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PubMed2002

The role of CD4 in regulating homeostasis of T helper cells.

Intrathymic T cell selection and peripheral activation of mature T cells are crucial for self-recognition and the general immune response to viral, bacterial, and tumor antigens. The T cell coreceptors, CD4 and CD8, contribute to the regulation of these processes. The importance of interactions between CD4 and molecules encoded by the class II major histocompatibility complex (MHC) for thymic T cell selection has been clearly established, however, the role of CD4-MHC class II interactions in T helper (TH) cell differentiation, in the maintenance of homeostasis in the peripheral immune system, and in the generation of memory TH cells is largely unclear. Here, we present evidence for a role of CD4 in controlling homeostasis in the peripheral immune system. We also demonstrate the importance of CD4-MHC class II interactions in inducing these previously not recognized functions of CD4.

Animals↗

PubMed2003

Molecular regulation of T lymphocyte homeostasis in the healthy and diseased immune system.

Lymphocyte homeostasis is achieved by a balance between the production and death of lymphocytes. In particular, T lymphocytes differentiate and mature in the thymus and are released into the peripheral circulation, where they can travel to sites of encounter with antigen. Once in the circulation, T lymphocytes have varying life spans depending on whether they remain resting, become activated by antigen and replicate, or they become memory cells. The regulation of lymphocyte fate, especially the induction of programmed cell death, or apoptosis, has become a focus of intense molecular research, and much has been learned. In particular, the Fas receptor and other members of the tumor necrosis factor receptors, as well as their respective ligands, have emerged as key regulators of T lymphocyte apoptosis. We are studying genetic abnormalities of this death pathway, which we have found to underlie the human disease, autoimmune lymphoproliferative syndrome (ALPS). The study of ALPS has revealed that inhibiting the death of lymphocytes can lead to autoimmune consequences. Also, the homeostasis of T lymphocytes can be powerfully affected by viruses and other infectious agents. In particular, the human immunodeficiency virus can cause the attrition of CD4+ T lymphocytes by inducing the premature death of such cells. We are studying the molecular mechanism by which the HIV causes CD4+ T cell destruction.

Animals↗

PubMed2004

The prolactin-releasing peptide receptor (GPR10) regulates body weight homeostasis in mice.

To identify new drug targets for the treatment of obesity, we employed a degenerate reverse transcriptasepolymerase chain reaction technique to isolate novel members of the G-protein coupled receptor superfamily from mouse hypothalamus. One of our clones was found to encode a protein with 90% amino acid identity to human GPR10, which was previously identified as the receptor for prolactin-releasing peptide (PrRP) and has been implicated in lactation, the regulation of food intake and other physiological functions. To investigate the role of GPR10 in food intake and body weight homeostasis, we generated mice carrying a targeted deletion of the GPR10 gene. First, using these knockout animals, we confirmed that GPR10 is the principle receptor for PrRP in the mouse hypothalamus because deletion of GPR10 completely abolished PrRP binding to isolated hypothalamic cell membranes. Second, we investigated the effect of normal and high-fat diets on energy intake, body weight, and glucose homeostasis in wild-type and GPR10 knockout mice. After fasting and refeeding, food intake in knockout animals was unchanged relative to control littermates. However, beginning at 16 wk of age on a normal diet, knockout mice became hyperphagic, obese, and showed significant increases in body fat and the levels of leptin and insulin, as well as decreased glucose tolerance. This metabolic profile was similar to the effect of a high-fat diet on wild-type animals. Our findings provide direct evidence that GPR10 is the receptor for PrRP and that it is involved in the regulation of energy balance in mice. GPR10 knockout mice will also prove useful for investigating other proposed activities for PrRP.

Animals↗

PubMed1998

Ion transport in chondrocytes: membrane transporters involved in intracellular ion homeostasis and the regulation of cell volume, free [Ca2+] and pH.

Chondrocytes exist in an unusual and variable ionic and osmotic environment in the extracellular matrix of cartilage and are responsible for maintaining the delicate equilibrium between extracellular matrix synthesis and degradation. The mechanical performance of cartilage relies on the biochemical properties of the matrix. Alterations to the ionic and osmotic extracellular environment of chondrocytes have been shown to influence the volume, intracellular pH and ionic content of the cells, which in turn modify the synthesis and degradation of extracellular matrix macromolecules. Physiological ion homeostasis is fundamental to the routine functioning of cartilage and the factors that control the integrity of this highly evolved and specialized tissue. Ion transport in cartilage is relatively unexplored and the biochemical properties and molecular identity of membrane transport mechanisms employed by chondrocytes in the control of intracellular ion concentrations and pH is not fully defined and this review focuses on these processes. Chondrocytes have been shown to express voltage and stretch activated ion channels, passive exchangers and ATP dependent ion pumps. In addition, recent studies of transport systems in chondrocytes have demonstrated the presence of isozyme diversity that includes Na+/H+ exchange (NHE1, NHE3), Na+, K(+)-ATPase (several isoforms) and others each of which possess considerably different kinetic properties and modes of regulation. This multitude of isozyme diversity indicates the highly specialized handling of ions and protons in order to accomplish a fine regulation of their transmembrane fluxes. The complexities of these transport systems and their patterns of isoform expression underscore the subtlety of ion homeostasis and pH regulation in normal cartilage. Perturbations in these mechanisms may affect the physiological turnover of cartilage and thus increase the susceptibility to degenerative joint disease.

Animals↗

PubMed2006

Role of the kinin B1 receptor in insulin homeostasis and pancreatic islet function.

Kinins are potent vasoactive peptides generated in blood and tissues by the kallikrein serine proteases. Two distinct kinin receptors have been described, one constitutive (subtype B2) and one inducible (subtype B1), and many physiological functions have been attributed to these receptors, including glucose homeostasis and control of vascular permeability. In this study we show that mice lacking the kinin B1 receptor (B1-/- mice) have lower fasting plasma glucose concentrations but exhibit higher glycemia after feeding when compared to wild-type mice. B1-/- mice also present pancreas abnormalities, characterized by fewer pancreatic islets and lower insulin content, which leads to hypoinsulinemia and reduced insulin release after a glucose load. Nevertheless, an insulin tolerance test indicated higher sensitivity in B1-/- mice. In line with this phenotype, pancreatic vascular permeability was shown to be reduced in B1 receptor-ablated mice. The B1 agonist desArg9bradykinin injected intravenously can induce the release of insulin into serum, and this effect was not observed in the B1-/- mice or in isolated islets. Our data demonstrate the importance of the kinin B1 receptor in the control of pancreatic vascular homeostasis and insulin release, highlighting a new role for this receptor in the pathogenesis of diabetes and related diseases.

Animals↗

PubMed1986

Hepatic glutaminase flux regulation of glutamine homeostasis. Studies in vivo.

The role of hepatic glutaminase flux in regulating plasma glutamine homeostasis was studied in the intact rat. Interorgan glutamine flow during chronic metabolic acidosis was away from the splanchnic bed and to the kidneys. Hindquarter and hepatic glutamine release were the major sources of glutamine removed by the kidneys. Interorgan glutamate flow was from the liver to the hindquarters and kidneys. Chronic metabolic acidosis reduced arterial glutamine concentration 30%. Acute respiratory acidosis (pH 7.12 +/- 0.02) returned arterial glutamine concentration to normal values, increasing and decreasing hepatic glutamine and glutamate release respectively; renal and gut glutamine removal rates were not decreased. Hepatic unidirectional glutamine utilization measured isotopically was decreased 51% by acute acidosis; unidirectional glutamine production was unchanged. The results are consistent with the proposed role of ammonia-activated hepatic glutaminase in the regulation of glutamine homeostasis during acute acidosis.

Acid-Base Equilibrium↗

PubMed2006

A behavioral homeostasis theory of habituation and sensitization: II. Further developments and predictions.

Habituation may be viewed as a decremental behavioral change to iterative stimuli of little immediate relevance. It is observed from protozoa to humans, indicating its evolutionary significance. If habituation is interpreted as the process of filtering out unimportant repetitive stimuli, then how should sensitization be interpreted? The 'behavioral homeostasis theory' of these two behaviors is based on the notion that organisms at a high level of 'alertness' prior to experiencing a new iterative stimulus will show a large initial response followed by a decrement (habituation) if the stimulus is of little significance. Conversely, the same organism at a low level of 'alertness' will show a small initial response to the same stimulus followed by an increase in 'alertness' and a larger response to the next stimulus (sensitization) in order to receive enough information to assess its significance. Circadian rhythmicity is hypothesized to play a role in determining 'alertness' to a new iterative stimulus at any given time. The level of responsiveness in initial habituaters and sensitizers, as an asymptote is approached, is a balance between being too 'alert' to an unimportant stimulus and missing other significant stimuli, and being too 'un-alert' and missing a change in the relevance of the present iterative stimulus. The concept of 'behavioral homeostasis' includes behaviors beyond habituation and sensitization across phylogeny. It includes instinctive as well as learned, and group as well as individual behavior. Such behavioral homeostatic processes to optimize detection and assessment of constantly occurring external stimuli are critical for organism survival. Clinical implications of this theory are also examined.

Animals↗

PubMed2005

Serotoninergic modulation of chloride homeostasis during maturation of the locomotor network in zebrafish.

During development, neural networks progress through important functional changes such as the generation of spontaneous activity, the expression of a depolarizing chloride gradient, and the appearance of neuromodulation. Little is known about how these processes are integrated to yield mature behaviors. We showed previously that, during the maturation of the locomotor network of the zebrafish, endogenous serotonin (5HT) increased motor activity by reducing intervals of inactivity, without affecting the active swim periods that are the target of 5HT in other and more mature preparations. Because membrane properties were constant during the rest intervals, we examined here whether 5HT modulates chloride homeostasis. We compared the effects of blocking (inward) chloride cotransport with bumetanide to the effects of 5HT and its antagonists, both behaviorally by video imaging and cellularly by whole-cell and gramicidin-perforated patch recordings. Bumetanide mimicked the effects of 5HT antagonists, by prolonging rest intervals without affecting the properties of swim episodes (duration; frequency; extent of depolarization) either behaviorally or during fictive swimming. Furthermore, bumetanide and 5HT antagonists suppressed the amplitude of depolarizing responses evoked by ionophoresis of glycine onto spinal neurons in the presence of tetrodotoxin and transiently suppressed the amplitude of responses to glycine measured after fictive swimming. The effects of bumetanide contrasted with and occluded the effects of 5HT. We suggest that, during development, endogenous 5HT modulates chloride homeostasis during the quiescent intervals and thereby offsets the long periods of quiescence commonly observed in developing networks to allow expression of sustained and behaviorally relevant activity.

Animals↗

PubMed2005

NMDA receptor activation mediates copper homeostasis in hippocampal neurons.

Copper is an essential transition metal with a critical role in the CNS. This requirement is underscored by Menkes disease, a fatal neurodegenerative disorder of childhood resulting from the absence or dysfunction of a copper-transporting P-type ATPase. To elucidate the cell biological mechanisms of copper homeostasis in the CNS, a polyclonal antisera against Menkes ATPase was used in immunoblot and immunohistochemical studies, demonstrating abundant expression of this copper transporter in hippocampal neurons. Consistent with this observation, immunofluorescent analysis revealed Menkes ATPase in the late Golgi of hippocampal neurons in primary culture. Glutamate receptor activation was found to result in the rapid and reversible trafficking of Menkes ATPase to neuronal processes, independent of the intracellular copper concentration and specific for activation of the NMDA- but not AMPA/kainate-type glutamate receptors. Metabolic studies revealed that trafficking of Menkes ATPase after NMDA receptor activation is associated with rapid release of copper from hippocampal neurons. Menkes ATPase is directly required for this copper efflux, because similar studies in hippocampal neurons derived from mice lacking a functional Menkes ATPase demonstrated no copper release. Together, these data reveal a critical role for Menkes ATPase in the availability of an NMDA receptor-dependent, releasable pool of copper in hippocampal neurons and demonstrate a unique mechanism linking copper homeostasis and neuronal activation within the CNS.

Adenosine Triphosphatases↗

PubMed2005

Downstream regulatory element antagonist modulator regulates Ca2+ homeostasis and viability in cerebellar neurons.

The Na+/Ca2+ exchangers NCX1, NCX2, and NCX3 are vital for the control of cellular Ca2+ homeostasis. Here, we show that a doublet of downstream regulatory element sites in the promoter of the NCX3 gene mediates transcriptional repression of NCX3 by the Ca2+-modulated transcriptional repressor downstream regulatory element antagonist modulator (DREAM). Overexpression of a DREAM EF-hand mutant insensitive to Ca2+ (EFmDREAM) in hippocampus and cerebellum of transgenic mice significantly reduced NCX3 mRNA and protein levels without modifying NCX1 and NCX2 expression. Cerebellar granules from EFmDREAM transgenic mice showed increased levels of cytosolic Ca2+ and were more vulnerable to increased Ca2+ influx after partial opening of voltage-gated plasma membrane Ca2+ channels induced by increasing K+ in the culture medium but survived better in the conditions of reduced Ca2+ influx prevailing in low extracellular K+. Overexpression of NCX3 in EFmDREAM transgenic granules using a lentiviral vector restored the normal survival response to high K+ observed in wild-type granules. Thus, the downregulation of the regulator of Ca2+ homeostasis NCX3 by Ca2+-regulated DREAM is a striking example of the autoregulatory property of the Ca2+ signal in neurons.

Amino Acid Motifs↗

PubMed2006

Are serum leptin and the Gln223Arg polymorphism of the leptin receptor determinants of bone homeostasis in elderly men?

OBJECTIVE: Across studies it has been suggested that leptin intervenes as a regulator of bone metabolism. This study assesses the contribution in elderly men of leptin and the Gln223Arg leptin receptor gene (LEPR) polymorphism to the variation in bone homeostasis, in relation to body composition and free estradiol as major confounders. DESIGN: We performed cross-sectional (n = 270) and longitudinal (mean follow-up 3.4 years, n = 214) evaluations in elderly men. METHODS: Serum leptin, LEPR genotype, baseline bone mineral density (BMD), longitudinal BMD changes at the hip and forearm, and biochemical markers of bone turnover were determined. RESULTS: In cross-sectional analyses absolute fat mass was the index of body composition most strongly associated with leptin (r = 0.74; P < 0.001). LEPR genotypes and serum leptin were not associated. Serum bone-specific alkaline phosphatase (S-BAP) was associated with LEPR genotypes (P = 0.05) and urinary C-terminal telopeptides of type I collagen (U-CTX) were associated with leptin levels (P = 0.03), independently from age, fat mass and free estradiol. Baseline BMD at the hip and forearm was neither associated with leptin nor with LEPR genotypes. Prospectively assessed BMD loss was not associated with serum leptin at the hip, whereas BMD loss was positively associated with leptin at the forearm (P = 0.01), independently from age, fat mass and free estradiol. Longitudinal changes in hip or forearm BMD were not associated with LEPR genotypes. CONCLUSION: The findings suggest a possible role for leptin as determinant of bone homeostasis in elderly men, but with only modest impact independently from body composition and free estradiol.

Aged↗

PubMed2001

Control of calcium homeostasis in Schistosoma mansoni.

Calcium signalling is fundamental for muscular contractility of Schistosoma mansoni. We have previously described the presence of transport ATPases (Na+,K+-ATPase and (Ca2+-Mg2+)-ATPase) and calcium channels (ryanodine receptors - RyR) involved in control of calcium homeostasis in this worm. Here we briefly review the main technics (ATPase activity, binding with specific radioligands, fluxes of 45Ca2+ and whole worm contractions) and results obtained in order to compare the distribution patterns of these proteins: thapsigargin-sensitive (Ca2+-Mg2+)-ATPase activity and RyR co-purified in P1 and P4 fractions mainly, which is compatible with a sarcoplasmic reticulum localization, while basal ATPase (along with Na+,K+-ATPase) and thapsigargin-resistant (Ca2+-Mg2+)-ATPase have a distinct distribution, indicative of their plasma membrane localization. Finally we attempt to integrate these contributions with data from other groups in order to propose the first synoptic model for control of calcium homeostasis in S. mansoni.

Animals↗

PubMed2026

Progress on the telomere-telomerase system in planarian neoblasts homeostasis and regeneration.

Planarians are flatworms with remarkable regenerative abilities, and their adult pluripotent stem cells, known as neoblasts, serve as the foundation for this regeneration. Neoblasts can rapidly migrate, proliferate, and undergo directed differentiation following tissue injury to complete regeneration. Telomeres are located at the ends of eukaryotic chromosomes and play a core role in maintaining chromosomal integrity. With each cell division, telomeres shorten. Telomerase is a reverse transcriptase that compensates for telomere loss during cell division by extending telomeric repeats. The telomere-telomerase system is one of the important mechanisms for maintaining stem cell homeostasis. As adult pluripotent stem cells of planarians, neoblasts are required to maintain a dynamic balance between high-frequency cell division and multilineage differentiation. The maintenance of their long-term proliferative capacity and genomic stability may depend on the precise regulation of the telomere-telomerase system. Thus, this system represents a critical entry point for understanding the remarkable regenerative ability of planarians. Integrating recent progress in regeneration, neoblast regulation, and the telomere-telomerase system, we systematically summarize the emerging evidence for telomere- telomerase involvement in neoblast homeostasis and regeneration. We aim to provide insights for research in regenerative medicine, stem cell regulation, and neural injury repair.

Animals↗

PubMed1997

The calcium-sensing receptor: insights into extracellular calcium homeostasis in health and disease.

The cloning of the BoPCaR1 gene has helped to elucidate many aspects of normal extracellular calcium homeostasis, particularly as applied to the regulation of PTH secretion, calcitonin secretion and renal calcium reabsorption. In addition, loss and gain of function mutations have been found to cause the clinical syndromes of FBH, NSHPT and ADHH respectively. The CaR has also been implicated in the mechanisms leading to primary and uraemic hyperparathyroidism, and autoimmune parathyroid destruction. The recent demonstration that the CaR regulates non-selective cation channel function in rat hippocampal neurones suggests that it may also have a role within the central nervous system that is entirely unrelated to calcium homeostasis (Ye et al. 1996). Finally, the prospect of CaR agonists and antagonists, which may allow PTH secretion to be regulated independently of the serum calcium concentration, also holds much promise for the medical treatment of hyperparathyroidism, renal osteodystrophy and osteoporosis.

Calcium↗

PubMed1997

Improvement of glucose homeostasis and hepatic insulin resistance in ob/ob mice given oral molybdate.

Molybdate (Mo) exerts insulinomimetic effects in vitro. In this study, we evaluated whether Mo can improve glucose homeostasis in genetically obese, insulin-resistant ob/ob mice. Oral administration of Mo (174 mg/kg molybdenum element) for 7 weeks did not affect body weight, but decreased the hyperglycaemia (approximately 20 mM) of obese mice to the levels of lean (L) (+/+) mice, and reduced the hyperinsulinaemia to one-sixth of pretreatment levels. Tolerance to oral glucose was improved: total glucose area was 30% lower in Mo-treated mice than in untreated ob/ob mice (O), while the total insulin area was halved. Hepatic glucokinase (GK) mRNA level and activity were unchanged in O mice compared with L mice, but the mRNA level and activity of L-type pyruvate kinase (L-PK) were increased in O mice by 3.5- and 1.7-fold respectively. Mo treatment increased GK mRNA levels and activity (by approximately 2.2-fold and 61% compared with O values), and had no, or only a mild, effect on the already increased L-PK variables. mRNA levels and activity of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK) were augmented in O liver (sixfold and by 57% respectively), and these were reduced by Mo treatment. Insulin binding to partially purified receptors from liver was reduced in O mice and restored by Mo treatment. Despite this correction, overall receptor tyrosine kinase activity was not improved in Mo mice. Moreover, the overexpression (by two- to fourfold) of the cytokine tumour necrosis factor alpha (TNF alpha) in white adipose tissue, which may have a determinant role in the insulin resistance of the O mice, was unaffected by Mo. Likewise, overexpression of the ob gene in white adipose tissue was unchanged by Mo. In conclusion, Mo markedly improved glucose homeostasis in the ob/ob mice by an insulin-like action which appeared to be exerted distal to the insulin receptor tyrosine kinase step. The blood glucose-lowering effect of Mo was unrelated to over-expression of the TNF alpha and ob genes in O mice, but resulted at least in part from attenuation of liver insulin resistance by the reversal of pre-translational regulatory defects in these mice.

Adipose Tissue↗

PubMed2002

Adaptation to sustained high plasma vasopressin in water and electrolyte homeostasis in the rat transgenic for the metallothionein-vasopressin fusion gene.

Prolonged exposure of tissues to a receptor agonist often leads to adaptive changes that limit the subsequent responsiveness of the tissue to the same agonist. Recently, we have generated rats transgenic for the metallothionein I-human arginine vasopressin (AVP) fusion gene (Tg), which produced high plasma AVP with relatively preserved renal water excretion, suggesting that there might be adaptive mechanism(s) for maintaining water and electrolyte homeostasis against chronic AVP oversecretion from the earliest stage of life. In this study, to investigate whether down-regulation of AVP V2 receptor (V2R), which could possibly be caused by long-standing high plasma AVP, participates in this adaptive mechanism(s), non-peptidic V2R antagonist OPC31260 was administered to reverse the down-regulation, and water loading was performed after V2R antagonist treatment had been withdrawn. Additionally, to confirm the down-regulation, Northern blotting analysis for V2R mRNA was carried out. Tg rats showed slightly decreased urine volume and water intake with an equivalent plasma [Na(+)] level (Tg 140.4 +/- 0.6 mEq/l; control 139.3 +/- 0.6 mEq/l) under basal conditions. After water loading using a liquid diet containing zinc, which stimulates the promoter region in the transgene, the urine increase showed only limited suppression with a dramatically increased plasma AVP level and mild hyponatremia (135.8 +/- 1.8 mEq/l) in Tg rats. When diet containing OPC31260 had been provided for 4 days until the day before the start of water loading, antidiuresis and hyponatremia (125.4 +/- 1.mEq/l) were significantly potentiated. V2R mRNA expression in kidney was significantly less in Tg rats than in control rats under basal conditions, and this suppression was restored by OPC31260 treatment to levels comparable with those of control rats. These results suggest that long-standing high plasma AVP causes V2R down-regulation, and it may play an important role in the adaptive mechanism(s) for maintaining water and electrolyte homeostasis in chronically AVP-overexpressing rats.

Adaptation, Physiological↗

PubMed2002

Direct effects of ciliary neurotrophic factor on brown adipocytes: evidence for a role in peripheral regulation of energy homeostasis.

Ciliary neurotrophic factor (CNTF) plays an important role in regulating neuronal growth. Recently, central anorexigenic effects of this cytokine have been characterized. However, peripheral effects on tissues that actively contribute to the regulation of energy homeostasis have not been described. Here, we report direct potent and selective effects of CNTF on growth factor and metabolic signalling intermediates in mouse brown adipocytes. CNTF stimulates STAT3, MAP kinase, Akt, and p70 S6 kinase. We find that, next to mediating Akt and p70 S6 kinase activation, both phosphatidylinositol 3-kinase and protein kinase C are separately acting, main intermediates for inducing mitogen-activated protein (MAP) kinase activation. On a functional level, CNTF enhances beta3-adrenergic induction of uncoupling protein-1. Thus, these results demonstrate direct effects of CNTF on adipose tissue signalling and metabolism and suggest a novel role for this cytokine in the peripheral regulation of energy homeostasis.

Adipocytes↗

PubMedDate not supplied

Optimal use of fluids of varying formulations to minimise exercise-induced disturbances in homeostasis.

The rationale underlying the development of various formulations of beverages for consumption before, during, and/or after physical exercise is that such formulations should minimise some of the disturbances in physiological homeostasis that occur during exercise and thereby prevent injury and/or enhance performance. Exercise- and dehydration-induced increases in core temperature, body fluid osmolality, heart rate, losses of plasma and other body fluid volumes, and carbohydrate depletion are probably the most important homeostatic disturbances that can be ameliorated by fluid consumption. With the exception of athletes subject to hyponatraemia after consumption of ordinary water during prolonged activity, changes in electrolyte concentrations in the body fluids of most athletes do not justify the inclusion of electrolytes in fluid replacement beverages to be consumed during exercise. However, small amounts of sodium added to water does speed gastric emptying and fluid absorption from the intestine. Recent evidence suggests that a precompetition meal high in easily digested carbohydrates should be consumed not later than 5 to 6 hours before competition. There is little published research on the optimal composition of this meal. Water ingestion 30 to 60 minutes before exercise seems to be of benefit to temperature regulation and cardiovascular homeostasis if the exercise is of moderate intensity (50 to 65% VO2max), but probably has little effect at the higher intensities of athletic performance. There is no systematic evidence to support the inclusion of calcium or sodium chloride in drinks consumed an hour or 2 before exercise. Furthermore, if glucose solutions are fed 15 to 45 minutes before prolonged exercise, they will probably cause a fall in blood glucose during exercise and may adversely affect performance. These adverse effects are not present when fructose is consumed before exercise. Contrary to the adverse effects of glucose feedings 15 to 60 minutes before exercise, the consumption of 18 to 50% solutions of glucose or glucose polymers 5 minutes before prolonged exercise seems to have potential for improving endurance performance. Similarly, the inclusion of caffeine in beverages consumed 60 minutes before prolonged exercise improves athletic performance for many subjects. Others may be hypersensitive to the effects of caffeine and are adversely affected by its use. For exercise leading to exhaustion in less than 30 minutes, neither caffeine nor carbohydrate ingestion is effective in minimising homeostatic perturbations or improving exercise performance.(ABSTRACT TRUNCATED AT 400 WORDS)

Drinking↗