Effect of hypoxia exposure on the recovery of skeletal muscle phenotype during regeneration.

Hypoxia impairs the muscle fibre-type shift from fast-to-slow during post-natal development; however, this adaptation could be a consequence of the reduced voluntary physical activity associated with hypoxia exposure rather than the result of hypoxia per se. Moreover, muscle oxidative capacity could be reduced in hypoxia, particularly when hypoxia is combined with additional stress. Here, we used a model of muscle regeneration to mimic the fast-to-slow fibre-type conversion observed during post-natal development. We hypothesised that hypoxia would impair the recovery of the myosin heavy chain (MHC) profile and oxidative capacity during muscle regeneration. To test this hypothesis, the soleus muscle of female rats was injured by notexin and allowed to recover for 3, 7, 14 and 28 days under normoxia or hypobaric hypoxia (5,500 m altitude) conditions. Ambient hypoxia did not impair the recovery of the slow MHC profile during muscle regeneration. However, hypoxia moderately decreased the oxidative capacity (assessed from the activity of citrate synthase) of intact muscle and delayed its recovery in regenerated muscle. Hypoxia transiently increased in both regenerated and intact muscles the content of phosphorylated AMPK and Pgc-1α mRNA, two regulators involved in mitochondrial biogenesis, while it transiently increased in intact muscle the mRNA level of the mitophagic factor BNIP3. In conclusion, hypoxia does not act to impair the fast-to-slow MHC isoform transition during regeneration. Hypoxia alters the oxidative capacity of intact muscle and delays its recovery in regenerated muscle; however, this adaptation to hypoxia was independent of the studied regulators of mitochondrial turn-over.

Ambient hypoxia enhances the loss of muscle mass after extensive injury.

Hypoxia induces a loss of skeletal muscle mass and alters myogenesis in vitro, but whether it affects muscle regeneration in vivo following injury remains to be elucidated. We hypothesized that hypoxia would impair the recovery of muscle mass during regeneration. To test this hypothesis, the soleus muscle of female rats was injured by notexin and allowed to recover for 3, 7, 14, and 28 days under normoxia or hypobaric hypoxia (5,500 m) conditions. Hypoxia impaired the formation and growth of new myofibers and enhanced the loss of muscle mass during the first 7 days of regeneration, but did not affect the final recovery of muscle mass at 28 days. The impaired regeneration under hypoxic conditions was associated with a blunted activation of mechanical target of rapamycin (mTOR) signaling as assessed by p70(S6K) and 4E-BP1 phosphorylation that was independent of Akt activation. The decrease in mTOR activity with hypoxia was consistent with the increase in AMP-activated protein kinase activity, but not related to the change in regulated in development and DNA response 1 protein content. Hypoxia increased the mRNA levels of the atrogene muscle ring finger-1 after 7 days of regeneration, though muscle atrophy F box transcript levels remained unchanged. The increase in MyoD and myogenin mRNA expression with regeneration was attenuated at 7 days with hypoxia. In conclusion, our results support the notion that the enhanced loss of muscle mass observed after 1 week of regeneration under hypoxic conditions could mainly result from the impaired formation and growth of new fibers resulting from a reduction in protein synthesis and satellite cell activity.

Effect of hypoxia exposure on the phenotypic adaptation in remodelling skeletal muscle submitted to functional overload.

AIM: To determine whether hypoxia influences the phenotypic adaptation of skeletal muscle induced by mechanical overload. METHODS: Plantaris muscles of female rats were submitted to mechanical overload following synergist ablation. After 3 days of overload, rats were exposed to either hypobaric hypoxia (equivalent to 5500 m) or normoxia. Muscles were collected after 5, 12 and 56 days of overload (i.e. after 3, 9 and 53 days of hypoxia). We determined the myosin heavy chain (MHC) distribution, mRNA levels of myocyte-enriched calcineurin-integrating protein 1 (MCIP1) to indirectly assess calcineurin activity, the changes in oxidative capacity from the activities of citrate synthase (CS) and cytochrome c oxidase (COX), and the expression of regulators involved in mitochondrial biogenesis (Pgc-1α, NRF1 and Tfam) and degradation (BNIP-3). RESULTS: Hypoxia did not alter the fast-to-slow MHC shift and the increase in calcineurin activity induced by overload; it only transiently slowed down the overload-induced transition in MHC isoforms. Hypoxia similarly decreased CS and COX activities in overloaded and control muscles. Nuclear respiratory factor 1 (NRF1) and transcription factor A (Tfam) mRNA and BNIP-3 protein were not influenced by hypoxia in overloaded muscles, whereas Pgc-1α mRNA and protein contents did not correlate with changes in oxidative capacity. CONCLUSION: Hypoxia is not a critical stimulus to modulate the fast-to-slow MHC transition associated with overload. Thus, the impairment of the fast-to-slow fibre shift often observed during post-natal development in hypoxia could be explained by the lower voluntary locomotor activity associated with hypoxia. Hypoxia alters mitochondrial oxidative capacity, but this adaptive response is similar in overloaded and control muscles.

Pitfalls in target mRNA quantification for real-time quantitative RT-PCR in overload-induced skeletal muscle hypertrophy.

Quantifying target mRNA using real-time quantitative reverse transcription-polymerase chain reaction requires an accurate normalization method. Determination of normalization factors (NFs) based on validated reference genes according to their relative stability is currently the best standard method in most usual situations. This method controls for technical errors, but its physiological relevance requires constant NF values for a fixed weight of tissue. In the functional overload model, the increase in the total RNA concentration must be considered in determining the NF values. Here, we pointed out a limitation of the classical geNorm-derived normalization. geNorm software selected reference genes despite that the NF values extensively varied under experiment. Only the NF values calculated from four intentionally selected genes were constant between groups. However, a normalization based on these genes is questionable. Indeed, three out of four genes belong to the same functional class (negative regulator of muscle mass), and their use is physiological nonsense in a hypertrophic model. Thus, we proposed guidelines for optimizing target mRNA normalization and quantification, useful in models of muscle mass modulation. In our study, the normalization method by multiple reference genes was not appropriate to compare target mRNA levels between overloaded and control muscles. A solution should be to use an absolute quantification of target mRNAs per unit weight of tissue, without any internal normalization. Even if the technical variations will stay present as a part of the intergroup variations, leading to less statistical power, we consider this method acceptable because it will not generate misleading results.

Hypoxic stimulus alters hypothalamic AMP-activated protein kinase phosphorylation concomitant to hypophagia.

Acute exposure to hypobaric hypoxia is known to decrease food intake, but the molecular mechanisms of such alteration in feeding behavior remain unknown. We tested the hypothesis that hypothalamic AMP-activated protein kinase (AMPK) phosphorylation is affected by acute exposure to hypobaric hypoxia and thus would be involved in initial anorexia. To address this issue, male rats weighing 255-270 g were either submitted to hypobaric hypoxia (H, equivalent altitude of 5,500 m), maintained under local barometric pressure conditions (N), or pair-fed an equivalent quantity of food to that consumed by H rats (PF), for 6, 24, or 48 h. Daily food intake dropped by 73% during the first day of hypoxia (P<0.01) and remained by 46% lower than in N rats thereafter (P<0.01). Hypoxia per se, as estimated by comparing experimental data between the H and PF groups, increased ob gene transcription and plasma leptin concentration. A transient increase in glucose availability occurred in the H group compared with PF animals (P<0.05). The hypoxic stimulus led to an early and transient decrease in hypothalamic AMPK and acetyl-CoA carboxylase (ACC) phosphorylation, concomitant with hypophagia and associated alterations in nutrients and hormones. An increase in NPY mRNA levels occurred from day 1, similarly in H and PF rats, and thus mainly related to food restriction alone (P<0.05). In conclusion, the present study demonstrates that hypoxia per se inhibited AMPK and ACC phosphorylation in the hypothalamus, concomitant with profound anorexia. A powerful counterregulation occurs rapidly, mediated by NPY and devoted to avoid prolonged anorexia.

Musclin gene expression is strongly related to fast-glycolytic phenotype.

Musclin has been described as a muscle-derived secretory peptide, responsive to insulin in vivo, and inducing insulin resistance in vitro. Because muscle fibers display very different metabolic properties and insulin sensitivity, we tested the hypothesis that musclin expression could depend on myofiber type. Musclin mRNA was detected at high level in fast gastrocnemius and plantaris muscles, but only as traces in soleus, a slow-twitch muscle. A single fiber analysis showed that musclin was produced by muscle fibers themselves, almost exclusively type IIb fibers. Slow to fast transition of soleus phenotype after hindlimb suspension increased musclin mRNA levels, whereas fast to slow transition of plantaris phenotype after functional overload decreased musclin mRNA levels. This clearly suggests that musclin transcription is strongly related to fast-glycolytic phenotype. We conclude that musclin is produced by myocytes in a highly fiber-type specific manner and that physiological changes in type IIb MHC lead to coordinated musclin expression.

[Cardiological aspects of fatigue states in athletes]. / Aspects cardiologiques des etats de fatigue du sportif.

The physical load increase during training can lead to the development of clinical patterns of intolerance differing according to their severity, prognosis and reversibility. However, they always include fatigue as a key symptom. The aim of this paper is to review recent data on fatigue states in sportsmen, their clinical presentation and diagnostic orientations. A continuum exists, from acute fatigue states after one or several highly-intensive training sessions, to overreaching, associated to performances alteration which can be easily reversed, and to overtraining, representing a severe clinical pattern which can hardly be reversed. Overreaching and overtraining are characterized by a persisting fatigue state, associated to performances alteration and mood disorders. In an athlete with unexplained alteration of performances associated to physical fatigue, the medical interrogation is critical, in order to check the durable character of sportive performances alteration, to describe the fatigue and identify risk factors of occurrence of overtraining (training program intensity, mental stress, diet factors, hypoxic training, etc.). The use of a validated and adapted questionnaire as the one proposed by the French Society of Sports Medicine is valuable. In majority, in athletes and those doing sports regularly, the cardiological alert signs are rare, and the clinical examination by a specialist is poorly contributive, except for eliminating an organic cause of fatigue.

Substrate utilization during prolonged exercise with ingestion of (13)C-glucose in acute hypobaric hypoxia (4,300 m).

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

Quantification by real-time PCR of developmental and adult myosin mRNA in rat muscles.

A real-time RT-PCR assay using newly designed primers was developed to analyze developmental and adult MHC mRNA expression both in skeletal muscles and single fibers. Only 4 ng of total RNA was necessary for the analysis of the relative mRNA expression of MHC genes. Different validation steps were realized concerning both specificity and sensitivity of each primer set, and linearity and efficiency of each real-time PCR amplification. Then, quantification of MHC mRNA in neonatal and adult muscles as well as in single fibers was done by the deltaC(T) method, with CycA gene as the reference gene. Due to a higher sensitivity than that of a competitive PCR method, we demonstrated that this assay is suitable to study very low level of MHC mRNA expression as developmental MHC in adult muscle and to quantify mRNA from very small samples.

Adaptive changes in cardiac myosin heavy chain and creatine kinase isozymic profiles in rats native of altitude.

AIM: The developmental changes in the myosin heavy chain (MHC) profile, creatine kinase (CK) and lactate dehydrogenase (LDH) activities and isozyme expression occurring in heart were examined in rats born and living at altitude (La Paz, Bolivia, 3700 m, H(LP)) for 16 generations. We hypothesized that H(LP) rats respond differently to hypoxia than rats born and living at sea level, and secondarily exposed to altitude during 3 weeks (H(3W)). METHODS: The cardiac expression of MHC, CK and LDH was studied in left (LV) and right ventricle (RV) of H(LP) animals 1, 2, 3, 4 and 18 weeks after birth, and compared with control normoxic (C groups) and H(3W) animals. RESULTS: Rats secondarily exposed to hypoxia showed a lower alpha-MHC content than C or H(LP) rats in both LV and RV, 3 weeks after birth (P < 0.05), consistent with a delay in the maturation of the heart contractile phenotype. A global increase in the total CK activity was observed in the LV of H(3W) animals in comparison with C rats (P < 0.05), while no change was reported in H(LP) animals. In both ventricles, M-LDH activity was higher in H(3W) than in H(LP) and C rats (P < 0.05). The relative amount of alpha-MHC decreased by 20% in RV of 18-week-old H(LP) and H(3W) rats in comparison with C animals, consistent with the hypoxia-induced ventricular enlargement (P < 0.01). An increased activity of the foetal B-CK subunit was observed in both LV and RV of H(3W) rats in comparison with H(LP) and C animals (P < 0.05). CONCLUSION: This study demonstrates that rats native and living at altitude for several generations present some features relevant to genetic selection to altitude.

Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?

The renin-angiotensin-aldosterone system plays an important role in the hydroelectrolytic balance, blood pressure regulation, and cell growth. In some studies, the insertion (I) allele of the angiotensin-converting enzyme (ACE) gene, associated with a lower ACE activity, has been found in excess frequency in elite endurance athletes, suggesting that decreased ACE activity could be involved in endurance performance (Myerson S, Hemingway H, Budget R, Martin J, Humphries S, and Montgomery H. J Appl Physiol 87: 1313-1316, 1999). To test this hypothesis, we evaluated whether ACE inhibition could be associated with improved endurance performance and muscle oxidative capacity in rats. Eight male Wistar rats were treated for 10-12 wk with an ACE inhibitor, perindopril (2 mg.kg-1.day-1), and compared with eight control rats. Endurance time was measured on a treadmill, and oxidative capacity and regulation of mitochondrial respiration by substrates were evaluated in saponin-permeabilized fibers of slow soleus and fast gastrocnemius muscles. Endurance time did not differ between groups (57 +/- 5 min for perindopril vs. 55 +/- 6 min for control). Absolute and relative (to body weight) left ventricular weight was 20% (P < 0.01) and 12% (P < 0.01) lower, respectively, in the treated group. No difference in oxidative capacity, mitochondrial enzyme activities, or mitochondrial regulation by ADP was observed in soleus or gastrocnemius. Mitochondrial respiration with glycerol 3-phosphate was 17% higher in gastrocnemius (P < 0.03) and with octanoylcarnitine 14% greater in soleus (P < 0.01) of treated rats. These results demonstrate that ACE inhibition was not associated with improved endurance time and maximal oxidative capacity of skeletal muscles. This suggests that ACE activity has no implication in endurance capacity and only minor effects on mitochondrial function in sedentary animals.

[Physical activity in the heat: physiology of hydration recommendations]. / L'activité physique à la chaleur: de la physiologie aux recommandations d'apport hydrique.

Physical exercise in the heat causes severe disturbances in homeostasis. The need for evaporative thermolysis is increased due to the combination of endogenous and exogenous heat production. Despite a marked increase in cardiac output, muscles and skin must compete for sufficient blood flow. In addition progressive dehydration can impair the ability of the cardiocirculatory to adjust adequately. The most serious risk associated with exercise in a hot environment is heat stroke. Although deleterious effects of dehydration occur only if large amounts of water and electrolytes are lost without being replaced, even moderate fluid depletion can reduce both physical and cognitive performance. Another mechanism by which heat exposure directly affects performance involves core temperature elevation which can induce profound changes in muscular activity and energy consumption, thereby accelerating exhaustion. Prevention of deleterious effects on health and performance requires an effective rehydration strategy to maintain body fluid balance. This strategy must optimize all three potentially limiting factors for fluid replacement, i.e., fluid intake, gastric emptying, and intestinal absorption. Practical guidelines are given to answer the questions of when, what and how much to drink.

Comparison of passive heat or exercise-induced dehydration on renal water and electrolyte excretion: the hormonal involvement.

The effects of hydromineral hormones and catecholamines on renal water and electrolyte excretion were examined during and after dehydration induced by either passive heat or exercise. Eight healthy young Caucasian subjects participated in three separate trials, each including three consecutive phases. Phases 1 and 3 involved a 90-min period at rest in a thermoneutral environment, while phase 2 involved a 120-min period designed to provide: (1) euhydration (control trial), (2) passive heat-induced dehydration of 2.8% body mass, or (3) exercise-induced dehydration of 2.8% body mass. During the two dehydration procedures, the decreases in urine flow and sodium excretion were more marked during exercise (P < 0.05). An increase in plasma catecholamines occurred only during exercise, together with a reduction in creatinine clearance and more marked increases in plasma renin and aldosterone than during passive heat exposure (P < 0.05). Although plasma vasopressin was elevated during the two dehydration procedures, urine osmolality did not change and, moreover, free water clearance increased during exercise (P < 0.05). Plasma levels of atrial natriuretic peptide increased markedly only during exercise compared to the other trials (P < 0.05). After the dehydration procedures, urine flow decreased again and urine osmolality increased markedly (P < 0.05), while plasma vasopressin remained elevated. These results suggest that sympathoadrenal activation during exercise plays a major role in the more marked reduction in diuresis and natriuresis than during passive heat exposure. Despite high plasma vasopressin concentrations during the two dehydrating events, the observed antidiuresis was not due to an increased renal concentrating ability, and the vasopressin was more effective after the dehydration procedures.

Use of bioelectrical impedance analysis to estimate body fluid compartments after acute variations of the body hydration level.

Physiological measurements including body mass, plasma osmolality, natremia, plasma volume measured by Evans Blue dilution, and total body water (TBW) and extracellular water (ECW) volumes estimated by bioelectrical impedance analysis (BIA) were recorded in eight healthy young Caucasian subjects before and after acute variations of their body hydration state on four separate occasions: 1) euhydration or control trial (C); 2) heat-induced dehydration of 2.8% body mass (D); 3) exercise-induced dehydration of 2.8% body mass (E); and 4) glycerol-hyperhydration (H). Heart rate, rectal and mean skin temperatures were also recorded throughout the experiment. The main result of the study is that BIA only half predicted the body water loss after exercise, although conditions were standardized (electrode placement, side of the body, limb position, posture, and ambient temperature). Differences in body temperatures cannot explain such an unexpected result, nor did the study of plasma osmolality and sodium concentration. If BIA appears to adequately predict changes in TBW after heat-induced dehydration and glycerol hyperhydration, further studies including measures of TBW and ECW by dilution tracer methods would be necessary to establish the validity of using the BIA method to measure such changes and to interpret ECW variations.

Plasma volume changes during and after acute variations of body hydration level in humans.

This study examined plasma volume changes (deltaPV) in humans during periods with or without changes in body hydration: exercise-induced dehydration, heat-induced dehydration and glycerol hyperhydration. Repeated measurements of plasma volume were made after two injections of Evans blue. Results were compared to deltaPV calculated from haematocrit (Hct) and blood haemoglobin concentration ([Hb]). Eight well-trained men completed four trials in randomized order: euhydration (control test C), 2.8% dehydration of body mass by passive controlled hyperthermia (D) and by treadmill exercise (60% of their maximal oxygen uptake, VO2max) (E), and hyperhydration (H) by glycerol ingestion. The Hct, [Hb], plasma protein concentrations and plasma osmolality were measured before, during and after the changes in body hydration. Different Hct and [Hb] reference values were obtained to allow for posture-induced variations between and during trials. The deltaPV values calculated after two Evans blue injections were in good agreement with deltaPV calculated from Hct and [Hb]. Compared to the control test, mean plasma volume declined markedly during heat-induced dehydration [-11.4 (SEM 1.7)%] and slightly during exercise-induced dehydration [-4.2 (SEM 0.9)%] (P < 0.001 compared to D), although hyperosmolality was similar in these two trials. Conversely, glycerol hyperhydration induced an increase in plasma volume [+7.5 (SEM 1.0)%]. These results would indicate that, for a given level of dehydration, plasma volume is dramatically decreased during and after heat exposure, while it is better maintained during and after exercise.

Effects of acute hypobaric hypoxia on the appearance of ingested deuterium from a deuterium oxide-labelled carbohydrate beverage in body fluids of humans during prolonged cycling exercise.

To determine whether or not acute hypobaric hypoxia alters the rate of water absorption from a carbohydrate beverage ingested during exercise, six men cycled for 80 min on three randomly assigned different occasions. In one trial, exercise was performed in hypoxia (barometric pressure, P(B) = 594 hPa, altitude 4,400 m) at an exercise intensity selected to elicit 75% of the individual's maximal oxygen uptake (VO2max) previously determined in such conditions. In the two other experiments, the subjects cycled in normoxia (P(B) = 992 hPa) at the same absolute and the same relative intensities as in hypoxia, which corresponded to 55% and 75%, respectively, of their VO2max determined in normoxia. The subjects consumed 400 ml of a 12.5% glucose beverage just prior to exercise, and 250 ml of the same drink at 20, 40 and 60 min from the beginning of exercise. The first drink contained 20 ml of deuterium oxide to serve as a tracer for the entry of water into body fluids. The heart rate (HR) during exercise was higher in hypoxia than in normoxia at the same absolute exercise intensity, whereas it was similar to HR measured in normoxia at the same relative exercise intensity. Both in normoxia and hypoxia, plasma noradrenaline concentrations were related to the relative exercise intensity up to 40 min of exercise. Beyond that duration, when exercise was performed at the highest absolute power in normoxia, the noradrenaline response was higher than in hypoxia at the same relative exercise intensity. No significant differences were observed among experimental conditions, either in temporal profiles of plasma D accumulation or in elimination of water ingested in sweat. Conversely, elimination in urine of the water ingested appeared to be related to the severity of exercise, either high absolute power or the same relative power combined with hypoxia. We concluded that water absorption into blood after drinking a 12.5% glucose beverage is not altered during cycling exercise in acute hypobaric hypoxia. It is suggested that the elimination of water ingested in sweat and urine may be dependent on local circulatory adjustments during exercise.

Effects of different carbohydrate-electrolyte beverages on the appearance of ingested deuterium in body fluids during moderate exercise by humans in the heat.

To determine whether different forms of glucose (free and polymer) associated with sodium chloride influence the rate of water absorption during exercise in the heat, six men took part in five trials. Each trial included a passive heating session which resulted in a 2% loss of body mass, followed by 1h of treadmill exercise (at 50% of maximal oxygen uptake) in warm conditions (dry bulb temperature 35 degrees C, relative humidity 20%-30%). Immediately before exercise, the subjects were given either no fluid or a volume equal to 50% of the fluid previously lost (about 650 ml), chosen from among four D2O-labelled beverages: mineral water, a 6% glucose-electrolyte solution (GS), a 6% maltodextrin solution and a 6% maltodextrin-electrolyte solution. No significant differences were observed among these various beverages so far as temporal accumulation of deuterium in plasma, sweat and urine was concerned. During GS, the plasma volume was completely restored and the drifts of heart rate and rectal temperature were less marked than during other trials. These results would suggest that rehydration with GS was more efficient, probably because of an internal redistribution of water. The proportion of ingested water was twice as high in sweat as it was in urine. These findings may reflect the essential part played by circulatory adjustments in the transfer of plasma water into sweat and urine.

Effects of various beverages on the hormones involved in energy metabolism during exercise in the heat in previously dehydrated subjects.

The objective of our study was to examine the effects of beverage content on hormone responses involved in fuel substrate metabolism (catecholamines, insulin and glucagon) in previously dehydrated subjects exercising at a moderate intensity in the heat. Six healthy men walked for 60-min on five occasions at 50% maximal oxygen uptake in a warm environment (dry bulb temperature 35 +/- 0.2 degrees C, relative humidity 20%). On each occasion, the subjects were dehydrated before exercise (loss of 2% body mass) by passive controlled hyperthermia, which led to a reduction in plasma volume (PV) of about -5% to -9%. In one session, the subjects exercised without rehydration (Dh). In the other sessions, four beverages (650 ml) were given just before the exercise: mineral water (W), a 60 g x l(-1) glucose and 1.2 g x l(-1) NaCl solution (GS), a 60 g x l(-1) maltodextrin solution, and a 60 g x l(-1) maltodextrin and 1.2 g x l(-1) NaCl solution. Compared to Dh and W, carbohydrate supply with or without NaCl induced a higher glycaemia (P < 0.05), a reduced increase in plasma adrenaline concentration (P < 0.05) and a higher plasma insulin concentration (P < 0.05), which lowered plasma free fatty acids and glycerol concentrations (P < 0.05). The lesser increase in plasma noradrenaline concentrations observed during GS compared to Dh and W sessions can be explained by a larger correction in PV which might have induced better haemodynamic conditions. However, the increase in plasma glucagon with carbohydrate supply--compared to Dh and W (P < 0.05)--remains unexplained.

Effect of ingestion pattern on rehydration and exercise performance subsequent to passive dehydration.

Six male volunteers performed three tests, each comprising a passive heating session to obtain dehydration (loss of 2.6% body mass), followed by exercise on a treadmill until exhaustion (50% of maximal oxygen consumption) in a warm environment (dry bulb temperature 35 degrees C, relative humidity 20%-30%). In one test, the subjects exercised without rehydration (Dh). In the two other tests, 50% of the fluid lost in the dehydration session was replaced by drinking mineral water given either in one amount [913 (SEM 23) ml] before the exercise (Rh1) or divided into four equal portions [228 (SEM 5) ml] before the exercise and on three occasions at 15-min intervals during exercise (Rh4). Rehydration increased exercise duration in Rh1 compared to Dh [112 (SEM 7) min and 82 (SEM 3) min, respectively; P < 0.05]. The difference was not significant with Rh4 [103 (SEM 9) min]. A restoration of the time course of changes in plasma volume, plasma osmolality, heart rate and rectal temperature occurred immediately in Rh1 and as delayed in Rh4 until after 60 min of exercise. Our results demonstrated that the swift replacement of the fluid loss in the dehydrated subjects was beneficial to exercise performance by rapidly correcting the disturbances in body fluid balance.