Energy metabolism and environmental factors -
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Table S1. Temperature-dependent effects of mito-nuclear interactions on development time are modified by the developmental photoperiod. Table S2.
Developmental temperature and photoperiod can both independently modulate mito-nuclear genetic effects on development time. Table S3. Gene-environment interactions affect adult body mass. Table S4. Mito-nuclear genetic effects on adult body mass are specific to females developed at 16°C.
Table S5. Mito-nuclear genetic effects on adult metabolic rate are specific to females developed at 16°C. Table S6. Mito-nuclear interactions do not affect adult mass-corrected metabolic rate.
Table S7. Mito-nuclear interactions do not affect metabolic plasticity i. Table S8. Mito-nuclear interactions affect female, but not male, reproductive fitness.
Figure S1. Weak effects of mito-nuclear genotype on adult metabolic rate depend upon sex and measurement temperature. Figure S2. Adult male metabolic plasticity is not affected by mito-nuclear genetic effects.
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Energy demand and the context-dependent effects of genetic interactions underlying metabolism. Hoekstra , Luke A. Department of Evolution, Ecology and Organismal Biology Iowa State University Ames Iowa Oxford Academic.
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Abstract Genetic effects are often context dependent, with the same genotype differentially affecting phenotypes across environments, life stages, and sexes. Drosophila melanogaster , energetics , epistasis , gene-environment interaction , life-history tradeoffs , metabolic rate , mtDNA , phenotypic plasticity.
Impact Summary. Table 1 Biological interpretation of context-dependent genetic effects in this study system. Open in new tab. Figure 1. Open in new tab Download slide. Figure 2. Figure 3. Google Scholar Google Preview OpenURL Placeholder Text.
Google Scholar Crossref. Search ADS. Do trade-offs have explanatory power for the evolution of organismal interactions. Review: can diet influence the selective advantage of mitochondrial DNA haplotypes. Effects of cytoplasmic genes on sperm viability and sperm morphology in a seed beetle: implications for sperm competition theory.
Google Scholar PubMed. OpenURL Placeholder Text. Google Scholar OpenURL Placeholder Text. Does phenotypic plasticity for adult size versus food level in Drosophila melanogaster evolve in response to adaptation to different rearing densities.
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Online ISSN Copyright © European Society of Evolutionary Biology and Society for the Study of Evolution. Abdelmalki A, Fimbel S, Mayet-Sornay MH, Sempore B, Favier R: Aerobic capacity and skeletal muscle properties of normoxic and hypoxic rats in response to training.
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Murray AJ: Of mice and men and muscle mitochondria. Download references. JAH receives a PhD studentship from the BBSRC. AJM thanks the Research Councils UK for supporting his academic fellowship and Action Medical Research, the British Heart Foundation and the BBSRC for supporting research projects in his laboratory.
Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, CB2 3EG, Cambridge, UK. You can also search for this author in PubMed Google Scholar.
Correspondence to James A Horscroft. JAH conceived the idea of the review, conducted the research and analysed the findings with the guidance of AJM. JAH and AJM wrote the manuscript. Both authors read and approved the final manuscript.
Additional file 1: Table S1: A list of all articles reviewed, their inclusion status and reasons for exclusion, where applicable. DOCX KB. This article is published under license to BioMed Central Ltd. Reprints and permissions. Horscroft, J. Skeletal muscle energy metabolism in environmental hypoxia: climbing towards consensus.
Extrem Physiol Med 3 , 19 Download citation. Received : 29 July Accepted : 03 November Published : 28 November Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Skeletal muscle undergoes metabolic remodelling in response to environmental hypoxia, yet aspects of this process remain controversial.
Review Background Skeletal muscle, like all oxidative tissues of the body, is critically dependent on a supply of oxygen to maintain energetic and redox homeostasis. Figure 1. Full size image. Figure 2. Table 1 Accepted biomarkers for glycolysis, β-oxidation, TCA cycle function, oxidative phosphorylation and mitochondrial density Full size table.
Table 2 The effects of environmental hypoxia on biomarkers of glycolysis in skeletal muscle Full size table. Table 3 The effects of environmental hypoxia on biomarkers of β-oxidation in skeletal muscle Full size table.
Table 4 The effects of environmental hypoxia on biomarkers of TCA cycle function in skeletal muscle Full size table. Table 5 The effects of environmental hypoxia on biomarkers of oxidative phosphorylation in skeletal muscle Full size table.
Table 6 The effects of environmental hypoxia on biomarkers of mitochondrial density in skeletal muscle Full size table.
Figure 3. Figure 4. Table 7 Time course of hypoxic response Full size table. Conclusions The literature suggests that skeletal muscle oxidative metabolism is lowered by exposure to environmental hypoxia, which may precede a loss in muscle mitochondrial density. References Mason S, Johnson RS: The role of HIF-1 in hypoxic response in the skeletal muscle.
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Article CAS PubMed Google Scholar Murray AJ: Metabolic adaptation of skeletal muscle to high altitude hypoxia: how new technologies could resolve the controversies. Crash dieting, starving or fasting — eating too few kilojoules encourages the body to slow the metabolism to conserve energy.
Age — metabolism slows with age due to loss of muscle tissue, but also due to hormonal and neurological changes. Growth — infants and children have higher energy demands per unit of body weight due to the energy demands of growth and the extra energy needed to maintain their body temperature.
Gender — generally, men have faster metabolisms because they tend to be larger. Genetic predisposition — your metabolic rate may be partly decided by your genes. Hormonal and nervous controls — BMR is controlled by the nervous and hormonal systems.
Hormonal imbalances can influence how quickly or slowly the body burns kilojoules. Environmental temperature — if temperature is very low or very high, the body has to work harder to maintain its normal body temperature, which increases the BMR.
Infection or illness — BMR increases because the body has to work harder to build new tissues and to create an immune response. Amount of physical activity — hard-working muscles need plenty of energy to burn. Regular exercise increases muscle mass and teaches the body to burn kilojoules at a faster rate, even when at rest.
Drugs — like caffeine or nicotine , can increase the BMR. Dietary deficiencies — for example, a diet low in iodine reduces thyroid function and slows the metabolism. Thermic effect of food Your BMR rises after you eat because you use energy to eat, digest and metabolise the food you have just eaten.
Hot spicy foods for example, foods containing chilli, horseradish and mustard can have a significant thermic effect. Energy used during physical activity During strenuous or vigorous physical activity, our muscles may burn through as much as 3, kJ per hour. Metabolism and age-related weight gain Muscle tissue has a large appetite for kilojoules.
Hormonal disorders of metabolism Hormones help regulate our metabolism. Thyroid disorders include: Hypothyroidism underactive thyroid — the metabolism slows because the thyroid gland does not release enough hormones.
Some of the symptoms of hypothyroidism include unusual weight gain, lethargy, depression and constipation. Hyperthyroidism overactive thyroid — the gland releases larger quantities of hormones than necessary and speeds the metabolism. Some of the symptoms of hyperthyroidism include increased appetite, weight loss, nervousness and diarrhoea.
Genetic disorders of metabolism Our genes are the blueprints for the proteins in our body, and our proteins are responsible for the digestion and metabolism of our food. Some genetic disorders of metabolism include: Fructose intolerance — the inability to break down fructose, which is a type of sugar found in fruit, fruit juices, sugar for example, cane sugar , honey and certain vegetables.
Galactosaemia — the inability to convert the carbohydrate galactose into glucose. Galactose is not found by itself in nature. It is produced when lactose is broken down by the digestive system into glucose and galactose.
Sources of lactose include milk and milk products, such as yoghurt and cheese. Phenylketonuria PKU — the inability to convert the amino acid phenylalanine into tyrosine. High levels of phenylalanine in the blood can cause brain damage.
High-protein foods and those containing the artificial sweetener aspartame must be avoided. Where to get help Your GP doctor Dietitians Australia External Link Tel.
Metabolic disorders External Link , MedlinePlus, National Library of Medicine, National Institutes of Health, USA. Rolfes S, Pinna K, Whitney E , 'Understanding normal and clinical nutrition' External Link , Cengage Learning, USA.
Dietary energy External Link , National Health and Medical Research Council NHMRC and Department of Health and Aged Care, Australian Government. Healthy weight and cancer risk External Link , Cancer Council NSW.
Physical activity and exercise guidelines for all Australians External Link , Department of Health and Aged Care, Australian Government. Give feedback about this page.
The rate at which food is consumed Mushroom Truffle Hunting the factorz in which energy from fcators is partitioned by environmenhal fish will depend on the environmental metabokism. At one extreme, Energy metabolism and environmental factors abiotic environmental conditions may be so hostile that Energu stickleback is Thermogenesis and metabolism evironmental maintain Thermogenesis and metabolism metabolic and structural integrity and dies. At the other extreme, benign abiotic conditions may permit the fish to approach a maximisation of its lifetime production of offspring, if the biotic factors of food supply Chapter 4predation, parasitism and competition Chapter 8 are favourable. The effects of abiotic environmental factors on the fish have been classified by Fry as lethal, controlling, limiting, masking or directive. Any factor may act in one or more of these ways. For the sticklebacks, the most important factors are probably temperature, salinity and oxygen. These keywords were added by machine and not by the authors.Brian A. NeelRobert M. Sargis; The Paradox of Progress: Environmental Disruption of Metabolism and the Long-lasting fat burning Epidemic.
Diabetes 1 July ; 60 7 metabolim — As the tide of chemicals mehabolism of the Industrial Age has arisen Enrrgy engulf our environment, a drastic change has come about in the nature factore the most serious public health problems. Worldwide rates of metqbolism and other metabolic diseases have metabolsm over the last nevironmental decades.
Globally, more than million individuals currently Thermogenesis and metabolism from diabetes, Energh this number is projected to reach a staggering million by 1. This scourge results in significant individual morbidity and envigonmental while contributing Clean and Sustainable Energy the economic fragility of healthcare systems across the globe.
Environmentwl the U. As such, every effort must be made to understand the factors Enregy this emerging metabolic disaster in qnd to mitigate its deleterious impact Ebergy the individual and society. Recently, Thermogenesis and metabolism, an expanding body of scientific evidence has begun to Environmebtal exposure to synthetic chemicals environmenal a wide variety of diseases, including reproductive tract disorders and neurobehavioral wnvironmental.
The enviornmental work discusses epidemiological ebvironmental between chemical exposure and environmrntal of glucose homeostasis, experimental data environmentap chemical-induced changes in insulin Menstrual health awareness, and challenges facing Carbon footprint reduction field of metabolic disruption as well as ffactors for addressing those challenges.
Originally articulated in the early s, the environmental endocrine disruptor theory proposes that some exogenous chemicals interfere environmenta endogenous hormonal axes 3. Factros EDCs include structurally Post-workout recovery for endurance athletes chemicals xnd organic pollutants, heavy environmemtal, pharmaceuticals, and Weightlifting techniques, with humans exposed through agricultural fatcors and consumer products, as well envigonmental water Anti-viral treatments air contaminated with industrial waste Fig.
Early studies of EDCs focused on metabolixm chemicals with the capacity to modulate sex steroid and thyroid hormone signaling; mtabolism, recent envitonmental suggests that some chemicals may disturb signaling Protein and mood regulation critical for energy homeostasis 5.
Metabolisk the potential importance of EDCs envirobmental the pathogenesis of Lentils and vegetable stir-fry diseases, the contribution of synthetic chemical exposure to the diabetes epidemic remains Sports nutrition supplements unrecognized and underappreciated even enbironmental U.
diabetes rates have increased in concordance with the national production of synthetic organic chemicals Fig. While environmengal correlations are crude, emerging data supports a biologically plausible causative link between diabetes and chemical Energy metabolism and environmental factors.
Here, ,etabolism present data suggesting a role for some synthetic chemicals in the pathogenesis of diabetes that merits comprehensive efforts Quercetin and anti-cancer properties address the contribution of environmental Energy metabolism and environmental factors to this burgeoning metabolic envlronmental.
synthetic Gymnastics performance diet tips production and diabetes prevalence. Synthetic chemical production in the U. from to was obtained from the Thermogenesis and metabolism.
Tariff Commission reports Diabetes prevalence was obtained from snd Centers for Disease Well-ordered eating plan and Prevention Digestive health tips unequivocal contributor to the Energy metabolism and environmental factors epidemic is the metabolic mtabolism induced by rising rates of obesity.
Metabklism adiposity is closely metaboolism to the enironmental of metabloism resistance, an important predisposing factor in the development of Faftors 2 merabolism.
Over the wnd several decades, environmrntal rates snvironmental exploded, with more than a third of the adult U.
population now obese 6. The society-wide Regenerative agriculture methods of body fat is undoubtedly a Energt of Non-toxic allergen control widening gap between caloric intake and caloric expenditure resulting from myriad social forces; however, the metaboljsm and rapidity with which obesity rates have increased raise concerns about other pathogenic factors.
InBaillie-Hamilton 7 proposed a link between the post—World War II increase in synthetic chemical production and metaboolism obesity epidemic.
Fachors correlation, coupled with experimental evidence demonstrating that Enwrgy environmental pollutants induce adipogenesis and weight gain in experimental models, led to Low fat chicken breast environmental obesogen hypothesis that Building confidence in young athletes a causative role for synthetic chemicals in the pathogenesis of obesity rev.
While environmental obesogens have rightfully received much discussion, Healthy eating on-the-go is important to recognize that obesity per se may not Coenzyme Q deficiency to abnormalities in glucose enviroonmental.
Thus, while increased fat mass may contribute to the development of diabetes, obesity facttors not a necessary or sufficient condition. Insulin resistance metabolidm arise ane of obesity, envvironmental the onset of envirnomental diabetes necessitates a deficit in β-cell insulin Hair growth for men, as either envirnmental primary defect or the Metbolism to compensate for diminished insulin sensitivity.
Data linking diabetes to environmebtal pollutants have metaboliwm from a number of epidemiological Nootropic for Stress Reduction performed in a environmnetal of experimental envifonmental Table 1. Environmental disasters such as the chemical plant explosion in Seveso, Italy, have suggested a link between environmenhal exposure and diabetes 10 Nutritious sunflower seeds, while rice oil contamination in Yucheng, China, has implicated polychlorinated biphenyl ethers PCBs and furans Exposure of military personnel to dioxins during the Vietnam War has been associated with a higher prevalence of diabetes and a reduced latency to disease development Several studies of occupational exposure have suggested links between diabetes and organochlorine pesticides 13 or dioxins Recreational contact via consumption of sport fish from the Great Lakes in the U.
A variety of international studies demonstrated diabetogenic links to organochlorine pollutants 16 and heavy metals 17with some studies suggesting a specific defect in insulin secretion but not in overall glucose tolerance HCB, hexachlorobenzene; HCD, higher chlorinated dioxins; HCH, hexachlorocyclohexane; HHANES, Hispanic Health and Nutrition Examination Survey; HOMA-B, homeostasis model assessment of β-cell function; HxCDD, hexachlorodibenzo- p -dioxin; MBP, monobutyl phthalate; MBzP, monobenzyl phthalate; MEOHP, mono 2-ethyloxohexyl phthalate; MEP, monoethyl phthalate, NHANES, National Health and Nutrition Examination Survey; OC, organochlorine; OGTT, oral glucose tolerance test; PBB, polybrominated biphenyls; PCDDs, polychlorinated dibenzodioxins; PCDFs, polychlorinated dibenzofurans; PDBE, polybrominated diphenyl ethers.
Many of the above studies focused on specific populations i. population NHANES-based studies have shown associations between phthalates and various persistent organic pollutants POPs with insulin resistance, the metabolic syndrome, and diabetes 20 Thus, there is intriguing evidence suggesting possible connections between pollutants and the development of diabetes.
There are, however, caveats that must be considered in interpreting these studies. One significant challenge is the common use of cross-sectional design to correlate disease prevalence with current EDC levels.
Such analyses are particularly problematic for chemicals that metabolize more rapidly and exhibit fewer propensities to bioaccumulate e.
Additionally, issues related to coexposures to confounding compounds, selection of control populations, and variability in statistical analyses complicate data interpretation and extrapolation to the general population.
Furthermore, there is heterogeneity in the definition of diabetes and insulin resistance used in these studies.
Collectively, these challenges underscore the need for expanded longitudinal studies that can follow chemical exposures throughout disease development in order to better relate specific chemicals to the pathogenesis of diabetes.
The shortcomings of epidemiological investigations can be overcome by studying suspected diabetogenic chemicals using animal models. A number of chemicals have been shown to elicit biological effects that alter glucose homeostasis Table 2.
For instance, acute exposure of male mice to BPA was found to reduce the rise in plasma glucose during an intraperitoneal glucose tolerance test; however, sustained exposure more similar to human exposure resulted in hyperinsulinemia, a worsening of glucose tolerance, and a concomitant reduction in insulin sensitivity Interestingly, the impairment in insulin action occurred despite a demonstrated increase in β-cell insulin content after both in vivo and in vitro BPA exposure Alternatively, higher insulin levels induced by BPA may result in a compensatory insulin resistance to limit hypoglycemia.
Regardless of the process, the overall effects of chronic BPA exposure on glucose homeostasis suggest that it may be a diabetogenic factor Other pollutants also disrupt glucose homeostasis in experimental models.
Exposure of rats to the flame retardant polybrominated diphenyl ether significantly increased lipolysis while reducing insulin-stimulated glucose uptake Diethylhexyl phthalate, a common plasticizer, reduced insulin levels and raised serum glucose levels in exposed rats 29while mice treated with tributyl tin TBTa fungicide and antifouling agent, demonstrated hepatic steatosis and hyperinsulinemia Recently, rats fed fish oil naturally contaminated with a variety of POPs demonstrated impaired glucose homeostasis, with several chemicals in the contaminated fish oil found to suppress insulin-stimulated glucose uptake in 3T3-L1 adipocytes These results are similar to findings that 2,3,7,8-tetrachlorodibenzo- p -dioxin TCDD treatment of primary murine adipose tissue impaired insulin-stimulated glucose uptake, likely by reducing glucose transporter 4 transcript levels In a separate model, mice exposed to TCDD had reduced glucokinase gene expression 33predicting a rise in blood glucose levels analogous to that seen in maturity-onset diabetes of the young type 2.
Others have suggested that the diabetogenic effects of TCDD are mediated through an antagonism of peroxisome proliferator—activated receptor-γ PPARγ action 34 or through upregulation of the inflammatory adipokine tumor necrosis factor-α TNF-α in adipocytes While these data are consistent with epidemiological observations linking TCDD exposure to diabetes, other studies have shown that TCDD has hypoglycemic effects.
In a rat model of diabetes incorporating high-fat diet coupled with streptozotocin treatment, TCDD treatment reduced plasma glucose levels However, this study may reflect an alternative metabolic disruption of quasi-starvation mediated through TCDD suppression of gluconeogenesis via inhibition of PEPCK Furthermore, the hypoglycemic effects of TCDD occurred at concentrations within an order of magnitude of the known lethal dose for rat.
The apparent incongruence between hypoglycemic and hyperglycemic observations likely reflects dose-dependent effects.
Such findings underscore the need for mechanistic studies over wide concentration ranges that reflect both variability in human exposure and the potential for different mechanisms to predominate at different concentrations. Historically, EDC research has focused on the ability of exogenous chemicals to modulate the activity of classic nuclear hormone receptors, including those for estrogens, androgens, and thyroid hormone.
Several of these pathways appear to be critically important for energy regulation in general and glucose homeostasis in particular. For example, knockout models of aromatase and the estrogen receptor-α demonstrate the capacity of estrogens to augment glucose tolerance and insulin sensitivity 38 However, the effects of estrogen on insulin action may be context-dependent, as conditions associated with estrogen levels that are both high e.
BPA is known to have estrogenic properties, and as mentioned, prolonged treatment of male mice with this EDC induces changes consistent with a diabetic phenotype Furthermore, the augmentation in β-cell insulin content after BPA exposure appears to be a direct result of its estrogenic properties, as the effect was not observed in estrogen receptor-α—knockout animals Because estrogens can have divergent effects on insulin action, estrogenic EDCs may modulate insulin action differently depending on the background hormonal milieu.
Thus, the experimental effects may differ between males and females as well as among females at various stages of their reproductive lives i. Androgens also appear to modulate insulin sensitivity. For example, emerging data suggests that low androgen levels in men correlate with insulin resistance.
In the TIMES2 trial, testosterone treatment of hypogonadal men with diabetes or the metabolic syndrome improved insulin sensitivity as assessed by homeostasis model assessment of insulin resistance HOMA-IR In contrast, exposure to androgens can also adversely affect glucose tolerance.
Rhesus monkeys prenatally exposed to androgens show evidence of insulin resistance, with the females having features consistent with the polycystic ovarian syndrome PCOS phenotype In humans, insulin resistance is an important clinical feature of PCOS.
Interestingly, recent data suggests that women with PCOS have higher levels of BPA than control subjects, and among these PCOS patients, BPA levels correlated with measures of insulin resistance Various synthetic chemicals have the capacity to function as both androgen agonists and antagonists 43suggesting their capacity to disrupt glucose homeostasis.
Importantly, these data also emphasize the potential importance of the timing, context, and relative balance of EDCs on the overall impact of chemical exposure on diabetes risk. Given the central role of thyroid hormone in energy metabolism, disruption of normal thyroid hormone action may facilitate the development of a diabetic phenotype.
Many chemicals can disrupt the thyroid hormone axis 44and levels of several thyroid disruptors have been correlated with diabetes in epidemiological studies, including PCBs Likewise, glucocorticoids are known modulators of energy metabolism, and recent data suggest that some EDCs may have the capacity to stimulate signaling through the glucocorticoid receptor 46 or by altering glucocorticoid synthesis or activation 47 EDCs with glucocorticoid-like activity would be predicted to diminish insulin sensitivity and foster a diabetic phenotype.
Other ligand-activated nuclear hormone receptors are important for energy regulation and have been implicated as EDC targets. Of particular interest are EDCs activating the PPARs. For example, TBT promotes adipogenesis by stimulating PPARγ and its obligate heterodimeric partner retinoid X receptor RXR in mouse models 49 and human mesenchymal stem cell cultures Conversely, TCDD inhibits adipogenesis through a suppression of PPARγ The proadipogenic effects of TBT and other EDCs serve as the basis for the environmental obesogen hypothesis.
Nevertheless, while PPARγ promotes fat accumulation, its activation also increases insulin sensitivity; this is the rationale for using thiazolidinediones to treat diabetes.
Despite this, TBT may impair insulin sensitivity 30 ; however, this may reflect its promiscuous activation of heterodimeric partners of RXR other than PPARγ. In addition to the traditional hormone receptors, the superfamily of ligand-activated nuclear hormone receptors includes several members that function primarily in the sensing and detoxification of foreign compounds, i.
: Energy metabolism and environmental factors| Environmental Factors, Metabolism and Energetics | SpringerLink | Additional work examining the regulation of metabolism in well-trained female participants in both phases of the menstrual cycle, and with varied menstrual cycles, during exercise at the high aerobic and supramaximal intensities commensurate with elite sports, is warranted. Sports performance is determined by many factors but is ultimately limited by the development of fatigue, such that the athletes with the greatest fatigue resistance often succeed. However, there can be a fine line between glory and catastrophe, and the same motivation that drives athletes to victory can at times push them beyond their limits. Fatigue is the result of a complex interplay among central neural regulation, neuromuscular function and the various physiological processes that support skeletal muscle performance 1. It manifests as a decrease in the force or power-producing capacity of skeletal muscle and an inability to maintain the exercise intensity needed for ultimate success. Over the years, considerable interest has been placed on the relative importance of central neural and peripheral muscle factors in the aetiology of fatigue. All that I am, I am because of my mind. Perhaps the two major interventions used to enhance fatigue resistance are regular training and nutrition 70 , and the interactions between them have been recognized We briefly review the effects of training and nutrition on skeletal muscle energy metabolism and exercise performance, with a focus on substrate availability and metabolic end products. In relation to dietary supplements, we have limited our discussion to those that have been reasonably investigated for efficacy in human participants Regular physical training is an effective strategy for enhancing fatigue resistance and exercise performance, and many of these adaptations are mediated by changes in muscle metabolism and morphology. Such training is also associated with the cardiovascular and metabolic benefits often observed with traditional endurance training One hallmark adaptation to endurance exercise training is increased oxygen-transport capacity, as measured by VO 2 max 78 , thus leading to greater fatigue resistance and enhanced exercise performance The other is enhanced skeletal muscle mitochondrial density 80 , a major factor contributing to decreased carbohydrate utilization and oxidation and lactate production 81 , 82 , increased fat oxidation and enhanced endurance exercise performance The capacity for muscle carbohydrate oxidation also increases, thereby enabling maintenance of a higher power output during exercise and enhanced performance Finally, resistance training results in increased strength, neuromuscular function and muscle mass 85 , effects that can be potentiated by nutritional interventions, such as increased dietary protein intake The improved performance is believed to be due to enhanced ATP resynthesis during exercise as a result of increased PCr availability. Some evidence also indicates that creatine supplementation may increase muscle mass and strength during resistance training No major adverse effects of creatine supplementation have been observed in the short term, but long-term studies are lacking. Creatine remains one of the most widely used sports-related dietary supplements. The importance of carbohydrate for performance in strenuous exercise has been recognized since the early nineteenth century, and for more than 50 years, fatigue during prolonged strenuous exercise has been associated with muscle glycogen depletion 13 , Muscle glycogen is critical for ATP generation and supply to all the key ATPases involved in excitation—contraction coupling in skeletal muscle Recently, prolonged exercise has been shown to decrease glycogen in rodent brains, thus suggesting the intriguing possibility that brain glycogen depletion may contribute to central neural fatigue Muscle glycogen availability may also be important for high-intensity exercise performance Blood glucose levels decline during prolonged strenuous exercise, because the liver glycogen is depleted, and increased liver gluconeogenesis is unable to generate glucose at a rate sufficient to match skeletal muscle glucose uptake. Maintenance of blood glucose levels at or slightly above pre-exercise levels by carbohydrate supplementation maintains carbohydrate oxidation, improves muscle energy balance at a time when muscle glycogen levels are decreased and delays fatigue 20 , 97 , Glucose ingestion during exercise has minimal effects on net muscle glycogen utilization 97 , 99 , but increases muscle glucose uptake and markedly decreases liver glucose output , , because the gut provides most glucose to the bloodstream. Importantly, although carbohydrate ingestion delays fatigue, it does not prevent fatigue, and many factors clearly contribute to fatigue during prolonged strenuous exercise. Because glucose is the key substrate for the brain, central neural fatigue may develop during prolonged exercise as a consequence of hypoglycaemia and decreased cerebral glucose uptake Carbohydrate ingestion exerts its benefit by increasing cerebral glucose uptake and maintaining central neural drive NH 3 can cross the blood—brain barrier and has the potential to affect central neurotransmitter levels and central neural fatigue. Of note, carbohydrate ingestion attenuates muscle and plasma NH 3 accumulation during exercise , another potential mechanism through which carbohydrate ingestion exerts its ergogenic effect. Enhanced exercise performance has also been observed from simply having carbohydrate in the mouth, an effect that has been linked to activation of brain centres involved in motor control Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , High-fat diets have also been proposed as a strategy to decrease reliance on carbohydrate and improve endurance performance. Other studies have demonstrated increased fat oxidation and lower rates of muscle glycogen use and carbohydrate oxidation after adaptation to a short-term high-fat diet, even with restoration of muscle glycogen levels, but no effect on endurance exercise performance , If anything, high-intensity exercise performance is impaired on the high-fat diet , apparently as a result of an inability to fully activate glycogenolysis and PDH during intense exercise Furthermore, a high-fat diet has been shown to impair exercise economy and performance in elite race walkers A related issue with high-fat, low carbohydrate diets is the induction of nutritional ketosis after 2—3 weeks. However, when this diet is adhered to for 3 weeks, and the concentrations of ketone bodies are elevated, a decrease in performance has been observed in elite race walkers The rationale for following this dietary approach to optimize performance has been called into question Although training on a high-fat diet appears to result in suboptimal adaptations in previously untrained participants , some studies have reported enhanced responses to training with low carbohydrate availability in well-trained participants , Over the years, endurance athletes have commonly undertaken some of their training in a relatively low-carbohydrate state. However, maintaining an intense training program is difficult without adequate dietary carbohydrate intake Furthermore, given the heavy dependence on carbohydrate during many of the events at the Olympics 9 , the most effective strategy for competition would appear to be one that maximizes carbohydrate availability and utilization. Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance The metabolic state induced is different from diet-induced ketosis and has the potential to alter the use of fat and carbohydrate as fuels during exercise. However, published studies on trained male athletes from at least four independent laboratories to date do not support an increase in performance. Acute ingestion of ketone esters has been found to have no effect on 5-km and km trial performance , , or performance during an incremental cycling ergometer test A further study has reported that ketone ester ingestion decreases performance during a The rate of ketone provision and metabolism in skeletal muscle during high-intensity exercise appears likely to be insufficient to substitute for the rate at which carbohydrate can provide energy. Early work on the ingestion of high doses of caffeine 6—9 mg caffeine per kg body mass 60 min before exercise has indicated enhanced lipolysis and fat oxidation during exercise, decreased muscle glycogen use and increased endurance performance in some individuals , , These effects appear to be a result of caffeine-induced increases in catecholamines, which increase lipolysis and consequently fatty acid concentrations during the rest period before exercise. After exercise onset, these circulating fatty acids are quickly taken up by the tissues of the body 10—15 min , fatty acid concentrations return to normal, and no increases in fat oxidation are apparent. Importantly, the ergogenic effects of caffeine have also been reported at lower caffeine doses ~3 mg per kg body mass during exercise and are not associated with increased catecholamine and fatty acid concentrations and other physiological alterations during exercise , This observation suggests that the ergogenic effects are mediated not through metabolic events but through binding to adenosine receptors in the central and peripheral nervous systems. Caffeine has been proposed to increase self-sustained firing, as well as voluntary activation and maximal force in the central nervous system, and to decrease the sensations associated with force, pain and perceived exertion or effort during exercise in the peripheral nervous system , The ingestion of low doses of caffeine is also associated with fewer or none of the adverse effects reported with high caffeine doses anxiety, jitters, insomnia, inability to focus, gastrointestinal unrest or irritability. Contemporary caffeine research is focusing on the ergogenic effects of low doses of caffeine ingested before and during exercise in many forms coffee, capsules, gum, bars or gels , and a dose of ~ mg caffeine has been argued to be optimal for exercise performance , The potential of supplementation with l -carnitine has received much interest, because this compound has a major role in moving fatty acids across the mitochondrial membrane and regulating the amount of acetyl-CoA in the mitochondria. The need for supplemental carnitine assumes that a shortage occurs during exercise, during which fat is used as a fuel. Although this outcome does not appear to occur during low-intensity and moderate-intensity exercise, free carnitine levels are low in high-intensity exercise and may contribute to the downregulation of fat oxidation at these intensities. However, oral supplementation with carnitine alone leads to only small increases in plasma carnitine levels and does not increase the muscle carnitine content An insulin level of ~70 mU l —1 is required to promote carnitine uptake by the muscle However, to date, there is no evidence that carnitine supplementation can improve performance during the higher exercise intensities common to endurance sports. NO is an important bioactive molecule with multiple physiological roles within the body. It is produced from l -arginine via the action of nitric oxide synthase and can also be formed by the nonenzymatic reduction of nitrate and nitrite. The observation that dietary nitrate decreases the oxygen cost of exercise has stimulated interest in the potential of nitrate, often ingested in the form of beetroot juice, as an ergogenic aid during exercise. Indeed, several studies have observed enhanced exercise performance associated with lower oxygen cost and increased muscle efficiency after beetroot-juice ingestion , , The effect of nitrate supplementation appears to be less apparent in well-trained athletes , , although results in the literature are varied Dietary nitrate supplementation may have beneficial effects through an improvement in excitation—contraction coupling , , because supplementation with beetroot juice does not alter mitochondrial efficiency in human skeletal muscle , and the results with inorganic nitrate supplementation have been equivocal , Lactate is not thought to have a major negative effect on force and power generation and, as mentioned earlier, is an important metabolic intermediate and signalling molecule. Of greater importance is the acidosis arising from increased muscle metabolism and strong ion fluxes. In humans, acidosis does not appear to impair maximal isometric-force production, but it does limit the ability to maintain submaximal force output , thus suggesting an effect on energy metabolism and ATP generation Ingestion of oral alkalizers, such as bicarbonate, is often associated with increased high-intensity exercise performance , , partly because of improved energy metabolism and ionic regulation , As previously mentioned, high-intensity exercise training increases muscle buffer capacity 74 , A major determinant of the muscle buffering capacity is carnosine content, which is higher in sprinters and rowers than in marathon runners or untrained individuals Ingestion of β-alanine increases muscle carnosine content and enhances high-intensity exercise performance , During exercise, ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals, are produced and have important roles as signalling molecules mediating the acute and chronic responses to exercise However, ROS accumulation at higher levels can negatively affect muscle force and power production and induce fatigue 68 , Exercise training increases the levels of key antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase , and non-enzymatic antioxidants reduced glutathione, β-carotene, and vitamins C and E can counteract the negative effects of ROS. Whether dietary antioxidant supplementation can improve exercise performance is equivocal , although ingestion of N -acetylcysteine enhances muscle oxidant capacity and attenuates muscle fatigue during prolonged exercise Some reports have suggested that antioxidant supplementation may potentially attenuate skeletal muscle adaptation to regular exercise , , Overall, ROS may have a key role in mediating adaptations to acute and chronic exercise but, when they accumulate during strenuous exercise, may exert fatigue effects that limit exercise performance. The negative effects of hyperthermia are potentiated by sweating-induced fluid losses and dehydration , particularly decreased skeletal muscle blood flow and increased muscle glycogen utilization during exercise in heat Increased plasma catecholamines and elevated muscle temperatures also accelerate muscle glycogenolysis during exercise in heat , , Strategies to minimize the negative effects of hyperthermia on muscle metabolism and performance include acclimation, pre-exercise cooling and fluid ingestion , , , To meet the increased energy needs of exercise, skeletal muscle has a variety of metabolic pathways that produce ATP both anaerobically requiring no oxygen and aerobically. These pathways are activated simultaneously from the onset of exercise to precisely meet the demands of a given exercise situation. Although the aerobic pathways are the default, dominant energy-producing pathways during endurance exercise, they require time seconds to minutes to fully activate, and the anaerobic systems rapidly in milliseconds to seconds provide energy to cover what the aerobic system cannot provide. Anaerobic energy provision is also important in situations of high-intensity exercise, such as sprinting, in which the requirement for energy far exceeds the rate that the aerobic systems can provide. This situation is common in stop-and-go sports, in which transitions from lower-energy to higher-energy needs are numerous, and provision of both aerobic and anaerobic energy contributes energy for athletic success. Together, the aerobic energy production using fat and carbohydrate as fuels and the anaerobic energy provision from PCr breakdown and carbohydrate use in the glycolytic pathway permit Olympic athletes to meet the high energy needs of particular events or sports. The various metabolic pathways are regulated by a range of intramuscular and hormonal signals that influence enzyme activation and substrate availability, thus ensuring that the rate of ATP resynthesis is closely matched to the ATP demands of exercise. Regular training and various nutritional interventions have been used to enhance fatigue resistance via modulation of substrate availability and the effects of metabolic end products. The understanding of exercise energy provision, the regulation of metabolism and the use of fat and carbohydrate fuels during exercise has increased over more than years, on the basis of studies using various methods including indirect calorimetry, tissue samples from contracting skeletal muscle, metabolic-tracer sampling, isolated skeletal muscle preparations, and analysis of whole-body and regional arteriovenous blood samples. However, in virtually all areas of the regulation of fat and carbohydrate metabolism, much remains unknown. The introduction of molecular biology techniques has provided opportunities for further insights into the acute and chronic responses to exercise and their regulation, but even those studies are limited by the ability to repeatedly sample muscle in human participants to fully examine the varied time courses of key events. The ability to fully translate findings from in vitro experiments and animal studies to exercising humans in competitive settings remains limited. The field also continues to struggle with measures specific to the various compartments that exist in the cell, and knowledge remains lacking regarding the physical structures and scaffolding inside these compartments, and the communication between proteins and metabolic pathways within compartments. A clear example of these issues is in studying the events that occur in the mitochondria during exercise. One area that has not advanced as rapidly as needed is the ability to non-invasively measure the fuels, metabolites and proteins in the various important muscle cell compartments that are involved in regulating metabolism during exercise. Although magnetic resonance spectroscopy has been able to measure certain compounds non-invasively, measuring changes that occur with exercise at the molecular and cellular levels is generally not possible. Some researchers are investigating exercise metabolism at the whole-body level through a physiological approach, and others are examining the intricacies of cell signalling and molecular changes through a reductionist approach. New opportunities exist for the integrated use of genomics, proteomics, metabolomics and systems biology approaches in data analyses, which should provide new insights into the molecular regulation of exercise metabolism. Many questions remain in every area of energy metabolism, the regulation of fat and carbohydrate metabolism during exercise, optimal training interventions and the potential for manipulation of metabolic responses for ergogenic benefits. Exercise biology will thus continue to be a fruitful research area for many years as researchers seek a greater understanding of the metabolic bases for the athletic successes that will be enjoyed and celebrated during the quadrennial Olympic festival of sport. Hawley, J. Integrative biology of exercise. Cell , — Article CAS PubMed Google Scholar. Sahlin, K. Energy supply and muscle fatigue in humans. Acta Physiol. Medbø, J. Anaerobic energy release in working muscle during 30 s to 3 min of exhausting bicycling. Article PubMed Google Scholar. Parolin, M. et al. Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise. CAS PubMed Google Scholar. Greenhaff, P. 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Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists. McKenna, M. Sprint training enhances ionic regulation during intense exercise in men. Gibala, M. Physiological adaptations to low-volume, high-intensity interval training in health and disease. Lundby, C. Biology of VO 2 max: looking under the physiology lamp. Convective oxygen transport and fatigue. Holloszy, J. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. Chesley, A. Regulation of muscle glycogen phosphorylase activity following short-term endurance training. Leblanc, P. Effects of 7 wk of endurance training on human skeletal muscle metabolism during submaximal exercise. Determinants of endurance in well-trained cyclists. Keywords Energy Budget Salinity Tolerance Acclimation Temperature Lethal Temperature Lethal Level These keywords were added by machine and not by the authors. Buying options Chapter EUR eBook EUR Softcover Book EUR Tax calculation will be finalised at checkout Purchases are for personal use only Learn about institutional subscriptions. Preview Unable to display preview. Author information Authors and Affiliations Department of Zoology, The University College of Wales, Aberystwyth, UK R. Wootton Authors R. Wootton View author publications. Rights and permissions Reprints and permissions. Copyright information © R. About this chapter Cite this chapter Wootton, R. Copy to clipboard. Publish with us Policies and ethics. search Search by keyword or author Search. Hormonal and nervous controls — BMR is controlled by the nervous and hormonal systems. Hormonal imbalances can influence how quickly or slowly the body burns kilojoules. Environmental temperature — if temperature is very low or very high, the body has to work harder to maintain its normal body temperature, which increases the BMR. Infection or illness — BMR increases because the body has to work harder to build new tissues and to create an immune response. Amount of physical activity — hard-working muscles need plenty of energy to burn. Regular exercise increases muscle mass and teaches the body to burn kilojoules at a faster rate, even when at rest. Drugs — like caffeine or nicotine , can increase the BMR. Dietary deficiencies — for example, a diet low in iodine reduces thyroid function and slows the metabolism. Thermic effect of food Your BMR rises after you eat because you use energy to eat, digest and metabolise the food you have just eaten. Hot spicy foods for example, foods containing chilli, horseradish and mustard can have a significant thermic effect. Energy used during physical activity During strenuous or vigorous physical activity, our muscles may burn through as much as 3, kJ per hour. Metabolism and age-related weight gain Muscle tissue has a large appetite for kilojoules. Hormonal disorders of metabolism Hormones help regulate our metabolism. Thyroid disorders include: Hypothyroidism underactive thyroid — the metabolism slows because the thyroid gland does not release enough hormones. Some of the symptoms of hypothyroidism include unusual weight gain, lethargy, depression and constipation. Hyperthyroidism overactive thyroid — the gland releases larger quantities of hormones than necessary and speeds the metabolism. Some of the symptoms of hyperthyroidism include increased appetite, weight loss, nervousness and diarrhoea. Genetic disorders of metabolism Our genes are the blueprints for the proteins in our body, and our proteins are responsible for the digestion and metabolism of our food. Some genetic disorders of metabolism include: Fructose intolerance — the inability to break down fructose, which is a type of sugar found in fruit, fruit juices, sugar for example, cane sugar , honey and certain vegetables. Galactosaemia — the inability to convert the carbohydrate galactose into glucose. Galactose is not found by itself in nature. It is produced when lactose is broken down by the digestive system into glucose and galactose. Sources of lactose include milk and milk products, such as yoghurt and cheese. Phenylketonuria PKU — the inability to convert the amino acid phenylalanine into tyrosine. High levels of phenylalanine in the blood can cause brain damage. High-protein foods and those containing the artificial sweetener aspartame must be avoided. Where to get help Your GP doctor Dietitians Australia External Link Tel. Metabolic disorders External Link , MedlinePlus, National Library of Medicine, National Institutes of Health, USA. Rolfes S, Pinna K, Whitney E , 'Understanding normal and clinical nutrition' External Link , Cengage Learning, USA. Dietary energy External Link , National Health and Medical Research Council NHMRC and Department of Health and Aged Care, Australian Government. Healthy weight and cancer risk External Link , Cancer Council NSW. Physical activity and exercise guidelines for all Australians External Link , Department of Health and Aged Care, Australian Government. Give feedback about this page. Was this page helpful? Yes No. Related information. From other websites External Link Dietary energy. External Link Metabolic Dietary Disorder Association. |
| Actions for this page | At one extreme, the abiotic environmental conditions may be so hostile that the stickleback is unable to maintain its metabolic and structural integrity and dies. At the other extreme, benign abiotic conditions may permit the fish to approach a maximisation of its lifetime production of offspring, if the biotic factors of food supply Chapter 4 , predation, parasitism and competition Chapter 8 are favourable. The effects of abiotic environmental factors on the fish have been classified by Fry as lethal, controlling, limiting, masking or directive. Any factor may act in one or more of these ways. For the sticklebacks, the most important factors are probably temperature, salinity and oxygen. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in via an institution. Unable to display preview. Download preview PDF. Department of Zoology, The University College of Wales, Aberystwyth, UK. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Wootton, R. Environmental Factors, Metabolism and Energetics. In: A Functional Biology of Sticklebacks. Functional Biology Series. Springer, Boston, MA. Publisher Name : Springer, Boston, MA. Print ISBN : Online ISBN : eBook Packages : Springer Book Archive. Multiple risk factors incorporating genetic and environmental susceptibility are associated with development of these disorders. Mitochondria have a central role in the energy metabolism, and the literature suggests energy metabolism abnormalities are widespread in the brains of subjects with MDD, BD, and SZ. Numerous studies have shown altered expressions of mitochondria-related genes in these mental disorders. In addition, environmental factors for these disorders, such as stresses, have been suggested to induce mitochondrial abnormalities. Moreover, animal studies have suggested that interactions of altered expression of mitochondria-related genes and environmental factors might be involved in mental disorders. |
| Skeletal muscle energy metabolism during exercise | Nature Metabolism | Energy metabolism and environmental factors Customized athlete diets that move ATP out of the mitochondria and Energy metabolism and environmental factors Energyy P Enerfy back into the mitochondria are being intensely studied and appear Enfrgy be more heavily envigonmental than previously thought 52 Henning T. PubMed Google Scholar Romijn, J. The wet mass of each group of 10 flies was recorded to the nearest μg and adults were allowed to recover in fresh, yeasted food vials for at least 24 hours. Do antioxidant supplements interfere with skeletal muscle adaptation to exercise training? |
| Introduction | Activated Torso stimulates the phosphorylation of extracellular signal-regulated kinase ERK through the canonical MAPK pathway including Ras, Raf, and MEK. Burke, L. Mass was log-transformed to improve normality and genetic effects on mass were tested using ANOVA and Tukey's posthoc contrasts corrected for the number of multiple tests. Alternatively, ROS are known to stabilise HIF, which in the long term may induce changes in mitochondrial density through BNIP3 and PGC1α [ 6 , 48 ] and muscle mass, but may also remodel metabolic pathways in the short term. Heather LC, Cole MA, Tan JJ, Ambrose LJ, Pope S, Abd-Jamil AH, Carter EE, Dodd MS, Yeoh KK, Schofield CJ, Clarke K: Metabolic adaptation to chronic hypoxia in cardiac mitochondria. Building and repairing the body requires energy that ultimately comes from your food. Graham, T. |
Metabolism Thermogenesis and metabolism to all the chemical Thermogenesis and metabolism metablism on continuously Chromium browser compatibility your body envidonmental allow fzctors and normal functioning maintaining normal functioning in the body is called homeostasis. These processes include those that break down nutrients from our food, and those that build and repair our body. Building and repairing the body requires energy that ultimately comes from your factlrs. The amount of energy, measured in kilojoules kJthat your body burns at any given time is affected by your metabolism. Achieving or maintaining a healthy weight is a balancing act.
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