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Biomedical subjects

T D Noakes

Publications and source records attributed to T D Noakes.

At least 55 records · Page 3Linked to original sources
PubMed2001

Sodium replacement and fluid shifts during prolonged exercise in humans.

In the study presented here, we examined the affects of a close to complete replacement of sweat water and Na+ losses on fluid shifts during exercise. Six cyclists performed three 4-h rides at 55% of their peak oxygen uptake in a 20 degrees C environment while consuming 3.85 l of an 8% carbohydrate solution containing 5, 50 or 100 mEq.l-1 of Na+. Increases in Na+ intake reduced renal free water clearance from around 40 ml.h-1 to -8 and -121 ml.h-1 and led to a decrease in urine volume from approximately equal to 1.0 to 0.5 l (P < 0.05). In contrast, the 3.5-3.9 l fluid and 150-190 mEq Na+ losses in sweat were similar in each trial, as were the approximately equal to 80 mEq K+ losses in sweat and urine and the 282-288 mosmol.kg-1 plasma osmolalities. During the low-Na+ trial, plasma osmolality was maintained by a approximately equal to 1.3 l contraction of extracellular fluid (ECF) with the loss of approximately equal to 200 mEq Na+. However, in the other trials, approximately equal to 1.3 l of water was lost from the intracellular fluid. During the medium-Na+ trial, a loss of only approximately equal to 40 mEq Na+ maintained ECF volume, and during the high-Na+ trial, a gain of approximately equal to 160 mEq Na+ expanded the ECF by approximately equal to 0.8 l. However, corresponding changes in plasma volumes from -0.20 to 0.15 l had no effect on cardiovascular drift or thermoregulation. These data suggest that during prolonged exercise of moderate intensity under mild environmental conditions when sweat rates are approximately equal to 0.9 l.h-1, complete Na+ replacement maintains plasma volume and reduces dehydration, but when fluid intake matches sweat rate, has little effect on plasma osmolality.

Administration, Oral↗
PubMed2001

Influence of ambient temperature on plasma ammonia and lactate accumulation during prolonged submaximal and self-paced running.

This study examined the effects of heat stress on the accumulation of plasma ammonia, lactate, and urate during prolonged running. Nine highly trained endurance runners completed two running trials in a counterbalanced fashion in cool (15 degrees C) and in hot (35 degrees C) humid (60% relative humidity) conditions. Subjects ran on a motorised treadmill at 70% of peak treadmill running speed for 30 min (submaximal) followed by a self-paced 8-km performance run. Blood was drawn at pre-exercise, end-submaximal and end-performance run and analysed for plasma ammonia, lactate, and urate. Four subjects failed to complete the performance run in the heat and the performance times for the rest of the subjects was increased from 27.3 (0.6) min in cool conditions to 31.3 (1.2) min in hot conditions (P < 0.05). The end-performance rectal temperature was 38.6 (0.1) and 39.2 (0.1) degrees C (P<0.05) in cool and hot conditions, respectively. Differences in plasma lactate at the end of submaximal running were not significant. However, at the end of performance runs lactate was 6.0 (0.9) m mol x l(-1) in cool and 3.1 (0.5) mmol x l(-1) in hot conditions, values that were significantly different (P<0.05). Plasma ammonia increased from pre-exercise to approximately equal to 59 micromol x l(-1) at the end-submaximal runs for both coditions and further at the end of performance runs to 108.5 (11) micromol x l(-1) (P<0.05) in hot but not in cool conditions. Plasma urate increased from pre-exercise to 311.2 (25.9) micromol x l(-1) at end-submaximal runs and to approximately equal to 320.4 micromol x l(-1) at end-performance runs in hot and cool environments. The findings that plasma urate accumulation was similar at the completion of running in both conditions, while ammonia was significantly augmented in hot conditions compared with cool, suggest that ammonia accumulation during heat stress exercise might be derived from sources other than purine catabolism.

Adult↗
PubMed2001

Effects of androgen manipulation on postprandial triglyceridaemia, low-density lipoprotein particle size and lipoprotein(a) in men.

Although androgenic hormones decrease HDLC concentration, no direct evidence has linked them to atherosclerosis. The present study was undertaken to extend our ability to assess risk associated with androgen induced lipoprotein(Lp) changes by simultaneously gathering information about postprandial triglyceridaemia (PPT), LDL particle size, HDL and Lp(a) in men either taking exogenous androgens or with suppressed endogenous androgen concentrations. The experimental groups comprised nine male bodybuilders who self-administered anabolic-androgenic steroids (AAS) for a mean period of 6.5 weeks, and 10 healthy men whose testosterone concentration had been reversibly suppressed for 5 weeks using the GnRH agonist triptorelin (Decapeptyl; D-Trp-6-LHRH). A separate group receiving no hormonal treatment provided analytical control (n=7). Lipoprotein size was assessed by gradient gel electrophoresis categorisation (GGE), lipoprotein concentrations by immuno and enzymatic assays and PPT by a standardised oral fat tolerance test (65g /m(2)). Testosterone concentration was significantly reduced on triptorelin from 7.32+/-1.92 to 1.15+/-0.57 ng/ml (P=0.002). High dose AAS use was confirmed by urinalysis. With AAS use, mean HDLC and Lp(a) concentrations and PPT decreased from 0.9+/-0.3 to 0.7+/-0.3 mmol/l (P=0.004), 125+/-128 to 69+/-73 U/l (P=0.008) and 11.6+/-10.0 mmol/l h to 7.5+/-5.4 mmol/l h (P=0.027) respectively. Mean total cholesterol and LDLC were unchanged. LDL size was unchanged in six AAS users, decreased in one but remaining in the normal size range, and increased in two from small LDL to the normal range. Size changes in the latter two subjects were associated with 42 and 58% reductions in PPT respectively. In the triptorelin group, mean total cholesterol, HDLC and Lp(a) were increased from 4.8+/-0.8 mmol/l to 5.2+/-1.0 mmol/l (P=0.039), 1.1+/-0.2 to 1.4+/-0.3 mmol/l (P=0.002) and 278+/-149 to 377+/-222 U/l (P=0.004) respectively. Mean LDLC concentration and PPT were unchanged. LDL particle size increased in four, decreased in two, and was unchanged in four subjects. LDL size decreased in two and showed no change in the other five control subjects. Other lipid measures were unchanged in the control group. Thus, apart from lowering HDLC concentrations, no other potentially atherogenic effects of endogenous androgens or AAS were observed. A suppression of Lp(a) as well as a reduced PPT and increased LDL size in predisposed individuals may be antiatherogenic effects of AAS.

Adult↗
PubMed2001

Exercise-associated hyponatremia: a review.

This paper reviews the extensive literature on hyponatremia, a common and potentially serious complication of ultra-distance exercise. Fluid overload is the likely aetiology. Fluid intakes are typically high in athletes who develop hyponatremia, although hyponatremia can occur with relatively modest fluid intakes. The development of fluid overload and hyponatremia in the presence of a modest fluid intake raises the possibility that athletes with this condition may have an impaired renal capacity to excrete a fluid load. The bulk of evidence favours fluid retention in the extracellular space (dilutional hyponatremia) rather than fluid remaining unabsorbed in the intestine. Female gender is an important risk factor for the development of hyponatremia. Management and prevention of exercise-associated hyponatremia are discussed.

Adolescent↗
PubMed2001

Insulin sensitivity measured by the minimal model: no associations with fasting respiratory exchange ratio in trained athletes.

The aim of this study was to examine the role of fasting insulin concentrations and tissue insulin sensitivity on whole-body substrate oxidation in 61 well-trained subjects. Subjects underwent a frequently sampled intravenous glucose tolerance test (FSIVGT) after a 10- to 12-hour overnight fast. Minimal model analysis was used to determine insulin sensitivity (S(i)). A week later, fasting (10- to 12-hour) respiratory exchange ratio (RER) was measured at rest and during exercise at 25%, 50%, and 70% of peak power output (W(peak)). Prior to these measurements, training volume, dietary intake, and muscle fiber composition, substrate concentrations, and enzyme activities were determined. The average fasting plasma insulin concentration was 7.3 +/- 2.4 microU/mL (4.0 to 10.5 microU/mL), and the mean S(i) was 14.0 +/- 6.1 x (10(-4) min(-1) x microU(-1) x mL(-1)) (2.6 to 26.3 x 10(-4) min(-1) x microU(-1) x mL(-1)). There was no significant correlation between fasting plasma insulin concentration and S(i) (r = -.14, P =.336) or between these measurements and fasting RER, measured at rest and during exercise at 25%, 50%, and 70% W(peak). Only VO(2max) and the proportion of type 1 muscle fibers were significantly correlated with S(i) (r =.30, P =.045 and r =.34, P =.026, respectively), and waist-to-hip ratio (WHR) was significantly correlated with fasting plasma insulin concentration (r =.35, P =.006). In conclusion, S(i) and fasting plasma insulin concentration were not associated with fasting RER at rest and during exercise of increasing intensity in trained athletes who have high S(i).

Adult↗
PubMed2001

Reliability of a 5-m multiple shuttle test.

The aim of the present study was to determine the reliability of a modified 5-m multiple shuttle test. The 'match-related fitness' of 23 female hockey players was assessed on four occasions within 4 weeks. The results of each test session and each shuttle were analysed using analysis of variance with repeated measures to determine the reliability of the test. The mean distance for each of the six shuttles decreased (121.2 +/- 7.5, 114.5 +/- 7.5, 112.2 +/- 7.5, 109.9 +/- 7.9, 108.4 +/- 8.1 and 108.7 +/- 8.3 m for shuttles 1-6, respectively; P < 0.001) similarly for each of the four sessions (P = 0.99). The total and peak distances covered during the tests were not significantly different (P = 0.99 and P = 0.12, respectively). The intra-class correlation coefficient (R) for these variables was 0.98 and 0.86, respectively. The delta distance and the fatigue index calculated post-test were significantly different (P = 0.001 and P = 0.006, respectively) between the four sessions. The intra-class correlation coefficient for both these variables was 0.74. Heart rate and rating of perceived exertion (RPE) were not significantly different between sessions (P = 0.42 and P = 0.095, respectively). The intra-class correlation coefficient for heart rate ranged from 0.65 to 0.97 and that for RPE from 0.85 to 0.91. We conclude that the 5-m multiple shuttle run test is a reliable measure of total and peak distances, heart rate and RPE response and is sufficiently reliabile to track changes in fitness over a season. The delta distance and fatigue index are not as reliable and should be interpreted with caution.

Adult↗
PubMed2001

Response to a fluid load in athletes with a history of exercise induced hyponatremia.

PURPOSE: To determine whether athletes who had previously developed hyponatremia during an ultradistance triathlon show an impaired ability to excrete a large fluid load compared with athletes who had completed the same race without developing hyponatremia. METHODS: Six athletes who had developed hyponatremia ([Na] < 135 mmol x L(-1)) in the 1997 Ironman Triathlon (study cases) were compared with six athletes who completed the same race without hyponatremia (controls). All participants consumed 3.4 L of water over 2 h at rest. Weight, urine output, urine electrolytes, serum [Na(+)], hemoglobin, and hematocrit were measured every 30 min. Changes in plasma volume and residual fluid volume in the gut were estimated from these data. RESULTS: There were no significant differences between cases and controls in any parameters measured. Maximal rates of urine production (+/- SD) (1043 +/- 331 mL x h(-1) for cases, 878 +/- 168 mL x h(-1) for controls) were substantially behind the rate of fluid intake (1500 mL x h(-1)). Consequent to fluid retention, serum [Na(+)] fell progressively in both groups. Five cases and four controls developed hyponatremia. There was an inverse correlation between change in body weight and change in [Na(+)] (r = -0.67). Estimated changes in the intra- and extra-cellular fluid volumes could account for all the retained fluid, and there was little evidence for fluid accumulation in the bowel. CONCLUSION: When evaluated at rest, there does not appear to be any unique pathophysiological characteristic that explains why some athletes develop hyponatremia in response to fluid overload during prolonged exercise. Rather, hyponatremia was induced with equal effect in both cases and controls, consequent to progressive fluid overload of all the body fluid compartments and without evidence for fluid retention in the small bowel.

Adult↗
PubMed2001

Fluid balance during and after an ironman triathlon.

OBJECTIVE: To record weight changes, fluid intake and changes in serum sodium concentration in ultradistance triathletes. DESIGN: Descriptive research. SETTING: Ironman triathlon (3.8 km swim, 180 km cycle, 42.2 km run). Air temperature at 1200 h was 21 degrees C, (relative humidity 91%). Water temperature was 20.7 degrees C. PARTICIPANTS: 18 triathletes. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Subjects were weighed and had blood drawn for serum sodium concentration [Na], hemoglobin, and hematocrit, pre-race, post-race, and at 0800 h on the morning following the race ("recovery"); subjects were also weighed at transitions. Fluid intake during the race was estimated by athlete recall. RESULTS: Median weight change during the race = -2.5 kg (p < 0.0006). Subjects lost weight during recovery (median = -1.0 kg) (p < 0.03). Median hourly fluid intake = 716 ml/h (range 421-970). Fluid intakes were higher on the bike than on the run (median 889 versus 632 ml/h, p = 0.03). Median calculated fluid losses cycling were 808 ml/h and running were 1,021 ml/h. No significant difference existed between pre-race and post-race [Na] (median 140 versus 138 mmol/L) or between post-race and recovery [Na] (median 138 versus 137 mmol/L). Plasma volume increased during the race, median + 10.8% (p = 0.0005). There was an inverse relationship between change in [Na] pre-race to post-race and relative weight change (r = -0.68, p = 0.0029). Five subjects developed hyponatremia ([Na] 128-133 mmol/L). CONCLUSIONS: Athletes lose 2.5 kg of weight during an ultradistance triathlon. most likely from sources other than fluid loss. Fluid intakes during this event are more modest than that recommended for shorter duration exercise. Plasma volume increases during the ultradistance triathlon. Subjects who developed hyponatremia had evidence of fluid overload despite modest fluid intakes.

Adult↗
PubMed2001

High-fat diet versus habitual diet prior to carbohydrate loading: effects of exercise metabolism and cycling performance.

We examined the effects of a high-fat diet (HFD-CHO) versus a habitual diet, prior to carbohydrate (CHO)-loading on fuel metabolism and cycling time-trial (TT) performance. Five endurance-trained cyclists participated in two 14-day randomized cross-over trials during which subjects consumed either a HFD (> 65% MJ from fat) or their habitual diet (CTL) (30 +/- 5% MJ from fat) for 10 day, before ingesting a high-CHO diet (CHO-loading, CHO > 70% MJ) for 3 days. Trials consisted of a 150-min cycle at 70% of peak oxygen uptake (VáO2peak), followed immediately by a 20-km TT. One hour before each trial, cyclists ingested 400 ml of a 3.44% medium-chain triacylglycerol (MCT) solution, and during the trial, ingested 600 ml/hour of a 10% 14C-glucose + 3.44% MCT solution. The dietary treatments did not alter the subjects' weight, body fat, or lipid profile. There were also no changes in circulating glucose, lactate, free fatty acid (FFA), and b-hydroxybutyrate concentrations during exercise. However, mean serum glycerol concentrations were significantly higher (p < .01) in the HFD-CHO trial. The HFD-CHO diet increased total fat oxidation and reduced total CHO oxidation but did not alter plasma glucose oxidation during exercise. By contrast, the estimated rates of muscle glycogen and lactate oxidation were lower after the HFD-CHO diet. The HFD-CHO treatment was also associated with improved TT times (29.5 +/- 2.9 min vs. 30.9 +/- 3.4 min for HFD-CHO and CTL-CHO, p <.05). High-fat feeding for 10 days prior to CHO-loading was associated with an increased reliance on fat, a decreased reliance on muscle glycogen, and improved time trial performance after prolonged exercise.

Adult↗
PubMed2001

Free living energy expenditure in post menopausal women before and after exercise training.

The aim of the study was to determine the effects of 8 weeks of moderate exercise training, on 24-hour free living energy expenditure in previously sedentary post-menopausal women. The experimental group (EX) included 9 women. Ten non-exercising control subjects (CON) were recruited to undergo pre- and post-testing. Estimated total daily energy expenditure (TDEE), total 24-hour heart beats (HB), total energy intake (TEI), resting metabolic rate, maximal oxygen consumption (VáO2max), body composition, and submaximal heart rate were measured before and after the exercise intervention. Body composition did not change (body fat % in CON 34.0 +/- 4.0% vs. 33.9 +/- 3.6% and EX 34.1 +/- 4.0% vs. 34.0 +/- 3.4%). Mean submaximal heart rate during steady-state exercise in EX was lower after training compared to CON (p < .05); however, VáO2max did not increase significantly (CON 1.96 +/- 0.23 vs. 1.99 +/- 0.24 l L O2/min and EX 1.86 +/- 0.39 vs. 1.94 +/- 0.30 L O2/min). Neither estimated TDEE (CON, 11.6 +/- 2.0 vs. 11.4 +/- 2.78 MJ; and EX 11.4 +/- 3.3 vs. 11.5 +/- 2.5 MJ, pre vs. post, respectively), RMR (CON 134.2 +/- 9.4 vs. 136.9 +/- 15.0 KJ/kgFFM/day, and EX 138.4 +/- 6.4 vs. 140.7 +/- 14.2 KJ/kgFFM/day, pre vs. post, respectively), TEI (CON 7.9 +/- 2.2 vs. 8.2 +/- 2.5 MJ, and EX 9.4 +/-1.6 vs. 8.3 +/- 2.8 MJ), nor HB (CON 110,808 +/- 12,574 vs. 107,366 +/- 12,864 beats, and EX 110,188 +/- 9,219 vs. 114,590 +/- 12,750 beats) change over 8 weeks in either group. These data suggest that a moderate exercise program may not impact on TDEE, RMR, TEI, or HB in previously sedentary, older women.

Basal Metabolism↗
PubMed2001

Reduced neuromuscular activity and force generation during prolonged cycling.

We examined neuromuscular activity during stochastic (variable intensity) 100-km cycling time trials (TT) and the effect of dietary carbohydrate manipulation. Seven endurance-trained cyclists performed two 100-km TT that included five 1-km and four 4-km high-intensity epochs (HIE) during which power output, electromyogram (EMG), and muscle glycogen data were analyzed. The mean power output of the 4-km HIE decreased significantly throughout the trial from 319 +/- 48 W for the first 4-km HIE to 278 +/- 39 W for the last 4-km HIE (P < 0.01). The mean integrated EMG (IEMG) activity during the first 4-km HIE was 16.4 +/- 9.8% of the value attained during the pretrial maximal voluntary contraction (MVC). IEMG decreased significantly throughout the trial, reaching 11.1 +/- 5.6% during the last 4-km HIE (P < 0.01). The study establishes that neuromuscular activity in peripheral skeletal muscle falls parallel with reduction in power output during bouts of high-intensity exercise. These changes occurred when <20% of available muscle was recruited and suggest the presence of a central neural governor that reduces the active muscle recruited during prolonged exercise.

Adult↗
PubMed2001

Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia.

An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed the existence of a 'governor' in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle. In contrast, if the function of the heart or some other oxygen-sensitive organ is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxia compared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.

Brain↗
PubMed2001

Neural control of force output during maximal and submaximal exercise.

A common belief in exercise physiology is that fatigue during exercise is caused by changes in skeletal muscle metabolism. This 'peripheral' fatigue results either from substrate depletion during submaximal exercise or metabolite accumulation during maximal exercise in the exercising muscles. However, if substrate depletion alone caused fatigue, intracellular ATP levels would decrease and lead to rigor and cellular death. Alternatively, metabolite accumulation would prevent any increase in exercise intensity near the end of exercise. At present, neither of these effects has been shown to occur, which suggests that fatigue may be controlled by changes in efferent neural command, generally described as 'central' fatigue. In this review, we examine neural efferent command mechanisms involved in fatigue, including the concepts of muscle wisdom during short term maximal activity, and muscle unit rotation and teleoanticipation during submaximal endurance activity. We propose that neural strategies exist to maintain muscle reserve, and inhibit exercise activity before any irreparable damage to muscles and organs occurs. The finding that symptoms of fatigue occur in the nonexercising state in individuals with chronic fatigue syndrome indicates that fatigue is probably not a physiological entity, but rather a sensory manifestation of these neural regulatory mechanisms.

Action Potentials↗
PubMed2001

The influence of sensory cues on the perception of exertion during exercise and central regulation of exercise performance.

The perception of effort during exercise and its relationship to fatigue is still not well understood. Although several scales have been developed to quantify exertion Borg's 15-point ratings of perceived exertion (RPE) scale has been adopted as a valid and reliable instrument for evaluating whole body exertion during exercise. However, Borg's category-ratio scale is useful in quantifying sensations of exertion related to those variables that rise exponentially with increases in exercise intensity. Previous research has examined the extent to which afferent feedback arising from cardiopulmonary and peripheral variables mediates the perception of exertion. However, the literature has not identified a single variable that consistently explains exertion ratings. It is concluded that effort perception involves the integration of multiple afferent signals from a variety of perceptual cues. In a process defined as teleoanticipation, the changes in perceived exertion that result from these afferent signals may allow exercise performance to be precisely regulated such that a task can be completed within the biomechanical and metabolic limits of the body. The accuracy with which individuals can regulate exercise intensity based upon RPE values, the decrease in muscle recruitment (central drive) that occurs before fatigue, and the extent to which perceived exertion and heart rate can be altered with hypnosis and biofeedback training all provide evidence for the existence of such a regulatory system. Future research is needed to precisely quantify the extent to which efferent feedforward commands and afferent feedback determine pacing strategies such that an exercise event can be completed without irreversible tissue damage.

Biomechanical Phenomena↗
PubMed2001

Peak rates of diuresis in healthy humans during oral fluid overload.

OBJECTIVE: To determine whether rates of intestinal fluid absorption and renal diuresis can match high rates of fluid ingestion in healthy humans exposed to oral fluid overload, thereby preventing the development of hyponatraemia either by reverse sodium movement across the intestine (the Priestley-Haldane effect) or by expansion of the extracellular fluid volume. METHODS: Changes in renal function and in plasma chemical measurements in response to an oral fluid overload (0.9-1.8 l/h x 3 h) were investigated in 6 healthy control subjects at rest, and in a subject with a history of exercise-induced symptomatic hyponatraemia, during both prolonged (160-minute) exercise and at rest. FINDINGS: All control subjects gained weight (2.7 +/- 0.2 kg, mean +/- standard error of mean (SEM)) because the rate of oral fluid intake exceeded the peak rate of urine production (778 +/- 39 ml/h). Blood volume rose by 7.1 (+/- 0.5)% and plasma sodium concentrations fell progressively from 144 +/- 2.6 to 136 +/- 1.1 mmol/l (P < 0.05) in the control subjects. Plasma potassium and angiotensin II concentrations were unchanged and creatinine clearance was normal (approximately 125 ml/min). Free water clearance reached a maximum of 11.2 +/- 0.9 ml/min after 2 hours. The increase in body mass could be accounted for by calculated or measured changes in extra- and intracellular fluid volumes. Similar changes were measured in the subject with a previous history of symptomatic hyponatraemia. CONCLUSION: The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was no evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraemia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of approximately 900 ml/h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision.

Adult↗
PubMed2000

[Improving performance and promoting health by sports participation].

The 20th century witnessed the globalization of international sporting competitions, most notably in Olympic Competition. Thus whereas fewer than 20 countries competed in the 1900 Olympic Games, close to 200 countries were represented at the 2000 Olympic Games in Sydney. There has also been a progressive improvement in athletic performance during the past century, for reasons that are described in this article. A question that needs to be asked is whether this increased global participation in competitive sport has improved the health of the general population in those countries in which international competitive sports have been promoted. There is little evidence to support this possibility. An important goal of the beginning century must be to globalize sporting participation amongst the general population specifically for health enhancement.

Competitive Behavior↗