THE HEMODYNAMIC AND METABOLIC ALTERATIONS ASSOCIATED WITH ACUTE HEAT STRESS INJURY IN MARATHON RUNNERS * Thomas F. O'Donnell, Jr. Departments of Surgery and Medicine Tufts University School of Medicine Tufts-New England Medical Center Hospital Boston, Massachusetts 021 11 Newton- Wellesley Hospital Newton, Massachusetts 02162 Naval Hospital Beaufort, South Carolina 29902

INTRODUCTION One of the key mechanisms in the body's defense against heat stress is the maintenance of a hyperdynamic circulatory response until the heat load is dissipated. As a result of a release of sympathetic vasomotor tone, cutaneous blood flow rises three or fourfold in order to facilitate external heat loss. Cardiac output increases 50% to 75% during heat stress, paralleling the elevated peripheral blood flow. In resting man, when skin temperature is kept constant but elevated, the increase in cardiac output is accounted for by elevated cutaneous flow.' Muscle blood flow is not enhanced appreciably. If exercise is superimposed on the heat gain from environmental sources, the endogenous heat load of 65 to 85 kcal/hr from basal metabolism may escalate to 400-600 kcallhr. Not only does the working muscle mass compound the total heat gain, but also it requires increased blood flow to supply oxygen and energy substrates. Thus, the circulatory stress of a man exercising in hot and humid conditions differs from that encountered by a resting subject in similar environmental situations. Metabolic needs may compete with thermoregulatory demands. The circulatory system of the marathon runner demonstrates certain adaptive responses to exercise that are characterized by lowered heart rate and increased stroke volume index. In effect, cardiac contractility is enhanced and may prove of benefit during periods of heat stress. In this manner, the conditioned athlete's cardiovascular response to heat stress probably differs from that of the nonconditioned but equally youthful subject.2 Because of the close relationship of the hemodynamic response to the metabolic response, biochemical changes during heat stress may also be different in these two groups. It is the purpose of this study to examine the hemodynamic and metabolic responses of eight marathon runners treated for heat stress injury during the 1976 Boston Athletic Association (BAA) Marathon. Dry bulb temperatures at that event were in the 90s (32"-38' C) and humidity was greater than 60%--conditions well recognized as conducive to the development of heat stress. Of the 2,000 participants, approximately 16 were treated at various hospitals for heat stress illnesses. The data on eight marathon runners will be compared to similar observations obtained on 15 young nonconditioned Marines previously reported by this author.$

* Opinions expressed in this article are those of the author and do not reflect those

of the Navy or Marine Corps at large.

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ODonnell: Heat Stress Injury

263

METHODSAND MATERIALS Eight participants in the 1976 BAA marathon were studied. All patients exhibited some form of heat stress injury, and all were brought immediately to the Newton-Wellesley Hospital by police ambulance. Our participants' heat stress injury occurred at a distance of between 13.75 and 19.5 miles of the marathon route. Upon arrival at the hospital, rectal temperature, heart rate, and blood pressure were obtained. The eight patients were triaged into two groups by clinical criteria: heat stroke or heat exhaustion.' Those subjects with heat stroke were cooled to 101" F (38.3" C) by packing in ice and vigorous massage, and received an infusion of Ringer's lactate.5 By contrast, those participants with heat exhaustion received an infusion of Ringer's lactate alone with volume replacement assessed by urine output and postural signs. Venous blood samples were drawn for electrolytes, blood urea nitrogen, and creatinine, as determined by standard laboratory measures." All patients were questioned as to their previous residence and training regimen when fully alert.

RESULTS Environmental Data. TABLE 1 presents the dry bulb temperatures at various distances along the marathon route at a time when humidity was approximately 62%, and wind velocity varied between 4 to 8 knots. Clinical Data. None of the patients were world class runners, and only two were "official" marathon entries. Seven of the eight patients resided in the north, where they had undergone their premarathon training. The mean age of the participants was 28 years (range: 17 through 38 years) and all were males. Six of the eight subjects demonstrated mental confusion on initial examination. None were anhidrotic, although the three patients with elevated rectal temperatures had flushed skin. Circulatory Data. TABLE 2 demonstrates the admission hemodynamic and temperature data for the eight patients. Three patients were hypotensive. No patient had a pulse pressure greater than 40 mmHg. Of note were the strikingly low heart rates, despite increased rectal temperatures in several of these patients. One patient was extremely bradycardic (patient No. 6 ) with a heart rate of TABLE1 ENVIRONMENTAL DATAALONG

THE COURSE OF THE

Distance (Miles)

1976 BOSTONMARATHON

Dry Bulb Temperature * (" C )

6.8

37.2 33.3

10.5

31.1

13.8 t 17.8 t

32.2 30.2

0

* Relative humidity was 62% for all temperatures. t Interval between which patients demonstrated acute heat stress syndrome.

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Annals New York Academy of Sciences TABLE2 HEMODYNAMIC DATA

Subject Number

Rectal Temperature (" C)

Mean Arterial Pressure (mmHg)

Pulse Pressure (mmHg)

Heart Rate (beatshin)

40.5 38.4 38.3 39.0 39.2 40.0 38.0 40.6

67 84 93 84 103 68 111 68

20 36 40 34 40 25 34 25

62 96 68 60 70 48 74 58

48 beatdmin. Electrocardiograms were performed in five patients and all

showed some minor abnormalities (atrial premature beat in one; S-Tsegment elevation, three; sinus bradycardia, two; voltage criteria for LVH, three; and first degree heart block, two.) Metabolic Data. Six and five patients, respectively, had serum sodium and chlorides at the upper range of normal, while four patients showed elevated HEMODYffAM/C AND EffVMOffMEff TAL DATA IN ACUTE n E A t s m m s MARATTnONLR5 h . 0 ) 0 NORYOTLNIIVL 0 HYPOTLN5IVE

MARINE5 (n * 181

0 40

30 20 10 Moan Artrriol Prraaurr (mm Ha)

Wort Rot. (Bratrlmin)

Rrctol limp.

WBGl (OC1

P C1

FIGURE1. This figure compares hemodynamic and environmental data from 15 Marine recruits to the 8 marathoners. Although mean arterial pressure and rectal temperature are comparable in the two groups, heart rate is markedly decreased in the marathoners. The environmental conditions, indicated by the wet bulb globe temperature (WBGT),were more severe for the marathoners than for the group of Marines.

O'Donnell: Heat Stress Injury

265

serum potassium levels. By contrast, carbon dioxide combining power was normal in all patients. Three patients had elevation of their blood urea nitrogen, one patient to 30 mg/100 rnl. Plasma hemoglobin levels were increased in two patients to 12.4 and 22 mg% , respectively.

DISCUSSION This study demonstrates that the responses of eight marathon runners to heat stress differs in many respects from those of the less conditioned subject. CAffDIAC DYffAM/CS /ff ACUT€ HEAT STffOK€ (MEAN f S. C M. I Cardiac Index L/min/mt

7 6 5 4 3

Stroke 6o Volumr Index 50 cc/beatr/me 40

120 Hrart Rate I00 (Brats/min) 80

-

1

1

ADM

I 2 HRS.

FIGURE 2. This figure demonstrates cardiac dynamics on admission with acute heat stroke (left side of panel) and twelve hours following treatment (right side of panel). Cardiac index, stroke volume index, and heart rate are all elevated on admission. The increase in cardiac index results from both an elevated heart rate and an enhanced stroke volume index. These differences are best appreciated by comparing our eight marathon runners to a group of 15 Marine recruits subjected to heat stress previously studied by this author.3 As will be appreciated in FIGURE1, environmental conditions during the marathon were more severe than those experienced by the Marine recruits. That not more than sixteen participants developed heat stress injuries during the 1976 BAA marathon despite the hot and humid condition may be

Annals New York Academy of Sciences

266

related to the constant cooling of the runners by water hoses along the route. Since seven of the eight marathoners resided and trained in the North prior to the race, lack of acclimatization played an important role in the development of heat stress injury. A similar prevalence of Northerners was observed in our study of 15 Marine recruits with heat stress injury. Because of the sudden change from a cool environmental condition to a hot and humid condition, the well-described endocrinologic, renal, and circulatory adaptations had not had time to d e ~ e l o p . ~Other major risk factors, such as fatigue and dehydration, may also have played a role in the development of heat stress injury in the marathoners. Lack of physical conditioning and obesity obviously were absent in the marathon runners but were present in several of the Marine recruits. Although two of the clinical manifestations of heat stress injury, confusion and weakness, were similar to those shown by the nonconditioned Marines, the TABLE 3

BIOCHEMICAL DATA ~

Subject Number Normal range 1 2 3 4 5 6 7 8

Blood Urea Carbon Nitrogen Dioxide (mg/ (meqlliter) 100 ml)

Potassium (meq/liter)

Sodium (meq/liter)

Chloride (meq/liter)

135-145 145 144 141 145 145 145 139 143

3.5-5.2 4.2 3.8 4.6 4.0 5.2 5.1 5.4 5.2

90-110

-

20-30

111 106 110 107 105 105 108

24.0 27.5 26.0 24.5 27.5 26.0 27.5

-

8-20 17 19 32 18 14 21 17 21

three marathoners with heat stroke differed in one major respect-they were sweating despite a markedly increased rectal temperature. This nonanhidrotic form of heat stroke has been described with prolonged exercise in highly acclimatized Israeli soldiers and in Army [email protected] Exercise-induced heat stroke may differ from that observed in the elderly population, which occurs generally at rest. Austin and Berry10 noted 100% of their cases were anhidrotic. By contrast, in the young athlete the endogenous heat load overwhelms the heat dissipating mechanisms before “sweat fatigue” may ensue. Of further interest was the cerebral symptom of confusion observed in the other five marathoners who did not have elevated rectal temperatures and were suffering from heat exhaustion. Rectal temperature, therefore, assumes an important differential finding in the clinical diagnosis of the various heat stress disorders.i The4hemodynamicresponses of the eight marathon runners are compared to the 15 Marine recruits in FIGURE1. Rectal temperature and mean arterial pressure are relatively comparable. Heart rate, however, is inappropriately low in seven of the eight marathoners, particularly in the three hypotensive subjects

O'Donnell: Heat Stress Injury

267

with heat stroke. Many authors I1-l3 have observed the close relationship between a central and peripheral circulatory response in heat stress. The marked increase in cutaneous flow acts like an arteriovenous shunt so that cardiac output is increased 3-4f0ld.I~ When exercise is combined with exposure to hot and humid conditions even greater stress is placed on circulatory homeostasis. Muscle blood flow is increased because of metabolic demands, but in turn muscle work results in a 7-1 0-fold increase in endogenous heat production. Deep muscle temperatures may rise to 41.1" C (106" F), so that the temperature of the blood draining from the muscle beds and the liver may be significantly higher than rectal temperature. Most investigators feel that the central circulatory response is determined by the resistances of the various regional vascular beds. Thus, in the exercising heat-stressed individual, splanchnic blood flow must decrease to compensate for the combination of increased skin and muscle blood flow. The limitations on venous return in the exercising heatstressed individual alters the central response. Cardiac output and stroke volume are less than in the resting heat-stressed subject.15 Controversy exists as to whether the central response, that is, increased cardiac output, results predominantly from an increased heart rate or from a concomitant increase in stroke volume. Koroxenides felt that cardiac output was increased principally as a result of an elevated heart rate, but Burch and Hyman l 6 observed that the 4-fold increase in cardiac output was accompanied by a 3-fold elevation in stroke volume. FIGURE 2 demonstrates the results of cardiodynamic studies in eight Marine recruits with acute heat stroke studied by this author." It will be noted that the markedly increased cardiac index resulted from both an elevated heart rate and an increased stroke volume index. It can be appreciated from this data that the limiting factor in the circulatory response to heat stress is the ability of the heart to meet the demands required by peripheral blood flow. Either cardiac failure or lack of selective shunting of blood within the splanchnic region may result in circulatory decompensation. On the other hand, the direct toxic effect of heat on thermally labile enzymes may also lead to decreased myocardial contractility as we have observed in one Marine recruit.Ii As has been demonstrated by the experimental work of Gold l 3 and of Daily and Harrison,'* circulatory failure results in high mortality in heat stress injuries. The cardiovascular response of the right marathoners to heat stress was unique. Mean arterial pressure and urine output were maintained at normal or near normal levels. In view of the low heart rate and the clinical evidence of vasodilatation, stroke volume index was apparently increased to maintain cardiac output. This would be consistent with previous circulatory studies in conditioned athletes where an increased stroke volume index was the main circulatory adaptation to repetitive exercise.* Further adaptive changes in the circulatory response may be related to selective regional shunting such as in the splanchnic or muscle beds.'@ Whether enhanced vagal tone was the basis for the bradycardia observed in the marathoners is unknown. The electrocardiographic findings, however, in several of the marathoners (increased P-R interval and first degree heart block) make increased parasympathetic activity a possibility. Whatever the cause of the bradycardia, it is in striking contrast to the tachycardia of the nonconditioned Marines. The metabolic data demonstrated in TABLE2 is in agreement with our previous findings and those of Schreier.'" The marginal elevations in sodium

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Annals New

York Academy of Sciences

are probably related to the hypotonic sweat loss, which was significant by the 15th mile of the marathon. Serum potassium levels, however, differ from those observed in the Marine recruits. Actual hyperkalemia was observed in four marathoners. The elevated potassium may be related to changes in muscle membrane permeability secondary to prolonged exercise.; Such a hypothesis is strengthened by the finding of myoglobinemia in previous studies of exercising man.*l The slight elevation in blood urea nitrogen is consistent with dehydration and with alterations in renal dynamics as described by Schreier and others.?", ?? SUMMARY Studies of clinical, metabolic, and hemodynamic responses to heat stress in eight marathon runners have demonstrated several important differences from those observed in nonconditioned subjects. Three marathoners manifested a nonanhidrotic form of heat stroke, a phenomenon not observed in our Marine recruits. Five patients with heat exhaustion evidenced signs of severe mental confusion despite apparently adequate hemodynamic function. Heart rate was significantly lower in all eight marathoners in comparison to the 15 Marine recruits. This latter observation suggests that either selective regional shunting of blood or increased stroke volume index occurs in marathoners subject to heat stress. ACKNOWLEDGMENTS The author wishes to express his gratitude for the help of the surgical, medical, resident, and nursing staffs of the Newton-Wellesley Hospital in caring expertly for these patients. REFERENCES 1. KOROXENIDIS, G. T., J. T. SHEPHERD & R. J. MARSHALL. 1961. Cardiovascular response to acute heat stress. J. Appl. Physiol. 16(5): 869-872. 2. GRIMBY, G. & B. SALTIN.1971. Physiological effects of physical training in different ages. Scand. J. Rehab. Med. 3: 6-14. 3. O'DONNELL, T. F. 1975. Acute Heat Stroke. J. Amer. Med. Assoc. 234: 824828. 4. ELNTORW.1968. Heat Stroke. Lancet u: 3 1-32. 5. ODONNELL, T. F. 1971. Medical problems of recruit training: A research approach. U. S. Navy Med. 586: 28-34. 6. BERGMEYER, H. U. 1965. Methods of enzymatic analysis. Academic Press.

New York, N.Y. 7. KNOCHEL, J. P. 1974. Environmental heat illness. Arch. Intern. Med. 133: 841-862. & E. SHOHAR. 1963. Mechanism of heat stroke. J. Trop. 8. GILAT,T., S. SHIBOLET Med. Hyg. 6 6 204-212. J. P., W.R. BEISEL,E. G. HERNDON, E. S. GERARD & K. G. BARRY. 9. KNOCHEL, 1961. The renal, cardovascular, hematologic, and serum electrolyte abnormalities of heat stroke. Amer. J. Med. 30: 299-309. 10. AUSTIN,M. G., J. W.BERRY.1956. Observations on 100 cases of heat stroke. J. h e r . Med. Assoc. 161: 1525-1529.

ODonnell: Heat Stress Injury 11. WILSON,G. 1940. The cardiopathology of heat stroke. J. Amer. Med. Assoc. 114: 557-558. 12. DAILY,W. M. & T. R. HARRISON.1948, A study of the mechanism and treatment of experimental heat pyrexia. Amer. J. Med. Sci. 215: 42-55. 13. GOLD,J. 1960. Development of heat pyrexia. J. Amer. Med. Assoc. 173: 11751182. 14. DETRY,J-M. R., G. L. BRENGELMANN, L. B. ROWELL& C. WYSS. 1972. Skin 15. 16. 17. 18. 19.

20. 21. 22.

and muscle components of forearm blood flow in directly heated resting man. J. Appl. Physiol. 32(4): 506-511. ROWELL,L. B., J. A. MURRAY, G. L. BRENGELMANN & K. K. KRANING.1969. Human cariovascular adjustments to rapid changes in skin temperature during exercise. Circ. Res. 24: 71 1-724. BURCH,G. E. & A. HYMAN.1977. Influence of a hot and humid envoironment upon cardiac output and work in normal man and in patients with chronic congestive heart failure at rest. Amre. Heart J. 53: 665-675. O'DONNELL, T. F. & G. H. A. CLOWES. 1972. The circulatory abnormalities of heat stroke. N. Engl. J. Med 287: 734-737. MOORE,F. T., S. A. MARABLE & E. OGDEN. 1966. Contractility of the heart in abnormal temperatues. Ann. Thor. Surg. 2(3 1: 446-450. ROWELL,L. B., G. L. BRENGELMANN, J. R. BLACKMON & J. A. MURRAY. 1970. Redistribution of blood flow during sustained high skin temperature in resting man. J. Appl. Physiol. 28: 415-420. SCHREIR, R. W., J. HANO,H. I. KELLER,R. M. FINKEL,P. F. GILLILAND, W. J. 1970. Renal, metabolic, and circulatory response CIRKSENA & P. E. TESCHAN. to heat and exercise. J. Int. Med. 73: 213-223. GREENBERG, J. & L. ARNENSON.1967. Exertional rabnomyolysis with myoglobinuria in a large group of military recruits. Neurology 17: 216-222. KEW, M. C., C. ABRAHAMS, N. W. LEVIN,er a/. 1967. The effects of heat stroke on the function and structure of the kidney. Quart. J. Med. 35: 277-300.

The hemodynamic and metabolic alterations associated with acute heat stress injury in marathon runners.

THE HEMODYNAMIC AND METABOLIC ALTERATIONS ASSOCIATED WITH ACUTE HEAT STRESS INJURY IN MARATHON RUNNERS * Thomas F. O'Donnell, Jr. Departments of Surge...
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