Changes in gastrointestinal cell integrity after marathon running and exercise-associated collapse.

PURPOSE: Endurance exercise and hyperthermia are associated with compromised intestinal permeability and endotoxaemia. The presence of intestinal fatty acid-binding protein (I-FABP) in the systemic circulation suggests intestinal wall damage, but this marker has not previously been used to investigate intestinal integrity after marathon running. METHODS: Twenty-four runners were recruited as controls prior to completing a standard marathon and had sequential I-FABP measurements before and on completion of the marathon, then at four and 24 h later. Eight runners incapacitated with exercise-associated collapse (EAC) with hyperthermia had I-FABP measured at the time of collapse and 1 hour later. RESULTS: I-FABP was increased immediately on completing the marathon (T0; 2593 ± 1373 ng·l-1) compared with baseline (1129 ± 493 ng·l-1; p < 0.01) in the controls, but there was no significant difference between baseline and the levels at four hours (1419 ± 1124 ng·l-1; p = 0.7), or at 24 h (1086 ± 302 ng·l-1; p = 0.5). At T0, EAC cases had a significantly higher I-FABP concentration (15,389 ± 8547 ng.l-1) compared with controls at T0 (p < 0.01), and remained higher at 1 hour after collapse (13,951 ± 10,476 ng.l-1) than the pre-race control baseline (p < 0.05). CONCLUSION: I-FABP is a recently described biomarker whose presence in the circulation is associated with intestinal wall damage. I-FABP levels increase after marathon running and increase further if the endurance exercise is associated with EAC and hyperthermia. After EAC, I-FABP remains high in the circulation for an extended period, suggesting ongoing intestinal wall stress.

Heat-Related Illnesses.

Heat-related illnesses comprise a spectrum of syndromes resulting from disruption of thermoregulation in people exposed to high environmental heat. Symptoms range from heat edema and exercise-associated muscle cramps to exercise-associated collapse, heat exhaustion, and life-threatening heat stroke. Athletes, outdoor laborers, and military personnel are at greatest risk. Several intrinsic and extrinsic factors increase the risk of heat-related illness, including medical conditions, environmental factors, medication use, and inadequate acclimatization. Proper recognition and treatment are effective in preventing adverse outcomes. Management of the mildest forms of heat-related illness (e.g., heat edema, exercise-associated muscle cramps) is largely supportive, and sequelae are rare. Heat exhaustion is characterized by cardiovascular hypoperfusion and a rectal core temperature up to 104°F without central nervous dysfunction. Mild cooling, rest, and hydration are recommended. Heat stroke is a medical emergency in which patients present with rectal core temperature of 105°F or greater, multiorgan damage, and central nervous dysfunction. Ice water or cold water immersion is recommended. Patients adequately cooled within 30 minutes have excellent outcomes. Patients with heat stroke generally require hospitalization to monitor for medical complications despite rapid cooling. People diagnosed with heat stroke or severe heat-related illness should refrain from physical activity for at least seven days after release from medical care, then gradually begin activity over two to four weeks. Acclimatization, adequate hydration, and avoidance of activities during extreme heat are the most effective measures to reduce the incidence of heat-related illnesses.

Effects of heat acclimation on endurance capacity and prolactin response to exercise in the heat.

We examined the effect of heat acclimation (HA) on endurance capacity and blood prolactin (PRL) response to moderate intensity exercise in the heat in young male subjects (n = 21). Three exercise tests (ET) were completed on a treadmill: H1 (walk at 60% VO(2)peak until exhaustion at 42°C), N (walk at 22°C; duration equal to H1) and H2 (walk until exhaustion at 42°C after a 10-day HA program). Heart rate (HR), skin (T (sk)) and core (T (c)) temperatures and body heat storage (HS) were measured. Blood samples were taken immediately before, during and immediately after each ET. HA resulted in lower HR, T (sk), T (c) and HS rate (P < 0.05) during ET, whereas endurance capacity increased from 88.6 ± 27.5 min in H1 to 162.0 ± 47.8 min in H2 (P < 0.001). Blood PRL concentration was lower (P < 0.05) during exercise in H2 compared to H1 but the peak PRL level observed at the time of exhaustion did not differ in the two trials. Blood PRL concentration at 60 min of exercise in H1 correlated with time to exhaustion in H1 (r = -0.497, P = 0.020) and H2 (r = -0.528, P = 0.014). In conclusion, HA slows down the increase in blood PRL concentration but does not reduce the peak PRL level occurring at the end of exhausting endurance exercise in the heat. Blood PRL response to exercise in the heat in non-heat-acclimated subjects is associated with their endurance capacity in the heat in a heat-acclimated state.

High work output combined with high ambient temperatures caused heat exhaustion in a wildland firefighter despite high fluid intake.

The purpose of this case study is to examine the physiological/behavioral factors leading up to heat exhaustion in a male wildland firefighter during wildland fire suppression. The participant (24 years old, 173 cm, 70 kg, and 3 years firefighting experience) experienced heat exhaustion following 7 hours of high ambient temperatures and arduous work on the fire line during the month of August. At the time of the heat-related incident (HRI), core temperature was 40.1 °C (104.2 °F) and skin temperature was 34.4 °C (93.9 °F). His work output averaged 1067 counts·min(-1) (arbitrary units for measuring activity) for the 7 hours prior to the HRI, a very high rate of work over an extended time period during wildfire suppression. In the 2.5 hours leading up to the heat incident, he was exposed to a mean ambient temperature of 44.6 °C (112.3 °F), with a maximum temperature of 59.7 °C (139.5 °F). He consumed an average of 840 mL·h(-1) in the 7 hours leading up to the incident and took an average of 24 ± 11 drinks·h(-1) (total of 170 drinks). The combined effects of a high work rate and high ambient temperatures resulted in an elevated core temperature and a higher volume and frequency of drinking than typically seen in this population, ultimately ending in heat exhaustion and removal from the fire line. The data demonstrate that heat-related incidents can occur even with aggressive fluid intake during wildland fire suppression.

Comparison of active cooling devices with passive cooling for rehabilitation of firefighters performing exercise in thermal protective clothing: a report from the Fireground Rehab Evaluation (FIRE) trial.

BACKGROUND: Thermal protective clothing (TPC) worn by firefighters provides considerable protection from the external environment during structural fire suppression. However, TPC is associated with physiologic derangements that may have adverse cardiovascular consequences. These derangements should be treated during on-scene rehabilitation periods. OBJECTIVE: To examine heart rate and core temperature responses during the application of four active cooling devices, currently being marketed to the fire service for on-scene rehabilitation, and compare them with passive cooling in a moderate temperature (approximately 24 degrees C) and with an infusion of cold (4 degrees C) saline. METHODS: Subjects exercised while they were wearing TPC in a heated room. Following an initial exercise period (bout 1), the subjects exited the room, removed the TPC, and for 20 minutes cooled passively at room temperature, received an infusion of cold normal saline, or were cooled by one of four devices (fan, forearm immersion in water, hand cooling, or water-perfused cooling vest). After cooling, the subjects donned the TPC and entered the heated room for another 50-minute exercise period (bout 2). RESULTS: The subjects were not able to fully recover core temperature during a 20-minute rehabilitation period when provided rehydration and the opportunity to completely remove the TPC. Exercise durations were shorter during bout 2 when compared with bout 1 but did not differ by cooling intervention. The overall magnitudes and rates of cooling and heart rate recovery did not differ by intervention. CONCLUSIONS: No clear advantage was identified when active cooling devices and cold intravenous saline were compared with passive cooling in a moderate temperature after treadmill exercise in TPC.

Pathophysiology of intense physical conditioning in a hot climate. I. Mechanisms of potassium depletion.

Serial estimations of exchangeable (42)K showed that six volunteer subjects undergoing intensive physical conditioning in a hot climate sustained a mean deficit of 517 mEq. This deficit occurred despite a daily potassium intake of 100 mEq. Simultaneous values for lean body mass rose suggesting that potassium deficiency was not the result of catabolism. Although sweating was the major avenue by which the deficit occurred, daily excretion of potassium into the urine when each subject was maximally deficient ranged from 46 to 75 mEq and thus was inappropriately high for potassium-depleted subjects. Despite high intakes of sodium and excretion of corresponding quantities into the urine, Na/K ratios in sweat were low thus indicating unsuppressed activity of aldosterone on sweat glands. Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. These findings suggest that intense physical work in the heat stimulates higher production of aldosterone than would occur in nonexercising subjects on similar sodium intakes. Similar to the phenomenon of mineralocorticoid escape, such overproduction of aldosterone in the presence of conditions permitting excretion of sodium into the urine could facilitate continued excretion of potassium by the kidney despite serious potassium depletion. As a consequence, the kidney played a role in the genesis of potassium depletion in these subjects. In contrast to subjects undergoing conditioning in the summer months, potassium depletion did not occur in 16 subjects during identical training under cooler environmental conditions.

High temperatures and nephrology: The climate change problem. / Altas temperaturas y nefrología: a propósito del cambio climático.

It is well known that climate change greatly affects human health, even though there are few studies on renal outcomes. Heat waves have been found to increase cardiovascular and respiratory morbidity and mortality, as well as the risk of acute renal failure and hospitalisation due to renal diseases, with related mortality. Recurrent dehydration in people regularly exposed to high temperatures seems to be resulting in an unrecognised cause of proteinuric chronic kidney disease, the underlying pathophysiological mechanism of which is becoming better understood. However, beyond heat waves and extreme temperatures, there is a seasonal variation in glomerular filtration rate that may contribute to the onset of renal failure and electrolyte disorders during extremely hot periods. Although there are few references in the literature, serum sodium disorders seem to increase. The most vulnerable population to heat-related disease are the elderly, children, chronic patients, bedridden people, disabled people, people living alone or with little social contact, and socioeconomically disadvantaged people.

Clinical Impact of Speed Variability to Identify Ultramarathon Runners at Risk for Acute Kidney Injury.

BACKGROUND: Ultramarathon is a high endurance exercise associated with a wide range of exercise-related problems, such as acute kidney injury (AKI). Early recognition of individuals at risk of AKI during ultramarathon event is critical for implementing preventative strategies. OBJECTIVES: To investigate the impact of speed variability to identify the exercise-related acute kidney injury anticipatively in ultramarathon event. METHODS: This is a prospective, observational study using data from a 100 km ultramarathon in Taipei, Taiwan. The distance of entire ultramarathon race was divided into 10 splits. The mean and variability of speed, which was determined by the coefficient of variation (CV) in each 10 km-split (25 laps of 400 m oval track) were calculated for enrolled runners. Baseline characteristics and biochemical data were collected completely 1 week before, immediately post-race, and one day after race. The main outcome was the development of AKI, defined as Stage II or III according to the Acute Kidney Injury Network (AKIN) criteria. Multivariate analysis was performed to determine the independent association between variables and AKI development. RESULTS: 26 ultramarathon runners were analyzed in the study. The overall incidence of AKI (in all Stages) was 84.6% (22 in 26 runners). Among these 22 runners, 18 runners were determined as Stage I, 4 runners (15.4%) were determined as Stage II, and none was in Stage III. The covariates of BMI (25.22 ± 2.02 vs. 22.55 ± 1.96, p = 0.02), uric acid (6.88 ± 1.47 vs. 5.62 ± 0.86, p = 0.024), and CV of speed in specific 10-km splits (from secondary 10 km-split (10th - 20th km-split) to 60th - 70th km-split) were significantly different between runners with or without AKI (Stage II) in univariate analysis and showed discrimination ability in ROC curve. In the following multivariate analysis, only CV of speed in 40th - 50th km-split continued to show a significant association to the development of AKI (Stage II) (p = 0.032). CONCLUSIONS: The development of exercise-related AKI was not infrequent in the ultramarathon runners. Because not all runners can routinely receive laboratory studies after race, variability of running speed (CV of speed) may offer a timely and efficient tool to identify AKI early during the competition, and used as a surrogate screening tool, at-risk runners can be identified and enrolled into prevention trials, such as adequate fluid management and avoidance of further NSAID use.

Hydration status and fluid intake of urban, underprivileged South African male adolescent soccer players during training.

BACKGROUND: Poor hydration compromises performance and heightens the risk of heat stress which adolescents are particularly susceptible to as they produce comparatively larger amount of metabolic heat during exercise. This study determined the hydration status and fluid intake of socio-economically disadvantaged, male adolescent soccer players during training. METHODS: A pilot study was conducted among 79 soccer players (mean age 15.9 ± 0.8 years; mean BMI 20.2 ± 2.1 kg/m(2)). Hydration status was determined before and after two training sessions, using both urine specific gravity and percent loss of body weight. The type and amount of fluid consumed was assessed during training. A self-administered questionnaire was used to determine the players' knowledge regarding fluid and carbohydrate requirements for soccer training. RESULTS: Players were at risk of developing heat illness during six of the 14 training sessions (60 - 90 minutes in length). Although on average players were slightly dehydrated (1.023 ± 0.006 g/ml) before and after (1.024 ± 0.007 g/ml) training, some were extremely dehydrated before (24%) and after (27%) training. Conversely some were extremely hyperhydrated before (3%) and after training (6%). The mean percent loss of body weight was 0.7 ± 0.7%. The majority did not consume fluid during the first (57.0%) and second (70.9%) training sessions. An average of 216.0 ± 140.0 ml of fluid was consumed during both training sessions. The majority (41.8%) consumed water, while a few (5.1%) consumed pure fruit juice. More than 90% stated that water was the most appropriate fluid to consume before, during and after training. Very few (5.0%) correctly stated that carbohydrate should be consumed before, during and after training. CONCLUSIONS: Approximately a quarter were severely dehydrated. Many did not drink or drank insufficient amounts. The players' beliefs regarding the importance of fluid and carbohydrate consumption did not correspond with their practices. A nutrition education programme is needed to educate players on the importance of fluid and carbohydrate to prevent dehydration and ensure appropriate carbohydrate intake.

Cardiovascular and metabolic manifestations of heat stroke and severe heat exhaustion.

We prospectively studied the clinical, biochemical (including creatine phosphokinase (CPK) isoenzymes) and electrocardiographic features of exertional heat stroke in 13 patients (group 1) and severe heat exhaustion in 14 patients (group 2). Despite initial presentations with severe hyperthermia, tachycardia and hypotension, only one patient with heat stroke had myocardial ischemia. The CPK isoenzymes were not indicative of myocardial damage in any patient. The patients with heat stroke were somewhat more dehydrated than those with heat exhaustion as measured by differences in serum creatinine, sodium and osmolality, and the former (group 1) had a significantly lower initial glucose level (P less than 0.05). Although significant differences in potassium were not observed in the pretreatment samples, at 12 hours the serum potassium was significantly lower in group 1 (P less than 0.05). This suggests that this group may have been more potassium-depleted at the time of heat stroke. Prompt recognition and vigorous therapy were successful in rapidly lowering high temperatures and in preventing serious complications.

Heat stress in motor vehicles: a problem in infancy.

Children have died from heat stress because they have been left in closed automobiles. Changes in the internal temperature of various sized automobiles left in the Brisbane summer sun were examined. With all windows and doors closed, this temperature rose from an ambient level of 36 C to a maximum of 67 C within 15 minutes and remained there until the doors were opened. Slightly lower temperatures were found for light colored sedans and station wagons. However, all readings were significantly above ambient and all produced an environment unacceptable for a child. Temperatures approaching ambient were only achieved with ventilation provided by windows at least 200 mm (half) open. A lesser gap (50 mm) resulted in interior temperatures exceeding 50 C, which is still too hot for children. Infants left in such an environment will lose fluid quickly from sweat and could become as much as 8% dehydrated in four hours. Subsequently the cerebral manifestations of heat stroke would ensue. Parents and pediatricians should be warned of the danger of heat stress if children are left in a closed automobile.

Invasive evaluation of patients with heat stroke.

Right-heart catheterization was performed in ten patients who suffered heat stroke on their pilgrimage to Mecca, Saudi Arabia. The group included seven men and three women who had mean rectal temperatures of 42.4 degrees C. Other findings included the following: heart rate (mean, 120 beats/min); cardiac output (mean, 8.2 ml/min/m2); arterial pressure (mean, 65 mm Hg); cardiac indices (mean, 4.4 ml/min/m2); right atrial pressure (mean, 6 mm Hg); pulmonary capillary wedge pressure (mean, 10 mm Hg); systemic vascular resistance (mean, 684 dyne.s.cm-5); pulmonary vascular resistance (mean, 86 dyne.s.cm-5); oxygen delivery (mean 837 ml/min/m2); oxygen consumption (mean 160 ml/min/m2); mixed venous oxygen tension (mean, 56 mm Hg); and shunt fraction (mean, 20 percent). Nine patients survived. One, who had a cardiopulmonary arrest before any treatment could be administered, died.

Hemodynamic alterations of heat stroke in the elderly.

Serial hemodynamic alterations were investigated in seven elderly patients with heat stroke. Their mean age was 72 +/- 6 years. The circulatory response to heat stroke was either hyperdynamic of hypodynamic. Two patients had increased cardiac index (4.3 and 4.4 L/min/m2), increased right atrial pressure (10 and 12 mm Hg), normal pulmonary capillary wedge pressure (10 and 12 mm Hg), and decreased systemic vascular resistance (542 and 738 dyne.sec.cm-5). Five patients had decreased cardiac index (mean 2.3 +/- 0.2 L/min/m2), decreased right atrial pressure (mean 2 +/- 1 mm Hg), normal pulmonary capillary wedge pressure (mean 6 +/- 3 mm Hg), and increased systemic vascular resistance (mean 2020 +/- 204 dyne.sec.cm-5). Circulatory failure appears to be secondary to peripheral pooling of blood or hypovolemia. The inability to compensate hemodynamically when stressed by heat may predispose certain elderly individuals to develop heat stroke.

Electrocardiographic abnormalities in patients with heat stroke.

Serial electrocardiograms were taken in 46 Hajj Pilgrims suffering from heat stroke immediately after cooling 12 and 24 h later. The collected data were analyzed and revealed that a statistically significant number of patients with heat stroke had sinus tachycardia (43 percent, p < 0.05), conduction defect (22 percent, p < 0.046), prolonged Q-T interval (61 percent, p < 0.007), diffuse nonspecific ST-T changes (26 percent, p < 0.036), and ST-T changes (localized to the ECG leads confirming to a territory of coronary artery) consistent with myocardial ischemia (21 percent, p < 0.02). Although adverse effects of heat stroke on the heart are multifactorial, the above data indicate that heat stroke predisposes to certain risk of myocardial ischemia and conduction disturbances. This may reflect the true cardiovascular status of these heat stroke victims.

Prevention of endotoxaemia by non-absorbable antibiotics in heat stress.

Four anaesthetised monkeys were given oral kanamycin (15 mg 1 kg 12 hourly) over five consecutive days before being heat stressed. Four other anaesthetised monkeys served as controls. The plasma lipopolysaccharide concentration in control primates increased initially from 0.044 (SEM 0.004) ng/ml to 0.062 (0.006) ng/ml as the rectal temperature increased from 37.5 to 39.5 degrees C. A second increase in lipopolysaccharides started at 42 degrees C and reached 0.308 (0.038) ng/ml (p less than 0.01) at 44.5 degrees C. Before heat stress the plasma lipopolysaccharide concentration in the primates who had been pretreated with kanamycin was 0.007 (0.006) ng/ml, and despite heating these animals to 44.5 degrees C no increase in plasma lipopolysaccharide concentrations were seen in this group. The cardiovascular variable during heat stress were more unstable in the control group and began to deteriorate at a lower temperature than in the group receiving antibiotic. These data suggest that the increased plasma lipopolysaccharide concentration during heat stress originates mainly from the gut.

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

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.

Endotoxemia and release of tumor necrosis factor and interleukin 1 alpha in acute heatstroke.

To determine whether endotoxemia and release of tumor necrosis factor (TNF-alpha) and/or interleukin 1 alpha (IL-1 alpha) are involved in the pathogenesis of heatstroke, 17 adult patients with a mean rectal temperature of 42.1 +/- 0.2 degrees C were studied. Blood samples were taken on admission and after cooling was completed. TNF-alpha and IL-1 alpha levels were measured by enzyme-linked immunosorbent assay, and lipopolysaccharide (LPS) content was measured by the chromogenic substrate modification of the Limulus amebocyte lysate. TNF-alpha, IL-1 alpha, and LPS were elevated in all patients [199 +/- 25 (SE) pg/ml, 480.5 +/- 68.3 pg/ml, and 8.60 +/- 1.19 ng/ml, respectively, compared with normal control values of 31.4 +/- 8.4 pg/ml, 53.7 +/- 5.32 pg/ml, and less than 9 pg/ml]. There was no significant correlation between temperature and the circulating concentration of TNF-alpha, IL-1 alpha, and LPS. Postcooling TNF-alpha, IL-1 alpha, and LPS concentrations were significantly decreased but still above normal control values. The findings suggest that these mediators may have a role in the pathogenesis of heatstroke that could change the strategy of management.

Peripheral vascular responses to hyperthermia in the rat.

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.

Physiological tolerance to uncompensable heat stress: effects of exercise intensity, protective clothing, and climate.

This study determined the influence of exercise intensity, protective clothing level, and climate on physiological tolerance to uncompensable heat stress. It also compared the relationship between core temperature and the incidence of exhaustion from heat strain for persons wearing protective clothing to previously published data of unclothed persons during uncompensable heat stress. Seven heat-acclimated men attempted 180-min treadmill walks at metabolic rates of approximately 425 and 600 W while wearing full (clo = 1.5) or partial (clo = 1.3) protective clothing in both a desert (43 degrees C dry bulb, 20% relative humidity, wind 2.2 m/s) and tropical (35 degrees C dry bulb, 50% relative humidity, wind 2.2 m/s) climate. During these trials, the evaporative cooling required to maintain thermal balance exceeded the maximal evaporative capacity of the environment and core temperature continued to rise until exhaustion from heat strain occurred. Our findings concerning exhaustion from heat strain are 1) full encapsulation in protective clothing reduces physiological tolerance as core temperature at exhaustion was lower (P < 0.05) in fully than in partially clothed persons, 2) partial encapsulation results in physiological tolerance similar to that reported for unclothed persons, 3) raising metabolic rate from 400 to 600 W does not alter physiological tolerance when subjects are fully clothed, and 4) physiological tolerance is similar when subjects are wearing protective clothing in desert and tropical climates having the same wet bulb globe thermometer. These findings can improve occupational safety guidelines for human heat exposure, as they provide further evidence that the incidence of exhaustion from heat strain can be predicted from core temperature.