Pyramid Science

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Monday, December 29, 2008

Eye Disorders

Complications of Orbital Fracture Repair

Most common complication of orbital floor fracture repair is diplopia. Up to 75% combined orbital floor and medial wall fractures may have clinically significant diplopia six months postoperatively. Damage directly to globe or to optic nerve, eyelid avulsion, damage to lacrimal apparatus, haemorrhage, damage to infraorbital nerve.

Eye Injuries

In the first 24 hours after an eye injury, blood leaking into skin around the eye usually produces a bruise (contusion): black eye. Damage to the inside of eye is more serious and injury to face can fracture any of several bones that form the orbits. The fracture may impair function of muscles that move the eye, producing double vision or inhibiting eye movement to the right, left, up or down.


The condition in which increased pressure around brain causes the optic nerve to swell where it enters the eye is known as papilloedema. This almost always occurs in both eyes and is usually caused by a brain tumour or abscess, head injury, bleeding in brain, infection of meninges, pseudotumour cerebri, cavernous sinus thrombosis or severe high blood pressure. Severe lung diseases can also lead to papilloedema and this may at first cause headaches without affecting vision.

If there is no papilloedema, there is no evidence or reason to necessarily suspect a tumour. In the case of injury to the eye (temporal bone area) there is a very high chance of an orbital floor fracture and muscle/nerve damage. The third cranial nerve controls the extrinsic muscles and the sixth cranial nerve controls the lateral rectus muscle and trochlear nerve by fourth cranial nerve. If vision is impaired upwards and to right extreme the 4th and 6th nerve/muscle to right eye are implicated. So, a fracture of the bone in the orbit floor and partial detachment or damage to the muscle cause restricted movement in a particular direction.


Cell metabolism involves many types of chemical reaction that often occur in a well defined sequence or metabolic pathway. The overall effect is to break down large molecules, usually nutrient molecules with the output of energy, then catabolism occurs through catabolic pathways or conversely anabolism: building up larger molecules from smaller ones. These usually require energy to be input. Enzymes are functional proteins that catalyse chemical reactions that do not normally occur or are too slow at body temperature. Catalysts participate in chemical reactions, but are not themselves changed or incorporated into products. Enzymes are usually tertiary of quaternary proteins of complex shape. Tertiary implies a three dimensional shape and quaternary the assembly of more than one protein in a cluster. Often their molecules contain a non-protein cofactor. Inorganic ions or vitamins may make up part of this and if it is an organic non-protein molecule is called a coenzyme.

A very important structural attribute of enzymes is the active site. This is a portion of the enzyme molecule that chemically "fits" the substrate molecule(s). The substrate is the molecule acted upon by the enzyme: the target molecule. The shape and electrochemical attractions of the active site complement some portion of the substrate(s). Often used is the lock and key model to describe enzyme action. The enzyme can lock (bind) or unlock substrates. The suffix -ase used with the root name of the chemical substance involved gives the name to the enzyme. Sucrase will be the enzyme that catalyses sucrose reactions. Sucrase may also be termed a hydrolase because it catalyses the hydrolysis of sucrose. Some enzymes are still known by their earlier trivial names (trypsin and pepsin). Oxidases, hydrogenases and dehydrogenases are all oxidation-reduction enzymes and release energy for muscular contractions. All physiological work relies on these enzymes. Hydrolases are hydrolysing enzymes usually active in digestion such as lipase, sucrase or maltase. Phosphorylating enzymes add or remove phosphate groups and are known as phosphorylases or phosphatases. The removal of carbon dioxide is by carboxylases or decarboxylases. Mutases or isomerases rearrange atoms within a molecule. Hydrases add water.

Enzymes are intracellular (majority) or extracellular. An important class of extracellular enzymes are the digestive enzymes and are all hydrolases. Generally, enzymes regulate cell function by regulating the metabolic pathways. Each reaction in the pathway requires one or more enzymes to permit that reaction to occur. The entire metabolic sequence can be turned on or off by the activation or inactivation of a single enzyme in the metabolic pathway. Most enzymes are highly specific in their action by acting only on a specific substrate. The configurations of the enzyme and the substrate make the active site unique. Various physical and chemical agents can easily disrupt enzyme action by altering the shape of the enzyme molecule. Such an agent is known as an allosteric effector. Enzyme inhibition may occur by distorting the active site or by giving it functional shape. Some may bind at an allosteric site on the enzyme molecule and thereby change the shape of the active site on a different part of the enzyme.

Antibiotic drugs, change in pH or temperature may act as allosteric effectors. Pepsin (protein-digesting enzyme gastric juice) operates within a low pH range (2-4) whereas trypsin (protein-digesting enzyme in pancreatic juice) operates within a higher pH range (6-8). Most enzymes work best in a fairly narrow range (40degC). Cofactors when they are added or removed from an enzyme molecule also have an allosteric effect.

End-product inhibition is a process where a chemical product at the end of a metabolic pathway binds to the allosteric site of one or more of the enzymes along the pathway that produced it thereby inhibiting synthesis of more product. This is a type of automatic negative feedback in the cell which prevents an accumulation of an extreme amount of a metabolic product. Most enzymes catalyse reactions in both directions, the rate and direction being governed by the law of mass action. An accumulation of a product slows the reaction and tends to reverse it. Enzymes are continually being destroyed and so have to be continually synthesised, even though they are not used up in the reactions they catalyse. Most enzymes are synthesized as inactive proenzymes. Kinases are the substances which activate enzymes. Commonly allosteric effects are the mechanism. Enterokinase changes the inactive trypsinogen into active trypsin by changing the shape of the molecule. A type of kinase (kinase A) within cells has been shown to activate enzymes that regulate certain pathways after a hormonal signal is received by the cell.

Saturday, December 27, 2008

Head Injury

The hard skull protects the soft brain (consistency of porridge) from many minor injuries. The scalp/skull may suffer bruising, lacerations and fractures, but apparently no damage to the neurological tissue that it covers. Head injuries usually mean damage to the brain even though this may only be transitory (concussive). Most head injuries are minor, though neurological injuries are the principal cause of death or lasting disability in the younger age groups who still play football, ride motorcycles and engage in contact sports. Head injuries are the main cause of death in the under 35's in America. In Britain, over one million people attend hospital each year with head injury with over 50% of these arising from road traffic accidents (RTAs) and 120,000 are classified each year as having suffered brain damage. The brain may be directly injured after the skull has been fractured, but may also be damaged by rapid acceleration or deceleration injuries.

The brain is able to slop about within the skull as gruel does in a bucket. When the brain moves violently to and fro, it suffers injury at two points: the impact site and at the opposite side of the brain as a result of rebound. The general shaking a brain receives (after a heavy blow or deceleration injury), causes widespread, but lesser damage throughout the frontal and temporal lobes. Further destruction of the brain is caused by the tearing of its covering (meninges) and blood vessels. Any subsequent haemorrhages cause extensive neurological damage, which is also accompanied by oedema and swelling. As the skull is rigid, any swelling can produce a dangerous rise in the intracranial pressure.

After any brain damage severe enough to cause unconsciousness, brain cells will have been permanently destroyed and therefore complete recovery is not possible. Even after concussion, patients may suffer for a time from ill-defined symptoms such as depression, apathy, headaches and dizziness. Many find the zest for life lessened. And difficulty in concentration. Serious head injuries with an apparent good recovery can be associated with loss of memory. Retrograde amnesia (loss of memory of events before an accident) is usually less extensive compared to loss afterwards.

It is unusual to suffer head injuries in accidents without associated injuries usually to the chest. This confuses the clinical picture after a head injury as damage to the lungs frequently reduces the oxygen supply to the brain. Likewise, difficulty in respiration and swelling within the lungs are sometimes the result of damage to the respiratory centre within the brain. Or injury to the spine.

Eating Disorder

Losing Weight

Rapid weight loss can result in excessive loss of lean tissue and reduction in aerobic capacity, strength, muscle endurance and dehydration. Prolonged dieting or food restriction can lead to menstrual irregularities and amenorrhea, reduced testosterone production in men and increased risk of stress fractures and bone loss (osteoporosis), chronic fatigue and disordered eating. Safe weight loss may be achieved by maintaining a high carb diet (60%), an adequate protein intake (15-20%) and a low fat intake (15-25%), together with an appropriate excercise programme. Recommended weight loss is 0.5-1kg/week so to make the weight for competition, it is essential to set a realistic goal and allow sufficient time to achieve it. High carb/low fat diet is the key to appetite control and long term weight management. The basal metabolic rate (BMR) is proportional to body weight, though there is no evidence that the BMR is reduced in overweight people. Food restriction causes only a temporary reduction in BMR, but this may be offset by exercise and, in any case, is restored once normal eating is resumed. Yo-yo dieting leads to a loss of lean tissue and an increased risk of heart disease and there is no permanent effect on BMR.

Gaining weight

Gaining weight involves a combination of strength training and a balanced diet. The rate of any weight gain depends on genetics, body type and hormonal balance. On average, a lean weight gain of 0.5-1kg/month is recommended and to gain muscle strength and size, there must be a slight positive energy balance. A recommended protein intake should range between 1.4-1.7g/kg.

Disordered eating

Disordered eating patterns are increasingly common among athletes and fitness participants and up to an estimated 62% female athletes may be affected. This is characterised by the preoccupation with food, food restriction and poor body image. It is regarded as a sub-clinical eating disorder as it includes some, though not all, of the criteria for defining a clinical eating disorder such as anorexia nervosa and bulimia nervosa. Athletes share many of the same personality characteristics as people with clinical eating disorders:
  • Obsessiveness
  • Compulsiveness
  • Perfectionism
The sports most 'at risk' include endurance sports (leanness is believed to be an advantage for performance), aesthetic sports (leanness is believed to be an important judging criterion in competition), and weight category sports. Many sports people appear to have a distorted body image and a higher level of body dissatisfction than the general population. There is no single cause of clinical or sub-clinical eating disorders, though it is likely that certain sports may precipitate an eating disorder in predisposed people, rather than be the cause of the eating disorder. Health consequences of disordered eating include chronic fatigue, reduction in performance, susceptibility to infection and injury, menstrual irregularities, amenorrhea, increased risk of stress fractures and osteoporosis. Sufferers should be approached with tact and sensitivity, rather than be guided towards professional help by an eating disorders specialist or counsellor.

Into practice

If "eating on the run", take a supply of healthy snacks to consume at regular intervals and an "eating on budget" diet should be around basic nutritious foods such as cereals, pulses, starchy vegetables and milk. Fruit and vegetables should be bought in season and in bulk. If there is little time to prepare meals they should be cooked in larger quantities and the remainder saved (frozen). Plan a weekly menu in advance and if eating late at night, consume most food during early part of day. A moderate-sized high carb snack/meal is then beneficial in the evening after training. A well-planned vegetarian diet can provide all the nutrients needed by athletes for good health and performance. Vegans may need to use more fortified foods. Female athletes may be at greater risk of deficient intakes of iron, calcium, riboflavin and folic acid, due to their lower intakes of food generally. The pre-competition diet should be high in carbs to ensure full glycogen stores. Include plenty of fluids to ensure good hydration. This meal should be taken 3-4hrs beforehand and be high in carbs, low in fat and fibre and easy to digest. Consuming an additional 50g high GI carb immediately before competition may delay fatigue in events lasting more than 1hr. Performance in events lasting >90mins may be increased by consuming 30-60g carb/hr in solid or liquid form.

Energy Fuels

Amino Acid - Protein Synthesis
Blood Flow Physics

Energy for exercise is provided by three main fuels:
  • Carbohydrate
    • 4kcal/g
  • Fat
    • 9kcal/g
  • Protein
    • 4kcal/g
The amount and proportion of each fuel used depends on the type, duration and intensity of exercise, your fitness level and your diet. For aerobic activities, all three fuels may be broken down (although protein makes a significantly smaller contribution than fat and carbohydrate). For anaerobic activities, only phosphocreatine (PC) and glycogen are broken down. The proportion of carbohydrate (glycogen) used increases with exercise intensity and decreases with exercise duration. The main cause of fatigue during aerobic exercise is usually glycogen depletion and/or dehydration. The main cause of fatigue during anaerobic exercise is initially PC depletion and/or lactic acid build up, but after several exercise sets, fatigue is eventually also due to glycogen depletion. For almost all types of exercise, performance is limited by the amount of glycogen in the muscles. Low pre-exercise stores lead to early fatigue, reduced training intensity and reduced training gains. Ensuring full glycogen stores before each training session can help delay fatigue and improve performance. This can be achieved by a high carbohydrate diet.

Summary - carbo power

For optimal training gains, ensure that muscle glycogen stores are fully restored during the period between training sessions. The length of time taken to refuel glycogen stores between training sessions depends on the intensity and duration of exercise (ie, the degree of depletion) and the amount and timing of carbohydrate intake and your fitness level. It takes longer to refuel following high intensity and/or prolonged exercise and will be increased by a low carbohydrate diet and low fitness levels. The recommended carb intake for athletes and active people is 60-70% of total energy intake. Practically, this means about 6-10g carb/kg body weight/day.

Glycogen refuelling is faster in the 2hr period following the exercise and a carb intake of at least 1g/kg body weight is recommended during this time. For efficient refuelling, continue to consume a minimum of 50g carb every 2hrs. Leave approx 2-3hrs between last meal and training. Consume a further 50g to help maintain blood sugar levels and delay fatigue and improve performance. For strenuous exercise lasting more than 60-90 mins consume 30-60g carb (liquid or solid form) to help maintain longer performance.

Choice of type depends on the nutritional package (and other contained nutrients). The glycemic index (GI) is a measure of the speed of absorption and the consequential rate of rising blood sugar. The nearer 100 the faster this absorption. The main part of any diet should comprise carb foods with an overall good nutritional package: bread, cereals, pulses, starchy vegetables, fruit and low fat dairy products. Carbs with high GI are good during and after exercise as they are absorbed quickly. Athletes with high energy and carb requirements should include mix of high and low bulk carbs in the diet.


Proteins make up part of the structure of every cell in the body including about three quarters of the dry weight of muscle. They also form enzymes and hormones and are continually broken down into their constituent amino acids and recycled as new proteins or energy substrates. Some protein is lost every day and must be replaced in the diet and most protein is broken down to provide energy when glycogen is in short supply (dieting and prolonged intense exercise). Exercise increases protein breakdown (catabolism) and therefore dietary requirements. The exact type depends on the type, frequency, duration and intensity of exercise, fitness level and energy and carb intake.

The protein needs of athletes is greater than those of sedentary people and intake is between 1.2 to 1.7g/kg body weight/day (12-15% energy intake is recommended). Strength training increases protein needs more than aerobic training. Intake of 1.4 to 1.7g/kg for strength athletes, 1.2 to 1.4g/kg for endurance athletes. Any increased protein needs should be able to be met from a balanced diet that is meeting energy needs. High protein intake surplus to requirements do not enhance muscle strength, size or mass and do not offer any advantage. Protein supplements are not necessary for most athletes and do not automatically enhance performace or strength, but may be useful if energy and protein requirements cannot be met by food alone.


There is no evidence to support claims for amino acid supplementation. Vitamin and mineral requirements depend on age, body size, activity level and individual metabolism. Dietary Reference Values (DRV) should be used only as a guide for the general population and not targets since they do not take into account the needs of the athlete. Regular and intense exercise increases the requirement for number of vitamins and minerals, though there is no official recommendation for athletes. A low intake can adversely affect health and performance and a high intake exceeding requirements will not necessarily improve performance. A well planned and balanced diet that meets energy needs is likely to provide sufficient vitamins and minerals.

Supplements should not take the place of a balanced diet

Supplements containing 100-200% Dietary Reference Intake (DRI) may be useful for athletes consuming less than 2000kcal/day and those with erratic eating habits, food intolerances or restrictive diets (vegan). Vitamins A, D and B6 and a number of minerals may be toxic in high doses (more than 10 x DRI). Indiscriminate supplementation may lead to nutritional imbalances and deficiences.

Vitamins - Overview

Increased free radicals are produced during exercise and these may be responsible for post exercise muscle soreness (DOMS: Delayed Onset Muscular Soreness). Excessive amounts may also increase the risk of heart disease, certain cancers and premature ageing. Antioxidant nutrients can help prevent free radical damage. High dietary intake of antioxidant rich foods is recommended: aim is at least 5 portions of fruit and vegetables a day, with moderate amounts of vegetables oils, oily fish, nuts and red wine. Optimal doses for antioxidant nutrients are unknown and the value of supplements not yet clear.

Vitamin A is essential for normal colour vision and for cells in the eye that enable sight in dim light. It promotes healthy skin and mucous membranes lining the mouth, nose and digestive system and is found in meat, eggs, whole milk, cheese, oily fish, butter and margarine.


Dehydration impairs performance and health and fluid losses depend on duration and intensity of exercise, temp and humidity, body size, fitness level. This can be as high as 1-2l/hr and always start well hydrated and continue drinking at regular intervals early on and drink plenty afterwards to replace fluid losses. Water suitable fluid for moderate exercise of up to 1hr. More intense exercise of more than 1hr should include dilute salt (sodium chloride). Carbohydrate can speed up water absorption and provide additional fuel. Optimal concentration for fluid replacement is 4-8g carb/100ml and 40-110mg sodium/100ml. A compromise should be made between function and taste as is often made in commercial drinks.

Tonicity is a measure of the ability of a solution to exert an osmotic pressure upon a membrane. Hypotonic and isotonic sports drinks are the most suitable when rapid fluid replacement is the priority. Carb drinks based on glucose polymers also replace fluids, but provide greater amounts of carb (10-20%) at lower osmolality (a measure of the number of dissolved particles in fluid). Most suitable for prolonged intense exercise (>90min) when fuel replacement is the priority and fluid losses are small.

Alcohol before any exercise has a negative effect on strength, endurance, co-ordination, power and speed. It raises the risk of injury. Excess body fat is a major disadvantage in most sports and fitness programmes and it reduces power, speed and performance. Very low body fat does not guarantee improved performance. There appears to be an optimal fat range for every individual and cannot be predicted by any standard linear relationship. There are three components to body fat:
  • Essential (tissue structure)
  • Gender specific (hormonal function)
  • Storage (energy)
The minimum %age fat for men is 5% and for women is 10%. In normal health these range 13-18% and 18-25%, respectively. Many athletes fall below these recommended ranges. Very low fat levels are associated with hormonal imbalance in both sexes (amenorrhea, infertility, reduced bone density, increased risk of osteoporosis). Very low fat diets can lead to deficient intakes of essential fatty acids and fat soluble vitamins. In the long term, fat and calorie restriction can result in other nutritional imbalances, depleted glycogen stores, chronic fatigue, loss of lean tissue and reduced performance. A fat intake of 15-30% of energy needs is recommended for athletes and active people. Unsaturated fatty acids should make up majority of the fat intake, with saturated fatty acids and trans fatty acids kept to a minimum.

Friday, December 26, 2008


The currency of all energy requirements involves the chemical adenosine triphosphate (ATP) and is one compound made up of a nitrogen base (adenosine) linked to three phosphate groups. The cleavage of one phosphate-adenosine chemical bond releases a large quantity of energy forming adenosine diphosphate (ADP). It is ATP -> ADP that produces the driving force to make muscle contract. All chemical reactions in the body require energy be they the formation of structural proteins or enzymes (proteins) through peptide bond formation between amino acids or breakdown of foodstuffs in digestion. All require energy. The combustion of fat, carbohydrate or protein will provide this energy to restore the ADP -> ATP. It is basically as simple as that. The complicated part is how this energy is provided, but still it remains a matter of breaking one adenosine-phosphate bond to energise other chemical reactions and reforming the bond to resynthesise ATP. Essentially, the ATP -> ADP + energy is the trigger for other processes.

There is a limited amount of ATP in the body so once ATP -> ADP has occurred, the ADP must be converted back into ATP to replenish these limited stores. Several mechanisms occur depending on the speed at which the energy is required. The complete and efficient combustion of fat, carbohydrate and protein is a relatively slow process. For aerobic (using oxygen) and anaerobic (without oxygen) activity a different series of chemical reactions occurs. Creatine phosphate is a stop gap chemical high-energy provider, but for a very short term period (30-60 secs). The restoration of all phosphate linkages to other chemicals requires energy and this must be provided from the large storage reserves of mostly fat and carbohydrate. Protein can also be destroyed to provide energy.

ATP is not synthesised in any one particular tissue and then transported around the body, but rather every cell has the capacity to synthesise and use ATP within itself. It is very important to appreciate that the processes which use ATP are closely matched with those that produce energy so that the greater the demand for energy the faster the energy must be produced. Otherwise a mismatch between ATP demand and supply will lead to an energy crisis and the cell couldn't function.

Before fat can be mobilised from the subcutaneous fat cells under the skin, the muscle must still be able to work. If cells did not contain there own store of energy then disaster would result. The substance creatine phosphate (CP) does this. Once the main source of energy is supplied to the working muscle the CP stores can then be repleted, its job over. Fat and carbohydrate are the two main foodstuffs which are oxidised. To a lesser extent, unless through prolonged endurance work or where carbohydrate and/or fat is in limited supply, protein will be utilised and this defines starvation conditions. The rate of energy requirement will determine the source of energy given that there are normal levels within the body. This energy is then trapped by ATP (from ADP) with carbon dioxide and water as the byproducts.

The mitochondria within cells are the engines which actually burn the fuel to produce the energy. These are highly specialised structures and are the powerhouses of all cellular activity and account for most of the oxygen used by the body. The chemical pathway by which energy is produced is called the Krebs cycle (after Sir Hans Krebs), sometimes referred to as the citric acid cycle, which describes the chemical fate (metabolism) of fat, carbohydrate and protein. In other words how nutrients provide ATP from ADP.

High rates of energy requirement must come from carbohydrate. They are capable of rapid release of energy where the slower oxidative processes cannot match the need. Glycogen stored within the liver can provide glucose which can be transported to glycogen starved muscle. Muscle glycogen cannot be mobilised in the same way to supply other muscles.

During high energy demanding activity the rate at which energy is required outstrips the rate at which normal oxidative processes work: carbohydrate combustion. Glycogen is broken down into a smaller chemical entity called pyruvate which can then enter the Krebs cycle. Glucose has 6 carbon atoms within the molecule and pyruvate has 3 carbon atoms. Each carbon atom will ultimately be lost completely as a single carbon dioxide molecule. Complete oxidation or effectively the combination of carbon with oxygen.

When demand is high and oxidative processes do not function properly because of the slowness of the process, pyruvate is converted to lactic acid. This can take place outside the mitochondria of the cell as it does not require oxygen and is therefore called anaerobic metabolism (without oxygen). Although ATP is generated very quickly, the process is very inefficient and only 2 ATP units are produced from a single glucose unit. Remember, the 6 -C atom unit of glucose gives two 3-C atom units of pyruvate. Lactic acid also has the same 3-C atoms from the pyruvate.

The glucose to lactic acid process is very important under high energy demand, but this process can only function for a very short period. Lactic acid dissociates or breaks down to produce hydrogen ions and lactate. This is very acidic and unless these products are removed, the cell will be destroyed. In reality fatigue and complete exhaustion set in before this occurs and this can be viewed as the body protecting itself from destruction.

Complete oxidation (aerobic) of glucose intermediates within the mitochondria produces a vastly greater yield of ATP per glucose unit. Respiration increases naturally to ensure a sufficiency of oxygen to do this. Between 36-38 units of ATP are produced aerobically compared to the 2 units in the anaerobic process. So, although the lactate route to ATP is fast it is clearly very inefficient and glycogen stores would be depleted very rapidly.

Biologically available energy is not utilised by the dissipation of heat in respiration, but the mitochondria within cells contain groups of organised enzymes and are responsible for the use of this biologically available energy. Inorganic phosphate phosphorylates the nucleotide ADP (adenosine 5-diphosphate) to the corresponding ATP (adenosine 5-triphosphate). The high free energy of hydrolysis of ATP comes from the two phosphoanhydride groups within. Direct hydrolysis of ATP would result in heat formation, but the pathway is different. This endergonic biochemical process requires energy, cannot occur spontaneously and is a coupled reaction.

The sequence is thermodynamically unfavoured and would require energy if it were to take place in one step. To render it favourable it can be carried out in two steps, one involving ATP. Phosphorylation by ATP generates energy and forms a very reactive intermediate. This would be catalysed by enzymes in the biological system. Enzymes do not alter the thermodynamic outcome of a reaction, favourable or otherwise, only its velocity.

ATP is regarded as a high energy compound like acetyl-coenzyme A and other nucleoside triphosphates, for example guanosine 5-triphosphate (GTP). Protein synthesis requires both ATP and GDP to trans-phosphorylate yielding ADP and GTP. Although many of these high energy compounds require ATP, the ATP itself can be formed by direct phosphorylation with inorganic phosphate.

Respiration is essentially the controlled oxidation of glucose to yield biologically available energy in the form of ATP. Just as some oxidations require the presence of oxygen and others can be effected in its absence, so respiration is of two types. Oxygen-dependent (aerobic) and oxygen-independent (anaerobic). In both types of respiration, high-energy organic phosphates are produced and serve as phosphate donors for the phosphorylation of ADP. This process is described as substrate phosphorylation.

In aerobic respiration, an additional and quantitatively more important phosphorylation mechanism operates to produce ATP from ADP. It utilises inorganic phosphate and is oxygen-dependent. This highly endergonic process of oxidative phosphorylation stems from an electron transport mechanism as in photosynthesis. However, the flow of electrons originates in the dehydrogenation of respiratory substrates and terminates in the reduction of oxygen to water.

The process by which glucose is degraded during anaerobic respiration is known as glycolysis (splitting of sugar). The biological pathway is referred to as the Embden-Meyerhof pathway after its original formulators. So, how does the process produce ATP?

During glycolysis (hydrolysis of starch or glycogen), glucose is phosphorylated by ATP which in turn loses one phosphate group and changes to ADP. The phosphorylated glucose then enzymatically rearranges (isomerises) to the fructose phosphate derivative, another sugar. The 6-C atom unit of glucose is contracted into a 5-C atom ring and an exocyclic (outside the ring) C-atom. It is again phosphorylated, but this time to fructose-1,6-diphosphate by another ATP to ADP transfer. Two molecules of ATP have been used to convert glucose to fructose-1,6-diphosphate, which is easily split into two 3-C fragments (glyceraldehyde-3-phosphate and dihydroxyacetone-1-phosphate) by an enzyme. These trioses are simple sugars and biochemically interconvertible by enzymatic action.

The dihydroxyacetone-1-phosphate is converted into another molecule of glyceraldehyde-3-phosphate. So far one glucose unit has been converted to two glyceraldehyde-3-phosphate molecules at the expense of two ATP molecules. The oxidation (removal of hydrogen: dehydrogenation) of the aldehyde gives an acid which is phosphorylated by inorganic phosphate (not ATP) to yield 1,3-diphosphoglycerate which is a mixed anhydride of a carboxylic acid and orthophosphoric acid and so has a high free energy of hydrolysis. What this means is that the compound can phosphorylate ADP back to ATP by transfer of one of the phosphate groups.

Two molecules of the glycerate are generated from the original glucose unit so providing two ATP molecules. The sum so far of ATP is zero since two molecules of ATP were consumed (giving ADP) to reach the two molecules of glycerate which now generate two ATP molecules from ADP. The resulting 3-phosphoglycerate is enzymatically isomerised to 2-phosphoglycerate which loses a molecule of water to give phosphoenolpyruvate, another high energy phosphate capable of transfer of the phosphate group to ADP forming ATP. Again two molecules of the high energy phosphate give two ATP molecules and pyruvic acid. Overall, the original glucose unit required two ATP molecules, but ultimately has provided four ATP molecules. A gain of two ATP molecules by the oxidation of glucose -> pyruvate. In humans the enzyme required to convert pyruvate to ethanol is absent so in the fatigued athlete where oxygen is deficient the pyruvate is reduced to lactate directly. The hydrogen removed in the earlier steps of glucose oxidation is transferred from the substrate to an acceptor called nicotinamide adenine dinucleotide (NAD+) forming the reduced acceptor NADH, which now enzymatically releases the hydrogen (REDOX reactions in biology).

Under aerobic conditions, where oxygen is in good supply, the pyruvate is not converted to lactate but undergoes a continuing oxidation to give ultimately carbon dioxide and water. This is called the Krebs cycle also known as the tricarboxylic acid cycle.

Current thinking is that lactate is not produced only in the anaerobic process where oxygen is unavailable. Lactate is formed under these conditions, but also its production is directly related to the rate at which energy is produced. So it would seem that under generally an aerobic state of low work output, some lactate is still formed within some cells, but is easily cleared from the system and no sign of fatigue results. This may be due to blood circulation insufficiency in some parts of the working muscle. However formed lactate is not a metabolic dead-end and the products of glucose cleavage from which it is derived are not wasted. Lactic acid can be reconverted to pyruvate in the same muscle cell by oxidation (loss of hydrogen) when the energy demand is reduced. This would then spare fresh glycogen being consumed or glucose removed from the blood transport system. Glycogen is stored within the muscle cell and cannot be used by other cells, but glucose is freely transported around the body in the blood and taken up as required. Pyruvate formed from lactic acid would be oxidised rather that from glucose or glycogen directly. The glycogen within parts of a muscle may be depleted so lactate could be used by these muscle cells instead of using glucose from the circulation. Lactate can be taken up by the liver and be converted back into glucose and finally end up back in muscle cells as glycogen.

The eventual metabolic fate of lactate can be oxidation or conversion back to glycogen depending on the prevailing energy demands. Cells do not suddenly switch from aerobic to anaerobic metabolism. Lactate formation during exercise is proportional to the rate of energy production and does not start at a certain threshold of intensity (an anaerobic threshold). Lactate is produced continually but only accumulates when the rate of production exceeds the clearance rate. It may be converted back to pyruvate within the same muscle cell when the rate of energy provision from oxidative metabolism is sufficient to meet the demands for energy. This would then spare glucose units from glycogen within the muscle as well as entry of glucose from the circulation, as the pyruvate that is formed could then be oxidised in place of pyruvate formed from glucose or glycogen.

Lactate may leave the muscle cell to be taken up by other muscle cells within the same muscle. Such cells may have exhausted their own supply of glycogen and be in need of suitable carbohydrate to convert back to pyruvate and then either oxidise to produce energy, or use to rebuild the glycogen store in the cell. Lactate may leave the muscle and be taken up by the liver and converted back to glucose. The glucose formed by this process can then be released back into the blood to be taken up by the muscle cell as further fuel for either energy production or glycogen repletion.

  • Therefore, while the eventual metabolic fate of any lactate formed will be oxidation, the immediate fate will depend on the energetic demands on the cell prevailing at that time. The idea that the cell suddenly switches over from aerobic to anaerobic metabolism is no longer tenable. Lactate formation during exercise now appears to be directly proportional to the rate at which energy is being produced and does not start suddenly at a certain point or threshold of exercise intensity (an 'anaerobic threshold'). Instead lactate is being produced continually and only accumulates when the rate at which it is produced exceeds the rate it can be cleared from the system.

Energy from fats

Stored triglycerides in adipose tissue and muscle cells are converted into energy in stages. Firstly, the triglyceride store is mobilised within the adipose tissue to bring about the release of free fatty acids into the circulation. Several hormones control this process the most important being adrenaline and noradrenaline which are released when energy is required - the fight or flight hormones which prepare the body for action. The free fatty acids are then transported in the blood to the working muscle by a carrier the protein called albumin. The glycerol that is released is taken up by the liver and converted to glucose by a process known as gluconeogenesis. The glucose so produced can then be taken up by working muscle to provide energy.

The blood supply containing increased free fatty acids (FFA) levels causes a corresponding increase in the uptake of FFA by the muscle and is related to the rate of blood flowing through the capillaries in the muscle. The FFA entering the muscle can then be oxidised immediately or stored in the muscle as additional triglyceride. To utilise the FFA energy is required so ATP is needed. The activated FFA are then transported to the mitochondria of the cell by a special carrier mechanism. The most critical stages of the utilisation of FFA are the transportation to the muscle and carriage to the mitochondria of the cell when in the muscle. The greater the number of mitochondria in the cell then the larger the capacity to take up fatty acids and oxidise them to produce energy. Once in the mitochondria the activated FFA are broken down and enter the Krebs cycle to be oxidised in the same way as carbohydrate. The number of ATP units depends on the number of carbon atoms in the fatty acid molecule. The longer the fatty acid the more carbon atoms there are and the more energy (number of ATP units) produced. This amount will be in the range 80-200 ATP units for FFA chain lengths of between 10-24 carbon atoms.

So whereas 36-38 ATP units are provided from glucose oxidation, the potential energy yield from fatty acid oxidation is much greater. Consequently any factor which can increase the utilisation of FFA will have a considerable impact on the overall energy generated. However, the rate of oxidation or energy resynthesis from triglyceride is determined by the mitochondria in the cell. The absolute rate may be large but the rate at which ATP is resynthesised is comparatively low.

The fatty acid chain is metabolised in 2-carbon units at a time in the Krebs cycle. The pyruvate from the degradation of glucose under aerobic conditions enters the cycle in the same way and is completely broken down to CO2 and water. The hydrogen that is removed from pyruvate is transferred to NAD+ which constitutes the coenzyme of almost all dehydrogenating enzymes (dehydrogenases). The Krebs cycle is such because the oxaloacetate required and consumed in the first step is regenerated at the end.

Pyruvate is oxidatively decarboxylated to yield an acetyl unit in the form of acetyl-coenzyme A and this undergoes an enzyme-catalyzed condensation with oxaloacetate to give citrate as the first step in the cycle. Fatty acid breakdown commences with the 2-carbon fragment entering the cycle at the same place as pyruvate and so form a common pathway from acetyl-coenzyme A Citrate is enzymatically isomerised via cis-aconitate to isocitrate and this is oxidised (hydrogen removed) and decarboxylated to yield oxoglutarate. This in turn is is oxidatively decarboxylated to succinyl-coenzyme A in a similar way that pyruvate is converted to acetyl-coenzyme A. This is a high energy compound and is used to drive the phosphorylation of GDP to guanosine 5-triphosphate (GTP) and in the process is converted to succinate. Dehydrogenation of succinate to fumarate, the enzymatic hydration of fumarate to malate and finally the dehydrogenation of malate to oxaloacetate complete the cycle.

The operation of the Krebs cycle is confined to small subcellular particles possessing internal structure and containing electron-acceptor systems. These mitochondria can be thought of as corridor containing shelves which hold the correct enzymes in the right sequence so passage down the pathway effects the conversion of acetyl-coenzyme A to oxaloacetate.

Tissues such as the heart and liver are well suited for energy resynthesis from fat oxidation, but the brain and red blood cells are dependent on glycolysis (from carbohydrate) for energy and exclusively use glucose. Skeletal muscle can use a whole variety of different fuels although the capacity to oxidise fatty acids does vary between the types of muscle fibre. The high oxidative capacity fibres are the Type I (or SO: slow, oxidative) fibres and are better able to oxidise fatty acids than the Type IIb (or FG: fast, glycolitic) fibres which are best suited to energy production from carbohydrate.


Another form of fat that can be used to provide energy is formed in the liver as ketones. Under extreme conditions of prolonged exercise or starvation or in diabetes, the excess free fatty acids are released into the circulation and converted by the liver to ketones. The importance of ketones is that they are the only alternative fuel source which can be used by the brain and nervous tissue other than glucose. ketones are taken up by the brain and skeletal muscle and enter the Krebs cycle to be oxidised to produce ATP.

Energy from proteins

Amino acids are metabolised as an energy source along with fat and carbohydrate. The protein does not form only structural tissue and enzymes, but through the process of gluconeogenesis, amino acids can be converted to glucose providing energy to tissues that rely on glucose as a fuel source. The nitrogen must first be removed (deamination) and this is converted to ammonia. The remaining carbon skeleton is then used as the energy source.

Most of the carbons form pyruvate or one of the Krebs cycle intermediates and can easily enter the oxidation pathway and be used to generate ATP within the mitochondria. The toxic ammonia is converted to urea in the liver transported to the kidneys in the blood and passed out of the body in the urine.

The carbon skeletons may be used as an energy source for those tissues that would normally use carbohydrate when this fuel source is reduced. In addition to providing energy, they also make it possible to supply the Krebs cycle intermediates required to replace those that have been lost from the cycle. These would normally be maintained from carbohydrate metabolism but as glycogen stores become depleted and the rate of carbohydrate metabolism reduced an alternative supply of the Krebs cycle intermediates is advantageous. Unless the supply of these intermediates is maintained it is not possible for the Krebs cycle to continue generating ATP from other substrates (fatty acids) if carbohydrate stores are limited. Under conditions where the supply of glucose exceeds the requirement for energy, the carbon skeletons may be converted to fatty acid and stored as triglyceride.

How is this energy used to move muscle?

Isotonic, isokinetic and isometric are different kinds of movements but are all muscle contractions. The same mechanism moves muscle regardless of the type. The Type I muscle fibre are slow to contract and are red in colour. They are relatively resistant to fatigue and have a high oxidative capacity. This means a high potential to generate ATP by the oxidation of carbohydrate, fat (and indirectly protein) in the mitochondria of the cell. They are referred to as the SO (slow, oxidative) fibres. The Type II muscle fibre are divided into IIa, IIb or IIab fibres.

Thursday, December 25, 2008


In mammals the blood is the transport mechanism of the human body and supplies nutrients to every cell. Poor circulation will cause some muscles to tire easily or at least not receive these nutrients. The main sources of energy in food are from protein, carbohydrate and fat. Calories are not eaten, but these food sources do provide energy. It is the energy potentially available if the food is burnt by the body as a fuel. If it is not needed then this potential fuel source is stored. Carbohydrate is converted into fat and stored by the body.

Consequently, the depot fat (stored by the body for later use) will increase if such foods are eaten and the energy requirement is not reached to consume this amount. The body is particularly efficient at doing this. Starvation diets do not work, and are dangerous for many reasons, because the body will go into starvation mode when it realises it is losing body material too fast. The metabolism slows to minimise this loss and the body fat is retained to some extent. So, when short term dieting is over, the old eating habits return, but with a slowed metabolism. What happens? You get fatter than you were! The availability of the potential for energy from these food sources is different. About 4kcal/g each from carbohydrate and protein but 9kcal/g from fat.

The fat content of food is a more compact form of energy. What this means is that for every 1g fat consumed, there is 9/4 = 2.25 times the energy available compared to 1g of each of the other two. Put another way, given a particular energy requirement needed for an activity, less than half the amount of fat would be burnt as fuel as would carbohydrate (the main muscle fuel) or protein. Indeed, to satisfy a balance of energy from food in work expended then less than half the weight of fat can be consumed as carbohydrate or again, put another way, over twice the carbohydrate g/g can be eaten. Consider the nutritional values of a typical chocolate cake.

Energy per 100g:
  • Protein 6.0g
  • Fat 16.0g
  • Carbohydrate 56.0g
The total weight is 78g (the 22g deficit is made up of water and other trace constituents). The fat content may only appear to be

16/78 = 20%

by weight. However, energy wise the picture is quite different.

  • Protein: 6 x 4 = 24kcal
  • Fat: 16 x 9 = 144kcal
  • Carbohydrate: 56 x 4 = 224kcal
  • Total = 392kcal
The fat content in energy terms is actually

144/392 =37%

nearly double. You must be very careful about how nutritional values are interpreted.

Intensity of Work

The intensity of muscle work can be estimated by using the modified Karvonen Equation to calculate your target heart rate (THR). Aerobic work is achieved in a muscle working at about 60-85% capacity. Such a muscle is able to completely burn the fat/carbohydrate fuel with the oxygen inhaled producing carbon dioxide and water as the only biproducts. The exhalation cycle in respiration removes the gaseous carbon dioxide and water as vapour.

Energy Pathways for Exercise

Anaerobic work at a higher intensity is when the need for energy cannot be supplied fast enough by the same mechanism and an alternative pathway is necessary. No oxygen is needed for this but the biproducts are different. Lactic acid is formed which causes the stiffness and soreness in muscle if it is allowed to build up in the anaerobic process. Lactic acid is completely removed but only much later after the muscle work is over.

Continued faster respiration, puffing or blowing depending on the actual intensity level, for an extended period after exercising ensures that sufficient oxygen is eventually supplied by the blood to do this. This is the oxygen debt - the deficiency of oxygen must be paid back. In some muscles the blood flow is not sufficient to supply enough oxygen for the aerobic mechanism to work in untrained muscles and lactic acid builds up as a result of anaerobic oxidation. This insufficiency also ensures that these biproducts are not removed completely and soreness and stiffness occurs. As the muscle is worked (trained) the blood supply improves so enough oxygen will be supplied to ensure aerobic oxidation so that stiffness does not occur. The training effect.

Tuesday, December 23, 2008


Nutrition is central to maximal performance. The short term is to reduce body fat and increase muscle mass. Recovery time between training sessions should be quicker so a higher volume of work is possible. In the longer term it is to improve the capacity to resist injury and illness, reduce common 'wear and tear' conditions like arthritis and osteoporosis, cancer and heart disease. Between 20-60 years, the aging effects are minimal if well nourished. Mostly, any decline is due to reduced activity, poor nutrition and stress.

Lean muscle tissue is hard and made of protein in origin. Consuming more protein cannot build more muscle. In terms of evolution there are three main threats to survival:
  • Starvation
  • Freezing
  • Predators
The production and regulation of energy has priority, metabolically speaking. No energy means no ability to drive the biochemical reactions that sustain life. In periods of starvation, the body firstly consumes fat then protein before itself (internal organs). Muscle mass and strength are not useful against cold conditions. Protein metabolism is intimately connected with energy metabolism.

To gain strength from muscle mass, the requirements for body must firstly be provided. Nutrition must be seen as an addition to strength training, not weight training by itself. Muscle has its constituents from protein from amino acids. Of the 20 in the human body, 8 must come from the diet as essential amino acids since the body cannot synthesise them.
Protein metabolism is closely linked to the biochemical energy-producing cycles.

Citric Acid Cycle

The Kreb Citric Acid Cycle generates adenosine triphosphate (ATP) from partially degraded carbohydrates, fats and proteins and is dependent on conditions. When carbohydrate is in short supply, the body will use proteins and fats. It is now known that proteins, or more exactly the amino acids from which they are constructed, provide a significant source of energy during periods of intense energy production: aerobic vs anaerobic exercise In particular the branched chain amino acids (Valine, Leucine and Isoleucine). Not just carbohydrates or fats. Muscle proteins are rich in these branched chain amino acids so can be utilised in intense activity: anaerobic weight training. They are easily broken down (oxidised) and once the branched chain amino acids have been used the rest of the protein is rendered useless. The amino acids then go back into the amino acid pool or provide energy, but are lost to the system. It is obvious that the energy requirements must be satisfied, but paradoxically intense training has the opposite of the desired effect.

High Grade Fuel

Carbohydrates (carbs) then fat or protein is the order of ease of oxidation. Ideally, these carbs should be of complex variety: whole grains, pulses, vegetables and fruit. This ensures a sustained and gradual release of sugars (low glycemic index). Muscle glycogen is maintained more efficiently and the need for protein oxidation is reduced. High glucose levels in blood assist transport of amino acids to muscle cells. Complex sugars (starches) provide a more stable and constant supply of blood glucose. Carbs and proteins are required together. Protein level of about 0.75g/kg is a probable minimum protein per day (World Health Organisation), but up to 2g/kg for heavy workloads according to research by the US National Research Council. Yet excess protein cannot be stored directly (deamination transforms the protein into carbon and hydrogen products by removal of the amino group as ammonia). This places an extra burden on the liver, so there is no advantage to be gained by consuming too much protein.

For most athletes between 1-1.5g/kg sufficient allowing the total calorie needs to be made upfrom carbs and fat. Most complex carbs contain around 10% protein so a high carb diet such as this could provide the protein requirements. A transaminase is an enzyme which interconverts amino acids. Excess amino acids from new and old protein matter can provide non-essential amino acids by transaminase. This requires zinc and vitamin B6 for activation. Zinc is also required for the action of the enzyme carboxypeptidase and is crucial for digestion of dietary proteins to amino acids. This is then used in the synthesis of muscle tissue. Vitamin B6 is required for absorption of amino acids across the intestine wall and into the bloodstream. Diets low in these essential nutrients lead to less efficient protein metabolism. A low level of nutrients prevents the efficient utilisation of proteins from the diet and results in a failure to build muscle tissue.

Chromium Requirements

Around 100mcgm daily appears to be crucial in the correct functioning of the insulin system and a chromium is a critical component of the Glucose Tolerance Factor (GTF). This enhances the activity of insulin in the body and it is insulin which promotes transport of glucose to muscle cells. An amino acid is taken into cell with a glucose molecule, so the importance of chromium is obvious: chromium is crucial in the metabolism of carbohydrate. An increase in chromium (as picolinate) produces lean body mass increases of 44% greater compared to athletes on standard intakes. These gains are accompanied by increased rates of fat loss. Other human studies have had only limited success in reproducing these results, although animal studies have consistently shown the same effect and it appears that extra chromium in poor diets can be of real benefit, but in a good diet this may be of limited benefit. Refined grains and sugars in modern diets may be low in chromium so supplementation should be considered. Low chromium also shown to increase blood cholesterol and circulating blood lipids with the consequent greater risk of cardiovascular disease.


After training, there is a one to four hour window to intake protein for absorption of amino acids and to repair and build muscle after strenuous training. Later than this and the propensity of muscle to absorb nutrients falls away and is eventually lost all together. Trained and untrained muscle are not different in this respect. Genetics play an important r├┤le in growth. Thinner and more wiry builds tend to have a faster metabolic rate and consequent higher energy requirements. There is a greater need for carbs. If slim there is a need for high carbs AND adequate protein. Eat frequent, small meals without too much aerobic exercise. Muscle will be catabolised. Fast gainers often carry a slightly higher level of body fat so adequate protein is matched by a lesser intake of carbs. The shortfall in the total calorie count is made up from fats. So wiry people need a greater carb:protein ratio (more protein) than do stockier builds (more carbs).

The benefits of creatine as a sports supplement are still unclear. Creatine should be regarded as the last addition to nutrition after everything else has been fixed if for no other reason than cost. It's expensive and the effects are questionable.

Reducing Body Fat

There are no shortcuts. There is no magic. A proper mixture is a diet consisting of unprocessed, natural and whole foods with regular (aerobic) exercise. Efficient mechanisms for storing energy in times of abundance evolved for use during those times of scarcity.

Storage of body fat

Fat is a very concentrated form of energy for its weight (muscle glycogen has around 75%. of its weight as water). It is also a good insulator against cold. These efficient pathways evolved against a background of the reverse situation and calories are burnt off to provide energy. Storage is easier than removing and so to reduce body fat the storage pathways should be stimulated as little as possible and the oxidation pathway to burn stored fat is stimulated as much as possible This last point arises from fact that carbs, not fat, are the preferred source of energy. Encouraging the body to use fat as a source is not easy and it can be seen why obesity is so prevalent. The abundance of nutritionally poor foods mixed with a lifestyle of inactivity. Calorie counting does not work and 'eating fewer calories' still results in the prevalence of obesity. Calories all carry the same chemical energy whether they originate from fat, carb or protein. Calories are not eaten, but they do result from food, but they do interact differently with the metabolism. Calories from some foods can be converted to stored body fat more easily than others.

The route back from stored fat is difficult. The enzyme is present in the human body to convert carbohydrate into fat, but the reverse process is not possible. The enzyme for that purpose is not present. The metabolism runs faster earlier in the day and a substantial breakfast is ideal. A decent lunch is beneficial, but a small evening meal should be consumed. Eating early actually increases the basal metabolic rate and evens out peaks and troughs in energy. Several small and frequent meals are better than one or two large ones and reduces the likelihood of excess calories being dumped as fat. Any excess fat is stored directly as body fat without biochemical transformation. So keep the actual fat intake low, <30% of total. However, some fat is essential for good health. Fatty acids in nuts, seeds, oily fish. This highlights the range of fats that are available. Animal fat (lard) is not the same as the fat from an avocado pear. A well nourished body can maintain lower levels of body fat when the diet contains some fat. It is important to realise that some biochemical reactions take place in a fatty medium and not water.

Calories from different types of carbohydrate have a different fate in the body. Refined sugar has a high glycemic index. Glucose = 100 and the speed of release into bloodstream is measured by the glycemic index. The faster the rate the more the insulin that is released, leading to fat storage (of the excess unburnt calories).

  • Cereals
    • cornflakes = 80
    • weetabix = 75
    • shredded wheat = 67
    • porridge oats = 49
    • fruit raisins = 64
    • bananas = 62
    • oranges = 40
    • apples = 39
  • Grain Products
    • white rice = 72
    • wholemeal bread = 72
    • brown rice = 66
    • oatcakes = 54
    • white pasta = 50
    • wholemeal pasta = 42
  • Sugars
    • glucose = 100
    • lucozade = 95
    • honey = 87
    • fructose = 59
  • Pulses
    • baked beans = 40 (no sugar)
    • butter beans = 36
    • chick peas = 36
    • kidney beans = 29
    • lentils = 29
    • soya beans = 15
Once fat is stored it is hard to get rid of. Refined carbs can also lead to poor glucose tolerance and this results in energy swings and sugar cravings. Complex and unrefined whole grain carbs have lower glycemic indeces, releasing calories gradually avoiding the insulin high. Additionally, a higher level of nutrients (some are crucial to fat metabolism) are present unlike the refined foods. Aerobic work enhances the oxygen-carrying capacity of the body and this increases the rate at which oxygen is delivered to the cells (see also mitochondria). Oxidation of fat requires an oxygen rich environment, which is encouraged by aerobic exercise.

Basal metabolism will be reduced if muscle mass is lost and is a common effect of crash diets. Chromium regulates of the blood sugar level and carbohydrate metabolism. How chromium works is unclear, but it is certainly implicated. Whole unprocessed grains are low in refined grains and should be part of a staple diet. Other fat metabolising components are vitamin B1, B2, B3, B5 and the minerals magnesium and manganese. A modest amount of calories taken as fat, but used in lower impact aerobic work, should result in an optimal loss of around 2 pounds/month. Fat is needed to lose fat.