Chapte

r4-
Medical 
problems 
of athletes

 
Part One:  The environment and sport 

• Introduction

• Heat

• WBGT

• Heat problems

○ Mild

○ Moderate

○ Severe

○ Classical heat stroke

○ Hyponatraemia
 
• Cold problems

○ Frostbite

○ Cold urticaria

○ Prevention of cold problems

• Altitude problems

○ Acute Mountain Sickness

○ High Altitude Pulmonary Oedema

○ High Altitude Cerebral Oedema

○ Retinal pathology

○ Chronic Mountain Sickness

Introduction

Athletes do battle with themselves, their competitors and the environment. The result maybe glory,
  injury or illness. In this chapter we describe the medical and environmental problems facing athletes.
Many are potentially serious but often maybe prevented by proper preparation and education.
  Heat

It is important to understand thermoregulatory factors. Thermoregulation results from reflex responses

from the various temperature receptors in the skin, central vessels, viscera, and (preoptic area) anterior
hypothalamus, signalling sympathetic shunting of blood and sweat gland stimulation when temp>37°C
(Benzinger reflex). It is well depicted in Fig 1.
The body maintains core temperature between the normal range of 36.1 to 37.8°C by balancing heat
production/gain and heat loss. Heat is produced by metabolic functions (65 to 85 kcal/hour at rest) and
work done by muscles (both smooth and skeletal; muscular contraction produces 300to 700 kcal/hour).
Heat is gained by radiant energy from the sun(100 to 200 kcal/hour).Fever can add at a rate of 15% rise
per degree F of fever.
Heat is lost to the environment in the following ways:

• Radiation (65% heat loss, only works when body temp>ambient temp)

• Evaporation (sweating, air-skin interface, the latent heat of evaporation is the amount of heat
passed to the environment by vaporization (0.6 kcal of heat/ml sweat), it is the major
physiological defense against over heating as the ambient temperature rises, reduced by high
humidity as the ambient vapour pressure approximates moist skin).

• Convection (needs air movement,12 to 15%)

• Conduction (direct contact)

• Reflected Radiation (from nearby surfaces)

WBGT (Fig 2)
It is important to evaluate all aspects of the exercise environment viz. temperature, humidity, air
movement (if outdoors) and solar radiation. This is done by the Wet Bulb Globe Temperature (WBGT)
which is a single temperature, which is dependent upon air temperature, solar & ground radiation,
humidity and wind velocity. It thus represents a sum of the impact of the environment upon the athlete. It
can be measured with cheap simple instrumentation or calculated with data from the weather bureau
(either degrees F or C).The WBGT calculation uses three measurements-natural wet-bulb temp(place a
wetted wick over the thermometer bulb), air temp, and globe temp (temp. inside a copper globe painted
flat black).
It is calculated thus:

• Indoor WBGT = (0.7 x natural wet-bulb temp) + (0.3 x globe temp)

• Outdoor WBGT=(0.7 x natural wet-bulb temp) + (0.2 x globe temp) + ( 0.1 x air temp)

Whether to or how to exercise in hot environments can be decided by considering the two criteria-RAL
(Recommended Alert Limit - above which action should be taken to reduce heat stress) and – C (Ceiling
Limit, above which exercise should not be undertaken without somehow changing the environment).
This is illustrated in Fig 2.. This graph presents limits based on exercise intensity (energy expenditure
per hour) and WBGT.
When the temperature is between C and RAL exercise is OK but with risk; therefore suggest this:

• Change the environment (fans or air conditioning) or move to area where WBGT is within
acceptable limits

• For the exercise session, decrease the intensity of the exercise (slow the pace and/or add rest
periods).Useful guide is the TARGET HEART RATE (unchanged from cool conditions)
.Exercise HR is increased one beat/min for every degree Centigrade above 25°C and two
beats/min for every mmHG above 20mmHg water vapour pressure. Stick to a determined HR.

1. MD Bracker 1992 Environmental and thermal injury Clin Sports Med 11(2) p 419-436

2. M J Leski 1994 Thermoregulation and safe exercise in the heat. Chap 18 in Sports Medicine Secrets Ed M B

Mellion Hanley and Belfus Phila p77-82

3. W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and

Williams Phila p288-293

4. National Institute for Occupational Safety and Health :Criteria for a recommended standard…occupational

exposure to hot environments.DHHS NIOSH Publ No 86-113 US Dept Health and Human Services Wash DC

1986

5. JT Marron JB Tucker 1994 Environmental Factors Chap 10 in Sports Medicine for the Primary Care Physician RB

Birrer Ed CRC Florida p83

6. WL Kenney E Kamon 1984 Comparative physiological responses of normotensive and essentially hypertensive

men to exercise in the heat Eur J Appl Physiol 52 196-201

7. JR Sutton Physiological and clinical consequences of exercise in heat an humidity Chap 2.4 in Oxford

8. D Richards R Richards et al 1979 Management of heat exhaustion in Sydney’s The Sun City-to-City fun

runner.Med J Aust 2 457-461

9. W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and

Williams Phila p294

10. E Sherry D Richards 1986 Hypothermia amongst resort skiers Nineteen cases from the Snowy Mountains Med J
Aust 144(9) 457-461

11. See US Air Force Survival Manual 64-3

12. Aceazolamide is banned from Olympic competition

13. R B Schoene 1994Mountaineering and climbing Chap 96 in Sports Medicine Secrets Ed MB Mellion Hanlet and
Belfus PA p430-434 with permission

14. PP Bartsch M Maggiorini C Ritter et al 1991 Prevention of high altitude pulmonary edema by nifedipine N Eng J
Med 325 1284-1289

Marron and Tucker have provided a useful guide for exercise in the heat: Table 1
 Table 1 Exercise in the Heat
Football practice WBGT reading (°F) Recommendations
60 Go ahead
61­66 Watch for >3% water loss
67­72 Take water onto field
73­77 Change schedule(30 min work/rest periods
78 Call off
Running  

WBGT
>82 Call off
73­82 red flag High risk, put off until after 4pm or before 

9am,not for those at risk
65­73 amber flag Moderate risk
50­65 green flag Minimal risk
<50 white flag Risk of hypothermia esp slow runners in the cold 

over long race

From Table 10-2 JT Marron JB Tucker 1994 Environmental factors In Sports Medicine for the Primary
Care physician RB Birrer Ed CRC Florida p83

It is important to acclimatize to exercise in a hot environment.25% of the thought-to-be healthy

population maybe heat intolerant if unacclimatized (but will decrease to 2% with proper preparation with
aerobic exercise starting with a 10-15 min and over a 10-14 day period). Especially for those > 60 years
(as thirst becomes less useful guide to hydration).
The following conditions predispose to heat stress:
• HBP (alters control of skin blood flow)
  • diabetes (because of neuropathy)
• drugs (diuretics, *-blockers, *-agonists, vasodilators, opiates, salicylates, thyroxine, CNS stimulants,
parasympatholytic or anticholinergics)
• alcohol
• obesity
• prior heat tolerance problems

The American College of Sports Medicine in 1984 recommended that endurance events were unsafe to
be held if the WBGT >28 degrees.

  Heat problems

These are a group of clinical presentations due to increased core temperatures which are generally
classified into mild, moderate or severe. There is an increased risk in children, female athletes (where
prolonged exercise in the luteal phase) and older athletes.

• Mild

Presents as heat fatigue, (heat) cramps or syncope. Symptoms include weakness, fatigue and muscle
cramps which occur during exercise, whereas fainting or dizziness usually occurs at the end of exercise
(when venous blood pools). Usually of short duration but maybe excruciating. Signs are muscle
tightness or cramps. Also see postural hypotension and tachycardia (heat syncope).

Treatment is rest, ice and message cramps. Oral fluids. Lie in cool area and elevate legs if syncope.
Remove excess clothing.

Note other terms used: Heat oedema (self-limited swelling of hands/feet, resolves with acclimatization);
heat tetany-carpopedal spasm; Miliaria rubra-maculopapular rash from keratin plugs over clothed areas,
need better hygiene.

• Moderate

Also known as heat exhaustion. There is headache, weakness, exhaustion, nausea, vomiting, ataxia
and mild confusion. Examination reveals increased sweating, hypotension (especially postural) and
tachycardia. Raised core temperature is present but its significance is doubtful since well marathon
runners can have temperatures up to 41 degrees Celsius. Rectal temperature should be measured to
monitor athlete’s true temperature status and to exclude heat stroke.

Treatment: Measures as for mild, as well as ice packs to groin and axillae and possibly intravenous
fluids.

• Severe (Heat Stroke)

Core temp > 41°C. There is collapse with impaired consciousness from exercise. Note: Clinical picture
may be masked by presence of hot, dry skin or cold and sweaty (therefore always take rectal
temperature).

• Classical heat stroke

Occurs in those at risk (old, homeless, poor, ill, fat, drunk, drugged); whilst exertional heat stroke occurs
in summer in those exercising.

Treatment - Initiate ABC of resuscitation. Start rapid cooling (cool packs over neck/groin/axilla; atomized
spray of warm air with fanning with warm air-The Mecca Cooling Unit) and intravenous fluids (one to
two litres of dextrose-saline solution). Transfer to nearest hospital as this is a medical emergency with
potentially life threatening multi-organ failure with DIC (with similarities to septic shock).

• Pathophysiology and complications

In severe heat illness, this chain of events is seen:

Heat injury * gut ischaemia * endotoxins enter portal circulation * hepatic clearance overwhelmed *
cytokine release

Dehydration and cytokines both contribute to hypotension and other complications. Complications of
severe head illness include:
 Cardiac Postural hypotension, conduction disturbances, 

myocardial infarct, and cardiac failure.
Neurological Convulsions, cerebro­vascular events and coma.
Abdominal Gastrointestinal bleeding, liver damage and renal 

failure.
Other Rhabdomyolysis or breakdown of skeletal 

muscle membrane. This results in toxic 
 
metabolites such as myoglobin which may lead 

to renal failure. Present with myoglobinuria 

(brown urine) and raised serum phosphokinase 

and potassium. An associated disseminated 

intravascular coagulation may also develop.
  
Prevention (Guidleines established from the City to Surf Race in Sydney dating from 1971)

• Wear appropriate cool, light coloured clothing

• Stay well hydrated before, during and after exercise ( 2 cups cold water 15-20 mins prior
exercise, one cup every 15 mins of exercise, and more than thirst demands afterwards).

• Adequate physical fitness preparation for sport/event/conditions is essential. This may include
heat acclimatization. The physiological adjustments in increased blood volume, venous tone
and especially sweating, seen during acclimatization usually requires two weeks to take effect
(although this is variable).
 
• Avoid exercise in extreme heat (and humidity). At risk events and sports should have
guidelines with medical advice.

• Do not exercise with intercurrent illness(such as fever, URTI or gastroenteritis).

• Proper planning with fluids, sunscreen and medical /or first aid cover.

• Education of the early signs of heat illnesses.

• Run within one’s capabilities

NOTE:ONE VICTIM OF HEAT STRESS MEANS OTHERS ARE AT RISK IN THE GROUP.
 

• Hyponatraemia

This can cause collapse associated with exercise, in heat and is commonly mistaken for heat stroke.
 Though only seen in ultra-endurance events (>34 hours),under extreme conditions, where profuse
sweating, not acclimatized, thought to be caused by fluid overload from hypotonic drinks.
  Cold problems

Though less of an immediate worry than heat stress, need to consider frostbite, exposure (hypothermia)
and masking of angina (cold air and/or cold peripheries may mask the onset of angina, lower the
threshold or cause angina at rest). Those involved in snow, water and mountaineering sports are at risk
as well as endurance events in cold temperatures. The wind chill factor accelerates temp loss through
convection and radiation. Hypothermia(defined as physiological state where core temp falls below
35oC) can be mild, moderate or severe and clinical features vary accordingly-

• Mild: Core temp (34-36ºC). Athlete usually displays cold extremities, shivering, tachycardia,
tachypnoea, urinary urgency, and slight incoordination. Patient is aware of this temperature
loss.

• Moderate: Core temp (32-34ºC). Blood sugars begin to fall and cerebral function begins to fail
at 35ºC, with unsteadiness, muscle weakness, cramps and increased coordination. If warmth,
shelter and food are found at this stage, recovery is rapid. If exposure to the cold continues, A
FAILURE OF SHIVERING (the critical difference between mild and moderate as when
shivering stops patient can no longer rewarm spontaneously and external heat is necessary)
and a loss of vasoconstrictor tone results in an accelerating loss of temperature control.
Speech becomes slurred, fatigue, dehydration, amnesia, poor judgement, drowsiness, anxiety
and irritability takes place.

• Severe: Core temp (<32ºC).Significant mortality with total loss of shivering, inappropriate
behaviour, impaired or loss of consciousness(coma), muscle rigidity, hypotension, pulmonary
oedema, extreme bradycardia, and cardiac arrhythmias ( especially ventricular fibrillation-VF).

Treatment: Measure the rectal temperature to assess the severity of hypothermia and to monitor
treatment(the diagnostic dilemma of unexpected confusion and agitation in the snow is solved by
measuring the rectal temp). Principles of treatment include basic life support measures (such as fluids,
nutrition, and cardiac support), minimizing further heat loss, re-warming in a controlled manner,
treatment of other injuries and transportation. It is a fallacy that voluntary activity increases body heat (in
fact, movement increases peripheral blood flow and so increases body surface area exposure to the
surrounding elements, resulting in increased heat loss and body heat requirements) Use full cardiac
and oximetric monitoring, establish an IV, start CPR,(if necessary. REMEMBER THAT A COLD
PATIENT IS NOT PRONOUNCEABLE AS DEAD UNTIL THEY ARE ‘WARM AND PINK’.CPR may need
to be continued for well over an hour until you are convinced there are no sustainable signs of life in the
rewarmed patient. This can be a difficult call-if possible talk to a more senior colleague).

In a severely hypothermic and pulseless patient(suspended animation) CPR, at half standard rates,
should only be started if full warming can be done.
Establish airway(may need to intubate).Then institute re-warming manoeuvres.
Re-warming maybe:
 • passive - insulation from wet, wind and cold. Removal of wet clothing and drying the body
(even in dry snow!). Allowing the body to gradually re-warm by its own metabolic heat.

• external active - hot packs and baths, heated aerosols, electric blankets, another body(such
measures are adequate for mild or moderate hypothermia). Caution should be exercised in
severe cases where shift of already reduced fluid volume to a warmed periphery may cause
hypotension and a cardiac event.

• internal active - warm drinks or food are reasonably simple measures. Most effective is venous
to venous haemodialysis (raise temp 1-2°F/hour).Otherwise use nasogastric tube, urinary
catheter, peritoneal catheter and enema tube with warm fluids. The rough handling of the
patient can precipitate irreversible ventricular fibrillation.

Frostbite
  Frostbite is a local destruction of superficial tissues caused by cold exposure (commonly toes, fingers,
ears), subdivided into:
Frost nip  Incipient frostbite with sudden blanching of skin 

and is painless
  Superficial Skin place, waxy and firm but not frozen 
Deep frostbite  Cold, pale, solid, fragile tissue

  

Treatment is local re-warming, analgesia, protection (with blanket cotton wool) and gentle handling.
Avoid rubbing area or applying snow and watch for secondary vascular occlusion by oedema, gangrene
and infection. Possible use of calcium channel blockers (peripheral vasodilatation) and NSAIDs (protect
against prostaglandin effects).

Cold urticaria

Where patients exposed to cold similarly develop urticarial eruptions which may evolve into angio-
oedema. In severe cases may go to hypotension and syncope. A mast cell mediated, IgE dependent
disorder, although cryoglobulins and cold agglutinins may be recognized in the blood. The urticaria may
affect only the exposed limb. Previous asymptomatic exposure to cold stimuli does not exclude cold
urticaria. Treatment is by re-warming, antihistamines and sympatheticomimetic agents if severe .

Prevention of cold problems

• Adequate preparation(clothing, communication, equipment, weather forecasts).

• Stay well hydrated and nourished(chocolate bar in pack).Caution with alcohol.

• Do not exercise to exhaustion.

• Adequate fitness level for required activity including cold and altitude acclimatization if
indicated. (NB. Cold acclimatization is less effective than heat acclimatization).
 Note: Death in snow avalanche is from suffocation, injury, hypothermia(in that order).
  Altitude problems

Distinct medical problems are encountered in sport at high attitudes and are made worse with rapid
ascent. Performances at high altitudes are helped by reduced wind resistance and gravity, and
worsened by the reduced oxygen pressure (FiO2 remains constant but *barometric pressure and so
*PiO2 and possibly *PaO2 and *SaO2) and by the dropping temperatures (temperatures reduce by
about 2C for every additional 300m above sea level).
Changes with physical activity (acclimatization) at high altitude include:

• *pulmonary ventilation (with breathlessness), variable, may not become apparent for several
days, leads to mild respiratory alkalosis(to counter the *PaO2)

• *HR in order to *CO and offset the *SaO2(to maintain oxygenation),this*HR is transient(returns
to N after 2-3 days however HRmax may remain below sea level value).Note target HR
guidelines developed at lower altitudes are still useful guide in presence of high heat and
humidity

• *Vo2 max(by 5% at 4,000 feet)with *physical work capacity(and greater above 4,000feet)

• *RBC(to*oxygen-carrying capacity blood)with shift of O2-haemoglobin curve over days to

weeks

• * capillary and *mitochondrial density over weeks

NOTE-Myocardial ischaemia may occur where CAD (because of relative hypoxia)

A resolution was made at the 20th World Congress of Sports Medicine (Melbourne 1974) urging
extreme caution at altitudes of more than 2290m (8700ft) and an absolute prohibition of contests above
3050m (10000ft). Various adaptations occur over varying time frames at altitude, including a reduction
in bicarbonate, an increase in haemoglobin levels, a restoration of blood volume and an increase in
various tissue enzymes. Problems encountered at altitudes include the following:
Acute Mountain Sickness (over 8,000 feet), AMS

With non-specific symptoms such as headache, dizziness, nausea, vomiting, irritability and insomnia
from hyperventilation and associated acid-base disturbances. It is usually a temporary condition
affecting the first 2 or 3 days of a rapid ascent over 2000m. There is mild tachycardia and peripheral
oedema. Symptomatic treatment is usually adequate (rest, hydration, analgesics), in severe cases
return to lower altitudes is advisable and the use of acetazolamide (125 mg bid) may help (beware
diuretic effect on plasma volume).

High Altitude Pulmonary Oedema (over 10,000 feet), HAPE

A life threatening (non-cardiac)condition occurring in the first few days of an ascent and manifests with
symptoms dyspnoea, blood-stained(pink) frothy sputum, coughing, and chest discomfort/pain. Signs of
tachycardia and tachypnoea, low grade fever and cyanosis.. It is more common in the presence of
intercurrent cardio-respiratory conditions.O2 desaturation (moderate to severe)with relative
 hypoventilation. Treatment is immediate descent, oxygen, nifedipine (20mg slow rel q8)and
dexamethasone (4mg q6h). Note both these drugs thought to be useful but not proven. Hyperbaric
therapy(if descent not possible).

High Altitude Cerebral Oedema (above 12,000 feet), HACE

A rare condition with severe headache, confusion, hallucination, impaired consciousness or coma.
Signs of ataxia, focal neurological/visual signs, retinal haemorrhage. Usually associated with rapid
ascents above 4000m. Moderate oxygen desaturation. Treatment is URGENT return to low altitude,
oxygen and intravenous corticosteroids (dexamethasone 8mg bolus then 4mg q6h), hyperbaric oxygen
bag (if descent not possible).

LT to check

Retinal pathology

These small retinal haemorrhages are mainly benign and occur above altitudes of 4000m. Visual
impairment can occur with central scotomata and impaired colour vision.

Chronic Mountain Sickness (above 10,000 feet),CMS

Takes months/years to develop. There is lethargy and reduced exercise capacity. Signs of plethora,
peripheral oedema and conjunctival injection. Polycythaemia, hypercapnia (relative) and oxygen
desaturation.

Treatment is descent,O2 and respiratory stimulants (acetazolamide, progesterone, phlebotomy).

Prevention is possible and essential.

• Avoid rapid ascents

• Altitude acclimatization. Approximately 3 weeks at a moderate altitude (2500 - 3000m).

• Appropriate medical screening(patients with pulmonary hypertension, uncompensated CHF,

unstable angina, recent MI or severe anaemia are at greater risk when travelling to higher
altitudes)

• Education of participants about early symptoms, signs and management of altitude illnesses.

• Susceptible patients(often young and healthy) need a slow gradual ascent with prophylactic
use of nifedipine

• Consider carrying a portable hyperbaric bag (In the USA, the Gamow Bag is available from
Chinook Medical Products in Boulder, CO)

Chapte
r4-
Medical 
problems 
of athletes
 
 Eugene Sherry, Sameer Viswanathan, Amitabha Das, and Lawrence Trieu

 
Part One:  The environment and sport 

• Introduction

• Heat

• WBGT

• Heat problems

○ Mild

○ Moderate

○ Severe

○ Classical heat stroke

○ Hyponatraemia
 
• Cold problems

○ Frostbite

○ Cold urticaria

○ Prevention of cold problems

• Altitude problems

○ Acute Mountain Sickness

○ High Altitude Pulmonary Oedema

○ High Altitude Cerebral Oedema

○ Retinal pathology

○ Chronic Mountain Sickness

Introduction

Athletes do battle with themselves, their competitors and the environment. The result maybe glory,
  injury or illness. In this chapter we describe the medical and environmental problems facing athletes.
Many are potentially serious but often maybe prevented by proper preparation and education.

Heat

It is important to understand thermoregulatory factors. Thermoregulation results from reflex responses

from the various temperature receptors in the skin, central vessels, viscera, and (preoptic area) anterior
 
hypothalamus, signalling sympathetic shunting of blood and sweat gland stimulation when temp>37°C
(Benzinger reflex). It is well depicted in Fig 1.
The body maintains core temperature between the normal range of 36.1 to 37.8°C by balancing heat
production/gain and heat loss. Heat is produced by metabolic functions (65 to 85 kcal/hour at rest) and
work done by muscles (both smooth and skeletal; muscular contraction produces 300to 700 kcal/hour).
Heat is gained by radiant energy from the sun(100 to 200 kcal/hour).Fever can add at a rate of 15% rise
per degree F of fever.
Heat is lost to the environment in the following ways:

• Radiation (65% heat loss, only works when body temp>ambient temp)

• Evaporation (sweating, air-skin interface, the latent heat of evaporation is the amount of heat
passed to the environment by vaporization (0.6 kcal of heat/ml sweat), it is the major
physiological defense against over heating as the ambient temperature rises, reduced by high
humidity as the ambient vapour pressure approximates moist skin).

• Convection (needs air movement,12 to 15%)

• Conduction (direct contact)

• Reflected Radiation (from nearby surfaces)

WBGT (Fig 2)
It is important to evaluate all aspects of the exercise environment viz. temperature, humidity, air
movement (if outdoors) and solar radiation. This is done by the Wet Bulb Globe Temperature (WBGT)
which is a single temperature, which is dependent upon air temperature, solar & ground radiation,
humidity and wind velocity. It thus represents a sum of the impact of the environment upon the athlete. It
can be measured with cheap simple instrumentation or calculated with data from the weather bureau
(either degrees F or C).The WBGT calculation uses three measurements-natural wet-bulb temp(place a
wetted wick over the thermometer bulb), air temp, and globe temp (temp. inside a copper globe painted
flat black).
It is calculated thus:

• Indoor WBGT = (0.7 x natural wet-bulb temp) + (0.3 x globe temp)

• Outdoor WBGT=(0.7 x natural wet-bulb temp) + (0.2 x globe temp) + ( 0.1 x air temp)

Whether to or how to exercise in hot environments can be decided by considering the two criteria-RAL
(Recommended Alert Limit - above which action should be taken to reduce heat stress) and – C (Ceiling
Limit, above which exercise should not be undertaken without somehow changing the environment).
This is illustrated in Fig 2.. This graph presents limits based on exercise intensity (energy expenditure
per hour) and WBGT.
When the temperature is between C and RAL exercise is OK but with risk; therefore suggest this:

• Change the environment (fans or air conditioning) or move to area where WBGT is within
acceptable limits

• For the exercise session, decrease the intensity of the exercise (slow the pace and/or add rest
periods).Useful guide is the TARGET HEART RATE (unchanged from cool conditions)
.Exercise HR is increased one beat/min for every degree Centigrade above 25°C and two
 beats/min for every mmHG above 20mmHg water vapour pressure. Stick to a determined HR.

1. MD Bracker 1992 Environmental and thermal injury Clin Sports Med 11(2) p 419-436

2. M J Leski 1994 Thermoregulation and safe exercise in the heat. Chap 18 in Sports Medicine Secrets Ed M B

Mellion Hanley and Belfus Phila p77-82

3. W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and

Williams Phila p288-293

4. National Institute for Occupational Safety and Health :Criteria for a recommended standard…occupational

exposure to hot environments.DHHS NIOSH Publ No 86-113 US Dept Health and Human Services Wash DC

1986

5. JT Marron JB Tucker 1994 Environmental Factors Chap 10 in Sports Medicine for the Primary Care Physician RB

Birrer Ed CRC Florida p83

6. WL Kenney E Kamon 1984 Comparative physiological responses of normotensive and essentially hypertensive

men to exercise in the heat Eur J Appl Physiol 52 196-201

7. JR Sutton Physiological and clinical consequences of exercise in heat an humidity Chap 2.4 in Oxford

8. D Richards R Richards et al 1979 Management of heat exhaustion in Sydney’s The Sun City-to-City fun

runner.Med J Aust 2 457-461

9. W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and

Williams Phila p294

10. E Sherry D Richards 1986 Hypothermia amongst resort skiers Nineteen cases from the Snowy Mountains Med J
Aust 144(9) 457-461

11. See US Air Force Survival Manual 64-3

12. Aceazolamide is banned from Olympic competition

13. R B Schoene 1994Mountaineering and climbing Chap 96 in Sports Medicine Secrets Ed MB Mellion Hanlet and
Belfus PA p430-434 with permission

14. PP Bartsch M Maggiorini C Ritter et al 1991 Prevention of high altitude pulmonary edema by nifedipine N Eng J
Med 325 1284-1289

Marron and Tucker have provided a useful guide for exercise in the heat: Table 1

Table 1 Exercise in the Heat

Football practice WBGT reading (°F) Recommendations
60 Go ahead
61­66 Watch for >3% water loss
67­72 Take water onto field
73­77 Change schedule(30 min work/rest periods
 78 Call off
Running  

WBGT
>82 Call off
73­82 red flag High risk, put off until after 4pm or before 

9am,not for those at risk
65­73 amber flag Moderate risk
50­65 green flag Minimal risk
<50 white flag Risk of hypothermia esp slow runners in the cold 

over long race

From Table 10-2 JT Marron JB Tucker 1994 Environmental factors In Sports Medicine for the Primary
Care physician RB Birrer Ed CRC Florida p83

It is important to acclimatize to exercise in a hot environment.25% of the thought-to-be healthy

population maybe heat intolerant if unacclimatized (but will decrease to 2% with proper preparation with
aerobic exercise starting with a 10-15 min and over a 10-14 day period). Especially for those > 60 years
(as thirst becomes less useful guide to hydration).
The following conditions predispose to heat stress:
• HBP (alters control of skin blood flow)
  • diabetes (because of neuropathy)
• drugs (diuretics, *-blockers, *-agonists, vasodilators, opiates, salicylates, thyroxine, CNS stimulants,
parasympatholytic or anticholinergics)
• alcohol
• obesity
• prior heat tolerance problems

The American College of Sports Medicine in 1984 recommended that endurance events were unsafe to
be held if the WBGT >28 degrees.

  Heat problems

These are a group of clinical presentations due to increased core temperatures which are generally
classified into mild, moderate or severe. There is an increased risk in children, female athletes (where
prolonged exercise in the luteal phase) and older athletes.

• Mild

Presents as heat fatigue, (heat) cramps or syncope. Symptoms include weakness, fatigue and muscle
cramps which occur during exercise, whereas fainting or dizziness usually occurs at the end of exercise
(when venous blood pools). Usually of short duration but maybe excruciating. Signs are muscle
tightness or cramps. Also see postural hypotension and tachycardia (heat syncope).
 Treatment is rest, ice and message cramps. Oral fluids. Lie in cool area and elevate legs if syncope.
Remove excess clothing.

Note other terms used: Heat oedema (self-limited swelling of hands/feet, resolves with acclimatization);
heat tetany-carpopedal spasm; Miliaria rubra-maculopapular rash from keratin plugs over clothed areas,
need better hygiene.

• Moderate

Also known as heat exhaustion. There is headache, weakness, exhaustion, nausea, vomiting, ataxia
and mild confusion. Examination reveals increased sweating, hypotension (especially postural) and
tachycardia. Raised core temperature is present but its significance is doubtful since well marathon
runners can have temperatures up to 41 degrees Celsius. Rectal temperature should be measured to
monitor athlete’s true temperature status and to exclude heat stroke.

Treatment: Measures as for mild, as well as ice packs to groin and axillae and possibly intravenous
fluids.

• Severe (Heat Stroke)

Core temp > 41°C. There is collapse with impaired consciousness from exercise. Note: Clinical picture
may be masked by presence of hot, dry skin or cold and sweaty (therefore always take rectal
temperature).

• Classical heat stroke

Occurs in those at risk (old, homeless, poor, ill, fat, drunk, drugged); whilst exertional heat stroke occurs
in summer in those exercising.

Treatment - Initiate ABC of resuscitation. Start rapid cooling (cool packs over neck/groin/axilla; atomized
spray of warm air with fanning with warm air-The Mecca Cooling Unit) and intravenous fluids (one to
two litres of dextrose-saline solution). Transfer to nearest hospital as this is a medical emergency with
potentially life threatening multi-organ failure with DIC (with similarities to septic shock).

• Pathophysiology and complications

In severe heat illness, this chain of events is seen:

Heat injury * gut ischaemia * endotoxins enter portal circulation * hepatic clearance overwhelmed *
cytokine release

Dehydration and cytokines both contribute to hypotension and other complications. Complications of
severe head illness include:
  Cardiac Postural hypotension, conduction disturbances, 

myocardial infarct, and cardiac failure.
Neurological Convulsions, cerebro­vascular events and coma.
Abdominal Gastrointestinal bleeding, liver damage and renal 

failure.
Other Rhabdomyolysis or breakdown of skeletal 
 muscle membrane. This results in toxic 

metabolites such as myoglobin which may lead 

to renal failure. Present with myoglobinuria 

(brown urine) and raised serum phosphokinase 

and potassium. An associated disseminated 

intravascular coagulation may also develop.
  
Prevention (Guidleines established from the City to Surf Race in Sydney dating from 1971)

• Wear appropriate cool, light coloured clothing

• Stay well hydrated before, during and after exercise ( 2 cups cold water 15-20 mins prior
exercise, one cup every 15 mins of exercise, and more than thirst demands afterwards).

• Adequate physical fitness preparation for sport/event/conditions is essential. This may include
heat acclimatization. The physiological adjustments in increased blood volume, venous tone
and especially sweating, seen during acclimatization usually requires two weeks to take effect
(although this is variable).
 
• Avoid exercise in extreme heat (and humidity). At risk events and sports should have
guidelines with medical advice.

• Do not exercise with intercurrent illness(such as fever, URTI or gastroenteritis).

• Proper planning with fluids, sunscreen and medical /or first aid cover.

• Education of the early signs of heat illnesses.

• Run within one’s capabilities

NOTE:ONE VICTIM OF HEAT STRESS MEANS OTHERS ARE AT RISK IN THE GROUP.

• Hyponatraemia
 
This can cause collapse associated with exercise, in heat and is commonly mistaken for heat stroke.
Though only seen in ultra-endurance events (>34 hours),under extreme conditions, where profuse
sweating, not acclimatized, thought to be caused by fluid overload from hypotonic drinks.
  Cold problems

Though less of an immediate worry than heat stress, need to consider frostbite, exposure (hypothermia)
and masking of angina (cold air and/or cold peripheries may mask the onset of angina, lower the
threshold or cause angina at rest). Those involved in snow, water and mountaineering sports are at risk
as well as endurance events in cold temperatures. The wind chill factor accelerates temp loss through
convection and radiation. Hypothermia(defined as physiological state where core temp falls below
35oC) can be mild, moderate or severe and clinical features vary accordingly-

• Mild: Core temp (34-36ºC). Athlete usually displays cold extremities, shivering, tachycardia,
tachypnoea, urinary urgency, and slight incoordination. Patient is aware of this temperature
loss.

• Moderate: Core temp (32-34ºC). Blood sugars begin to fall and cerebral function begins to fail
at 35ºC, with unsteadiness, muscle weakness, cramps and increased coordination. If warmth,
shelter and food are found at this stage, recovery is rapid. If exposure to the cold continues, A
FAILURE OF SHIVERING (the critical difference between mild and moderate as when
shivering stops patient can no longer rewarm spontaneously and external heat is necessary)
and a loss of vasoconstrictor tone results in an accelerating loss of temperature control.
Speech becomes slurred, fatigue, dehydration, amnesia, poor judgement, drowsiness, anxiety
and irritability takes place.

• Severe: Core temp (<32ºC).Significant mortality with total loss of shivering, inappropriate
behaviour, impaired or loss of consciousness(coma), muscle rigidity, hypotension, pulmonary
oedema, extreme bradycardia, and cardiac arrhythmias ( especially ventricular fibrillation-VF).

Treatment: Measure the rectal temperature to assess the severity of hypothermia and to monitor
treatment(the diagnostic dilemma of unexpected confusion and agitation in the snow is solved by
measuring the rectal temp). Principles of treatment include basic life support measures (such as fluids,
nutrition, and cardiac support), minimizing further heat loss, re-warming in a controlled manner,
treatment of other injuries and transportation. It is a fallacy that voluntary activity increases body heat (in
fact, movement increases peripheral blood flow and so increases body surface area exposure to the
surrounding elements, resulting in increased heat loss and body heat requirements) Use full cardiac
and oximetric monitoring, establish an IV, start CPR,(if necessary. REMEMBER THAT A COLD
PATIENT IS NOT PRONOUNCEABLE AS DEAD UNTIL THEY ARE ‘WARM AND PINK’.CPR may need
to be continued for well over an hour until you are convinced there are no sustainable signs of life in the
rewarmed patient. This can be a difficult call-if possible talk to a more senior colleague).

In a severely hypothermic and pulseless patient(suspended animation) CPR, at half standard rates,
should only be started if full warming can be done.
Establish airway(may need to intubate).Then institute re-warming manoeuvres.
Re-warming maybe:

• passive - insulation from wet, wind and cold. Removal of wet clothing and drying the body
(even in dry snow!). Allowing the body to gradually re-warm by its own metabolic heat.

• external active - hot packs and baths, heated aerosols, electric blankets, another body(such
measures are adequate for mild or moderate hypothermia). Caution should be exercised in
severe cases where shift of already reduced fluid volume to a warmed periphery may cause
hypotension and a cardiac event.

• internal active - warm drinks or food are reasonably simple measures. Most effective is venous
to venous haemodialysis (raise temp 1-2°F/hour).Otherwise use nasogastric tube, urinary
 catheter, peritoneal catheter and enema tube with warm fluids. The rough handling of the
patient can precipitate irreversible ventricular fibrillation.

Frostbite
  Frostbite is a local destruction of superficial tissues caused by cold exposure (commonly toes, fingers,
ears), subdivided into:
Frost nip  Incipient frostbite with sudden blanching of skin 

and is painless
  Superficial Skin place, waxy and firm but not frozen 
Deep frostbite  Cold, pale, solid, fragile tissue

Treatment is local re-warming, analgesia, protection (with blanket cotton wool) and gentle handling.
Avoid rubbing area or applying snow and watch for secondary vascular occlusion by oedema, gangrene
and infection. Possible use of calcium channel blockers (peripheral vasodilatation) and NSAIDs (protect
against prostaglandin effects).

Cold urticaria

Where patients exposed to cold similarly develop urticarial eruptions which may evolve into angio-
oedema. In severe cases may go to hypotension and syncope. A mast cell mediated, IgE dependent
disorder, although cryoglobulins and cold agglutinins may be recognized in the blood. The urticaria may
  
affect only the exposed limb. Previous asymptomatic exposure to cold stimuli does not exclude cold
urticaria. Treatment is by re-warming, antihistamines and sympatheticomimetic agents if severe .

Prevention of cold problems

• Adequate preparation(clothing, communication, equipment, weather forecasts).

• Stay well hydrated and nourished(chocolate bar in pack).Caution with alcohol.

• Do not exercise to exhaustion.

• Adequate fitness level for required activity including cold and altitude acclimatization if
indicated. (NB. Cold acclimatization is less effective than heat acclimatization).

Note: Death in snow avalanche is from suffocation, injury, hypothermia(in that order).
  Altitude problems

Distinct medical problems are encountered in sport at high attitudes and are made worse with rapid
ascent. Performances at high altitudes are helped by reduced wind resistance and gravity, and
worsened by the reduced oxygen pressure (FiO2 remains constant but *barometric pressure and so
*PiO2 and possibly *PaO2 and *SaO2) and by the dropping temperatures (temperatures reduce by
about 2C for every additional 300m above sea level).
Changes with physical activity (acclimatization) at high altitude include:
 • *pulmonary ventilation (with breathlessness), variable, may not become apparent for several
days, leads to mild respiratory alkalosis(to counter the *PaO2)

• *HR in order to *CO and offset the *SaO2(to maintain oxygenation),this*HR is transient(returns
to N after 2-3 days however HRmax may remain below sea level value).Note target HR
guidelines developed at lower altitudes are still useful guide in presence of high heat and
humidity

• *Vo2 max(by 5% at 4,000 feet)with *physical work capacity(and greater above 4,000feet)

• *RBC(to*oxygen-carrying capacity blood)with shift of O2-haemoglobin curve over days to

weeks

• * capillary and *mitochondrial density over weeks

NOTE-Myocardial ischaemia may occur where CAD (because of relative hypoxia)

A resolution was made at the 20th World Congress of Sports Medicine (Melbourne 1974) urging
extreme caution at altitudes of more than 2290m (8700ft) and an absolute prohibition of contests above
3050m (10000ft). Various adaptations occur over varying time frames at altitude, including a reduction
in bicarbonate, an increase in haemoglobin levels, a restoration of blood volume and an increase in
various tissue enzymes. Problems encountered at altitudes include the following:
Acute Mountain Sickness (over 8,000 feet), AMS

With non-specific symptoms such as headache, dizziness, nausea, vomiting, irritability and insomnia
from hyperventilation and associated acid-base disturbances. It is usually a temporary condition
affecting the first 2 or 3 days of a rapid ascent over 2000m. There is mild tachycardia and peripheral
oedema. Symptomatic treatment is usually adequate (rest, hydration, analgesics), in severe cases
return to lower altitudes is advisable and the use of acetazolamide (125 mg bid) may help (beware
diuretic effect on plasma volume).

High Altitude Pulmonary Oedema (over 10,000 feet), HAPE

A life threatening (non-cardiac)condition occurring in the first few days of an ascent and manifests with
symptoms dyspnoea, blood-stained(pink) frothy sputum, coughing, and chest discomfort/pain. Signs of
tachycardia and tachypnoea, low grade fever and cyanosis.. It is more common in the presence of
intercurrent cardio-respiratory conditions.O2 desaturation (moderate to severe)with relative
hypoventilation. Treatment is immediate descent, oxygen, nifedipine (20mg slow rel q8)and
dexamethasone (4mg q6h). Note both these drugs thought to be useful but not proven. Hyperbaric
therapy(if descent not possible).

High Altitude Cerebral Oedema (above 12,000 feet), HACE

A rare condition with severe headache, confusion, hallucination, impaired consciousness or coma.
Signs of ataxia, focal neurological/visual signs, retinal haemorrhage. Usually associated with rapid
ascents above 4000m. Moderate oxygen desaturation. Treatment is URGENT return to low altitude,
oxygen and intravenous corticosteroids (dexamethasone 8mg bolus then 4mg q6h), hyperbaric oxygen
bag (if descent not possible).

LT to check

Retinal pathology

These small retinal haemorrhages are mainly benign and occur above altitudes of 4000m. Visual
impairment can occur with central scotomata and impaired colour vision.

Chronic Mountain Sickness (above 10,000 feet),CMS

Takes months/years to develop. There is lethargy and reduced exercise capacity. Signs of plethora,
peripheral oedema and conjunctival injection. Polycythaemia, hypercapnia (relative) and oxygen
desaturation.

Treatment is descent,O2 and respiratory stimulants (acetazolamide, progesterone, phlebotomy).

Prevention is possible and essential.

• Avoid rapid ascents

• Altitude acclimatization. Approximately 3 weeks at a moderate altitude (2500 - 3000m).

• Appropriate medical screening(patients with pulmonary hypertension, uncompensated CHF,

unstable angina, recent MI or severe anaemia are at greater risk when travelling to higher
altitudes)

• Education of participants about early symptoms, signs and management of altitude illnesses.

• Susceptible patients(often young and healthy) need a slow gradual ascent with prophylactic
use of nifedipine

• Consider carrying a portable hyperbaric bag (In the USA, the Gamow Bag is available from
Chinook Medical Products in Boulder, CO)