The body utilizes energy in the form of energy-rich chemical compounds to perform work that is required to maintain normal function ( Fig. 21.1 ).

Regeneration of ATP for source of energy in muscle contraction. The body utilizes energy in the form of energy-rich chemical compounds to perform the work that is required to maintain normal body function.

Conversion from chemical bond energy to gross motor energy is inefficient; a majority of reactions produce heat.

Sources of nonexercising heat production include involuntary smooth muscle contraction, myocardial contraction, muscle group contraction to maintain posture, shivering, digestion, and baseline cellular metabolism.

Heat production increases to 15–20 times of the resting rate as a result of increased muscular contraction and cellular metabolism.

At maximum exercise, the work efficiency of the body is only 15%–30%; thus, 70%–85% of muscle energy consumption is converted to heat and must be dissipated .

The thermoregulatory system is unable to maintain a homeostatic environment when heat production is increased beyond the body’s ability to effectively transfer heat, resulting in an elevated core temperature.

The consequence is heat injury.

During excess heat production, the body must constantly dissipate heat in order to maintain core temperature.

Without regulation, the heat generated by the body at rest would increase core temperature by 1°C every 5 minutes; the rate of core temperature elevation accelerates in a hot environment.

Thermoregulation requires complex interactions among the central nervous system (CNS), cardiovascular system, and integumentary system to maintain a core body temperature of approximately 37°C (98.6°F).

The CNS temperature regulatory center is located in the hypothalamus.

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  The hypothalamus receives inputs regarding the core body and skin temperature from peripheral skin receptors and circulating blood volume.

  
  
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  Increases in core temperature are sensed and centrally regulated by thermal detectors in the hypothalamus, which then provide stimulus via the sympathetic nervous system to initiate sweating and increased peripheral blood flow ( Fig. 21.2 ).

  
  

  
  

  
  

  

  
  

  
  

  Temperature regulation. Increases in core temperature are sensed and centrally regulated by thermodetectors in the hypothalamus, which then provide stimulus via the sympathetic nervous system to initiate sweating and increase peripheral blood flow.

  
  

Core body temperature is determined by the net balance of metabolic heat production and the transfer and exchange of heat to/from the surrounding environment. This can be expressed in the heat balance equation described below ( 21.1 ).

S = amount of stored heat

M = metabolic heat production

E = evaporative heat loss

R = radiant heat loss or gain

C = convection heat loss or gain

K = conductive heat loss or gain

Heat loss can be divided into:

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  Nonevaporative heat loss

  
  
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  Evaporative heat loss

Nonevaporative heat loss dissipates most body heat when the ambient temperature is below 20°C (68°F).

Evaporation accounts for a majority of heat loss when the temperature is above 20°C (68°F).

Evaporation occurs when liquid converts to gas.

Heat is transferred through the evaporation of sweat and respiratory moisture.

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  Insensate loss of moisture equals 600 mL per day.

Sweating

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  Sweating usually begins when the body temperature is above 37°C (98.6°F).

  
  
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  Amount is proportional to body surface area

  
  
  
  
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    Rate is dependent on acclimatization and level of conditioning.

    
    
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    Sweat rates vary between 600 and 3500 mL per hour.

  
  
  
  
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  Heat of vaporization of water governs the cooling effect of perspiration.

  
  
  
  
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    Normal rate of heat vaporization of water is 540 calories per gram but from the skin surface is 580 calories per gram.

  
  

Cooling as a result of the evaporation of perspiration is directly related to

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  Sweat rate (L/h): multiplied by 580 calories per gram (heat of vaporization of water on skin)

  
  
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  Total body surface area (TBSA)

  
  
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  Velocity of air crossing the skin surface area

Problems with heat dissipation in a hot and humid environment:

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  Evaporative cooling is indirectly related to humidity.

  
  
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  Evaporation can account for 98% of heat loss in a hot dry environment.

  
  
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  At temperatures above 35°C (95°F), convection and radiation do not contribute to heat loss, whereas sun radiation causes heat gain.

  
  
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  In heat-acclimated athletes, equilibrium between heat production and heat dissipation results in core temperatures during exercise ranging between 37°C (98.6°F) and 40°C (104°F) without diminished performance.

  
  
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  If heat-dissipating mechanisms fail or if there is overwhelming heat stress, core temperature will continue to rise to dangerous levels.

Specific demands for cardiac output (CO) and plasma volume must be met for heat dissipation during exercise in a hot environment.

15% of CO is shunted to working muscles early during exercise.

In addition, 15%–25% of CO is shunted from the central circulation to the skin for cooling, which effectively lowers the central plasma volume.

A bout of exercise decreases plasma volume, venous return, and stroke volume.

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  Conversely, a known training effect of regular exercise is an increase in plasma volume, venous return, and stroke volume—all of these result in improved heat regulation with exercise.

Sweat rate during exercise results in 500–2000 mL loss of plasma volume per hour.

To maintain the necessary CO in order to maintain exercise intensity (and core temperature), heart rate must increase to compensate for the reduced stroke volume.

If plasma volume is not maintained while exercise intensity and environmental conditions remain constant, work and exercise performance will be adversely affected, cooling efficiency decreases, and hypotension occurs.

Process can be favorably changed by reducing exercise intensity (slowing down), building plasma volume (drinking), and improving nonevaporative heat loss mechanisms (e.g., improving convection by increasing skin surface exposure or circulating local wind/water speed and reducing radiation exposure).

Signs and Symptoms: Progressive, painful involuntary muscle contraction of skeletal muscles during or after intense, prolonged exercise; large lower limb muscles are commonly affected, but any muscle may be involved, including abdominal and intercostal muscles

Etiology: Although commonly referred to as heat cramps, they are not directly related to an elevated core body temperature. Exercise-associated muscle cramps (EAMCs) can occur in warm, cool, or temperature-controlled environmental conditions. EAMCs often begin with early muscle fasciculation in an affected muscle group and may progress to severe and diffuse muscle spasm. Although the exact mechanism is not known, muscle fatigue, dehydration, high sweat rates, high sodium sweat concentration, electrolyte imbalance, and altered neuromuscular control have been implicated in the development of EAMCs.

Predisposing Factors: Lack of acclimatization and/or conditioning, ongoing negative sodium balance (“salty sweaters”), history of EAMCs, faster competition performance times, and prior local muscle or tendon injury

Treatment:

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  Rest and cooling

  
  
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  Passive, static muscle stretching

  
  
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  Ice and muscle massage

  
  
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  Oral hydration with an electrolyte and carbohydrate solution

  
  
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  Oral intake of salt-containing foods

  
  
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  In refractory individuals who are nonresponsive to oral hydration or in those who are unable to consume oral fluids, intravenous (IV) normal saline bolus may be indicated.

  
  
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  Refractory muscle cramps may require IV medications

  
  
  
  
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    Diazepam 1–5 mg IV

    
    
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    Midazolam 1–2 mg IV

    
    
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    Magnesium sulfate 2 g intravenous piggyback (IVPB)

  
  

Prevention: Conditioning and heat acclimatization, maintaining fluid and salt balance; recurrent crampers, particularly “salty sweaters,” may benefit from liberal use of salt within their diet, particularly in warmer environments

Complications: Rare, but may be a warning sign for impending heat exhaustion; development of rhabdomyolysis should be expected in severe, prolonged episodes of muscle cramping that involves multiple muscle groups

Signs and Symptoms: Syncope, near-syncope, or lightheadedness often seen in unfit or nonheat-acclimatized individuals who stand for extended periods of time in a warm environment

Etiology: Often attributed to dehydration, venous pooling in peripheral-dependent extremities, decreased preload, and reduced cardiac output with resultant decreased cerebral blood flow leading to syncope; is generally a self-limited condition

Treatment: (General treatment of heat illness)

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  Assess ABCs

  
  
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  Lie down and elevate legs (Trendelenburg position)

  
  
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  Rest in a cool, shaded environment

  
  
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  Oral hydration

Signs and Symptoms: Difficulty with standing and/or ambulating without assistance, faintness, dizziness, or syncope following the completion of a bout of prolonged, strenuous activity; accounts for approximately 85% of medical visits following marathons, ultramarathons, or triathlon events

Etiology: Normal response to aerobic exercise is an increase in cardiac output in response to the increase in O ₂ demand and redistribution of blood flow to working muscles. During exercise, the repetitive contraction of skeletal muscles helps to maintain venous return to the heart: often referred to as the “second heart” mechanism. As the intensity of muscle contraction decreases during the end of the event, vasodilatation persists, leading to blood pooling in the peripheral circulation and decreased preload. This combined with inadequate sympathetic tone results in decreased overall cerebral perfusion pressure, which results in an altered mental status.

Predisposing Factors: Heat stress, abruptly ending exercise without cool down, dehydration, lack of acclimatization, and advanced age

Evaluation and Treatment:

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  General treatment of heat illness (3.b.11)

  
  
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  Rest in a cool, shaded environment with air movement

  
  
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  Initiate oral hydration

  
  
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  Before confirming the diagnosis of EAC, exertional heat stroke (EHS) and exercise-associated hyponatremia (EAH) must be ruled out.

  
  
  
  
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    Core temperature <40°C, normal mental status, and normal sodium levels are consistent with EAC.

  
  
  
  
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  With treatment, symptoms should resolve in <30 minutes.

  
  
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  Follow vital signs closely

Complications: Rare, but may be a warning sign for impending heat exhaustion or another more ominous cause of syncope

Definition: Hyponatremia (serum sodium ≤135 mEq/L) observed in athletes that is usually associated with endurance/ultraendurance exercise

Incidence: Observed in 5%–13% of marathon participants and 0.3%–27% of ultraendurance participants, most of whom are minimally symptomatic or asymptomatic

Presenting postevent symptoms: Complaints of “not feeling right,” nausea, lightheadedness, malaise, lethargy, and cramps; vomiting is an extremely common postmarathon symptom of EAH

Signs of fluid overload: Edema (e.g., ring or wrist band fitting more tightly), weight gain, and emesis; more ominous signs of fluid overload are indicative of early pulmonary and cerebral edema and include tachypnea, tachycardia, and mental status changes (confusion, seizure, coma, and death)

Etiology: Thought to be caused by a combination of excessive intake of hypotonic fluids, loss of sodium in sweat, and an inappropriate exercise-elevation of antidiuretic hormone (ADH)

Predisposing Factors:

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  Endurance activity lasting >4 hours

  
  
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  Body mass index (BMI) <20 kg/m ²

  
  
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  Weight gain during endurance event: Runners who fail to lose 0.75 kg of body weight during a marathon are seven times more likely to develop hyponatremia than are those who lose >0.75 kg.

  
  
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  Female gender (likely secondary to lower BMI): Women in the postluteal phase of their menstrual cycle have also been found to be at an increased risk of EAH because of the influence of progesterone on fluid retention and increased sensitivity to ADH during this phase.

  
  
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  Inexperience with endurance events

  
  
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  Use of nonsteroidal anti-inflammatory medications (NSAIDs) and selective serotonin reuptake inhibitors (SSRIs): Etiology remains controversial; may result from decreased glomerular filtration rate

  
  
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  Prolonged activity in a hot and humid environment

Evaluation/Treatment (Houston Marathon Protocol):

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  Level 1 prerace assessment:

  
  
  
  
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    Prerace education includes:

    
    
    
    
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      Stress importance of measuring prerace and postrace weights

      
      
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      Prerace questionnaire to self-assess the risk of hyponatremia

      
      
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      List of postrace symptoms associated with hyponatremia

      
      
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      Encourage salty food and fluid intake in a cool environment

      
      
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      Dilute urine production offers favorable prognosis

    
    

  
  
  
  
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  Level 2 assessment (serum sodium <135 mEq/L with few or no symptoms):

  
  
  
  
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    Participant presents with weight gain or postevent symptoms of hyponatremia and no mental status changes.

    
    
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    Obtain vital signs, weight, serum electrolytes, and glucose

    
    
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    Observe closely while encouraging oral fluid intake

    
    
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    IV fluids are typically not needed unless oral fluids cannot be tolerated—consider 3% NS (hypertonic saline) if mental status is deteriorating.

    
    
    
    
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      Production of dilute urine indicates progress toward normal sodium levels.

    
    

  
  
  
  
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  Level 3 assessment (serum sodium <135 mEq/L with markedly mental status changes—seizures, coma, or increasing delirium):

  
  
  
  
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    Usually not seen unless sodium levels are <128 mEq/L

    
    
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    Usually, worsening mental status is followed by rapid deterioration of respiratory status.

    
    
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    Establish and monitor airway; be prepared for intubation

    
    
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    Establish IV access and use hypertonic saline: 3% NS, 100 mL for over 10 minutes, and follow with 1 mL/min/kg, up to 70 mL/hour, until symptoms improve

    
    
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    Arrange for immediate transport to a medical facility

    
    
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    In a critical care setting with central pressure monitoring, loop diuretics and mannitol may be needed to reduce pulmonary and cerebral edema.

  
  

Prevention of EAH: Educate athletes not to drink more than their sweat rate (usually 600–1200 mL/hour). Athletes can be taught the following method to predetermine their own sweat rate (see “calculate sweat loss under similar conditions” in the Prevention of Heat Illness section below). Hypotonic carbohydrate (6%–8%) fluids may be more beneficial for prevention of EAH than water. Event organizers can reduce the distance between drinking stations for endurance events.

Overview: Heat exhaustion is the most common exertional heat-related illness . It is characterized by the inability to effectively exercise in the heat secondary to a combination of cardiovascular insufficiency, hypotension, energy depletion, and central fatigue.

Signs:

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  Elevated core temperature usually ≤40.5°C (≤105°F)

  
  
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  Decreased cardiac output (tachycardia, orthostatic hypotension, tachypnea, and syncope)

  
  
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  Mild mental status changes (mild confusion, agitation, and incoordination)

  
  
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  If a majority of mental status changes are severe, proceed to heat stroke evaluation and management.

Symptoms:

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  Fatigue/inability to continue exercise

  
  
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  Headaches

  
  
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  Nausea and vomiting

  
  
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  Muscle cramps

  
  
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  Chills or piloerection

  
  
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  If dehydration is present as well, thirst may be present, but it is not a reliable indicator of hydration status.

Etiology: Failure of the cardiovascular system’s response to workload. Usually, a combination of exertional heat stress and dehydration, which results in inability to adequately dissipate heat; occurs most frequently in hot and humid conditions but can occur in normal environmental conditions with intense physical activity; heat exhaustion most commonly affects unacclimatized or dehydrated individuals with a BMI of >27 kg/m ² .

Evaluation and Treatment:

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  General treatment of heat illness (3.b.11)

  
  
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  Obtain vital signs and core body temperature

  
  
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  If core body temperature is <40°C (104°F)

  
  
  
  
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    Remove clothing and sports equipment that restrict heat dissipation

    
    
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    Use ice towels and ice bags to assist cooling

    
    
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    Initiate oral hydration with an electrolyte-containing solution

    
    
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    If unable to tolerate oral fluids, IV fluids may be necessary.

    
    
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    Closely monitor vital signs, core temperature, and mental status

    
    
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    Initiate rapid cooling protocol if status deteriorates

    
    
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    Symptoms usually resolve within 2–3 hours. Slow recovery should prompt transfer to a medical facility for further evaluation.

  
  

Complications: No long-term sequelae of heat exhaustion have been reported; however, evidence suggests that one episode of marked heat illness may increase the risk of future episodes of heat illness or complications thereafter.

Definition: Exertional heat stroke ( EHS) is a life-threatening condition characterized by extreme hyperthermia ( core temperature >40.5°C or 105°F ) with eminent thermoregulatory failure, multiorgan failure, and profound CNS dysfunction.

Signs and Symptoms:

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  Core temperature >40.5°C (105°F); may be as high as 41.7°C–43.3°C (107°F–110°F)

  
  
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  Markedly impaired cardiac output (hypotension, tachycardia, and tachypnea)

  
  
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  Pronounced mental status changes (irritability, ataxia, confusion, disorientation, syncope, hysterical or psychotic behavior, seizures, and/or coma)

  
  
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  Diminished peripheral cooling ability

  
  
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  Unlike classic heat stroke, which generally affects children and the elderly, patients with EHS will usually have hot and wet skin.

  
  
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  Life-threatening conditions such as disseminated intravascular coagulation (DIC), acute renal failure (ARF), and neurologic sequelae are associated with prolonged elevated core body temperature.

  
  
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  Morbidity and mortality increases as the duration of critically elevated core body temperature (>40.5°C or 105°F) is prolonged.

  
  
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  Rapid cooling has a marked impact on the survivability of critically ill individuals.

Etiology: Total thermoregulatory failure that will not spontaneously reverse itself; the risk of EHS is greatest when the wet bulb globe temperature (WBGT) is >28°C (82°F) during higher-intensity exercises and when strenuous exercise lasts for >1 hour ( Eq. 21.2 ). WBGT index is calculated using the following formula:

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