Showing posts with label Respiratory Exchange Ratio. Show all posts
Showing posts with label Respiratory Exchange Ratio. Show all posts

Tuesday, 22 September 2015

How we lose weight: Oxidation of carbohydrate & fat in the body.



1. Oxidation of Carbohydrate in the body.

Glucose is C6H12O6, or 6(CH2O)

6(CH2O)+ 6(O2) → 6(CO2) + 6(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 6 molecules of Oxygen produce 6 molecules of Carbon Dioxide, the Respiratory Exchange Ratio (RER) is 6/6 = 1

Converting molecular weights into their gram equivalents, 180g of Glucose combines with 192g of Oxygen to produce 264g of Carbon Dioxide plus 108g of water plus ~3,012kJ of energy. I'm using kJ rather than kcal, as the human body expends energy as mechanical energy (force x distance) and heat energy.

2. Oxidation of Fat in the body.

Fat is three fatty acids (Stearic Acid, say) attached to a Glycerol backbone. As ~95% of the energy released from a fat is from the three fatty acids, I'm ignoring the Glycerol backbone, to keep the maths as easy as possible.  Stearic Acid is CH3(CH2)16COOH. I'm approximating it to 18(CH2), to keep the maths as easy as possible.

54(CH2) + 81(O2) → 54(CO2) + 54(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 81 molecules of Oxygen produce 54 molecules of Carbon Dioxide, the RER is 54/81 = 0.67

Note: The RER for fats is actually 0.7, as the Glycerol backbone is converted into Glucose by the liver. As the RER for Glucose is 1, this raises the RER of my approximated fat by ~5%.

Converting molecular weights into their gram equivalents, 756g of approximated fat combines with 2,592g of Oxygen to produce 2,376g of Carbon Dioxide plus 972g of water plus ~28,468kJ of energy.

We lose weight by breathing, weeing, pooing, sweating etc. See also Majority of weight loss occurs 'via breathing'.

This doesn't invalidate Energy Balance, as the kcal/kJ values for foods merely represents the amount of chemical energy that can be released by oxidation of the various fuels in the foods. See Why Calories count (where weight change is concerned).

We gain weight by consuming fuels & water.

Saturday, 1 June 2013

Metabolic Inflexibility: What it really means.

Here's a picture from Metabolic Flexibility and Insulin Resistance.

The Metabolically-Inflexible (MI) & Insulin Resistance

Here's another picture.
Fig 2. ● = Metabolically-Flexible (MF). ○ = Metabolically-Inflexible (MI).
Salient points:
1) Excessively high serum FFA a.k.a. NEFA is bad.
2) Respiratory Quotient (RQ) a.k.a. Respiratory Exchange Ratio (RER) changes due to dietary changes are more sluggish in the MI than in the MF.
3) Under Insulin Clamp conditions, RQ/RER is lower in the MI than in the MF, due to impairment of glucose oxidation and non-oxidative glucose disposal.

I have posted this because of Danny Roddy's post Is Supplemental Magnesium A Surrogate For Thyroid Hormone? , which leads onto A Bioenergetic View of High-Fat Diets.

In the first article, Danny Roddy writes:-
"Additionally, taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient (e.g., high-fat diet, light deficiency, excessive exercise) seems pretty silly. For example, as a rule, diabetics have a reduced respiratory quotient (Simonson DC, et al. 1988), tend to have higher levels of free fatty acids or NEFA (Kahn SE, 2006), and are often deficient in magnesium (De Valk HW, 1999)."

The second sentence (diabetics have a reduced respiratory quotient...and are often deficient in magnesium) seems to contradict the first sentence (...taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient seems pretty silly).

Simonson DC, et al. 1988 is Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin-dependent) diabetic patients.
"In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal."

Impaired glucose oxidation with normal lipid oxidation lowers RQ/RER. Therefore, lower RQ/RER must be bad, right? Wrong. From the above study:-
"...euglycaemic insulin clamp studies were performed..."
Remember Salient point 3)? Simonson DC, et al. 1988 is an insulin clamp study, the results of which don't apply to free-living people (who aren't insulin clamped).

See also Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. RER/RQ increases & decreases with increases & decreases in exercise intensity. This is Metabolic Flexibility (MF). Sorry, Danny.

Thursday, 2 May 2013

Respiratory Exchange Ratio (RER) explained.

Science!
What the heck is this?
RER has been mentioned a few times on this blog. By measuring the rate of CO2 exhaled and the rate of O2 inhaled, it's possible to work out how many kcals/min the body is generating from food at any instant and from what fuel mixture.

An RER of 0.700 means that 100% of energy is being generated from fat.
An RER of 1.000 means that 100% of energy is being generated from carbohydrate aerobically.
An RER of >1.000 means that 100% of energy is being generated from carbohydrate, some aerobically and some anaerobically.

How does this work? Fats are an ester of fatty acids + glycerol. Acid + Alcohol = Ester + Water.

Saturated fatty acids (the easiest type to calculate) have the generic formula CH3(CH2)nCOOH, where n can be from 0 to 16. Here are some saturated fatty acids and their n values:- Acetic (0), Propionic (1), Butyric (2), Lauric (10), Myristic (12), Palmitic (14) and Stearic (16). The total number of carbon atoms in each fatty acid is n+2. Stearic acid is mostly CH2s, so I'll approximate fat to n(CH2).

n(CH2) + 3/2n(O2) = n(CO2) + n(H2O) + Heat. The ratio of CO2 to O2 is 2/3, so RER = 0.666.

As fats contain things other than CH2 (e.g. glycerol CH2OHCHOHCH2OH), this raises RER to 0.700. Burning protein gives an RER = 0.800.

Carbohydrates have the generic formula n(CH2O), where n = 6 for glucose.

n(CH2O) + n(O2) = n(CO2) + n(H2O) + Heat. The ratio of CO2 to O2 is 1.000, so RER = 1.000.

So how on earth can Eskimos have an RER = 0.600? I have a theory. When hydrogen is oxidised, water only is produced. There is no CO2, so RER = 0.000. Therefore, if some hydrogen was being burned (by gut bacteria, say), this could result in RER falling below 0.700. Maybe...

Saturday, 20 December 2008

Everyone is Different.

If there's one thing I've learned over the years of research into Diet and Nutrition, it's this: Everyone is Different. When I first discovered low-carbohydrate diets (thanks to the late Dr Robert C. Atkins M.D.), I thought that it was the One True Diet, and I became a bit of an "Atkins bore" telling everyone how wonderful it was and suggesting that everyone should be on it. I now know that what suits me* doesn't necessarily suit everyone else.

*It only suited me because I had Insulin Resistance/Metabolic Syndrome/Syndrome-X. I reversed it in 2008. See Insulin Resistance: Solutions to problems for how I did it.

Here's Fig. 2 from Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Used with permission.


Respiratory Exchange Ratio (RER) (a.k.a. Respiratory Quotient (RQ)) is the ratio of carbon dioxide breathed out to oxygen breathed in. This ratio depends on the fuels that the body is burning for energy. For example, if the body is burning 100% fats, RER = 0.7. If the body is burning 100% carbohydrates aerobically, RER=1.0. If the body is burning 100% carbohydrates, with some aerobically and some anaerobically (e.g. sprinting flat-out), RER > 1.0. To understand why this is so, see Respiratory Exchange Ratio (RER) explained.

RER varies with intensity of exercise, food intake (increasing protein &/or carbohydrate intake increases it and fasting or reducing protein &/or carbohydrate intake reduces it) and cardiovascular fitness. Increasing cardiovascular fitness reduces RER.

The top diagram is a histogram of fasted RER and % fat oxidation vs. number of subjects. At the left-hand end of the histogram, there are two cyclists with a fat oxidation of 93 - 100%. At the right-hand end of the histogram, there is one cyclist with a fat oxidation of 20 - 27%. Average fat oxidation is ~60%.

As exercise intensity increases, the peak in the histogram shifts to the right as shown in the lower diagram. At 25% of maximum intensity, mean fat oxidation is ~53%. At 50% of maximum intensity, mean fat oxidation is ~37% and at 75% of maximum intensity, mean fat oxidation is ~13%. At maximum intensity, mean fat oxidation is ~0% i.e. 100% of energy is obtained from carbohydrates when sprinting flat-out. Somebody on a very-low-carbohydrate, high fat ketogenic diet e.g. Atkins induction (~20g net carbs/day) could keel over with hypoglycaemia if they exercise for too long at too high an intensity.

As there is variation from person to person, you must find out for yourself your own optimum proportions of proteins, fats & carbohydrates, and these depend upon the intensity & volume of exercise you do. It sounds complicated, but it isn't really.

Apply the principle of "Eat, monitor & adjust accordingly" as Toxic Toffee (ex-Muscletalk member) always used to say. The eating bit will be covered in future Blog posts. The monitoring bit doesn't necessarily involve bathroom scales.

Hang on. Isn't "dieting" all about losing excess weight? Not necessarily. Remember the old joke?
Q. What's the best way to lose 5lbs of ugly flab?
A. Cut off your head.
As your body contains water, muscle, bodyfat, bones, cartilage, tendons, organs, glycogen, skin etc and your scales can't tell the difference between them, losing weight the wrong way can make you less healthy. However, losing weight the right way will make you more healthy.

If you starve, skip breakfast or go for a long run before breakfast, as your body is lacking glycogen reserves & amino acids, a large amount of a corticosteroid hormone called cortisol is secreted, which increases the conversion of muscle into amino acids, then glucose. As muscle has an energy density of ~600kcal/lb, a deficit of 3,500kcal (which would result in a bodyfat loss of 1lb) results in a muscle loss of 5.8lb. For more information, see The Energy Balance Equation.

Chronically-high cortisol also suppresses the immune system and weakens skin & bones.

Unless you have a lot of muscle mass to spare, it's bodyfat that you should be losing, and to monitor this, either use a tape-measure around your waist, check how loose/tight your clothes are, or strip-off and jump up & down in front of a full-length mirror. As Big Les (Muscletalk Moderator) says, "If it jiggles, it's fat.".

2016 EDIT: Scales that can calculate bodyfat % etc are now inexpensive, e.g. Body Analysis Scale.

So, what happens if you eat too much carbohydrate but your body doesn't burn it fast enough? Initially, carbohydrate intake tops-up liver and muscle glycogen stores, which increases carbohydrate-burning to compensate. The liver can store about 70g of glycogen and muscles can store about 400g of glycogen. If, despite increased carbohydrate-burning, more carbohydrate is consumed than is burned, glycogen stores continue to fill. When glycogen stores become full, RER increases to 1.0 and 100% of energy is derived from carbohydrate. Getting 100% of energy from carbohydrate means that zero fat is burned, so keeping glycogen stores filled to the brim by chronically overeating carbohydrate is not a good idea if you want to burn some body-fat.

Once glycogen stores are full, any additional intake of carbohydrate beyond that which is burned passes through the lipogenesis pathway - this basically means that carbs are turned into fat - which may end up as liver fat. But there's even worse news. Fat is secreted by the liver into the blood as triglycerides. This is bad for the cholesterol particles in your blood. See Cholesterol and Coronary Heart Disease. What happens if you eat too few carbs? As stated above, someone exercising at a highish intensity taking in insufficient carbohydrates could get hypoglycaemia & keel over.

How many grams of carbohydrate per day does it take to promote lipogenesis? Someone at rest burns ~1kcal/minute. If this is derived 100% from carbohydrate, this is equivalent to 0.25g of carbohydrate/minute, or 15g of carbohydrate/hour, or 360g of carbohydrate/day. Therefore, sedentary people who chronically consume more than 360g of carbohydrate/day may produce significant triglycerides. People who have The Metabolic Syndrome/Syndrome-X (a high proportion of people who have excess belly fat) have increased lipogenesis and higher serum triglycerides than healthy people.

Discussing weight again for a moment, it's often said that all diets are the same, as weight loss is all about calories. This is true. See Is a Calorie a Calorie? However, body composition is determined by a combination of macro-nutrient proportions (i.e. the relative amounts of proteins, carbohydrates and fats in the diet) and the intensity & volume of exercise. Health is determined by a combination of micro-nutrient proportions (i.e. vitamins, minerals & anutrients) and exercise. See On burning, storing and recomposing.

If you're only interested in weight loss, just count calories. If  you wish to lose bodyfat without losing muscle mass, you need to know what proportions of proteins, carbohydrates & fats to eat (it's really not that critical, but many people get it wrong). You need to know the difference between good carbs & bad carbs, and good fats & bad fats. You need to know the best times to eat proteins, carbohydrates & fats relative to exercise (it's also really not that critical, but many people get it wrong). You need to know the difference between good exercise & bad exercise.

Continued on We are not all the same.