loss was examined by per- formance blocking within treatment groups, the analysis revealed that runners drinking GE sweat more (P<0.01) than those drinking either water or 1/2GE. A signifi- cant (P< 0.01) effect of time was also observed.

Control 14 29 42

km

Fig. 1. Changes in rectal temperature of athletes at varyous dis- tances during the marathon race. The groups are designated in the figure. GE, glucose/electrolyte solution (see Methods); 1/2GE, half-strength GE. I~---------Q H20; A . . . . -A 1/2 GE; O . . . . O GE

0 w uJ c~ (5 q9

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29 43 Km

Fig. 2. Cumulative fluid intake, sweat loss and fluid deficit of ath- letes after 14.5, 29 and 42.3 km of a marathon race. Groups are designated in the figure. • Intake; [] sweat loss; [] fluid deficit

Table 2. Mean running speed of the three groups during each 4.5-kin segment of the marathon

Fluid Running speed (m s -1)

0-14.5 km 14.5-29 km 29-42.3 km

Change (%) 14.5-29 km: 29-42.3 km

t-I20 4.29 4.29 2.82 34.3 (0.54) (0.49) (0.56)

1/2GE 4.13 4.02 2.87 28.6 (0.57) (0.60) (0.47)

GE 4.15 3.99 3.46 13.3 (0.76) (0.55) (0.77)

H20 vs 1/2GE P < 0 . 9 9 P<0 .84 P<0 .98 1/2GE vs GE P<0 .99 P<0 .98 P<0 .28 H20 vs GE P<0 .98 P<0 .89 P<0 .06

488

Analysis of the cumulative deficit of fluid (intake less sweat loss) during the entire race showed a highly signif- icant (P<0.001) effect among the matched subjects (performance grouping) within each treatment group, and a significant (P<0.01) effect of time. When per- formance blocking was done within each treatment group, the results revealed that runners ingesting GE so- lution had less (P< 0.05) fluid deficit than either of the other two groups.

Figure 3 shows the cumulative loss of sodium and po- tassium for each segment of the race. The total loss of sodium averged almost 400 mmol. The mean loss of po- tassium at the end of the race was 46 mmol, with almost equal amounts being lost during each segment of the race.

The concentrations of sodium and potassium in se- rum during each segment of the run are shown in Fig. 4. There were significant (P<0.01) differences in serum sodium concentrations both between and within groups

E 400

o ~ 300 13- o - o E ~g E 200

-(3 O co 100

b 14 29 42

I H2o }E= [ ] 1/2 GE

[ ] GE co

[ ] Potassium

km

Fig. 3. Cumulative loss of sodium and potassium during the entire race, as well as during each segment of it. Groups are designated in the figure

147

E 146

• 145 S~ $ E 144 03

E

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S v 09

143 5,8 5.6 5.4

5.2

5.0 4.8

4.6 4.4

4.2 4.0

.~ .~ H20 - [ Z:,-----,'~ 1/2 GE / , r ~ _ ~ _ . ~ o.----O GE / . . . [

I I I I

L I I I

Control 14 29 42

km

Fig. 4. Plasma sodium and potassium concentration of athletes during the race. Groups are designated in the figure

during the race. There Was also a significant (P< 0.01) effect of time. There were no significant differences among groups in serum sodium concentration prior to the race. However, at 14, 29 and 42 km, the group given GE solution had serum sodium concentrations that were significantly (P<0.05) greater than those of the group ingesting water.

There were significant (P<0.01) differences in plas- ma potassium concentration both between and within groups during the race. There was also a significant (P<0.01) effect of time and a significant (P<0.05) group × time interaction. There were no significant dif- ferences among groups in plasma potassium concentra- tion prior to the race. At 14 km and 29 km, the group ingesting GE solution had potassium concentrations that were significantly (P< 0.01) less than those of the group drinking water. At 14 km and 29 km, the group ingest- ing 1/2GE solution had significantly (P<0.01) lower concentrations of potassium in their serum than the group ingesting water. At 42 km, there were no signifi- cant differences in potassium concentration among the three groups.

Figure 5 shows the changes that occurred in plasma volume in the three groups. The decrement was signifi- cantly (P<0.05) greater in the group drinking water than in either group ingesting a GE solution. The two- way analysis of variance (ANOVA) revealed significant (P<0.01) differences both between and within groups, and a significant (P< 0.01) effect of time. The results of the two-way ANOVA also indicated that the reduction of plasma volume in the group ingesting GE was signifi- cantly less at 14 (P<0.01), 29 and 42 (P<0.05) km than in the group ingesting water. The group ingesting 1/ 2GE had less reduction in plasma volume (P<0.05) than the group ingesting water only at 14 km.

km

0

2 CO

o 4 tm (1) Eo~" 6

O

> 8 E

~ 10 h--

12

14 29 42

Fig. 5. Deficit in plasma volume of athletes during the marathon run. Groups are designated in the figure. • H20; [] 1/2GE; [] GE

Figure 6 shows the calculated mean blood pressure during the race. Mean blood pressure in all groups was highest at the 14-km study point and declined thereafter. The decline during the last segment of the race was sig- nificantly (P< 0.05) greater in those athletes who drank water than in those who drank either full- or half- strength GE (H20 vs GE P<0.05 at 42 km).

110

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0 ~ o .~ 90 rn

® 80

70

~ ' ' ~ \ \ 7 " \ , \

I I I I 0 14 29 42

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Fig. 6. Change in mean blood pressure of athletes during the ma- rathon run. Groups are designated in the figure. -~ ~ H20; A - - - - - A 1/2 GE; O - - - - - - © GE

489

Figure 7 shows the concentration of glucose in the plasma of the three groups before the race and the changes that occurred as a result of running. The mean concentration of glucose in the plasma of all groups was significantly higher at the 14-km checkpoint than it had been before the race. In runners who drank water there was a sharp, progressive decrease in plasma glucose aft- er 14 km as there was in those who drank 1/2GE (2.5°70 glucose). The concentration of glucose in runners who drank GE was well maintained throughout the race and was significantly (P<0.05) different from that of either of the other two groups.

The concentration of insulin in all groups decreased significantly from control values at the 14-km study point and continued to fall throughout the race (Fig. 8). The concentration of insulin in the plasma of subjects drinking water declined more rapidly and to a greater degree than in either of the groups drinking a solution containing glucose. The insulin concentration in plasma of subjects drinking GE was significantly higher (P<0.05) than in subjects drinking water at 14, 29 and 42 kin.

The predicted time for each runner from pre-race es- timates of ability and training and the actual time each runner achieved are shown in Table 3. Among runners

6 . 0

~L 8 - 5.0 ~ 0

40

I I I I

Control 14 29 42

km

Fig. 7. Blood glucose concentration of athletes during the mara- thon run. Groups are designated in the figure. • H20; a 1/2 GE; © GE

C '

v

14

12

10

8

6

4

2

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-....

I I I Control 14 29 42

km

Fig. 8. Serum insulin concentration of athletes during the mara- thon run. Groups are designated in the figure. • H20; a 1/2 GE; O GE

Table 3. Comparison of pre-race predicted time (PT) and actual running time (AT)

H20 1/2 GE GE

Pace a PT (min) AT (rain) Pace PT (min) AT (min) Pace PT (min) AT (rain)

1 W 150-160 165 1 SP 150-160 2 W 160-170 185 2 W 160-170 3 W 170-180 181 3 W 170-180 4 SP 180-190 185 4 W 180-190 5 SP 190-200 194 5 SP 190-200 6 - - - - - - 6 SP 200-210 7 W 210-220 276 6 SP 200-210

7 W 210-220 Mean 173.3-183.3 197.6 182.5-192.5 (SD) (36.1)

153 176 205 202 203 203 214 245

201.1 (25.1)

1 SP 150-160 158 2 SP 160-170 160 3 SP 170-180 163 4 SP 180-190 169 5 W 190-200 246 6 W 200-210 219 7 SP 210-220 204

180-190 188.4 (32.1)

a W, walk/run/walk; SP, steady pace

490

who drank water, only 2 of 6 finished within their pre- dicted time range while the group as a whole averaged 14 min slower than the upper end of their predicted time. Among those who drank 1/2GE only 2 of 8 fin- ished within their predicted range while the group aver- aged 8.5 rain outside their predicted range. Among those who drank GE 3 of 7 ran faster than predicted, 2 fin- ished within their predicted range, and 2 ran slower than predicted. For the group as a whole the average time fell within the predicted range.

Perusal of these data also shows that among the run- ners who maintained a steady pace the pre-race estimate was either achieved or exceeded while among walk/run/ walk subjects only 2 achieved their pre-race goals and none ran faster than the pre-race estimate. The data show that the reason for performance differences be- tween the H20, 1/2GE, and GE groups was the number of runners in each group who were forced to a walk/ run/walk pace.

Discussion

Three physiological defects, hypoglycemia (Levin et al. 1924; Gordon et al. 1925), hyperthermia (Benzinger 1959; Cade et al. 1972; Hanson and Zimmerman 1979; Wyndham and Strydom 1969; Syndham 1977 and Wyndham 1977), and vascular hypovolemia (Cade et al. 1971, 1972; Cohen and Zimmerman 1969; Costill et al. 1970; Wyndham and Strydom 1969; Wyndham 1977) have been reported frequently in athletes who were in physical distress at the end of an athletic endurance event. In the present study each of these abnormalities occurred with increased frequency as early as after 29 km of running in athletes who later were forced to adopt an alternating walk/run/walk pace.

Hommen (1985), Nadel et al. (1980) and Rowell et al. (1966) have shown clearly that, as blood volume de- creases during exercise with thermal stress, there is a progressive decrease in stroke volume and cardiac out- put. Hommen (1985), in addition, found that when car- diac output falls, skin blood flow falls, heat delivery to the skin is diminished and body temperature increases rapidly.

The rectal temperature of all of our subjects in- creased significantly during the first 14 km of running. Those who replaced their fluid loss with water, however, had a significantly higher rectal temperature than either the group who replaced their deficit with GE or those who drank 1/2GE. As running speeds in matched run- ners and presumably, therefore, heat production, were similar in the three treatment groups during the first 29 km of the race, the differences in rectal temperature seem best explained by a decreased efficiency of heat dissipation in athletes replacing their fluid deficit with water.

Effective dissipation of heat requires vaporization of water (sweat) from the skin and vaporization is more ef- ficient when the skin is well perfused and therefore warm (Hommen 1985). While we cannot estimate the amount of sweat actually vaporized from the surface of

the skin or the amount dropped on the ground, we pos- tulate that more sweat was produced and, more impor- tantly, evaporated by athletes drinking GE than by those drinking water. Increased vaporization due to bet- ter perfusion and higher skin temperature increased the effectiveness of heat dissipation and, thus, moderated the rise in body temperature. The group drinking water had the greatest deficit of vascular volume throughout the race (Fig. 5). In this study we used plasma proteins to calculate change in plasma volume rather than the widely accepted hemoglobin/hematocrit formulation of Dill and Costill (1974) because significant hemolysis oc- curred in 12 of our 21 subjects and hemolysis would cause a spurious apparent expansion of blood and plas- ma volume. On the other hand, use of plasma proteins underestimates the true change because a small amount of protein leaks from the vascular space early in exercise (van Beaumont 1972). Since the same error occurs in all the runners and, as the work of van Beaumont shows, this is not very great, we elected to calculate plasma vol- ume on the basis of protein concentration. The data in Fig. 5, showing a 3% reduction in plasma volume in subjects ingesting GE and a 6% reduction in subjects in- gesting water after 14 km of running, do not mean that the actual reductions in volume were exactly 3% and 6%. However, it is good evidence that the reduction in plasma volume of subjects ingesting water was twice as great as it was in GE subjects. The deficit in plasma vol- ume was initiated when exercise began. As cardiac out- put and flow through true capillaries increased, fluid was lost from the vascular space (Hommen 1985; Nadel et al. 1980). When sweating began (visible sweating was observed by the bicycle rider accompanying each runner before 12 min in 19 of our subjects), loss of sodium and water in sweat resulted in a further progressive depletion of vascular volume, which adversely affected perfusion of the skin and the ability to dissipate heat. The reduced vascular volume could not be repaired by ingestion of water (Nose et al. 1988) since distribution of water be- tween the intracellular and extracellular space is regul- ated by osmotic forces (Nose et al. 1988; Pitts 1974) and the principal osmotically active agent in the extracellular space is sodium (Nose et al. 1988; Pitts 1974). Thus, when lost sodium and water in sweat are replaced by wa- ter, the extracellular sodium osmotic pressure is reduced and a greater proportion of the ingested water is distri- buted along osmotic gradients into the intracellular space. When the replacement fluid contains sodium, most of the sodium remains in the extracellular fluid (Pitts 1974; Schlein et al. 1973) and a larger proportion of the water remains in the extracellular compartment so that the vascular space is better maintained. Our data clearly show that athletes replacing fluid losses with GE, even though they sweat more than runners who replaced lost fluid with water, still maintained their vascular vol- ume much better. The physiological importance of maintaining vascular volume is also strongly suggested by the marked fall in blood pressure that occurred in athletes who had a severe deficit in vascular volume and were forced to a walk/run/walk pace toward the end of the race.

491

The concentration of glucose in plasma rose, as has been reported by others (Bergstrom et al. 1975; Cade et al. 1971), in all groups during the first 14 km of the race. In the group replacing fluid losses with water, however, a striking and significant fall in the concentra- tion of glucose in plasma occurred by 29 kin. While the concentration of glucose in plasma was better main- tained in runners who ingested 2.5°70 glucose throughout the race, a significant reduction still occurred in that group. Thus, 7 of 11 runners who "hit the wall" and only 1 of 10 runners who kept a steady pace had a re- duced blood glucose concentration. Only those runners who ingested a 507o solution of glucose throughout the race consistently maintained a constant concentration of glucose in plasma.

An interesting consequence of the failure to ingest glucose during exercise is apparent in the data (Fig. 4). While the concentration of potassium in plasma in- creased in all subjects during exercise, the increase in athletes replacing their fluid losses with water was much greater than in either of the groups replacing their losses with a solution containing glucose. It has been shown that accumulation of potassium by active cells is greatly facilitated by insulin (Briggs and Koechig 1923; Zierler 1966). It seems reasonable to postulate that the higher concentration of insulin in plasma (Fig. 8) induced by glucose ingestion facilitated reaccumulation of potas- sium by working muscles. It also points out the futility and possible danger of administering a high-potassium replacement fluid to athletes during exercise.

The development of physiological perturbations, in- cluding reduction in blood volume, increase in body temperature, and reduction of plasma glucose concen- tration, occurred with much greater frequency in run- ners who replaced their fluid deficit with water than in those who replaced it with GE. Likewise, the almost to- tal collapse of athletes in the last one-third of the race occurred with great frequency (8307o) in those replacing their fluid deficit with water while only 2907o of those using GE and 50% of those replacing with 1 /2GE ex- perienced this phenomenon.

The data suggest that poor performance (Tables 2 and 3) late in the race was due either to exhaustion of carbohydrate stores or to marked reduction of blood volume with its consequent elevation of body tempera- ture, or both. The data also suggest that ingestion of a glucose/electrolyte solution in adequate amounts can either ameliorate or prevent both the energy substrate depletion and the thermal consequences of prolonged vigorous exercise.

Acknowledgements. The authors wish to thank Mr. Kelly W. Campbell and Mrs. Patricia J. Powers for technical assistance, and Ms. Jacqueline Harris for her diligence and unfailing enthu- siasm in the preparation of the manuscript.

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