Three Metabolic Energy Systems
Personal Training 101
How You Get Energy & How You Use It
We usually talk of energy in general terms, as in �I don�t have a lot of energy today� or �You can feel the energy in the room.� But what really is energy? Where do we get the energy to move? How do we use it? How do we get more of it? Ultimately, what controls our movements? The three metabolic energy pathways are the�phosphagen system, glycolysis�and the�aerobic system.�How do they work, and what is their effect?
Albert Einstein, in his infinite wisdom, discovered that the total energy of an object is equal to the mass of the object multiplied by the square of the speed of light. His formula for atomic energy, E = mc2, has become the most recognized mathematical formula in the world. According to his equation, any change in the energy of an object causes a change in the mass of that object. The change in energy can come in many forms, including mechanical, thermal, electromagnetic, chemical, electrical or nuclear. Energy is all around us. The lights in your home, a microwave, a telephone, the sun; all transmit energy. Even though the solar energy that heats the earth is quite different from the energy used to run up a hill, energy, as the first law of thermodynamics tells us, can be neither created nor destroyed. It is simply changed from one form to another.
ATP Re-Synthesis
The energy for all physical activity comes from the conversion of high-energy phosphates (adenosine�triphosphate�ATP) to lower-energy phosphates (adenosine�diphosphate�ADP; adenosine�monophosphate�AMP; and inorganic phosphate, Pi). During this breakdown (hydrolysis) of ATP, which is a water-requiring process, a proton, energy and heat are produced: ATP + H2O ���ADP + Pi�+ H+�+ energy + heat. Since our muscles don�t store much ATP, we must constantly resynthesize it. The hydrolysis and resynthesis of ATP is thus a circular process�ATP is hydrolyzed into ADP and Pi, and then ADP and Pi�combine to resynthesize ATP. Alternatively, two ADP molecules can combine to produce ATP and AMP: ADP + ADP ���ATP + AMP.
Like many other animals, humans produce ATP through three metabolic pathways that consist of many enzyme-catalyzed chemical reactions: the phosphagen system, glycolysis and the aerobic system. Which pathway your clients use for the primary production of ATP depends on how quickly they need it and how much of it they need. Lifting heavy weights, for instance, requires energy much more quickly than jogging on the treadmill, necessitating the reliance on different energy systems. However, the production of ATP is never achieved by the exclusive use of one energy system, but rather by the coordinated response of all energy systems contributing to different degrees.
1. Phosphagen System
During short-term, intense activities, a large amount of power needs to be produced by the muscles, creating a high demand for ATP. The phosphagen system (also called the ATP-CP system) is the quickest way to resynthesize ATP (Robergs & Roberts 1997). Creatine phosphate (CP), which is stored in skeletal muscles, donates a phosphate to ADP to produce ATP: ADP + CP ���ATP + C. No carbohydrate or fat is used in this process; the regeneration of ATP comes solely from stored CP. Since this process does not need oxygen to resynthesize ATP, it is anaerobic, or oxygen-independent. As the fastest way to resynthesize ATP, the phosphagen system is the predominant energy system used for all-out exercise lasting up to about 10 seconds. However, since there is a limited amount of stored CP and ATP in skeletal muscles, fatigue occurs rapidly.
2. Glycolysis
Glycolysis is the predominant energy system used for all-out exercise lasting from 30 seconds to about 2 minutes and is the second-fastest way to resynthesize ATP. During glycolysis, carbohydrate�in the form of either blood glucose (sugar) or muscle glycogen (the stored form of glucose)�is broken down through a series of chemical reactions to form pyruvate (glycogen is first broken down into glucose through a process called�glycogenolysis). For every molecule of glucose broken down to pyruvate through glycolysis, two molecules of usable ATP are produced (Brooks et al. 2000). Thus, very little energy is produced through this pathway, but the trade-off is that you get the energy quickly. Once pyruvate is formed, it has two fates: conversion to lactate or conversion to a metabolic intermediary molecule called acetyl coenzyme A (acetyl-CoA), which enters the mitochondria for oxidation and the production of more ATP (Robergs & Roberts 1997). Conversion to lactate occurs when the demand for oxygen is greater than the supply (i.e., during anaerobic exercise). Conversely, when there is enough oxygen available to meet the muscles� needs (i.e., during aerobic exercise), pyruvate (via acetyl-CoA) enters the mitochondria and goes through aerobic metabolism.
When oxygen is not supplied fast enough to meet the muscles� needs (anaerobic glycolysis), there is an increase in hydrogen ions (which causes the muscle pH to decrease; a condition called acidosis) and other metabolites (ADP, Pi�and potassium ions). Acidosis and the accumulation of these other metabolites cause a number of problems inside the muscles, including inhibition of specific enzymes involved in metabolism and muscle contraction, inhibition of the release of calcium (the trigger for muscle contraction) from its storage site in muscles, and interference with the muscles� electrical charges (Enoka & Stuart 1992; Glaister 2005; McLester 1997). As a result of these changes, muscles lose their ability to contract effectively, and muscle force production and exercise intensity ultimately decrease.
3. Aerobic System
Since humans evolved for aerobic activities (Hochachka, Gunga & Kirsch 1998; Hochachka & Monge 2000), it�s not surprising that the aerobic system, which is dependent on oxygen, is the most complex of the three energy systems. The metabolic reactions that take place in the presence of oxygen are responsible for most of the cellular energy produced by the body. However, aerobic metabolism is the slowest way to resynthesize ATP. Oxygen, as the patriarch of metabolism, knows that it is worth the wait, as it controls the fate of endurance and is the sustenance of life. �I�m oxygen,� it says to the muscle, with more than a hint of superiority. �I can give you a lot of ATP, but you will have to wait for it.�
The aerobic system�which includes the�Krebs cycle�(also called the�citric acid cycle or TCA cycle) and the�electron transport chain�uses blood glucose, glycogen and fat as fuels to resynthesize ATP in the mitochondria of muscle cells (see the sidebar �Energy System Characteristics�). Given its location, the aerobic system is also called�mitochondrial respiration.�When using carbohydrate, glucose and glycogen are first metabolized through glycolysis, with the resulting pyruvate used to form acetyl-CoA, which enters the Krebs cycle. The electrons produced in the Krebs cycle are then transported through the electron transport chain, where ATP and water are produced (a process called�oxidative phosphorylation) (Robergs & Roberts 1997). Complete oxidation of glucose via glycolysis, the Krebs cycle and the electron transport chain produces 36 molecules of ATP for every molecule of glucose broken down (Robergs & Roberts 1997). Thus, the aerobic system produces 18 times more ATP than does anaerobic glycolysis from each glucose molecule.
Fat, which is stored as triglyceride in adipose tissue underneath the skin and within skeletal muscles (called�intramuscular triglyceride), is the other major fuel for the aerobic system, and is the largest store of energy in the body. When using fat, triglycerides are first broken down into free fatty acids and glycerol (a process called�lipolysis). The free fatty acids, which are composed of a long chain of carbon atoms, are transported to the muscle mitochondria, where the carbon atoms are used to produce acetyl-CoA (a process called�beta-oxidation).
Following acetyl-CoA formation, fat metabolism is identical to carbohydrate metabolism, with acetyl-CoA entering the Krebs cycle and the electrons being transported to the electron transport chain to form ATP and water. The oxidation of free fatty acids yields many more ATP molecules than the oxidation of glucose or glycogen. For example, the oxidation of the fatty acid palmitate produces 129 molecules of ATP (Brooks et al. 2000). No wonder clients can sustain an aerobic activity longer than an anaerobic one!
Understanding how energy is produced for physical activity is important when it comes to programming exercise at the proper intensity and duration for your clients. So the next time your clients get done with a workout and think, �I have a lot of energy,� you�ll know exactly where they got it.
Energy System Characteristics
Energy System Workouts
Have clients warm up and cool down before and after each workout.
Phosphagen System
An effective workout for this system is short, very fast sprints on the treadmill or bike lasting 5�15 seconds with 3�5 minutes of rest between each. The long rest periods allow for complete replenishment of creatine phosphate in the muscles so it can be reused for the next interval.
- 2 sets of 8 x 5 seconds at close to top speed with 3:00 passive rest and 5:00 rest between sets
- 5 x 10 seconds at close to top speed with 3:00�4:00 passive rest
Glycolysis
This system can be trained using fast intervals lasting 30 seconds to 2 minutes with an active-recovery period twice as long as the work period (1:2 work-to-rest ratio).
- 8�10 x 30 seconds fast with 1:00 active recovery
- 4 x 1:30 fast with 3:00 active recovery
Aerobic System
While the phosphagen system and glycolysis are best trained with intervals, because those metabolic systems are emphasized only during high-intensity activities, the aerobic system can be trained with both continuous exercise and intervals.
- 60 minutes at 70%�75% maximum heart rate
- 15- to 20-minute tempo workout at lactate threshold intensity (about 80%�85% maximum heart rate)
- 5 x 3:00 at 95%�100% maximum heart rate with 3:00 active recovery
References:
Brooks, G.A., et al. 2000.�Exercise Physiology: Human Bioenergetics and Its Applications.Mountain View, CA: Mayfield.
Enoka, R.M., & Stuart, D.G. 1992. Neurobiology of muscle fatigue.�Journal of Applied Physiology, 72�(5), 1631�48.
Glaister, M. 2005. Multiple sprint work: Physiological responses, mechanisms of fatigue and the influence of aerobic fitness.�Sports Medicine, 35�(9), 757�77.
Hochachka, P.W., Gunga, H.C., & Kirsch, K. 1998. Our ancestral physiological phenotype: An adaptation for hypoxia tolerance and for endurance performance?�Proceedings of the National Academy of Sciences, 95,�1915�20.
Hochachka, P.W., & Monge, C. 2000. Evolution of human hypoxia tolerance physiology.�Advances in Experimental and Medical Biology, 475,�25�43.
McLester, J.R. 1997. Muscle contraction and fatigue: The role of adenosine 5′-diphosphate and inorganic phosphate.�Sports Medicine, 23�(5), 287�305.
Robergs, R.A. & Roberts, S.O. 1997.�Exercise Physiology: Exercise, Performance, and Clinical Applications.�Boston: William C. Brown.
Nutrition is increasingly recognized as a key component of optimal sporting performance, with both the science and practice of sports nutrition developing rapidly.1 Recent studies have found that a planned scientific nutritional strategy (consisting of fluid, carbohydrate, sodium, and caffeine) compared with a self-chosen nutritional strategy helped non-elite runners complete a marathon run faster2 and trained cyclists complete a time trial faster.3 Whereas training has the greatest potential to increase performance, it has been estimated that consumption of a carbohydrate�electrolyte drink or relatively low doses of caffeine may improve a 40 km cycling time trial performance by 32�42 and 55�84 seconds, respectively.4
Carbohydrate ingestion has been shown to improve performance in events lasting approximately 1 hour.6 A growing body of evidence also demonstrates beneficial effects of a carbohydrate mouth rinse on performance.22 It is thought that receptors in the oral cavity signal to the central nervous system to positively modify motor output.23
The �train-low, compete-high� concept is training with low carbohydrate availability to promote adaptations such as�enhanced activation of cell-signaling pathways, increased mitochondrial enzyme content and activity, enhanced lipid oxidation rates, and hence improved exercise capacity.26 However, there is no clear evidence that performance is improved with this approach.27 For example, when highly trained cyclists were separated into once-daily (train-high) or twice-daily (train-low) training sessions, increases in resting muscle glycogen content were seen in the low-carbohydrate- availability group, along with other selected training adaptations.28 However, performance in a 1-hour time trial after 3 weeks of training was no different between groups. Other research has produced similar results.29 Different strategies have been suggested (eg, training after an overnight fast, training twice per day, restricting carbohydrate during recovery),26 but further research is needed to establish optimal dietary periodization plans.27
There has been a recent resurgence of interest in fat as a fuel, particularly for ultra endurance exercise. A high-carbohydrate strategy inhibits fat utilization during exercise,30 which may not be beneficial due to the abundance of energy stored in the body as fat. Creating an environment that optimizes fat oxidation potentially occurs when dietary carbohydrate is reduced to a level that promotes ketosis.31 However, this strategy may impair performance of high-intensity activity, by contributing to a reduction in pyruvate dehydrogenase activity and glycogenolysis. 32 The lack of performance benefits seen in studies investigating �high-fat� diets may be attributed to inadequate carbohydrate restriction and time for adaptation.31 Research into the performance effects of high fat diets continues.
While protein consumption prior to and during endurance and resistance exercise has been shown to enhance rates of muscle protein synthesis (MPS), a recent review found protein ingestion alongside carbohydrate during exercise does not improve time�trial performance when compared with the ingestion of adequate amounts of carbohydrate alone.33
The purpose of fluid consumption during exercise is primarily to maintain hydration and thermoregulation, thereby benefiting performance. Evidence is emerging on increased risk of oxidative stress with dehydration.34 Fluid consumption prior to exercise is recommended to ensure that the athlete is well-hydrated prior to commencing exercise.35 In addition,�carefully planned hyperhydration ( fluid overloading) prior to an event may reset fluid balance and increase fluid retention, and consequently improve heat tolerance.36 However, fluid overloading may increase the risk of hyponatremia 37 and impact negatively on performance due to feelings of fullness and the need to urinate.
Performance supplements shown to enhance performance include caffeine, beetroot juice, beta-alanine (BA), creatine, and bicarbonate.40 Comprehensive reviews on other supplements including caffeine, creatine, and bicarbonate can be found elsewhere.41 In recent years, research has focused on the role of nitrate, BA, and vitamin D and performance. Nitrate is most commonly provided as sodium nitrate or beetroot juice.42 Dietary nitrates are reduced (in mouth and stomach) to nitrites, and then to nitric oxide. During exercise, nitric oxide potentially influences skeletal muscle function through regulation of blood ow and glucose homeostasis, as well as mitochondrial respiration.43 During endurance exercise, nitrate supplementation has been shown to increase exercise efficiency (4%�5% reduction in VO at a steady attenuate oxidative stress.42 Similarly, a 4.2% improvement in performance was shown in a test designed to simulate a football game.44
Consuming carbohydrates immediately 
An acute bout of intense endurance or resistance exercise can induce a transient increase in protein turnover, and, until feeding, protein balance remains negative. Protein consumption after exercise enhances MPS and net protein balance,58 predominantly by increasing mitochondrial protein fraction with endurance training, and myofibrillar protein fraction with resistance training.59
Fluid and electrolyte replacement after exercise can be achieved through resuming normal hydration practices. However, when euhydration is needed within 24 hours or substantial body weight has been lost (.5% of BM), a more structured response may be warranted to replace fluids and electrolytes.77
The availability of nutrition information for athletes varies. Younger or recreational athletes are more likely to receive generalized nutritional information of poorer quality from individuals such as coaches.78 Elite athletes are more likely to have access to specialized sports-nutrition input from qualified professionals. A range of sports science and medicine support systems are in place in different countries to assist elite athletes,1 and nutrition is a key component of these services. Some countries have nutrition programs embedded within sports institutes (eg, Australia) or alternatively have National Olympic Committees that support nutrition programs (eg, United States of America).1 However, not all athletes at the elite level have access to sports-nutrition services. This may be due to financial constraints of the sport, geographical issues, and a lack of recognition of the value of a sports-nutrition service.78
Supplement use is widespread in athletes.86,87 For example, 87.5% of elite athletes in Australia used dietary supplements88 and 87% of Canadian high-performance athletes took dietary supplements within the past 6 months85 (Table 2). It is difficult to compare studies due to differences in the criteria used to define dietary supplements, variations in assessing supplement intake, and disparities in the populations studied.85
A positive drug test in an athlete can occur with even a minute quantity of a banned substance.41,87 WADA maintains a �strict liability� policy, whereby every athlete is responsible for any substance found in their body regardless of how it got there.41,86,87,89 The World Anti-Doping Code (January 1, 2015) does recognize the issue of contaminated supplements.91 Whereas the code upholds the principle of strict liability, athletes may receive a lesser ban if they can��show �no significant fault� to demonstrate they did not intend to cheat. The updated code imposes longer bans on those who cheat intentionally, includes athlete support personnel (eg, coaches, medical staff), and has an increased focus on anti-doping education.91,99
Allostasis: The process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPATG axis hormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term. It is essential in order to maintain internal viability amid changing conditions.
Chronic Care Model: Developed by Wagner and colleagues, the primary focus of this model is to include the essential elements of a healthcare system that encourage high-quality chronic disease care. Such elements include the community, the health system, self-management support, delivery system design, decision support and clinical information systems. It is a response to powerful evidence that patients with chronic conditions often do not obtain the care they need, and that the healthcare system is not currently structured to facilitate such care.�
Complementary and Alternative Medicine (CAM): A group of diverse medical and healthcare systems, practices, and products that are not presently considered to be part of conventional, mainstream medicine. The list of what is considered to be CAM changes frequently, as therapies demonstrated to be safe and effective are adopted by conventional practitioners, and as new approaches to health care emerge. Complementary medicine is used with conventional medicine, not as a substitute for it. Alternative medicine is used in place of conventional medicine. 
Cytochromes P450 (CYP 450): A large and diverse group of enzymes, most of which function to catalyze the oxidation of organic substances. They are located either in the inner membrane of mitochondria or in the endoplasmic reticulum of cells ans play a critical role in the detoxification of endogenous and exogenous toxins. The substrates of CYP enzymes include metabolic intermediates such as lipids, steroidal hormones, and xenobiotic substances such as drugs.
Dysbiosis: A condition that occurs when the normal symbiosis between gut flora and the host is disturbed and organisms of low intrinsic virulence, which normally coexist peacefully with the host, may promote illness. It is distinct from gastrointestinal infection, in which a highly virulent organism gains access to the gastrointestinal tract and infects the host.�
Functional Medicine Matrix: The graphic representation of the functional medicine approach, displaying the seven organizing physiological systems, the patient�s known antecedents, triggers, and mediators, and the personalized lifestyle factors that promote health. Practitioners can use the matrix to help organize their thoughts and observations about the patient�s health and decide how to focus therapeutic and preventive strategies.
Lifestyle Medicine: The use of lifestyle interventions such as nutrition, physical activity, stress reduction, and rest to lower the risk for the approximately 70% of modern health problems that are lifestyle-related chronic diseases (such as obesity and type 2 diabetes), or for the treatment and management of disease if such conditions are already present. It is an essential component of the treatment of most chronic diseases and has been incorporated in many national disease management guidelines.
Single Nucleotide Polymorphism or SNP (pronounced �snip�) is a DNA sequence variation occurring when a single nucleotide�A, T, C, or G�in the genome differs between members of a species or between paired chromosomes in an individual. Almost all common SNPs have only two alleles. These genetic variations underlie differences in our susceptibility to, or protection from, several diseases. Variations in the DNA sequences of humans can affect how humans develop diseases. For example, a single base difference in the genes coding for apolipoprotein E is associated with a higher risk for Alzheimer’s disease. SNPs are also manifestations of genetic variations in the severity of illness, the way our body responds to treatments, and the individual response to pathogens, chemicals, drugs, vaccines, and other agents. They are thought to be key factors in applying the concept of personalized medicine.
Triage Theory: Linus Pauling Award winner Bruce Ames� theory that DNA damage and late onset disease are consequences of a �triage allocation mechanism� developed during evolution to cope with periods of micronutrient shortage. When micronutrients (vitamins and minerals) are scarce, they are consumed for short-term survival at the expense of long-term survival. In 2009, Children�s Hospital and Research Center Oakland concluded that triage theory explains how diseases associated with aging like cancer, heart disease, and dementia (and the pace of aging itself) may be unintended consequences of mechanisms developed during evolution to protect against episodic vitamin/mineral shortages.
Xenobiotics: Chemicals found in an organism that are not normally produced by or expected to be present in that organism. This may also include substances present in much higher concentrations than usual. The term xenobiotics is often applied to pollutants such as dioxins and polychlorinated biphenyls, because xenobiotics are understood as substances foreign to an entire biological system, i.e. artificial substances that did not exist in nature before their synthesis by humans. Exposure to several types of xenobiotics has been implicated in cancer risk.
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Chronic undernutrition is characterized by a progressive reduction of the�fat-free mass (FFM) and fat mass (FM)�and �which has deleterious consequences on health. Undernutrition is insufficiently screened and treated in hospitalized or at-risk patients despite its high prevalence and negative impact on mortality, morbidity, length of stay (LOS), quality of life, and costs [1�4]. The risk of underestimating hospital undernutrition is likely to worsen in the next decades because of the increasing prevalence of overweight, obesity, and chronic diseases and the increased number of elderly subjects. These clinical conditions are associated with FFM loss (sarcopenia). Therefore, an increased number of patients with FFM loss and sarcopenic obesity will be seen in the future.
Academic societies encourage systematic screening of undernutrition at hospital admission and during the hospital stay [14]. The detection of undernutrition is generally based on measurements of weight and height, calculations of BMI, and the percentage of weight loss. Nevertheless, screening of undernutrition is infrequent in hospitalized or nutritionally at-risk ambulatory patients. For example, in France, surveys performed by the French Health Authority [15] indicate that: (i) weight alone, (ii) weight with BMI or percentage of weight loss, and (iii) weight, BMI,�and percentage of weight loss are reported in only 55, 30, and 8% of the hospitalized patients� records, respectively. Several issues, which could be improved by specific educational programs, explain the lack of implementation of nutritional screening in hospitals (table 1). In addition, the accuracy of the clinical screening of undernutrition could be limited at hospital admission. Indeed, patients with undernutrition may have the same BMI as sex- and age- matched healthy controls but a significantly decreased FFM hidden by an expansion of the FM and the total body water which can be measured by bioelectrical impedance analysis (BIA) [13]. This example illustrates that body composition evaluation allows a more accurate identification of FFM loss than body weight loss or BMI decrease. The lack of sensitivity and specificity of weight, BMI, and percentage of weight loss argue for the need for other methods to evaluate the nutritional status.
In 2008, twelve and thirty percent of the worldwide adult population was obese or overweight; this is two times higher than in 1980 [16]. The prevalence of overweight and obesity is also increasing in hospitalized patients. A 10-year comparative survey performed in a European hospital showed an increase in patients� BMI, together with a shorter LOS [17]. The BMI increase masks undernutrition and FFM loss at hospital admission. The increased prevalence of obesity in an aging population has led to the recognition of a new nutritional entity: �sarcopenic obesity� [18]. Sarcopenic obesity is characterized by increased FM and reduced FFM with a normal or high body weight. The emergence of the concept of sarcopenic obesity will increase the number of situations associated with a lack of sensitivity of the calculations of BMI and�body weight change for the early detection of FFM loss. This supports a larger use of body composition evaluation for the assessment and follow-up of nutritional status in clinical practice (fig. 1).
Fig. 2. Current and potential applications of body composition evaluation in clinical practice. The applications are indicated in the boxes, and the body composition methods that could be used for each application are indicated inside the circles. The most used application of body composition evaluation is the measurement of bone mineral density by DEXA for the diagnosis and management of osteoporosis. Although a low FFM is associated with worse clinical outcomes, FFM evaluation is not yet implemented enough in clinical practice. However, by allowing early detection of undernutrition, body composition evaluation could improve the clinical outcome. Body composition evaluation could also be used to follow up nutritional status, calculate energy needs, tailor nutritional support, and assess fluid changes during perioperative period and renal insufficiency. Recent evidence indicates that�a low FFM is associated with a higher toxicity of some chemo- therapy drugs in cancer patients. Thus, by allowing tailoring of the chemotherapy doses to the FFM in cancer patients, body com- position evaluation should improve the tolerance and the efficacy of chemotherapy. BIA, L3-targeted CT, and DEXA could be used for the assessment of nutritional status, the calculation of energy needs, and the tailoring of nutritional support and therapy. Further studies are warranted to validate BIA as an accurate method for fluid balance measurement. By integrating body composition evaluation into the management of different clinical conditions, all of these potential applications would lead to a better recognition of nutritional care by the medical community, the health care facilities, and the health authorities, as well as to an increase in the medico-economic benefits of the nutritional evaluation.
Body Composition Techniques For FFM Measurement
Body composition evaluation allows measurement of the major body compartments: FFM (including bone mineral tissue), FM, and total body water. Table 2 shows indicative values of the body composition of a healthy subject weighing 70 kg. In several clinical situations, i.e. hospital admission, chronic obstructive pulmonary dis- ease (COPD) [21�23], dialysis [24�26], chronic heart failure [27], amyotrophic lateral sclerosis [28], cancer [5, 29], liver transplantation [30], nursing home residence [31], and Alzheimer�s disease [32], changes in body compartments are detected with the techniques of body composition evaluation. At hospital admission, body composition evaluation could be used for the detection of FFM loss and undernutrition. Indeed, FFM and the FFM index (FFMI) [FFM (kg)/height (m2)] measured by BIA are significantly lower in hospitalized patients (n = 995) than in age-, height-, and sex-matched controls (n = 995) [3]. Conversely, clinical tools of nutritional status assessment, such as BMI, subjective global assessment, or mini-nutritional assessment, are not accurate enough to estimate FFM loss and nutritional status [30, 32�34]. In 441 patients with non-small cell lung cancer, FFM loss deter- mined by computerized tomography (CT) was observed in each BMI category [7], and in young adults with all�types of cancer, an increase in FM together with a de- crease in FFM were reported [29]. These findings reveal the lack of sensitivity of BMI to detect FFM loss. More- over, the FFMI is a more sensitive determinant of LOS than a weight loss over 10% or a BMI below 20 [3]. In COPD, the assessment of FFM by BIA is a more sensitive method to detect undernutrition than anthropometry [33, 35]. BIA is also more accurate at assessing nutrition- al status in children with severe neurologic impairment than the measurement of skin fold thickness [36].
FFM loss is correlated with survival in different clinical settings [5, 21�28, 37]. In patients with amyotrophic lateral sclerosis, an FM increase, but not an FFM in- crease, measured by BIA, was correlated with survival during the course of the disease [28]. The relation between body composition and mortality has not yet been demonstrated in the intensive care unit. The relation between body composition and mortality has been demonstrated with anthropometric methods, BIA, and CT. Measurement of the mid-arm muscle circumference is an easy tool to diagnose sarcopenia [38]. The mid-arm muscle circumference has been shown to be correlated with survival in patients with cirrhosis [39, 40], HIV infection [41], and COPD in a stronger way than BMI [42]. The relation between FFM loss and mortality has been extensively shown with BIA [21�28, 31, 37], which is the most used method. Recently, very interesting data suggest that CT could evaluate the disease prognosis in relation to muscle wasting. In obese cancer patients, sarcopenia as assessed by CT measurement of the total skeletal muscle cross-sectional area is an independent predictor of the survival of patients with bronchopulmonary [5, 7], gastrointestinal [5], and pancreatic cancers [6]. FFM assessed by measurement of the mid-thigh muscle cross- sectional area by CT is also predictive of mortality in COPD patients with severe chronic respiratory insufficiency [43]. In addition to mortality, a low FFMI at hospital admission is significantly associated with an in- creased LOS [3, 44]. A bicentric controlled population study performed in 1,717 hospitalized patients indicates that both loss of FFM and excess of FM negatively affect the LOS [44]. Patients with sarcopenic obesity are most at risk of increased LOS. This study also found that ex- cess FM reduces the sensitivity of BMI to detect nutritional depletion [44]. Together with the observation that the BMI of hospitalized patients has increased during the last decade [17], these findings suggest that FFM and�FFMI measurement should be used to evaluate nutritional status in hospitalized patients.
Numerous methods of body composition evaluation have been developed: anthropometry, including the 4-skinfold method [58], hydrodensitometry [58], in vivo neutron activation analysis [59], anthropogammametry from total body potassium-40 [60], nuclear magnetic resonance [61], dual-energy X-ray absorptiometry (DEXA) [62, 63], BIA [45, 64�66], and more recently CT [7, 43, 67]. DEXA, BIA, and CT appear to be the most convenient methods for clinical practice (fig. 2), while the other methods are reserved for scientific use.
The evaluation of FFM could be used for the calculation of energy needs, thus allowing the optimization of nutritional intakes according to nutritional needs. This could be of great interest in specific situations, such as severe neurologic disability, overweight, and obesity. In 61 children with severe neurologic impairment and intellectual disability, an equation integrating body composition had good agreement with the doubly labeled water method. It gave a better estimation of energy expenditure than did the Schofield predictive equation [36]. However, in 9 anorexia nervosa patients with a mean BMI of 13.7, pre- diction formulas of resting energy expenditure including FFM did not allow accurate prediction of the resting energy expenditure measured by indirect calorimetry [76]. In overweight or obese patients, the muscle catabolism in response to inflammation was the same as that observed�in patients with normal BMI. Indeed, despite a higher BMI, the FFM of overweight or obese individuals is similar (or slightly increased) to that of patients with normal BMI. Thus, the use of actual weight for the assessment of the energy needs of obese patients would result in over- feeding and its related complications. Therefore, the ex- perts recommend the use of indirect calorimetry or calculation of the energy needs of overweight or obese patients as follows: 15 kcal/kg actual weight/day or 20�25 kcal/kg ideal weight/day [77, 78], although these predictive formulas could be inaccurate in some clinical conditions [79]. In a US prospective study conducted in 33 ICU medical and surgical ventilated ICU patients, daily measurement of the active cell mass (table 2) by BIA was used to assess the adequacy between energy/protein intakes and needs. In that study, nutritional support with 30 kcal/ kg actual body weight/day energy and 1.5 g/kg/day protein allowed stabilization of the active cell mass [75]. Thus, follow-up of FFM by BIA could help optimize nutritional intakes when indirect calorimetry cannot be performed.
Body composition evaluation allows a qualitative assessment of body weight variations. The evaluation of body composition may help to document the efficiency of nutritional support during a patient�s follow-up of numerous clinical conditions, such as surgery [59], anorexia nervosa [76, 80], hematopoietic stem cell transplantation [81], COPD [82], ICU [83], lung transplantation [84], ulcerative colitis [59], Crohn�s disease [85], cancer [86, 87], HIV/AIDS [88], and acute stroke in elderly patients [89]. Body composition evaluation could be used for the follow-up of healthy elderly subjects [90]. Body composition evaluation allows characterization of the increase in body mass in terms of FFM and FM [81, 91]. After hematopoietic stem cell transplantation, the increase in BMI is the result of the increase in FM, but not of the increase in FFM [81]. Also, during recovery after an acute illness, weight gain 6 months after ICU discharge could be mostly related to an increase in FM (+7 kg) while FFM only increased by 2 kg; DEXA and air displacement plethysmography were used to measure the FM and FFM [91]. These two examples suggest that body composition evaluation could be helpful to decide the modification and/or the renewal of nutritional support. By identifying the patients gaining weight but reporting no or insufficient FFM, body composition evaluation could contribute to influencing the medical decision of continuing nutrition- al support that would have been stopped in the absence of body composition evaluation.
In clinical situations when weight and BMI do not reflect the FFM, the evaluation of body composition should be used to adapt drug doses to the FFM and/or FM absolute values in every patient. This point has been recently illustrated in oncology patients with sarcopenic obesity. FFM loss was determined by CT as described above. In cancer patients, some therapies could affect body com- position by inducing muscle wasting [92]. In patients with advanced renal cell carcinoma [92], sorafenib induces a significant 8% loss of skeletal muscular mass at 12 months. In turn, muscle wasting in patients with BMI less than 25 was significantly associated with sorafenib toxicity in patients with metastatic renal cancer [8]. In metastatic breast cancer patients receiving capecitabine treatment, and in patients with colorectal cancer receiving 5-fluorouracile, using the convention of dosing per unit of body surface area, FFM loss was the determinant of chemotherapy toxicity [9, 10] and time to tumor progression [10]. In colorectal cancer patients administered 5-fluoruracil, low FFM is a significant predictor of toxicity only in female patients [9]. The variation in toxicity between women and men may be partially explained by the fact that FFM was lower in females. Indeed, FFM rep- resents the distribution volume of most cytotoxic chemo- therapy drugs. In 2,115 cancer patients, the individual variations in FFM could change by up to three times the distribution volume of the chemotherapy drug per body area unit [5]. Thus, administering the same doses of chemotherapy drugs to a patient with a low FFM compared to a patient with a normal FFM would increase the risk of chemotherapy toxicity [5]. These data suggest that FFM loss could have a direct impact on the clinical outcome of cancer patients. Decreasing chemotherapy doses in case of FFM loss could contribute to improving cancer patients� prognosis through the improvement of the tolerance of chemotherapy. These findings justify the systematic evaluation of body composition in all cancer patients in order to detect FFM loss, tailor chemotherapy doses according to FFM values, and then improve the efficacy- tolerance and cost-efficiency ratios of the therapeutic strategies [93]. Body composition evaluation should also be used to tailor the doses of drugs which are calculated based on patients� weight, e.g. corticosteroids, immuno-suppressors (infliximab, azathioprine or methotrexate), or sedatives (propofol).
The implementation of body composition evaluation in routine care presents a challenge for the next decades. Indeed the concomitant increases in elderly subjects and patients with chronic diseases and cancer, and in the prevalence of overweight and obesity in the population, will increase the number of patients nutritionally at risk or undernourished, particularly those with sarcopenic obesity. Body composition evaluation should be used to improve the screening of undernutrition in hospitalized patients. The results of body composition should be based on the same principle as BMI calculation, towards the systematic normalization for body height of FFM (FFMI) and FM [FM (kg)/height (m)2 = FM index] [94]. The results could be expressed according to previously de- scribed percentiles of healthy subjects [95, 96]. Body com- position evaluation should be performed at the different stages of the disease, during the course of treatments and the rehabilitation phase. Such repeated evaluations of body composition could allow assessment of the nutritional status, adjusting the calculation of energy needs as kilocalories/kilogram FFM, following the efficacy of 
Anabolic-Androgenic Steroids
Anabolic-androgenic steroids (AAS) are testosterone derivatives that exert anabolic (tissue building) and androgenic (masculinizing) influences on the body.3 Since the discovery of the chemical structure of testosterone in 1935, attempts to separate the anabolic and androgenic effects of AAS�have been unsuccessful.3 
Dehydroepiandrosterone (DHEA) is a precursor to testos- terone produced primarily in the adrenal glands.4,14 Natural sources of DHEA include wild yams. The FDA banned sale of DHEA in 1996 due to insuf cient evidence of safety and value; however, DHEA remains a legal and popular item sold as a nutritional supplement.14,15
Androstenedione is a testosterone pre-cursor produced in the adrenal glands and gonads. Several professional athletes have used this substance, bringing it to national attention.2 Androstenedione is found naturally in the pollen of Scottish pine trees.19
The increased visibility of ergogenic aids in the last de- cade has occurred primarily because of the passage of the United States Dietary Supplement Health and Education Act (DSHEA) of 1994.22 Certain vitamins, minerals, amino acids, herbs, and other botanical preparations can be classified as a �dietary supplement� under the DSHEA guidelines. Dietary supplements, as a result of DSHEA, are no longer under the direct regulatory control of the FDA. In fact, substances sold as a dietary supplement do not require FDA evaluation for safety or efficacy, and do not have to meet quality control standards expected of approved drugs.5 The content and purity of dietary supplements are not regulated and can vary widely.5,23 Since androstenedione and DHEA have been found to occur naturally in plant sources, these testosterone precursors can be labeled as �dietary supplements� and sold legally over-the-counter.
Dietary supplements containing Chinese ephedra, also known as Mahaung, are marketed as performance enhancers and weight-loss aids.24 Ephedra species of herb have been used for over 5,000 years for respiratory ailments.25 Currently, ephedrine alkaloids are found in hundreds of prescriptions and over-the-counter products, such as antihistamines, decongestants, and appetite suppressants.24-26 Ephedra and related ephedrine alkaloids are sympathomimetic agents that�mimic epinephrine effects.
Creatine use in athletes has grown as a result of a 1992 study that showed that creatine supplementation produced a 20% increase in skeletal muscle creatine concentration.2,35 In the phosphorylated form, creatine serves as an energy substrate that contributes to adenosine triphosphate (ATP) re-synthesis during high-intensity exercise.36 Creatine re- mains popular with power and resistance athletes as it is thought to produce increases in strength, muscle mass, and to delay fatigue.2,14,36
Human growth hormone (hGH) is a polypeptide produced in the anterior pituitary gland. After its release from the pituitary, hGH can exert its effect in all cells of the body via tissue specific receptors. Human growth hormone is shown to promote protein anabolism, carbohydrate tolerance, lipolysis, natriuresis, and bone and connective tissue turnover.4,50
Recombinant EPO (r-EPO) was approved by the FDA for manufacture in 1989 after the EPO gene was cloned in 1985.14 Since its approval, r-EPO has been abused for athletic personal gain as an alternative to blood doping.3,14 Recombinant EPO has largely replaced the practice of blood doping, as r-EPO produces a dose-dependent increase in hematocrit.2 In theory, r-EPO should provide all of the benefits of blood doping without the risks involved in blood transfusion.3
The antioxidant capabilities of certain vitamins are believed by many to counter-act the production of free-radials that occurs during exercise.14 Most of the research to date involves vitamin E, vitamin C, and beta carotene.2 The existing literature does not support the notion that antioxidants have significant ergogenic capabilities.2,14,57 There are currently no recommendations for antioxidant use in athletes that exceeds the normal adult recommended daily allowance (RDA).
Beta-hydroxy-beta-methylbutyrate (HMB) is a metabolite of the branched-chain amino acid leucine. HMB is theorized to inhibit muscle breakdown during strenuous exercise but its exact mechanism of action remains unknown.14,58 Studies show that HMB supplementation may significantly lower serum lactate dehydrogenase (LDH), lower serum creatine phosphokinase (CPK) levels and delay blood lactate accumulation after endurance training compared to placebo.59,60 Furthermore, short-term HMB use has been shown to significantly increase strength gains with resistance-exercised training over placebo in one double-blinded study.61
Caffeine is a methylxanthine occurring naturally in many species of plants. Caffeine is thought to work through a variety of mechanisms. The central nervous system effect of caffeine is probably the result of adrenergic receptor antagonism.3 Its use by athletes stems from the theory that caffeine may delay fatigue by enhancing skeletal muscle contractility and spare muscle glycogen levels by enhancing fat metabolism.6 Multiple studies have reported an improved endurance time with caffeine use.6,62,63 There is evidence that caffeine use may enhance performance with more intense short-duration exercise as well.2 The caffeine dosages most associated with an ergogenic effect range in the literature from 3 to 9 mg per kilogram of body weight.2,6
Signs Of IT Band Syndrome
If you are a runner, you will be able to distinguish ITBS by:
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