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S N Cheuvront

Publications and source records attributed to S N Cheuvront.

7 recordsLinked to original sources
PubMed2006

Exercise associated hyponatraemia: quantitative analysis to understand the aetiology.

BACKGROUND: The development of symptomatic hyponatraemia consequent on participation in marathon and ultraendurance races has led to questions about its aetiology and prevention. OBJECTIVES: To evaluate: (a) the assertion that sweat sodium losses cannot contribute to the development of hyponatraemia during endurance exercise; (b) the adequacy of fluid replacement recommendations issued by the International Marathon Medical Directors Association (IMMDA) for races of 42 km or longer; (c) the effectiveness of commercial sports drinks, compared with water, for attenuating plasma sodium reductions. METHODS: A mathematical model was used to predict the effects of different drinking behaviours on hydration status and plasma sodium concentration when body mass, body composition, running speed, weather conditions, and sweat sodium concentration were systematically varied. RESULTS: Fluid intake at rates that exceed sweating rate is predicted to be the primary cause of hyponatraemia. However, the model predicts that runners secreting relatively salty sweat can finish ultraendurance exercise both dehydrated and hyponatraemic. Electrolyte-containing beverages are predicted to delay the development of hyponatraemia. The predictions suggest that the IMMDA fluid intake recommendations adequately sustain hydration over the 42 km distance if qualifiers-for example, running pace, body size-are followed. CONCLUSIONS: Actions to prevent hyponatraemia should focus on minimising overdrinking relative to sweating rate and attenuating salt depletion in those who excrete salty sweat. This simulation demonstrates the complexity of defining fluid and electrolyte consumption rates during athletic competition.

Body Composition↗
PubMed2001

Ad libitum fluid intakes and thermoregulatory responses of female distance runners in three environments.

Ad libitum fluid intakes and thermoregulatory responses were compared in eight female marathon runners during a 30 km treadmill run at individual best marathon race pace (range = 2.45-4.07 m x s(-1)) under three wet bulb globe temperature conditions (25 degrees C, 17 degrees C and 12 degrees C, corresponding to hot, moderate and cool conditions, respectively). Rectal temperature, mean skin temperature and heart rate were recorded at 10 min intervals and expired air was collected every 5 km during exercise. Simulated water stations were also provided at 5 km intervals with voluntary fluid intake being recorded. Blood was drawn before and after exercise for the determination of plasma volume changes and osmolarity. Ad libitum fluid intakes in the hot trial (0.70+/-0.31 l x h(-1); mean+/-s) were greater (P< 0.05) than in the cool (0.47+/-0.13 l x h(-1)) but not the moderate (0.54+/-0.26 l x h(-1)) trial. Each volume replaced 63%, 68% and 73% of total sweat losses in each condition, respectively, and kept dehydration below approximately 3% of body mass. After the initial 30 min of exercise, rectal temperature was maintained well below 39 degrees C for > 2 h of continuous running. The results demonstrate that the thermoregulatory responses of female distance runners to exercise in variable, but compensable, weather conditions is well maintained when ad libitum fluid intakes replace approximately 60-70% of sweat losses.

Adult↗
PubMed2001

Thermoregulation and marathon running: biological and environmental influences.

The extreme physical endurance demands and varied environmental settings of marathon footraces have provided a unique opportunity to study the limits of human thermoregulation for more than a century. High post-race rectal temperatures (Tre) are commonly and consistently documented in marathon runners, yet a clear divergence of thought surrounds the cause for this observation. A close examination of the literature reveals that this phenomenon is commonly attributed to either biological (dehydration, metabolic rate, gender) or environmental factors. Marathon climatic conditions vary as much as their course topography and can change considerably from year to year and even from start to finish in the same race. The fact that climate can significantly limit temperature regulation and performance is evident from the direct relationship between heat casualties and Wet Bulb Globe Temperature (WBGT), as well as the inverse relationship between record setting race performances and ambient temperatures. However, the usual range of compensable racing environments actually appears to play more of an indirect role in predicting Tre by acting to modulate heat loss and fluid balance. The importance of fluid balance in thermoregulation is well established. Dehydration-mediated perturbations in blood volume and blood flow can compromise exercise heat loss and increase thermal strain. Although progressive dehydration reduces heat dissipation and increases Tre during exercise, the loss of plasma volume contributing to this effect is not always observed for prolonged running and may therefore complicate the predictive influence of dehydration on Tre for marathon running. Metabolic heat production consequent to muscle contraction creates an internal heat load proportional to exercise intensity. The correlation between running speed and Tre, especially over the final stages of a marathon event, is often significant but fails to reliably explain more than a fraction of the variability in post-marathon Tre. Additionally, the submaximal exercise intensities observed throughout 42 km races suggest the need for other synergistic factors or circumstances in explaining this occurrence. There is a paucity of research on women marathon runners. Some biological determinants of exercise thermoregulation, including body mass, surface area-to-mass ratio, sweat rate, and menstrual cycle phase are gender-discrete variables with the potential to alter the exercise-thermoregulatory response to different environments, fluid intake, and exercise metabolism. However, these gender differences appear to be more quantitative than qualitative for most marathon road racing environments.

Body Mass Index↗
PubMed1999

Effect of ENDUROX on metabolic responses to submaximal exercise.

Claims that ENDUROX enhances performance by altering metabolic responses to exercise were tested. In a double-blind crossover design, 10 male subjects were randomly assigned to consume 400 mg of placebo or 800 mg ENDUROX for 7 days. Cycle ergometry was performed for 30 minutes at 25%, followed by 10 min at 65% of peak oxygen consumption. After a 1-week washout period, subjects performed the identical exercise protocol following 7 days of reciprocal supplemental conditions. Expired gases were collected and analyzed continuously for oxygen consumption, minute ventilation, and respiratory exchange ratio. Heart rate, blood pressure, rating of perceived exertion, blood lactate, and serum glycerol data were also collected at regular intervals. A two-way ANOVA with repeated measures revealed no significant main or interaction effects involving group differences (p > 0.05) between trials for any variable during rest, 25% or 65% (VO2 peak), or recovery. Our findings do not support the ergogenic claims for ENDUROX.

Adult↗
PubMed1999

The zone diet and athletic performance.

The Zone diet is the latest eating regimen marketed to improve athletic performance by opposing traditional high carbohydrate sports diets. The 40/30/30 diet is centred primarily on protein intake (1.8 to 2.2 g/kg fat free mass; i.e. total bodyweight-fat weight) and promises a change in the body's insulin to glucagon ratio through its macronutrient alterations. Changes in the existing hormonal milieu are said to result in the production of more vasoactive eicosanoids, thus allowing greater oxygen delivery to exercising muscle. This favourable condition, known as the Zone, is anecdotally reported to benefit even the most elite endurance athletes. Applying the Zone's suggested protein needs and macronutrient distributions in practice, it is clear that it is a low carbohydrate diet by both relative and absolute standards, as well as calorie deficient by any standard. Reliable and abundant peer reviewed literature is in opposition to the suggestion that such a diet can support competitive athletic endeavours, much less improve them. The notion that a 40/30/30 diet can alter the pancreatic hormone response in favour of glucagon is also unfounded. The Zone is a mixed diet and not likely to affect pancreatic hormone release in the same way individual nutrients can. Although the postprandial insulin response is reduced when comparing a 40% with a 60% carbohydrate diet, it is still a sufficient stimulus to offset the lipolytic effects of glucagon. Many of the promised benefits of the Zone are based on selective information regarding hormonal influences on eicosanoid biology. Contradictory information is conveniently left out. The principle of vasodilating muscle arterioles by altering eicosanoid production is notably correct in theory. However, what little human evidence is available does not support any significant contribution of eicosanoids to active muscle vasodilation. In fact, the key eicosanoid reportedly produced in the Zone and responsible for improved muscle oxygenation is not found in skeletal muscle. Based on the best available scientific evidence, the Zone diet should be considered more ergolytic than ergogenic to performance.

Diet↗
PubMed1999

Oxidative stress during a 3.5-hour exposure to 120 kPa(a) PO2 in human divers.

We examined the effect of a prolonged dive on measures of oxidative stress in human divers. Ten subjects, wearing dry suits, completed mental tasks while lying quietly at 4.6 m fresh water for 3.5 h. Subjects (9 male, 1 female) were active, experienced divers ranging in age from 19 to 54 yr. Subjects breathed an enriched air nitrox mixture yielding a P(O2) of approximately 120 kPa(a) for the duration of the dive. Venous blood was drawn before and after the dive for measurements of hemoglobin (Hb), hematocrit (Hct), plasma osmolarity (O(SM)), red blood cell osmotic fragility (Frag), superoxide dismutase activity (SODa), and thiobarbituric acid reactive substances (TBARS). Plasma volume (PV) shifts were calculated from the changes in Hb and Hct. Significant increases in Hb, Hct, Osm, Frag, and TBARS were found along with significant decreases in PV and SODa (P < or = 0.05). We conclude that hyperbaric exposures encountered by technical divers are sufficient to cause significant oxidative stress.

Adult↗