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CAUSES OF HYPONATREMIA IN NEW ZEALAND 

FEMALE UL TRADISTANCE TRIATHLETES 

Nichola Tui Hart 

A thesis submitted in partial fulfilment of the requirements for the degree of 

Master of Science 

In 

Nutritional Science 

Massey University, Albany, Auckland, New Zealand 

2001 



Abstract 

The lronman Triathlon is an ultradistance event typically dominated by male 

competitors. However, the event has become increasingly popular and is now 

attracting greater female participation [1, 2]. While hyponatremia (plasma sodium 

concentration < 135mmol/L) has been recognised as a serious complication of 

prolonged exercise, the aeitology remains unclear and controversial. The 

postulated causes of hyponatremia include the consumption and retention of 

excessive volumes of fluid or large unreplaced sodium losses in the sweat. 

This study was undertaken to investigate the nutritional, biochemical, hormonal 

and physical status of New Zealand female ultradistance triathletes, specifically, 

those competing in the New Zealand lronman Triathlon, on 3 March 2001. The 

study was to determine the causes of hyponatremia in these athletes. 

Twenty-seven (n=27) ultradistance female triathletes training for the New 

Zealand lronman Triathlon were recruited for the study. Participants completed: 

(a) a brief demographic questionnaire; (b) two 7-day food diaries to evaluate 

dietary intake during the peak of training (6-7 weeks prior to the event) and 

during the taper (1 week before the event); and (c) a menstrual status 

questionnaire. Body composition was assessed by calibrated digital scales and 

bioelectrical impedance analysis (BIA) 19 hours before the race and within 15 

minutes of each individual completing the race. Blood and urine samples were 



collected and analysed 19 hours before the race and within 15 minutes of each 

individual completing the race. 

Complete medical information was available for 19 of the 27 recruited female 

triathletes (70%). Post-race plasma sodium concentrations were inversely related 

to body weight changes. A mean weight loss of 1.6 ± 1.1 kg (p= < 0.001) equated 

to a percentage dehydration of 2.4 ± 1.8%. One athlete from the study group had 

asymptomatic hyponatremic (post-race plasma sodium concentration 

134mmol/L). The athlete was the smallest subject in the study (53.4kg), finished 

the race 1 kg heavier and was moderately overhydrated by 1.9%. A lowered post­

race plasma sodium concentration was also related to lowered haematocrit (Hct). 

The lowered Hct indicated that the fluid was retained in the extracellular space, 

which caused dilutional hyponatremia. 

The athlete with the asymptomatic hyponatremia was the only athlete taking a 

progesterone only, oral contraceptive pill. Progesterone is believed to contribute 

to postovulatory fluid retention. 

The mean daily energy intake (MOEi) results for the study group from the first 

and second 7 -day food diaries were 10811 ± 211 kJ/day (2672 ± 511 kcal/day) 

and 10155 ± 1820 kJ/day (2487 ± 410 kcal/day) respectively. This was between 

22-35% lower than the expected daily energy expenditure (EDEE) 1387 4 -

15610 kJ (3319 - 3734 kcal). It has been suggested that the difference may be 

ii 



due to inaccurate reporting of intake. The lower MOEi resulted in carbohydrate 

(CHO) intake expressed as grams of CHO per kilogram (kg) body weight (BW) 

per day appearing below the recommended 7-10g CHO/kg BW/day. All subjects 

had a fat intake below the 30-33%, and a protein intake above the 12-15% 

recommended for the general New Zealand population. Most of the athletes met 

or exceeded the Recommended Dietary Intake (ROI) for most micronutrients. 

The study concluded that the likely cause of exercise associated hyponatremia 

was probably dilutional hyponatremia due to the consumption and retention of 

large volumes of low sodium or sodium free fluids before and during the race. 

Many subjects would benefit from individualised dietary advice to balance the 

increased energy expenditure of heavy training and to determine the volume of 

fluids needed for ultradistance events. 

Ill 



Acknowledgments 

I would like to thank the following people for the valuable assistance they have 

provided during the completion of this research project: 

Dr Clare Wall Lecturer, Institute of Food, Nutrition and Human Health, 

Massey University 

Dr Dale Speedy 

Keith Thorpe 

Jane Patterson 

Medlab Taupo 

Medlab Hamilton 

Sports Physician, Sports Care, Manurewa, Auckland 

lronman New Zealand Race Director 

lronman New Zealand Event Manager 

Nurse/phlebotomists Beverley Garmey & Nancy Stratford 

Biochemistry Manager Graeme Broad 

I would also like to thank the New Zealand Dietetic Association and the late 

Neige Todhunter, and Susie Cropper Heinz/Watties Australasia for providing 

funding for this research project. 

IV 



Table of Contents 

1 Introduction 1 

2 Literature Review 3 

2.1 lronman Triathlon 3 

2.1.1 New Zealand lronman Triathlon 3 

2.2 Water and Sodium Regulation 4 

2.2.1 Water and Sodium Regulation Under Normal 

Conditions 4 

2.2.2 Water and Sodium Regulation in Endurance 

Exercise 6 

2.2.3 Sweating - Body Heat Dissipation During Exercise 6 

2.2.4 Sweat Rate 7 

2.2.5 Heat Acclimatisation 8 

2.3 Fluid Balance During Exercise 9 

2.3.1 Fluid Ingestion Before and During Exercise 9 

2.3.2 Gastric Emptying 13 

2.3.3 Intestinal Absorption 15 

2.4 Hyponatremia 17 

2.4.1 Clinical Features and Symptoms 18 

2.4.2 Aetiology - Postulated Causes of Hyponatremia 18 

2.4.3 Incidence 23 

2.4.4 Incidence of Hyponatremia at New Zealand lronman 

Triathlon over 3 Consecutive Years (1996-1998) 26 

v 



2.4.5 Hyponatremic Encephalopathy 29 

2.5 The Female Athlete 30 

2.5.1 Menstrual Phase 30 

2.5.2 Neuroendocrinology of the Menstrual Cycle 31 

2.5.3 Heat Tolerance and Thermoregulation 34 

2.6 Body Composition 38 

2.6.1 Bioelectrical Impedance Analysis (BIA) 38 

2.6.2 BIA and the Female Athlete 40 

2.7 Dietary Assessment 43 

3 Aims of the Study 46 

4 Methodology 47 

4.1 Dietary Assessment 47 

4.2 Body Composition/Blood Pressure 48 

4.3 Medical/Hormonal Assessment 49 

4.4 Temperature/Relative Hum id ity Assessment 51 

4.5 Statistical Methods and Delivery of Data to Participants 51 

5 Results 52 

5.1 Physical Characteristics and Demographic Data 52 

5.2 Body Composition, Bioelectrical Impedance Analysis 

and Blood Pressure 53 

5.3 Medical/Hormonal Assessment 57 

5.4 Dietary Assessment 66 

5.4.1 Energy and Macronutrient Intake 66 

VI 



5.4.2 Micronutrient Intake 

5.5 Temperature/Relative Humidity Assessment 

6 Discussion 

6.1 Body Composition and Medical Assessment 

6.2 Hormonal Assessment 

6.3 Dietary Assessment 

6.4 Recommendations 

6.5 Limitations 

7 Conclusions 

References 

Appendices 

72 

76 

77 

77 

83 

85 

96 

97 

99 

103 

1 Invitation to Participate in a Research Study (Information Sheets) 122 

2 Consent Form 123 

3 Food Diary 124 

4 Supplement/Medication List 125 

5 Site Map Displaying Location of Testing Facility at lronman Race 127 

6 Technical Description of the Seac - Bioelectrical Impedance 

7 

8 

Ananlysis 

Pre-Event/Post-Event Participant Identification Forms 

Menstrual Status Questionnaire Form 

9 Participant Result Form (Correlated and Tabled Medical, 

Anthropometrical and Nutritional Data) 

128 

129 

130 

131 

Vll 



1 OA Individual Subjects' Calculated Resting Metabolic Rate (RMR) 

and Expected Daily Energy Expenditure (EDEE) Table 135 

1 OB Individual Subjects' EDEE Values Compared with Mean Daily 

Energy Intake (MOEi) Results for the First, and Second 7-day 

Food Diaries 137 

Vlll 



List of Tables 

2.1 Race Conditions for Three Consecutive New Zealand lronman 

Triathlons ( 1996 - 1998) 26 

2.2 Incidence of Hyponatremia (HN) over Three Consecutive New 

Zealand lronman Triathlons (1996- 1998) 27 

2.3 Incidence of Hyponatremia (HN) in Female Triathletes 

Competing in the 1996 and 1997 New Zealand lronman 

Triathlon 29 

5.1 Demographic Data for Each Subject 53 

5.2 Pre-race Anthropometric Data for the Study Group 54 

5.3 Post-race Anthropometric Data for the Study Group 54 

5.4 Pre-race BIA for the Study Group 56 

5.5 Pre- and Post-race Blood Pressure Readings for the Study 

Group 57 

5.6 Results from Pre- and Post-race Blood Tests 58 

5.7 Results from Pre- and Post-race Urine Tests 64 

5.8 Individual Hormonal Assessment 65 

5.9 Oral Contraceptive (OC) Details for Individual OC Users 66 

5.10 Nutritional Data Collected 6-7-weeks Prior to the Event 67 

5.11 Nutritional Data Collected 1-week Prior to the Event 67 

5.12 Mean water intake for 151 and 2nd 7-day period 71 

5.13 Analysis of the First 7-day Food Diary Micronutrient 

Intake and Comparison to the ROI for New Zealanders 73 

IX 



5.14 Analysis of the Second 7-day Food Dairy Micronutrient 

Intake and Comparison to the ROI for New Zealanders 74 

5.15 Temperature/Relative Humidity with Relation to Race 

Times 76 

6.1 Incidence of Hyponatremia (HN) in Female Triathletes 

compared from 1996, 1997 and 2001 78 

6.2 Equations for Estimating RMR 86 

6.3 Estimation of RMR Using Mean Body Compositional 

Data 86 

6.4 Expected Daily Energy Expenditure (EDEE) 87 

6.5 Difference Between EDEE and Mean Daily Energy 

Intake (MOEi) 89 

6.6 Race Conditions for Three Consecutive New Zealand lronman 

Triathlon (1996-1998) Compared with the Conditions for 2001 95 

x 



List of Figures 

2.1 Fluid and Electrolyte Regulation 5 

5.1 Pre- and Post-race Weight for the Study Group 55 

5.2 Pre- and Post-race Plasma Sodium Concentration 

Comparisons 59 

5.3 Post-race Plasma Sodium Concentration vs Percentage 

Dehydration 60 

5.4 Difference in Serum Albumin for the Hyponatremic Athlete 

vs Mean Value for All Normonatremic Athletes 61 

5.5 Difference in Serum Protein for the Hyponatremic Athlete 

vs Mean Value for All Normonatremic Athletes 62 

5.6 Comparison of the Post-race Haematocrit and Haemoglobin 

Results 63 

5.7 The First 7-day Food Diary Mean Energy Contribution 68 

5.8 The Second 7-day Food Diary Mean Energy Contribution 69 

XI 



1 Introduction 

Since its creation in the late 1970s, the lronman Triathlon event has been 

dominated by male competitors. Over the last few years the event has become 

increasingly popular and is now attracting greater female participation [1, 2]. The 

lronman Triathlon by definition is an aerobic, ultradistance race involving three 

consecutive disciplines: swimming 3.8km (2.4 miles), cycling 179.2km (112 

miles) and running 42.2km (26 miles, 385 yards). 

Maintenance of fluid balance, muscle fuel stores (glycogen) and blood glucose 

by the athlete is challenged because of the duration of the event. Although races 

usually start early morning to avoid the heat, an lronman Triathlon takes 

considerably longer than eight hours to complete. As the temperature increases 

over the course of the race sweat losses can be substantial so that fluid intake 

becomes more critical. 

Hyponatremia (plasma sodium concentration < 135mmol/L) has been recognised 

as a serious complication of prolonged exercise. However, no reference to 

'exercise associated' hyponatremia can be found in the literature prior to the 

1980s. The aeitology of hyponatremia remains unclear and controversial; the 

postulated causes include the consumption and retention of excessive volumes 

of fluid or large unreplaced sodium losses in the sweat. 

Male and female hormones influence anatomy and physiology after puberty. 

Collected data on the male endurance athlete therefore can not be applied to the 

female endurance athlete because potential exists for these different hormonal 

and physiological processes to influence athletic performance. Consequently, it is 

important to be aware of the physical, biochemical, hormonal, and nutritional 

status of the female endurance triathlete competing in ultradistance events in 

order to study and determine the cause of hyponatremia in these athletes. 



Assessment of body compositional changes and biochemical alterations that 

occur during prolonged exercise (and the relationship to each other) could help 

identify risks associated with the development of hyponatremia and provide a 

protocol for the reduction of incidence. 

The nutritional requirements of female ultradistance triathletes are different when 

compared to sedentary females due to the effect of exercise on the physiology. 

The estimation of daily energy requirements, the carbohydrate (CHO) and protein 

intakes based on kilogram (kg) body weight (BW). and fluid and micronutrient 

(especially sodium) intakes will be greater due to the increased energy 

expenditure. 

Recommendations for food and fluid intake during heavy training, the taper 

leading into an event, as well as the day of the competition should be designed 

for each individual based on assessment of body composition, biochemical and 

hormonal status, and energy expenditure. 

2 



2 Literature review 

2.1 lronman Triathlon 

Triathlon races typically involve three consecutive disciplines (swim, bike, run) 

and were developed as endurance events for individual competitors. The 

triathlon season extends over the summer months and races usually start early 

morning to avoid the heat. The lronman Triathlon is an aerobic event that is 

raced over long distances. Navy Commander John Collins developed the ultra 

distance event in Hawaii in the late 1970s. Collins proposed the combination of 

the annual Waikiki Roughwater Swim (2.4 miles). the Around Oahu bike race 

(112 miles, then a two day event) and the Honolulu marathon (26.2 miles). He 

said that, "Whoever finishes first we'll call the lronman". Fifteen men participated 

in the first event February 18, 1978; 12 finished. The lronman event went on to 

become an annual race in Hawaii and eventually became so popular it required a 

number of qualifying races around the world. This included lronman New 

Zealand, which first took place March 24, 1985 [1]. 

2.1.1 New Zealand lronman Triathlon 

Statistical information from lronman New Zealand shows that 214 athletes 

competed in 1985 compared with 779 athletes in 2000. The number of female 

athletes competing has also increased from 20 females in 1985 to 106 females in 

2000 [2]. Female athletes race the same course as male athletes. 

The New Zealand lronman Triathlon was raced for 14 years in Auckland but was 

relocated in 1999, to Taupo, a premier holiday destination in the middle of the 

North Island of New Zealand. The swim course is 3.8km (2.4 miles) in a fresh 

water lake, the bike course is 179.2km (112 miles) and the run course is 42.2km 

(26 miles, 385 yards). 

3 



At best, ultra distance events like lronman Triathlon take approximately eight 

hours and 30 minutes to complete but most competitors take considerably 

longer. The duration of the event poses a challenge for the athlete with regard to 

maintenance of fluid balance, muscle fuel stores (glycogen) and blood glucose 

levels. As the temperature increases over the course of the race, sweat losses 

can be considerable so that fluid intake becomes critical. 

2.2 Water and Sodium Regulation 

2. 2. 1 Water and sodium regulation under normal conditions 

The body water of healthy individuals is conserved on a daily basis by factors 

that control input and output of both water and electrolytes [3]. There are wide 

variations in the amount of water and sodium consumed daily yet the 

composition, volume and distribution of body fluids in normal individuals is 

maintained within a narrow range. Water balance is regulated by hypothalamic 

control over anti-diuretic hormone (ADH) release from the posterior pituitary as 

presented in figure 2.1 [4]. ADH is released in response to increased osmolality 

of the blood, a decrease in plasma volume or left atrial pressure, and angiotensin 

II. In the kidney, ADH increases the permeability of the distal tubules and 

collecting ducts, thus increasing water re-absorption [4). 

Sodium is the principal electrolyte in the extra-cellular fluids and is the major 

contributor to serum osmolality. Serum osmolality regulates ADH and therefore 

water balance. If sodium concentration decreases in the blood, angiotensin II 

stimulates the release of ADH, which regulates the secretion of aldosterone. 

Aldosterone acts to increase sodium re-absorption in the distal tubules of the 

kidney as well as in the intestine [4, 5). 

4 



t g 

t 

soc 

ma ----@lie-t 

Figure 2.1 Fluid and Electrolyte Regulation. [4] 

5 



2.2.2 Water and sodium regulation in endurance exercise 

Even before significant sweat losses have occurred, mechanisms for the 

conservation of water and sodium have been activated in the body [4]: 

(a) There is a marked drop in plasma volume at the onset of exercise because 

water from the plasma moves into the exercising muscle, 

(b) The decrease in plasma volume decreases renal blood pressure, and 

stimulates ADH release and water re-absorption, 

(c) The decrease in renal blood pressure stimulates renin release from the 

kidney, which results in aldosterone secretion and sodium re-absorption [4, 

6], 

(d) As exercise continues, the production and evaporation of sweat is the major 

means for dissipating body heat [6]. 

2. 2. 3 Sweating - body heat dissipation during exercise 

During exercise in a cold or cool environment, body heat is lost mainly through 

radiation and convection via the air movement around the body. Some 

evaporation of sweat and evaporative heat loss from the lungs may also 

contribute to maintenance of the heat balance [5]. However, when the ambient 

temperature is higher than skin temperature, the only mechanism to control the 

excessive rise in the core temperature is the evaporation of water from the skin 

and respiratory tract [7]. 

The transfer of heat to the skin is achieved by vasodilation of cutaneous 

circulation, thereby displacing blood to the periphery [8]. As much as 75% of heat 

loss is achieved by the evaporation of sweat, with approximately 2424 kJ 

(580kcal) of heat dissipated for each litre of sweat evaporated [7]. In hot, humid 

environments, where sweat drops from the body without evaporating, actual 

sweat rates will be higher than predicted. In windy, mild conditions, in which 

sweat can be dissipated by convection, actual rates may be somewhat lower [4]. 

6 



2.2.4 Sweat Rate 

Sweat is mostly water, about 99 percent, but it also contains a number of major 

electrolytes and other nutrients [5, 6, 9]. The major electrolytes found in sweat 

are sodium and chloride. These electrolytes are present because sweat is 

derived from extra-cellular fluid, such as plasma, and intercellular fluid [5]. Sweat 

is hypotonic in comparison to the fluids in the body and the net effect of sweat 

loss is an increase in plasma osmolality [7]. 

The degree to which an athlete sweats depends on temperature, humidity, solar 

radiation, exercise intensity, heat acclimatisation and cardio-respiratory fitness 

[9]. In an observational case study by Armstrong et al [1 O] ten subjects performed 

eight hours of moderate, intermittent exercise (40-45% V02max) in hot 

conditions (41°C, 21% Relative Humidity (RH)) daily for 10 days to measure the 

effects of dietary sodium consumption on heat acclimatisation and physical 

performance. 

Volunteers had to live continuously for 17.5 days in a research facility which 

contained sleeping and dining quarters, and an environmentally controlled 

chamber. The daily diet (3600 kilocalories) had a specified sodium composition 

of 137 mEq (8g NaCl/day). The prescribed salt consumption fell within the normal 

range of the adult daily intake in the United States of (137-223 mEq sodium 

daily). At the conclusion of each day's exercise regimen, the volunteers returned 

to the 21"C environment. On the initial day of exercise-heat exposure, the body 

mass was measured (+/- 50g) immediately prior to exercise and at the end of 

each hour of exercise to allow the calculation of sweat rate (corrected for water 

intake, urine output, faecal excretion, and food consumption). To maintain body 

weight, volunteers were encouraged to drink pure water and flavoured water(< 1 

mmol sodium/L) ad libitum from canteens, during both exercise and rest. An 

average sweat rate of 0. 7 L per hour was reported [1 O]. 

7 



One volunteer experienced symptomatic hyponatremia during the research 

investigation. It was suggested that the volunteer was moderately hyper-hydrated 

at the beginning of the research - plasma indices (plasma sodium 134mmol!L, 

osmolality 282 mmol/kg, haemoglobin 15.6g/dl and haematocrit 0.45) were more 

than 2 Standard Deviations (2SD) from the means of the control subjects (1 OJ. 

The 'low normal' initial plasma sodium has been suggested to have predisposed 

the volunteer to hyponatremia. The total sodium loss (urine and sweat) and 

sweat volume of the hyponatremic volunteer were within ± 1 SD of the mean of 

the control subjects during hours 0-4. The authors have reported that sodium 

loss was not critical to the development of hyponatremia but that excessive fluid 

retention was (1 OJ. 

The 1985 retrospective evaluation of three athletes who completed the 

'Comrades ultra marathon' were reported to have similar sweat rates (11 J. This 

was considerably lower than when Alberto Salazar (a well-conditioned, world­

class athlete), competing in the 1984 Olympic marathon, in Los Angeles, USA, 

was reported to have had a sweat rate of 3. 7 L per hour (12J. 

It has been reported that women have more subcutaneous fat and have lower 

sweat rates than men and should monitor their body weight loss as a result of 

endurance exercise in order to calculate the required volume of fluid replacement 

(13, 14]. 

2. 2. 5 Heat acclimatisation 

The composition of sweat may vary somewhat from individual to individual and 

will even be different in the same individual when acclimatised to the heat, as 

contrasted to the non-acclimatised state [5]. In trained athletes many of the 

body's adaptations to cope with heat can happen quite quickly i.e. within 5 days. 

The majority of adaptations take place within 10 days but complete 

acclimatisation may take up to three weeks (14J. Wenger reported that well­

conditioned, heat acclimatised athletes, have sweat sodium concentrations in the 

8 



range of 5-30 mmol/L sweat (115-690 mg sodium/L sweat); typically non­

acclimatised athletes lose much more sodium and have sweat sodium 

concentrations in the range of 40-100 mmol/L sweat (920-2300mg sodium/L 

sweat) [15]. 

2. 3 Fluid Balance during Exercise 

Fluid balance during exercise is dependent upon the rates of fluid ingestion, 

gastric emptying, and intestinal absorption [16]. 

2. 3. 1 Fluid ingestion before and during exercise 

It is difficult to make recommendations for fluid ingestion during endurance and 

ultra endurance exercise that encompass the specific physiological issues and 

practical considerations of various sports events. Previous attempts have met 

with criticism for their failure to suit extremes of exercise or to understand 

practical issues in sport [17]. For example, the American College of Sports 

Medicine (ACSM) ( 1987) position paper [18] entitled 'The Prevention of Thermal 

Injuries During Distance Running' emphasised the need for regular fluid intake 

during races of 1 Okm and longer, and encouraged runners to ingest 100-200ml at 

every aid station (every 2-3km). Coyle and Montain reported that if the 

recommendation were taken literally fluid intake could range from 300ml/hour for 

a slower runner (10km/hour; 100ml/3km) to 2000ml/hour for a faster runner 

(20km/hour; 200ml/2km) [19]. Thus dehydration could occur at one extreme and 

gastrointestinal discomfort at the other. The uncertainty from the 1987 position 

paper is said to have been addressed in the most recent ACSM ( 1996) position 

paper, 'Exercise and Fluid Replacement' [20]. 

The first ACSM recommendation from the 1996 paper stated that individuals 

should consume a nutritionally balanced diet and drink adequate fluids during the 

24-hour period before an event, especially during the period that includes the 

meal prior to exercise, to promote proper hydration before exercise or 

competition [20]. The New Zealand Food and Nutrition Guidelines, though not 

9 



specific for athletes, are in agreement with the ACSM recommendation. The 

guidelines include the recommendations "Prepare meals with minimal added fat 

and salt" and "Choose pre-prepared foods, drinks and snacks that are low in fat, 

and salt" [21]. The recommended daily dietary allowances for sodium are 

approximately 11 OOmg to 31 OOmg. 

In a small (eight subjects - five male and three female - all well trained cyclists), 

observational, crossover designed study, Barr et al. [22) compared the responses 

during 6-hours of exercise in the heat (30°C, 50% RH) with three fluid 

replacement conditions. The three interventions included were no fluid, plain 

water to balance sweat and urinary losses and similar amounts of a saline 

solution containing sodium in amounts greater than is found in commercially 

available beverages (25 mmol/L). The no fluid condition resulted in decreased 

plasma volume (plasma sodium rose steadily and was significantly higher than 

both plain water and saline trials at 2-hour, 4-hour and post-exercise). In addition 

the study group experienced other deleterious effects of dehydration and the trial 

was terminated 1.5 hours prior to its scheduled completion. Conversely, plasma 

volume was maintained during the plain water and saline trials. Saline ingestion 

was not associated with significantly higher plasma sodium levels. Sodium losses 

were substantial in both the plain water and saline trials but were not large 

enough to present a risk of hyponatremia (low blood salt/sodium) (plasma 

sodium concentration <135 mmol/L) during 6-hours of exercise. The observed 

post-exercise plasma sodium level for the water trial was 135 mmol/L (+/- 0.5), 

and for the saline trial 137.3 mmol/L (+/- 0.7). However, the authors reported that 

had the subjects continued to exercise the risk of hyponatremia would not be 

inconceivable. The authors concluded that those athletes who restricted their 

sodium intake in accordance with nutrition recommendations aimed at the 

general public and who also engaged in prolonged exercise over several days 

with resultant excessive sodium loss through sweat were at greater risk [22]. The 

observational study by Armstrong et al. [1 O], reported that a "low normal" initial 

10 



plasma sodium and subsequent sodium losses contributed to the rapid onset of 

hyponatremia in the athlete. 

A recent report stated that simply adding salt to the diet (or eating high-salt 

foods) and consuming a selected volume of a salt-containing beverage (sports 

drink) would ensure better fluid retention and could prevent a sodium deficit [9]. 

However, in the Barr et al. [22) study, saline ingestion (sodium concentration 25 

mmol/L) did not prevent a decrease in plasma sodium. The saline solution 

contained sodium in amounts higher than generally found in commercial sports 

drinks. The higher sodium concentration needed (2-4 times greater than that of 

commercial beverages) to support pre-exercise sodium levels would reduce 

palatability of the solution and could lead to the risk of dehydration as a result of 

inadequate fluid ingestion [22). 

It has been reported that athletes may benefit from consuming a large 

volume/bolus of fluid as they can comfortably tolerate (e.g. 300-500ml) just prior 

to exercise (e.g. 15 minute before starting exercise). In addition to providing fluid, 

advocates suggest that this strategy helps "prime the stomach" to stimulate a 

more rapid gastric emptying of subsequent fluid intake during activity [23]. 

The second and perhaps most significant ACSM recommendation from 1996, 

stated that: during exercise, athletes should start drinking early and at regular 

intervals in an attempt to consume fluids at a rate sufficient to replace all the 

water lost through sweating, or consume the maximal amount that can be 

tolerated [20). Ideally, a fluid intake plan should replace about 80% of your sweat 

losses to ensure greater cardiac output, lower core temperature and reduce the 

rate of perceived exertion [24, 25). The recommendation recognises that an 

optimal intake may be difficult to achieve and that some degree of dehydration 

may be inevitable when sweat rates are sustained in excess of 1 L/hour [20, 26]. 

However, athletes should be warned that very high rates of fluid ingestion (> 1.5 

L/hour) or sodium-free fluid ingestion to match sweat loss sustained for many 

11 



hours, can lower plasma sodium concentration and precipitate the development 

of hyponatremia [27, 28]. 

In a randomised crossover designed trial, Vrijens and Rehrer [28] assessed 

whether replacing sweat losses with sodium-free fluid would lower the plasma 

sodium concentration and thereby precipitate the development of hyponatremia. 

Ten male endurance athletes cycled for 1-hour pre-trial (to estimate fluid needs) 

and two 3-hour experimental trials at 55% V02 max at 34°C, 65% RH. Water or 

Gatorade (63g/L carbohydrate, 18-mmol/L sodium) was given every 15 minutes 

at a rate equal to the estimated fluid loss. Plasma sodium concentrations 

decreased to a greater extent with water ingestion than with the ingestion of the 

Gatorade. One subject developed hyponatremia (plasma sodium 128 mmol/L) at 

2-hour 30-minutes in the water trial. 

The study by Barr et al. [22] is the most comparable to this study, however there 

was no significant difference between the two fluid replacement conditions in the 

Barr et al study. The difference in the results compared to the Barr et al. study 

may be explained by environmental differences. In the Vrijens et al. study [28] 

the environmental chamber was set at 34°C, 65% RH, whereas the chamber in 

the Barr et al. study was set at 30°C, 50% RH. 

In the Vrijens et al. study [28], more fluid was lost and replaced with ingested 

fluids. The sweat rate was 1.36 +/- 0.20 L/hour with water and 1.38 +/- 0.21 

L/hour with Gatorade. This can be compared with the lower sweat rate in the Barr 

et al. study [22] of 0.79 L/hour with water and 0.81 L/hour with saline solution. 

Although the exercise intensity was the same in both studies 55% V02 max, the 

temperature and humidity was greater in the Vrijens et al. study [22, 28]. The 

sodium content of sweat increases with an increased sweat rate [6]. The greater 

temperature and humidity of the Vrijens et al. study was, therefore, likely to have 

caused greater sodium loss through increased sweat rate [22,28]. 

12 



2.3.2 Gastric Emptying 

Gastric emptying is considered to be the first limiting step in making fluid 

available to the circulation [29]. Several descriptive studies involving running and 

cycling, at the same relative intensities, have shown that there is no difference in 

the regulation of gastric emptying rate (GER) between rest and exercise up to 

intensity levels of 70-80% V02 max [30, 31 ]. 

The GER is determined by the volume and the composition/energy content of the 

fluid consumed (16]. The common assumption that frequent small sips is the best 

pattern of fluid ingestion is not supported by the fact that ingesting a large fluid 

volume results in greater gastric emptying (32]. After the ingestion of a fluid bolus 

there is a rapid emptying phase followed by a phase of reduced emptying once 

the volume in the stomach has been reduced to about 30% of the initial content 

(29, 31, 33]. 

The chemical composition/energy density of the fluid is undoubtedly the most 

significant factor influencing GER [34]. In a small (six subjects - male) 

observational, crossover designed study Vis! and Maughan [34] compared the 

half-emptying time of four different solutions on four separate occasions. A 

double sampling gastric aspiration method (which makes it possible to follow the 

time course of gastric emptying) was used to investigate the relative importance 

of osmolality and carbohydrate content. The method compared the rate of gastric 

emptying of isoenergetic solutions of glucose and glucose polymer at high and 

low concentrations (34]. The four solutions studied were: 

(a) A dilute (40 g/L) monomeric glucose solution (LG, 230 mosmol/kg), 

(b) A dilute (40 g/L) glucose polymer solution (LP, 42 mosmol/kg), 

(c) A 188 g/L glucose solution (HG, 1300 mosmol/kg), and 

(d) A 188 g/L glucose polymer solution (HP, 237 mosmol/kg). 

Tests were conducted 3-5 days apart and subjects were seated throughout the 

study. 

13 



The dilute solutions (40 g/L) of glucose and glucose polymer were both rapidly 

emptied from the stomach. The glucose polymer solution (LP) emptied faster (14 

minutes) than the free glucose solution (LG) (17 minutes) [34]. Increasing the 

carbohydrate content of the solution decreased the rate of gastric emptying [34]. 

Both of the concentrated solutions (HP and HG) had a slower rate of gastric 

emptying than the dilute solutions. Although HP and HG had the same 

carbohydrate content, the osmolality was different. The greater osmolality of HG 

may have contributed to its slower rate of gastric emptying when compared to HP 

[34]. The dilute glucose solution (LG) emptied faster than the concentrated 

glucose polymer solution (HP) with the same osmolality (LG, 230 mosmol/kg; 

HP, 237 mosmol/kg) [34]. The results indicate that carbohydrate content appears 

to have greater influence than osmolality in gastric emptying of liquids and that 

the addition of carbohydrate in quantities up to 4% did not inhibit GER [34]. 

A sports drink is defined as a solution with 4-8% (4-8g/1 OOml) carbohydrate and 

500-700mg/L (20-30mmol) sodium [21]. A high content of electrolytes may 

reduce GER but the sodium content observed in most sports drinks mimics the 

sweat content of athletes and will not reduce GER [35]. Fructose, the sweetest 

monosaccharide, is often added to sports drinks to increase the sweetness 

without the addition of more glucose or polymers [36] but has been reported to 

cause gastrointestinal distress [7]. 

GER has been measured in 50 young (18-31 years) healthy subjects (32 males, 

18 females) by means of sequential scitigraphy with two radioactive markers [37]. 

Significant differences were found in gastric emptying of both solids and liquids 

among sexes; women emptied the stomach more slowly than men regardless of 

age, weight, height, or body surface. A relationship was found to exist between 

gastric emptying and the phase of the menstrual cycle. The authors observed 

that women have slower GER when compared to men, but during ovulation this 

is reversed [37]. A progesterone effect was suggested to be responsible for the 

faster emptying during ovulation reported in this study [37]. 

14 



2.3.3 Intestinal absorption 

Fluid loss during exercise can impair thermoregulatory function. Fluids ingested 

during activity must be absorbed to promote rehydration. As there is little net 

absorption of water and solutes in the stomach, the rate at which a drink is 

delivered to the absorptive surface of the proximal small intestine (duodenum 

and jejunum) will influence how quickly absorption occurs [38]. At rest the 

maximal fluid absorptive capacity of the proximal small intestine is reported to be 

about 1.9 to 2.3 L/hour (this is similar to the highest values ever recorded for 

gastric emptying) [39]. Currently the maximum rates of fluid absorption by the 

small proximal bowel during exercise are not known. However, Noakes has 

estimated that intestinal water absorption during exercise is limited to between 

750-1 OOOml/hour [26]. 

The proximal small intestine absorbs about 50-60% of any given fluid load, the 

ileum absorbs 20% and the colon 15% [39]. Absorption of water in the intestine is 

a passive process caused by the creation of local osmotic gradients. Introduction 

of water into the intestine places water in contact with the brush border 

membrane of the enterocytes covering the intestinal villi i.e. the presence of an 

osmotic gradient across a semi-permeable membrane. Water (0 mosmol. /kg) 

moves into the plasma (280 mosmol /kg) to dissipate the osmotic gradient, 

plasma is diluted by the entering water [16]. 

Plain drinking water is hypotonic, with osmolalities generally in the order of 

between 5-15 mosmol/ kg; they would be expected to promote the most effective 

rates of water absorption [38]. However, water absorption from an isotonic or 

hypotonic solution containing a transported monosaccharide such, as D-glucose, 

is more rapid than from water itself [40]. The relatively poor rates of water 

absorption from water is thought to be due to the efflux of electrolytes down 

concentration gradients pulling water across the mucosa into the intestinal lumen 

[38]. 

15 



The brush border membrane is the major barrier for absorption of carbohydrate. 

Within the membrane there are energy dependent active transporters. These 

transporters usually require the presence of the cation sodium (Na+) which are 

co-transported with the carbohydrate [38]. Other electrolytes do not appear to 

affect water and solute absorption to the same extent as sodium [16, 38]. 

Drinks with an osmolality greater than 290-mosmol/ kg are effectively hypertonic 

and when ingested they cause an efflux of water into the proximal small intestine, 

which reduces the rate of net water absorption. This effect renders the solution 

ineffective as a rehydration beverage [38]. 

The most effective osmolality range for solutions containing carbohydrate and 

sodium is between 200-260 mosmol/kg [38]. Increasing the concentration of 

glucose in the intestinal lumen to 10% (550 mosmol/kg) can cause fluid secretion 

and gastrointestinal distress [41 ]. Glucose polymers taste less sweet than mono­

or disaccharides and offer the potential advantage of increasing the quantity of 

glucose delivered to the intestine at decreased osmolality [36, 39, 42]. 

Endogenous sodium is secreted into the intestinal lumen rapidly when sodium­

free or low sodium solutions are perfused [16, 38]. It has, therefore, been 

postulated that exogenous sodium added to rehydration fluids, intended for use 

during exercise, is not required to activate the energy dependent transporters in 

the brush border membrane of the proximal small intestine [43]. While no 

perfusion studies have shown that the exclusion of sodium from glucose 

solutions has a detrimental effect on net water absorption, substitution of 

mannitol or magnesium for sodium results in a 23% and 45% reduction 

respectively in glucose absorption [38]. 

The addition of sodium to drinks intended for consumption during prolonged 

exercise such as ultraendurance events may be necessary. Hyponatremia has 

16 



been reported in these events where large sweat losses can be expected and the 

exercise intensity is necessarily low, making it possible to consume and absorb 

large volumes of fluid [11]. 

2.4 Hyponatremia 

The first hyponatremia study was published in 1916 by Haldane [44]. Compulsive 

water drinking was reported to have induced the complications of hyponatremia 

in psychiatric patients who subsequently died [44]. 

Hyponatremia was not a condition commonly associated with exercise until 

recently. Traditionally it was believed that all persons who collapsed during or 

after exercise were dehydrated and would require intravenous fluid therapy [26, 

45]. 

The most commonly encountered medical condition at endurance events is 

exercise-associated collapse (EAC) [45, 46, 47, 48]. EAC is not in itself a 

diagnosis, as it gives no indication of the cause of the condition [47]. Roberts 

describes the main complaint of EAC as the inability to stand or walk unaided as 

a result of dizziness, light-headedness or faintness [48]. Most collapsed runners 

were believed to suffer from exercise-induced dehydration with or without 

hyperthermia [46]. Because serum sodium concentration is not frequently 

measured in collapsed athletes, the diagnosis of hyponatremia is often missed or 

mistaken for exercise-induced hypoglycaemia or exertional 'heat-stroke' [48,49]. 

The development of hyponatremia requires that fluid must be ingested at high 

rates for many hours, probably for at least four to six hours (see section 2.4.2 for 

aeitology - postulated causes of hyponatremia). Hence the condition will be 

extremely uncommon in any race that finishes in less than four hours and 

becomes more evident in races lasting longer than eight hours [49]. The 

condition could develop after a race, however, if the athlete continues to ingest 

fluid at high rates [49]. 

17 



Hyponatremia usually occurs in athletes of average ability (recreational, as 

opposed to highly trained - competitive athletes), and is reported predominantly 

in those athletes who finish the race with the last 25-50% of entrants [27]. 

Female athletes have been reported to be at significantly increased risk of the 

development of hyponatremia [27, 51 ]. 

2. 4. 1 Clinical features and symptoms 

No reference to 'exercise associated hyponatremia' can be found in the literature 

prior to the 1980's. Symptomatic hyponatremia during prolonged exercise was 

first reported in 1981 by Noakes, in two athletes competing in the 1981, 90km 

Comrades Marathon footrace in South Africa [50]. In 1985 Noakes et al, provided 

the first clinical histories of these two cases plus reported another two cases in 

the medical literature [11]. 

Symptoms of hyponatremia may be mild and non-specific. They include: fatigue, 

nausea and malaise. The athlete may only become aware of the symptoms upon 

completion of the race [49, 51]. Symptoms of moderate severity include 

headache, confusion, restlessness, and disorientation [49]. More specific and 

severe symptoms include raised intracranial pressure, grand mal seizures, 

pulmonary edema, respiratory arrest, coma and death [11, 49, 52, 53]. It has 

been recognised from the aforementioned symptoms that exercise associated 

hyponatremia is a serious complication of prolonged exercise that has the 

potential to be life-threatening if misdiagnosed [11, 49, 51, 52, 53, 54, 55]. 

2.4.2 Aetiology- Postulated causes of hyponatremia 

The aetiology remains unclear and controversial. 

(a) Excessive losses of sodium through urine and sweat (either chronically 

before, or acutely during exercise); or 

(b) The consumption and retention of large volumes of low-sodium or sodium­

free fluids; or 

18 



(c) A combination of these two factors, 

are the factors that are most often debated in the literature [4]. 

Hiller and other authors have postulated that 'massive', unreplaced sodium 

losses, in the presence of dehydration is important in the development of 

hyponatremia [46, 56, 57, 58]. Hiller reported that the combination of dehydration 

and hyponatremia was easily understandable if one considered that sweat rates 

of 1.5 litres per hour with 0.25 normal saline solution (NSS) sweat concentration 

were usual [46,56]. Hiller stated that with an average lronman finish time of 13 

hours, an athlete would lose about 19.5 litres of water and about 39g of sodium 

chloride [46]. In a survey of 39 lronman finishers in 1985, the average fluid intake 

was much less than 19.5 litres and water (sodium-free fluid) was the commonly 

chosen drink. It is therefore possible that the athletes can finish the race both 

dehydrated and hyponatremic [46]. Hiller et al. reported that this is salt depletion 

heat exhaustion and the appropriate treatment for this condition is volume 

replacement with a solution such as 5% dextrose in normal saline solution 

(D5NSS) [46,56]. Hiller et al. also reported that 3 to 4 pints of fluid (571 ml = 1 

pint) per hour is required to maintain fluid balance under typical race conditions 

[46]. 

Sixty-four athletes (53 male and 11 female) from the 1984 Hawaiian lronman 

Triathlon participated in the first observational study of ultraendurance triathletes 

[57]. The study by Hiller et al. [57] assessed plasma electrolyte and glucose 

changes during the 1984 Hawaiian lronman Triathlon. Pre-race (21 to 24 hours 

before the race) and post-race (within 5 minutes of the subject completing the 

race) blood samples were taken from each subject. Blood was drawn from the 

brachia! vein while the subject was supine. During the 1984 race, environmental 

conditions were particularly severe: land air temperatures exceeded 34°C 

(100°F), Relative Humidity (RH) was high coupled with bright sunlight and high 

wind [46]. All 64 athletes had normal pre-event sodium levels that ranged from 

plasma sodium 141.8 mmol/L to 137.8 mmol/L. The post-race sodium levels 

19 



ranged from plasma sodium 114 mmol/L to 145 mmol/L. Seventeen of the 64 

athletes (27%) were hyponatremic. One of the top ten finishers had a post-race 

plasma sodium level of 125 mmol/L - indicating that this is not a problem of 

under-training or inexperience [46]. Hyponatremia was defined as a blood 

sodium concentration of <135 mmol/L. The pre- or post-race weight of the 

subjects was not recorded in this study. 

In a recently published article, Speedy et al. [59] recommended that weight 

measurements for all athletes before the race be a compulsory requirement of 

race registration, and subsequent inclusion of a post-race weight in the athlete's 

triage assessment if they present for medical care. Speedy et al. [59] also 

reported that knowing the weight change an athlete has sustained during a race 

is particularly helpful in deciding whether an athlete's symptoms are due to 

dehydration or over-hydration. 

The interpretation of Hiller has met with opposition from Noakes and others who 

documented weight gain or diuresis during recovery in hyponatremic athletes and 

therefore reported that hyponatremia developed from fluid retention or fluid 

overload [10, 11, 27, 51, 53, 59, 60, 61, 62, 63]. Detailed studies by Nose and 

colleagues concluded that it is the sodium content of the extracellular space that 

regulates the extracellular volume [64, 65]. The normal response to uncorrected 

sodium chloride losses during exercise would be a reduction in the extracellular 

volume in proportion to the sodium chloride deficit [64, 65]. Noakes has reported 

that the proponents of the theory that large, unreplaced, sodium chloride losses 

induce acute hyponatremia of exercise have ignored the fundamental 

physiological findings of Nose et al. [27]. 

Alternatively, Noakes and others postulated that hyponatremia developed from 

fluid retention or fluid overload. What they did not resolve is the issue of the 

location of the retained fluid. There are two possible mechanisms: 

20 



(a) The first possible mechanism is that the "missing" sodium chloride is not 

irreversibly lost in sweat or urine but is translocated into a 'third space' [27]. 

Unabsorbed fluid may pool in the gastrointestinal tract (the third space) with 

movement of sodium ions from the extracellular fluid into the gastrointestinal 

tract [26, 27]; or 

(b) The expansion of the extracellular volume, causing hyponatremia by dilution 

of a normal or slightly reduced total extracellular sodium chloride content 

(because of sweat or urine sodium losses or both) [27]. 

Until recently reports of changes in plasma sodium concentration and the 

relationship of hyponatremia to changes in body weight had included case 

studies [10, 11, 60] and smaller studies [58]. The theory of fluid retention was 

also supported by the findings of Vrijens and Rehrer [28]. The authors showed an 

inverse correlation between the rate of urine production and the rate of plasma 

sodium change - urinary losses were less than the mean in the hyponatremic 

subject [28]. 

Fluid overload - as a result of an expansion of the extracellular volume was 

confirmed in the largest observational, cohort study of ultraendurance triathletes 

[51]. Six hundred and five athletes from the 1997 New Zealand lronman Triathlon 

participated in the study by Speedy et al. [51 ]. Participating subjects were 

weighed 2-days before the race (because of time constraints) wearing minimal 

clothing, without shoes (in addition 323 athletes were weighed again immediately 

prior to the race to establish the extent of any weight change). Subjects were re­

weighed post-race at the finish line or at the medical tent wearing race clothing 

including shoes. The mean weight of a pair of running shoes was made as an 

adjustment to the post-race weight. Blood was collected by routine venipuncture 

within 15 minutes of subjects finishing the race. Blood was not collected before 

the race. Urgent assays for plasma sodium concentrations were carried out on 

89 athletes presenting for medical care. Samples collected from 284 well athletes 

were analysed the following morning. The race conditions were 21°C, 91% RH. 

21 



Water, Powerade, and Coca-Cola were the fluids available at the support 

stations (every 12km on the cycle course and every 1.8km on the run course) 

[51]. 

For the purposes of the study, mild hyponatremia was defined as a plasma 

sodium concentration of 130-134 mmol/L. Severe hyponatremia was defined as a 

plasma sodium concentration below 130 mmol/L. Athletes who presented to the 

medical tent with symptoms of hyponatremia and a plasma sodium concentration 

below 135mmol/L were categorised as "symptomatic" for hyponatremia. 

Hyponatremic athletes who did not present for medical care after the race were 

defined as "asymptomatic" for hyponatremia [51]. 

Full data on pre- and post-race weights, and post-race plasma sodium 

concentration were available on 330 race finishers (55%) (292 male, 38 female); 

58 (18%) of these finishers were hyponatremic. Fluid overload was reported in 

eight of the 11 athletes (73%) diagnosed with severe hyponatremia (plasma 

sodium concentration <130 mmol/L). The subjects either gained weight or 

maintained their pre-race weight. Relative weight change in those athletes with 

severe hyponatremia ranged from -2.4% to +5%. Lower post-race plasma 

sodium concentrations were also related to the lower haematocrit levels. This 

suggested that exercise associated hyponatremia was a result of the expansion 

of the extracellular space [51]. It was reported in the study by Speedy et al. [51] 

however, that those athletes defined as 'mild hyponatremic' (plasma sodium 

concentration 130-134 mmol/L) had a wide range of weight changes; some were 

overhydrated and some were dehydrated. 

In the small 1991 Hawaiian lronman Triathlon study (30 subject - 26 male, 4 

female) O'Toole et al. [58] observed that although the hyponatremic athletes 

were slightly dehydrated, they lost significantly less weight (fluid) than did the 

normonatremic athletes. Nine of the 30 athletes (30%) were diagnosed with 

hyponatremia. Hyponatremia in this study was defined as <130 mmol/L [58]. The 

22 



authors suggest that inappropriate retention or compartmentalisation of fluid may 

occur in combination with mild dehydration and without gross overload [58]. 

This suggestion may explain the 'mild hyponatremia' seen in the athletes with a 

wide range of weight changes in the Speedy et al. [51] study. However, 

hyponatremia defined as <130mmol/L in the O'Toole et al. [58] study, would have 

classified those athletes with 'severe hyponatremia' in the Speedy et al. [51] 

study. The majority of the athletes (73%) with severe hyponatremia in the 

Speedy et al. [51] study were overhydrated not dehydrated as seen 1n the 

O'Toole et al. [58] study. 

2.4.3 Incidence 

The incidence of hyponatremia is unclear, and varies considerably among 

studies. Part of the problem is definition. Some studies include mild cases (<135 

mmol/L) while others only report severe cases ( <130 mmol/L) [49]. 

Environmental conditions also impact on the prevalence of hyponatremia. Hiller 

et al. [57] reported the incidence of hyponatremia at the 1984 Hawaiian lronman 

Triathlon as high as 27%. The land course temperature at the event exceeded 

34°C (100°F). Speedy et al. [61] reported hyponatremia to be present in 9% of 

athletes requiring medical care after the 1996 New Zealand lronman Triathlon. 

The land course temperature at the event was between 17-24°C (68-80°F). Both 

studies defined hyponatremia as plasma sodium concentration < 135 mmol/L. 

Since the 1980's the drinking practices of competitors in ultraendurance events 

contrast to those ultraendurance athletes, who, up until 1969 were actively 

discouraged from drinking during exercise [26]. Indeed, the International Amateur 

Athletic Federation (IAAF) rules in force in 1953 stated that "refreshments (water 

was the only drink available) shall only be provided by the organisers of the race 

after 15 kilometres (km) or 10 miles, and thereafter every 5 km or 3 miles. No 

other refreshment may be carried or taken by the competitor other than that 

23 



provided by the organisers" [66]. Noakes reported the 1991 personal 

communication between himself and J. Mekler, world record holder at the 

ultramarathon distance [66]. J Mekler said, "In those days, it was quite 

fashionable not to drink, until one absolutely had to. After a race, runners would 

recount with pride 'I only had a drink after 30 or 40 kilometres'. To run a complete 

marathon without any fluid replacement was regarded as the ultimate aim of 

most runners, and a test of their fitness" [67]. 

The 1969 Wyndham and Strydom study [68] provided the stimulus to change the 

IAAF rules governing the conduct of international distance races (26]. The 

authors measured the rate of fluid ingestion and the levels of dehydration that 

developed in runners in 32-km footraces and reported that athletes drank less 

than they sweated [68]. Wyndham and Strydom stated that there was a linear 

relationship between levels of dehydration of >3% and the athletes' post-exercise 

rectal temperature [68]. The authors concluded that to prevent heat injury during 

exercise weight loss, dehydration must be avoided [68]. However, the most 

dehydrated runners of the 32-km footraces won the races, and despite 

inadequate fluid intake, showed no evidence of having a greater health risk or 

being predisposed to heat-stroke [26]. Noakes reported that no study had yet 

shown that dehydration to the levels present in endurance athletes (1-4% of body 

weight), exercising under more moderate environmental conditions poses any 

major health risks [67]. 

Several authors have reported that it is metabolic rate that determines sweat rate 

and body temperature during exercise [4, 11]. Barr and Costill stated that fluid 

loss at a given body weight is greater as running speed increases and that fluid 

loss at a given running speed increases with body weight [4]. Thus heavier 

runners will sweat heavily only if they also run fast and maintain high metabolic 

rates during exercise; in reality, heavier runners tend to run slower than lighter 

runners (27]. 

24 



The IAAF rule changes, stimulated by the Wyndham and Strydom study [68], 

allowed for fluid consumption every 2.5 km after the first 5 km of long distance 

races [66). The American College of Sports Medicine (ACSM) supported the rule 

change and produced a position statement in 1975 that emphasised a high fluid 

intake during exercise to prevent dehydration [69). In support of this paper sports 

medicine practitioners have counselled athletes to avoid dehydration during 

exercise by drinking more than their thirst dictates, as thirst may be an unreliable 

index of fluid needs during exercise [61). The IAAF rules were changed again in 

1990 to allow carbohydrate drinks and water to be provided at aid stations, every 

3 km, for long distance races [70). 

Hyponatremia was not a condition commonly associated with exercise until it was 

first recognised at the 1981 88-km Comrades Marathon and the 1982 through 

1985 Hawaiian lronman Triathlon [27). At this time ultradistance events became 

extremely popular with Time Magazine (September 2, 1985) calling triathlon the 

"sport of the eighties". Participation was reported as 3665 finishers (1981 

Comrades Ultra-endurance footrace) and, 4583 starters (1982-1985 Hawaiian 

lronman Triathlon) [11, 46]. The popularity attracted an increasingly large number 

of less competitive participants (the athlete competing in the lronman Triathlon 

for example would cycle 180 km in approximately 7 hours (26 km/hour) and run 

42 km in 4 hours (10.5 km/hour)) [27]. Noakes has stated that these less 

competitive athletes were exercising at slower paces so their sweat losses were 

low (0. 7 L/hour) and they were making ample use of the multiple aid stations 

(provided by the IAAF rule changes), taking plenty of time to stop and drink [11, 

27, 70]. The rule changes have increased the average fluid intake during 

competition from 1 OOml/hour in the late 60's and early ?O's [68] to between 500 -

2000ml/hour from the mid 1980's to the present time [53, 60). Noakes has 

postulated that multiple aid stations, combined with the inclusion of less 

competitive athletes has a close temporal relationship to the exercise associated 

hyponatremia cases reported in the mid-1980's [27]. 

25 



2.4.4 Incidence of hyponatremia at New Zealand lronman Triathlon over 3 

consecutive years (1996-1998) 

Hyponatremia was defined as (plasma sodium < 135 mmol/L) for all three races. 

Environmental conditions for the three races were comparable. At the 1996 race, 

ambient air temperature was between 17-24°C with a relative humidity (RH) 

97.6%. Ambient air temperature was 21°C with RH 91% for the 1997 race and 

19.4°C with RH 87% at the 1998 race (Table 2.1) [51, 59, 61]. 

Table 2.1 Race conditions for three consecutive New Zealand lronman 

Triathlons (1996 - 1998) 

Sports Drink 

NZ Temperature Relative Aid Station Brand Sodium CHO 

Iron man Humidity Frequency 

oc % Cycle Run (mg/L) (mmol/L) 

(km) (km) 

1996 17-24.0 97.5 12 1.8 Sports 391 17 

Schweppes 

Plus 

1997 21.0 91 12 1.8 Powerade 250 10.9 

1998 19.4 87 20 2.5 Powerade 250 10.9 

The frequency of the aid stations was the same in 1996 as in 1997, every 12 km 

on the cycle course and every 1.8 km on the run course [51, 61]. The proprietary 

sports drink in 1996 was Schweppes Sportsplus containing 391 mg/L of sodium 

(17 mmol/L) and 7% carbohydrate) [61]. The sports drink available in 1997 was 

Powerade (containing 250mg/L of sodium (10.9 mmol/L) and 8% carbohydrate) 

(Table 2.1) [51]. 

One hundred and nineteen of the 689 race starters in the 1996 race sought 

medical care (17%). Consent was obtained from 95 of those athletes to use their 

medical information for the study. A diagnosis of hyponatremia was made in eight 

26 

(g/L) 

7 

8 

8 



of the 95 athletes presenting for medical care (9%). Hyponatremia was 

calculated in 1.2% of race starters (Table 2.2) [61]. 

Table 2.2 Incidence of hyponatremia (HN) over three consecutive New 

Zealand lronman Triathlons (1996 -1998) 

NZ Number of Number of Number of Number of Percentage Percentage 

Iron man race athletes consenting athletes of HN of HN 

starters seeking athletes or with HN found in found in 

medical (complete consenting race 

care data on athletes starters 

race 

finishers) 

1996 689 119 95 8 9.0 1.2 

1997 660 115 330 58 18.0 8.8 

1998 650 134 117 4 3.4 0.6 

Six hundred and five of the 660 race starters in the 1997 race consented to 

participate in a hyponatremia study. Complete data was available for 330 

consenting participants (292 men and 58 women). One hundred and fifteen of 

the 660 race starters in the 1997 race sought medical care (17%), twenty-six of 

these athletes (23%) were hyponatremic. Fifty-eight of the 330 athletes with 

complete data available were hyponatremic (18%). Hyponatremia was calculated 

in 8.8% of race starters (Table 2.2) [51]. 

One hundred and thirty four of the 650 race starters at the 1998 race sought 

medical care (20%). One hundred and seventeen of the 134 consented to having 

their medical information used for the study. Four of the 117 athletes presenting 

for medical care (3.4%) were hyponatremic. Hyponatremia was calculated in 

0.6% of race starters (Table 2.2) [59]. 

There was a significant reduction in the number of athletes receiving medical 

care for hyponatremia from 1997 to 1998. The drinking practices of the athletes 

27 



were altered from 1997 to 1998. The frequency of aid stations was decreased on 

the cycle course from every 12km to every 20km, and the frequency of the run 

course aid stations decreased from every 1.8km to every 2.5km (Table 2.1) [59]. 

Speedy et al. [59] conclude that although it is difficult to prove a causal 

relationship, the interventions (reduced access to fluid and warnings of the 

dangers of drinking too much) were associated with a significant reduction in the 

number of athletes diagnosed with hyponatremia. The authors also 

acknowledged that confounding factors, including the awareness of the research 

project on the incidence of hyponatremia, may have accounted for the greater 

percentage of athletes who had plasma sodium concentrations measured in 

1997 than in 1998 [59]. 

The incidence of hyponatremia in female ultradistance triathletes competing in 

the 1998 New Zealand lronman was not specifically documented in the published 

material. However, in the 1996 New Zealand lronman there were 83 female race 

starters. Nineteen of the 95 athletes who consented to have their medical 

information studied were female. Three of the 19 female athletes were diagnosed 

with hyponatremia (16%). Three of the 83 female race starters were 

hyponatremic (3.6%) (Table 2.3) [61]. Permission was granted from the Auckland 

Ethics Committee and the author, Dr Dale Speedy, to review collected data from 

the 1997 New Zealand lronman. There were 79 female race starters in the 1997 

event. Complete medical information was available for 38 female participants 

(48%). Seventeen of the 38 female athletes were hyponatremic (45%). 

Seventeen of the 79 female race starters were diagnosed with hyponatremia 

(22%). There was complete medical information gathered on 22 New Zealand 

female ultradistance triathletes competing in the 1997 New Zealand lronman. 

Ten New Zealand female athletes of the 38 female participants with complete 

medical information were hyponatremic (26%). Ten of the 22 New Zealand 

female athletes were diagnosed with hyponatremia (45%). Ten New Zealand 

female athletes of the 79 female race starters were hyponatremic (13%) (Table 

2.3). 

28 



Table 2.3 Incidence of hyponatremia (HN) in female triathletes 

competing in the 1996 and 1997 New Zealand lronman Triathlons 

NZ lronman Number of Number of Number of Percentage of Percentage of 

female race consenting female HN found in HN found in 

starters female athletes with consenting female race 

athletes or HN female starters 

(complete athletes with 

data on race complete 

finishers medical data 

1996 83 19 3 16 3.6 

1997 79 38 17 45 22.0 

22 consenting 10 NZ female 10138 = 26 13.0 

NZ female athletes with 10122 = 45 

athletes with HN 

full data 

2.4. 5 Hyponatremic encephalopathy 

Women and men are equally likely to develop hyponatremia and hyponatremic 

encephalopathy post-operatively [71 ]. However, in a case-control study. Ayus et 

al. [71] observed those of the 34 case patients who developed permanent brain 

damage or died 33 (97%) were women. Among the women with brain damage, 

25 (76%) were menstruant Case patients included 40 women (62%) and 25 men 

(38%) - with postoperative hyponatremic encephalopathy; control patients 

included 367 women (54%) and 307 men (46%) - who had postoperative 

hyponatremia without encephalopathy. The much higher mortality from 

postoperative hyponatremia in menstruant women relative to that of 

postmenopausal women (or men) was thought to result from a diminished ability 

of the female brain to adapt to hyponatremia by limiting the amount of brain 

swelling [71]. As a person ages, brain volume declines progressively, whereas 

skull size remains constant in adult life. Thus, elderly people of either gender 

29 



have more room in the skull for the brain to expand than do younger people. The 

increased risk for menstruant women to develop hyponatremic encephalopathy 

did not depend on either the speed of development or the magnitude of the 

hyponatremia. The authors suggest that since elevated plasma levels of 

vasopressin are essentially a universal postoperative occurrence (2-4 days 

postoperative) it may be important to avoid the use of hypotonic intravenous 

solutions in the immediate postoperative period [71 ]. 

2.5 The Female Athlete 

Very little work has focused on the influence of hormonal cycles on exercise 

performance. The female athlete is exposed to a rhythmic variation in either 

endogenous hormones (as during a regular ovulatory menstrual cycle). or 

exogenous hormones (administered as the oral contraceptive pill). Given that 

oestrogens and progestogens can have individual or interactive effects on a 

variety of metabolic processes, the potential exists for an influence on athletic 

performance [72]. 

2.5.1 Menstrual Phases 

For women aged 20 to 40 years an average menstrual cycle lasts 28 days but 

may range from 20 to 45 days [73, 74]. The menstrual cycle is typically divided 

into three phases. The first, the period of menstrual bleeding (menses), is called 

the menstrual phase and occurs from Days 1 to 4 (or 5) Menstrual bleeding, or 

endometrial regression, is usually referred to as the first phase of the cycle 

because of the simplicity of noting Day 1 (it actually marks the completion of the 

menstrual cycle). The second phase is called the follicular, proliferative or 

regenerative phase. This phase is characterised by the development of a mature 

follicle under the primary influence of the gonadotropins, Juteinising hormone 

(LH) and follicle-stimulating hormone (FSH), and by a thickening of the 

endometrial lining of the uterus under the influence of oestrogen. The third phase 

is dominated by the hormone progesterone and is called the /uteal, 

30 



progestational, or secretory phase. This phase follows ovulation and continues 

until menstrual flow occurs again [75). 

2. 5. 2 Neuroendocrinology of the menstrual cycle 

The menstrual cycle is under the hormonal control of the endocrine system as 

well as the neurogenic stimulus of the nervous system [75]. This interaction 

occurs primarily between the hypothalamus and the pituitary gland [75]. The 

hypothalamus, located beneath the cerebral hemisphere, secretes gonadotropin­

re/easing hormone (GnRH) into the hypothalamic-pituitary portal vessels. The 

blood to the anterior pituitary gland transports GnRH, where it stimulates the 

release of the anterior pituitary hormones, LH and FSH [75]. Cyclic fluctuations of 

LH and FSH act on the ovary to release the steroid hormones, oestrogen and 

progesterone [75]. 

Estradiol (E2) is the major oestrogen, while estrone (E1) and estriol (E3) are less 

potent oestrogens [72]. The primary function of the oestrogens in the menstrual 

cycle is to stimulate the growth of the uterine endometrium. Oestrogens also 

exert major feedback effects on the secretion of GnRH, LH and FSH 

(complicated positive and negative feedback mechanisms) [75]. The facilitation of 

calcium uptake into bone, as well as the fat deposition around breasts, buttocks 

and thighs, is promoted by oestrogen [72]. Oestrogens contribute to a protective 

effect against atheroscelrosis by decreasing the total and low-density lipoprotein 

(LDL) cholesterol levels and by increasing the high-density lipoprotein (HDL) 

cholesterol level [72]. 

The main function of progesterone is to prepare the endometrial lining of the 

uterus for the implantation of a fertilised ovum (egg) (75]. Like oestrogen, 

progesterone also exerts a feedback effect on the secretion of GnRH, LH and 

FSH [75). The increase in progesterone levels during the luteal phase is 

responsible for 

31 



(a) The biphasic basal body temperature curve and increased core body 

temperature (of 0.3°C - 0.5°C); and 

(b) Greater basal metabolic rate during this time [72, 73]. 

Progesterone is believed to also contribute to postovulatory fluid retention 

through a complex feedback mechanism involving aldosterone and the renin and 

angiotensin system [73]. Under the influence of progesterone there is an 

increased excretion of water and sodium from the kidney as a consequence of 

antagonism of aldosterone. The resultant stimulation of the renin and angiotensin 

system then paradoxically increases aldosterone secretion and promotes an 

increase in ADH [72] and thus water re-absorption [6]. 

Twenty-eight studies were performed on thirteen normotensive male volunteers 

(22-44 years of age) to determine the effect of progesterone on renal sodium 

handling in man [76]. Male subjects were chosen to avoid cyclic changes in 

endogenous oestrogen and progesterone secretion. It was demonstrated that 

administration of progesterone consistently produced an increase in sodium 

excretion to normal subjects on either low (13-40 mmol of sodium/day) or high 

(240 mmol of sodium/day) sodium intakes and that progesterone inhibits sodium 

reabsorption in the proximal tubule in the nephron [76]. 

Water conservation via alteration in osmotic regulation of plasma ADH by 

endurance training was also suggested in twelve males (24-49 years of age) 

participating in the case-control study by Freund et al. [77]. The study addressed 

ADH levels in relation to hydration status at rest in six endurance-trained and six 

untrained subjects. The endurance trained subjects regularly ran 32miles/week 

(50km/week) and were capable of running 1 Okm in under 40 minutes. No 

differences between groups for base-line hormonal, electrolyte or renal 

measurements were found. Following the ingestion of 1 % of lean body weight as 

water, there were no significant differences in plasma aldosterone or renin 

activity between the groups. However, ADH levels were higher in trained than 



untrained subjects at 30 minutes post-drink. The higher plasma ADH values in 

the trained subjects is probably responsible for the blunted diuresis and is in spite 

of similar plasma osmolality values between the groups. 

The majority of previous studies examining hormonal and renal responses have 

used male subjects. Recent developments in our understanding of an athlete's 

physiology (mainly in relation to the male endurance runner) have revealed new 

areas of interest that need to be assessed with specific reference to the female 

athlete [74]. 

Sixteen females (18-37 years of age) who had been running a minimum of 35 

miles/week (56km/week) for at least 1 year participated in the observational 

study by De Souza et al. [78]. The effects of menstrual cycle phase (early 

follicular vs. midluteal) and menstrual status (eumenorrhea vs. amenorrhea) on 

plasma arginine vasopressin (AVP), renin activity, and aldosterone were studied 

before and after 40 minutes of submaximal running (80% maximal 02 uptake). 

Eumenorrhea was defined as the consistent recurrence of menstruation at 

intervals of 23-33 days. Amenorrhea was defined as the absence of menstruation 

for 3 or more consecutive months. Menstrual phase was associated with no 

significant differences in pre-exercise plasma AVP or renin activity in the 

eumenorrheic runners. Plasma AVP and renin activity were significantly elevated 

at 4 minutes after exercise in the eumenorrheic runners during both menstrual 

phases and returned to pre-exercise levels by 40 minutes post-exercise. 

Menstrual status was associated with no significant differences in pre-exercise 

AVP or renin activity, however amenorrheic runners had elevated resting levels 

of aldosterone. Post-exercise responses in the amenorrheic runners were 

comparable with the eumenorrheic runners during the early follicular phase. Pre­

exercise plasma aldosterone was significantly elevated during the midluteal 

phase in the eumenorrheic runners. Plasma aldosterone, post-exercise resulted 

33 



in a greater response during the midluteal phase, and was greater when 

compared to the amenorrheic runners [78]. The authors suggested that 

progesterone was the factor responsible for the observed differences, because 

progesterone is highest at this time [78]. Other studies have also shown that 

plasma aldosterone peaks during the midluteal phase of the menstrual cycle due 

to elevated levels of progesterone [79, 80]. 

In a more recent observational study, twelve healthy adult, pre-menopausal, 

normal-cycling women, aged 20-23 years, were studied over the follicular (6-10 

days) and luteal (19-22 days) phases of the menstrual cycle to determine AVP 

responses to exercise [81]. Peeke and colleagues demonstrated similar findings 

to that of De Souza et al. [78]: there was a significant increase in AVP 

concentrations after exercise, in both phases of the menstrual cycle, but the 

responses in the two phases were not significantly different (81]. Aldosterone 

was not measured in this study. 

2. 5. 3 Heat tolerance and thermoregulation 

Women generally have a large surface area to mass ratio, relatively great 

adiposity, and a menstrual cycle. All these properties may influence 

thermoregulation with regard to its effectiveness and therefore may affect heat 

tolerance [82]. 

The phase of the menstrual cycle has an impact on thermoregulation in women 

[83]. During the luteal phase of the menstrual cycle, core temperature is 

approximately 0.4°C higher than during the follicular phase, at least in non-heat 

acclimatised women [83, 84]. 

The adaptations that occur with heat acclimatisation include decreased heart 

rate, decreased rectal temperature, increased plasma volume, and increased 

sweating rate [83). Heat tolerance depends on the cardiovascular fitness of an 

individual more than gender. Young girls tolerate exercise in hot climates less 

34 



effectively than adult women because of the young girls' larger ratio of surface 

area to body mass and slower onset of sweating and sweating rate [83]. 

Hessemer and Bruck documented differences between the follicular and luteal 

phases in thresholds for sweating [85]. Ten healthy adult, pre-menopausal, 

normal-cycling women, aged 20-29 years, were studied over the follicular (4-7 

days after the onset of menstrual flow) and luteal (4-8 days after elevation of 

waking rectal temperature) phases of the menstrual cycle. Cycle phases were 

verified by progesterone determinations in venous blood. The ten women 

exercised for 15 minutes on a cycle ergometer in the mid-luteal phase and early 

follicular phase at the same constant work rates (mean 122 W) and an ambient 

temperature of 18°C [85]. Exercise was performed between 3:00am and 4:3aam 

(after a 4-hour resting period), when the luteal-follicular difference in body 

temperature is at its maximum. Pre-exercise oesophageal, tympanic and rectal 

temperatures averaged a.6°C higher in the luteal phase. During the exercise 

period these temperatures were significantly higher in the luteal than the follicular 

phase (average a.5°C). The thresholds for chest sweating and cutaneous 

vasodilation at the thumb and forearm were elevated in the luteal phase by an 

average of 0.47°C. The heart rate level during the exercise was significantly 

increased in the luteal phase by an average of 6.2 beats per minute. The mean 

exercise V02 in luteal was 5.2% higher than in follicular, the metabolic rate was 

increased in luteal by 5.6%, but the net efficiency was 5.3% lower [85]. 

The authors reported that the elevated vasodilation and sweating thresholds 

could account for the observed postovulatory increases in core temperature 

during rest, as well as for the sustained temperature elevation during exercise 

[85]. Hessemer and Bruck also stated that the higher heat production during 

exercise in the luteal phase might also have contributed to the temperature 

elevation [85]. The authors alternatively postulated that the 5.6% elevation in 

exercise metabolic rate may be secondary to the a.5°C higher core temperature 

35 



which could explain the increase in heart rate by 6.2 beats per minute in the 

luteal phase [85]. 

It was concluded from the Hessemer and Bruck study that during the luteal 

phase, short-lasting heavy exercise (15 minutes) is performed with higher core 

temperature and higher thermoregulatory, circulatory and aerobic-metabolic 

strain than during the follicular phase [72, 85]. 

Others have noted that the tests by Hessemer and Bruck were conducted 

between 3:00am and 4:30am when the deep body temperature difference 

between menstrual phases is at its maximum, and thus has little consequence in 

the sporting world [74]. 

In a more recent study involving short-duration heavy exercise, Lynch and 

Nimmo studied 15 women (five women using low-dose, monophasic oral 

contraceptive (OC) agents and ten normally menstruating women (Non-OC)) to 

determine the effect of OC's and the menstrual cycle (MC) on intermittent 

exercise performance [86]. The intermittent exercise involved repeated 20-

second sprints starting at 14.3km/h, increasing by 1.2km/h until exhaustion, on 

an incline of 10.5% [86]. Like the results found in the Hessemer and Bruck study 

[85] temperatures were higher in the luteal phase when compared to the follicular 

phase of the menstrual cycle. Unlike the increase in heart rate by 6.2 beats per 

minute in the luteal phase reported in the Hessemer and Bruck study [85], Lynch 

and Nimmo revealed no significant difference in heart rate between menstrual 

phases or between the groups [86]. The study by Lynch and Nimmo [86] is in 

accordance with the majority of reports published to date, that state that heart 

rate, both at rest and during exercise, is not affected by the menstrual phase [87, 

88, 89]. 

These reports however have all been completed using short duration activity. 

The current literature may not be applicable to extreme conditions, where there 

36 



may be potential implications for women participating in prolonged endurance 

events (e.g. marathons, ultra-marathons, and triathlons) at high ambient 

temperature during the luteal phase of their cycle [73). 

Pivarnik et al. [90] investigated whether menstrual cycle phase would affect 

temperature regulation during an endurance exercise bout at 22°C with 60% RH. 

Nine eumenorrheic, aerobically trained, heat acclimated women aged 27.2 ± 3.7 

years performed 60 minutes of cycling exercise at 65% of peak V02, and 

subjects were tested in both follicular and luteal phases [90). Sweat loss, V02 

and skin temperatures were not affected by menstrual cycle phase. Pre-exercise 

rectal temperature was 0.3°C higher during the luteal than during the follicular 

conditions, and this difference increased to 0.6°C by the end of the exercise. 

Pivarnik and colleagues reported that heart rate during luteal conditions were 10 

beats greater when compared to follicular conditions [90]. These results support 

the findings of Hessemer and Bruck [85]. De Souza et al (88), found no menstrual 

phase effect on heart rate response in a group of runners who performed a 40 

minute treadmill exercise at 80% V02 max. However, neither ambient conditions 

nor pre-exercise heart rate values were reported. Although Pivarnik et al. [90] did 

not document alterations in performance, higher ratings of perceived exertion at 

the same level of exercise during the luteal phase as compared with the follicular 

phase were reported. 

Pivarnik et al. (90], concluded that temperature regulation, cardiovascular strain 

and perceptual responses to steady-state exercise were adversely affected 

during the luteal phase of the menstrual cycle. Because the subject's V02 values 

during exercise were similar in follicular and luteal conditions, a difference in 

heart rate response suggests that the subjects were exercising at a higher 

percentage of their aerobic capacities in the luteal phase. Each subject's peak 

V02 was measured only once, and tests were performed randomly with respect 

to the menstrual cycle - therefore it can not be said for sure that V02max was 

not affected by the experimental conditions' [90). Subjects were not able to 

37 



achieve thermal equilibrium during exercise performed after ovulation, despite 

similar sweat loss and skin temperatures in follicular and luteal conditions [90]. 

Pivarnik et al. [90] suggested that the effects were mediated by progesterone, 

because they were not seen in a subject whose P4 levels did not increase after 

her lutenizing hormone surge had occurred. 

It has been postulated by Pivarnik et al. [90] there may be potential implications 

for prolonged athletic activity at high ambient temperature, as the woman is 

beginning to exercise at an already elevated core temperature. 

2.6 Body Composition 

The ability to accurately determine body composition would greatly enhance 

health-professionals understanding of the nutritional status of population groups. 

Methods for the in vivo assessment of body composition have progressed 

considerably in recent years. There are now many techniques available to 

estimate body composition in humans. There is anthropometry, bioelectrical 

impedance analysis (BIA), hydrodensitometry, dual energy X-ray absorptiometry 

(DEXA) and total body potassium (TBK). Many of these procedures have been 

limited to laboratory and clinical environments due to cumbersome, time 

consuming, expensive procedures. The development of newer procedures such 

as BIA, are more appropriate for field use and epidemiological studies [91 ]. 

2. 6. 1 Bioelectrical Impedance Analysis (BIA) 

Bioelectrical impedance methods have the advantage of convenience, rapidity 

and non-invasiveness [92]. Bioelectrical impedance analysis is based on two 

theories: 

1. The body consists of two compartments: 

(a) A lean compartment which contains virtually all the water and conducting 

electrolytes of the body; and 

38 



(b) A fat compartment which contains little water and is hence 

non-conducting. 

2. The Thomassett [93, 94] principles that state that the electrical impedance of 

a single geometric system is a function of conductor configuration, length, 

cross-sectional area and measurement signal frequency [91, 95]. 

The accuracy and precision of the BIA method are affected by instrumentation, 

subject factors, technician skill, environmental factors, and the prediction 

equation used to estimate fat-free mass (FFM) [96]. 

Multiple regression analysis has been used extensively to derive prediction 

equations to estimate body composition [97]. The publication of many regression 

equations for men [98, 99, 100, 101] and women [98, 99, 102, 103, 104] have 

resulted from the variance of body composition and anthropometric measures 

related to age and gender. Many of the regression equations however were 

derived on sample sizes of normally less than 75 [97]. Cooley and Lohnes have 

stated that equations derived on sample sizes of under 200 subjects should be 

viewed with caution [105]. 

If BIA is to be of use in estimating body composition, it must be accurate and 

valid. Lukaski et al. [106], and Segal et al. [107] have published conflicting data 

on the validity of the BIA method. Lukaski et al. [106] reported their standard 

errors for estimating (SEE) hydrostatically measured percent body fat (% fat) 

with BIA were low: 2.7% fat for males and 3.1% fat for females. The authors used 

gender-specific regression equations that estimated fat-free weight (FFW) from 

the ratio of height squared to bioelectrical resistance (ht2/R). In contrast, Segal et 

al. [107] reported SEE of 6.1 % fat for a combined sample of men and women, 

and used empirically derived equations provided by the manufacturer of the BIA 

system (R. J. L. Systems, Detroit, Ml). 

39 



Jackson et al. [108] designed a study to examine the reliability and validity of the 

BIA method and compare its accuracy with results obtained by standard 

anthropometric methods. BIA, skinfold fat, and hydrostatically measured % fat 

were obtained on 44 female and 24 male subjects, and each subject was tested 

four times by two testers on two different days [108]. An additional 26 men (n = 

50) and 38 women (n = 82) were tested once and combined with the data used 

for the reliability analysis to cross-validate BIA estimates of % fat with 

hydrostatically determined % fat [108]. The BIA prediction accuracy reported by 

Lukaski et al. (106] was not confirmed by the Jackson et al. study [108]. The SEE 

for the BIA methods ranged from 4.6 to 6.4% fat compared with 2.6 and 3.6% fat 

for the sum of seven (I7) skinfolds equations [108]. The results of the Jackson et 

al. study [108] are in agreement with the findings reported by Segal et al. [107], 

who showed that the BIA method was less accurate than other anthropometric 

models. The authors stated that the results suggest that weight/height2 is the 

major source of variance in BIA prediction models [108]. 

2.6.2 BIA and the female subject 

The study by Eaton et al. [109] compared the accuracy of four methods to assess 

body composition of seventy-seven caucasian women (age: 31.8 ± 8.6 years, 

weight: 59.5 ± 9.1kg, height: 162.4 ± 6.9 cm). Compared to% fat with hydrostatic 

weighing (24.9 ± 6.5%) an analysis of variance revealed no mean difference to 

BIA (25.7 ± 5.8%) and the SEE value for the BIA method was 4.2%. The authors 

concluded that the mean % fat differences between hydrostatic weighing and BIA 

were small and would allow for its use in assessing body composition even with a 

SEE value of 4.2% [109]. The authors also reported that % fat obtained from the 

BIA machine readings versus those computed from the manufacturer's equation 

indicated significant differences (machine 25.7%, equation 27.8%) [109]. 

In a more recent study Stout et al. [11 O] did not support the suggestion of Eaton 

et al. [109] that the equation supplied by the manufacturer is not the same as 

used by the BIA machine to calculate % fat. The estimated % fat values from the 

40 



BIA machine and BIA equation were highly correlated (r = 0.97) [110J. Stout et al. 

[11 OJ investigated the validity of methods for estimating % fat in 41 non-athletic 

young women (age: 20.1 ± 2.3 years). The authors reported that the limited 

number of studies on the validity of BIA procedures [108, 109, 111] for estimating 

% fat in women have resulted in disparate findings. Results from the Stout et al. 

[11 OJ study found Total Error (TE) values ranging from 4.3 to 7.2% fat, which 

indicated that the errors associated with all the BIA equations were substantially 

greater than those from (l.:7: 2.3% fat) and (L.:3: 2.4% fat). The authors reported 

that the accuracy with which BIA equations can estimate % fat may be partly a 

function of subject characteristics or the difference in BIA machines used for 

various investigations [11 O]. 

Adult women often report noticeable fluctuations in body weight (BW) related to 

the menstrual cycle. Temporary water retention has been assumed as the cause 

of the weight gain [111 J. Because water content is the largest component of the 

fat-free body (FFB) (approximately 73%) it can have a significant influence on the 

FFB [112J. Thus, temporary increases in body water can affect a female's body 

density and lead to variable estimations of body fatness when using an indirect 

method such as hydrostatic weighing (HW) [112]. 

Bunt et al. [112J investigated the possibility that variability in body weight in 

females due to water retention causes differences in body density (Db) values 

determined by HW. Seven females were measured when they felt they were at 

their lowest (LO) and highest (HI) body weights (BW) during a menstrual cycle 

[112J. Significant mean differences were found in BW (kg) (LO = 58.9, HI = 61.1 ), 

Db (g. cc -1) (LO= 1.0430, HI= 1.037), and% fat as determined by HW alone 

(LO = 24.8%, HI = 27.6%) [112]. The authors concluded that changes in total 

body water (TBW) can in part result in significantly different Db values obtained 

from HW in females who did experience perceptible changes in BW during the 

menstrual cycle [112J. Lohman [113J has shown that variation in water content of 

41 



the FFB is the greatest contributor to variation in the density of the FFB among 

subjects. 

In contrast to the findings by Bunt et al. [112], Lebrun et al. [89] found no 

significant differences in weight or% fat when 16 eumenorrheic women had their 

body composition measured by HW. 

Eating, drinking, dehydration, exercise, and menstrual cycle stage may affect BIA 

measures [96]. Individual females who experience significant changes in BW 

during the menstrual cycle are believed to have varying states of hydration (114]. 

Fluctuating levels of estradiol and progesterone are believed to be the cause of 

this and are related to their influences on sodium and water retention (114]. Such 

fluid alterations may be expected to impact on BIA since the method relies on 

distinguishing hydrated lean body mass (LBM) or TBW from relatively anhydrous 

fat (106]. 

There have been conflicting results reported in the two studies that assessed the 

effects of the menstrual cycle on BIA Chumlea et al. (115] investigated the 

effects of timing of the menstrual cycle and of oral contraceptive usage on BIA in 

29 women aged 21 to 38 years (11 women were taking oral contraceptive). The 

type of oral contraceptive (combination or progestogen only) was not discussed 

in the paper. The ratio of height squared to bioelectrical resistance (ht2/R) did not 

vary significantly during the menstrual cycle. However, the detection of significant 

variations was reduced because parts of two successive menstrual cycles were 

used instead of one complete menstrual cycle. 

In a more recent study Gleichauf and Roe (116] reported that BW and resistance 

changed significantly between the immediate post-menstruum and both the 

menses and the pre-menstruum in 25 women aged 20 to 41 years. The authors 

stated that the validity of the BIA technique for assessing body composition 

remains unconfirmed (116]. The study's results suggested that the effect on 

42 



resistance and fat-free mass estimates obtained during the menstrual cycle are 

related to changes in body weight, presumably caused by changes in water 

retention [ 116]. 

McKee and Cameron [117] included male control subjects in an attempt to 

discern variations in BIA associated with the menstrual cycle in women from 

those due to other physiological variables affecting both sexes. Body weight and 

BIA were measured two to five times per week for one menstrual cycle (21-34 

days) using 42 women (6 taking an oral contraceptive, OC), aged 19.0-34.4 

years, and for 22-32 days using 28 men aged 18.9-24.1 years [117]. Body weight 

in the non-OC women decreased significantly between menses and the late 

follicular phase, and increased significantly between the late follicular phase and 

the pre-menstrum. These changes were not correlated with matching BIA 

changes. BIA in the non-OC women, and body weight and BIA in the OC women 

and the men, did not differ significantly over the measurement period [117]. The 

authors concluded that body composition assessments based on BIA are not 

affected by the menstrual cycle [117]. 

Thorn et al [111] have also reported that females who experience significant 

changes in BW may encounter fluctuation in appetite (due to changes in 

estrogen and progesterone levels) and this may lead to significant shifts in caloric 

intake. 

2.7 Dietary Assessment 

It is useful to evaluate the dietary intake of the athletic population as they may 

have different eating habits to the general population - in terms of food choices, 

serve sizes, frequency of consumption, food preparation and even language 

about food. Athletes, particularly adolescents and those involved in endurance 

training, have higher nutrient requirements and turnover of nutrients than the 

sedentary population [118]. 

43 



Dietary evaluation involves collecting information on dietary intake and evaluating 

and interpreting dietary intake using the 'common' reference guidelines or 

standards available [118]. Dietary intake can be assessed by a number of data 

collection methods. Current food consumption methods include 1-7 day food 

record/diaries (using weighed - scales or estimated - household measures), or 

duplicate food collection [118]. Methods for collecting food consumption in the 

past (retrospectively) include 24-hour recall, food frequency questionnaires 

(FFQ) and diet histories (combination of 24-hour recall and FFQ) [118]. 

The diet record is considered the most 'accurate' and feasible method for 

research [119]. Although the weighed diet record is considered the 'gold' 

standard, a recent review of dietary intakes of athletes by Burke et al. [120], 

reported that 3 or 4 day diet records using household measures were 

predominantly the method of choice. Other authors have also reported that the 

estimated method using household measures was acceptable for research 

because of better compliance than the weighed method [121, 122]. It has been 

suggested that seven days of continuous recording was the most accurate 

method [123]. However, periods of recording for longer than 3 to 4 days have 

shown reduced accuracy, associated with memory interference, incomplete 

records and a high drop-out rate [124]. 

Collection of reliable and accurate dietary intakes of individuals and groups is 

difficult because of the influence of confounding effects and errors inherent in all 

dietary survey methods [118]. A number of errors are introduced at each stage of 

dietary assessment: from collection of food intake data to analysis and 

interpretation of these data [118]. 

There are several limitations when collecting nutritional data via the estimated 

method using household measures. Diet records are not representative of 

measuring usual diet unless repeated several times, two to three months apart 

[125]. Self-recording food intake changes an individual's eating behaviour by 

44 



discouraging snacking, inhibiting spontaneous food selection and consumption of 

mixed meals (because of difficulties estimating individual ingredients) [118]. 

Under-reporting of actual food intake either intentionally or unintentionally is 

higher in food records than other methods. Authors have reported that energy 

intake can be under-estimated by 20-50% [126, 127]. Under-reporting of food 

has been documented especially for women who are overweight [128], and 

endurance female athletes [129, 130]. 

The number of days needed to measure nutrient intakes reliably varies for 

different subjects and different nutrients. Basiotis et al. [131] have provided 

estimates for the number of days required to measure true average intake of a 

range of nutrients with given statistical confidence (95% confidence). Intakes of 

protein, fat and CHO required four, six and five to six days respectively to 

estimate true average intake in both males and females [131]. The accuracy of 

estimated dietary intake might also be affected by seasonal changes in food 

intake due to variation in food supply [132]. 

The number of days required to measure true average intake of micronutrients is 

much longer. Due to significant intraindividual variability, 5 to 10 days of urine or 

food collection, or more than 14 days of dietary recalls are necessary to 

characterise dietary sodium intake [133, 134]. Mean sodium intake obtained from 

food analysis and food composition tables were correlated to the measurement 

of urinary sodium excretion in a study by Sowers and Stumbo [135]. 

45 



3 Aims of the Study 

This study investigated the nutritional, biochemical, hormonal and physical status 

of New Zealand female ultradistance triathletes competing in the New Zealand 

lronman Triathlon, 3 March 2001. The aim of the study was to determine the 

causes of hyponatremia in these athletes. 

To ensure homogeneity, New Zealand female ultradistance triathletes competing 

in the New Zealand lronman Triathlon were selected because gender, heat 

acclimation, type and intensity of training and level of fitness would be similar_ 

The first aim of the study was to calculate the nutritional intake of the athletes 

(via 7-day food diaries) eight weeks and one week prior to competition. The 

second aim was to assess body composition (using digital scales and 

bioelectrical impedance) and to determine water content shifts before and after 

competition. The third aim was to investigate biochemical status (via blood and 

urine tests) before and after the race. The fourth aim was to determine menstrual 

status (via blood test and questionnaire) and investigate whether there is a 

correlation between the incidence of hyponatremia and different stages of the 

menstrual cycle. 

The overall aim of the study was to determine why female ultradistance 

triathletes are at increased risk from developing hyponatremia and to provide 

practical advice on how to lower the incidence. 

46 



4 Methodology 

The subjects for this study were recruited from female athletes who competed in 

either of the two Half lronman Triathlon competitions (Taupo Half lronman 

Triathlon - Saturday 16 December 2000 and Mt Maunganui Half lronman 

Triathlon - Saturday 6 January 2001). Those female athletes who then intended 

to go on and compete in the New Zealand lronman Triathlon, 3 March 2001 were 

asked to participate in the study. 

Subjects were invited to participate in the study by the provision of information 

sheets at the two venues and by contacting triathlon coaches who informed 

athletes in their regions about the study (appendix 1 ). The researcher was 

present at the two Half lronman Triathlon venues to provide further information 

about the study. Athletes who agreed to participate gave their informed consent 

before the start of the study (appendix 2). 

All New Zealand women who were participating in t