Lecture 6
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Lecture 6. Energy Stores and Whole Body Energy Balance. Intake and Expenditure. Fuel oxidation rate is beautifully matched to ATP demand Well coupled at the molecular level But fuel intake is totally mismatched from ATP demand Ie, we don’t eat at the same time as we consume energy!

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Lecture 6

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Lecture 6

Lecture 6

Energy Stores and Whole Body Energy Balance


Intake and expenditure

Intake and Expenditure

  • Fuel oxidation rate is beautifully matched to ATP demand

    • Well coupled at the molecular level

  • But fuel intake is totally mismatched from ATP demand

    • Ie, we don’t eat at the same time as we consume energy!

    • See Frayn, fig 1.2

      • Like the discordance in petrol intake into a car

  • On a daily basis, energy intake does not match energy expenditure

    • Excess in energy consumed over energy expenditure will be stored as fuel reserves

    • Despite this, weight (fuel reserves) stay remarkably constant over time


Fuel stores

Fuel Stores

  • Fat

    • Three fatty acids esterified to glycerol

    • Hydrophobic

      • Stored in absence of water

    • 37 kJ/g

      • Very efficient

    • Stored in white adipose tissue (WAT)

      • Know the properties of WAT

        • What adipocytes look like

        • Where fat cells are located

        • How they are considered to be endocrine (hormone releasing)

    • We store about 10-15 kg fat (females > males)

  • Carbohydrate

    • Stored as glycogen

      • Branched polymer of glucose, formed on the protein glycogenin

    • Hydrophilic

      • All the –OH groups on glycogen make it very water-attracting and it is associate with lots of water

    • 6 kJ/g ‘wet’ – NB. Textbooks say that ‘dry’ carbs are 16 kJ/g but remember, in the cell, it is stored in association with water

    • Stored mainly in Liver (100 g) and muscle (250 g)


Why fat

Why Fat?

  • Useful to compare the size of the stores

    • Cup of flour vs 20 litres of cooking oil 

  • Seems strange that we store nearly all our energy as fat

    • Brain has obligatory requirement for glucose

    • We can’t convert fatty acids into glucose (or any carbohydrate!)

    • Also, muscle glycogen is not available to rest of the body

      • Only liver glycogen can be released for use by other tissues.

  • Note about Protein

    • Not really a stored fuel

      • We don’t have a specific protein that represents a store of amino acids

      • Protein is broken down under extreme conditions, but it is expensive to make so it is not suited as a fuel store


Intake and expenditure1

Intake and Expenditure

  • Weight (fuel stores) are kept relatively constant

    • Even though intake and expenditure are highly mistmatched on a day-to-day basis

  • We seem to have a ‘set point’

    • Over months the two sides are VERY finely matched

    • We are good at ‘defending’ our weight

  • Weight normally regulated to within about 1 kg/year

    • A 1 kg rise would represent an imbalance of about 30 MJ per year

    • Ie, 70 kJ per day

      • 2 g fat per day

      • 5 g carbohydrate (a teaspoon of sugar!)

    • These are imperceptible amounts in dietary analysis

      • <1% of daily energy intake

      • Over that year we would have consumed about 4000 MJ

  • So what are the key components and regulators of intake and expenditure?


Expenditure

Expenditure

  • Three main components (see Frayn Ch 11)

    • Basal metabolic rate (BMR) – 60%

      • Resting metabolic rate (RMR)

    • Physical activity - 30%

      • Voluntary and Non-exercise activity thermogenesis (NEAT)

    • Diet-induced thermogenesis – 10%

      • Thermic effect of food

  • Obviously the contributions will vary in individuals

    • We can do something about physical acitvity but

    • Can we do anything about BMR…

      • Does BMR vary between individuals?


Measuring ee

Measuring EE

  • Indirect calorimetry

    • Measuring oxygen consumption

      • Because energy expenditure linked to the rate of the electron transport chain and the latter involves oxygen consumption

      • Energetic value of oxygen consumption always 20 J/ml regardless of fuel used

    • Inconvenient and ‘short-term’

    • Could use empirical equations

      • Harris-Benedict

  • Doubly labelled water

    • Measure of carbon dioxide production


The harris benedict equation

The Harris Benedict Equation

Estimate BMR 

  • Women:

    • BMR = 655 + ( 9.6 x weight in kilos ) + ( 1.8 x height in cm ) - ( 4.7 x age in years )

  • Men:

    • BMR = 66 + ( 13.7 x weight in kilos ) + ( 5 x height in cm ) - ( 6.8 x age in years )

      The only factor omitted by the Harris Benedict Equation is lean body mass. So it is quite accurate in all

      but the very muscular (where it will under-estimate BMR) and the very fat (will over-estimate BMR)

      Multiply by 4.184 to get into kJoules.

      Multiply BMR by the appropriate activity factor:Sedentary (little or no exercise) : = BMR x 1.2 Lightly active (light exercise/sports 1-3 days/week) :  = BMR x 1.375 Moderatetely active (moderate exercise/sports 3-5 days/week) :  = BMR x 1.55 Very active (hard exercise/sports 6-7 days a week) :  = BMR x 1.725 Extra active (very hard exercise/sports & physical job or 2x training) :  = BMR x 1.9 Note how the activity doesn't make as much difference as you might expect.

      See also Frayn Table 8.4 for a list of how various activities increase metabolic rate.


Lecture 6

BMR

  • BMR is almost totally dictated by LEAN BODY MASS

    • Ie, the mass of metabolically active tissue

    • Muscle metabolically active because it is continually pumping ions, even when it is ‘still’

    • Adipose tissue is relatively inactive

    • So plots of metabolic rates vs fat free mass (FFM) are linear

      • Slope is 4 ml O2 consumed per min per kg FFM (ie, about 100 kJ/day/kg FFM)

    • Overweight people do not have lower BMRs (see Frayn Fig 11.5)

      • Inded the extra weight makes whole body metabolic rate higher

  • Factors that could potentially change BMR

    • Uncoupling proteins

      • Brown adipose tissue UCP-1, but also maybe UCP-2 and UCP-3 in muscle

    • More lean body mass

    • Substrate cycles (futile cycles)

      • Fuel synthesis then breakdown

        • Eg, make protein from amino acids consuming ATP, then dismantle the protein (with no gain of ATP)

      • Leaky membranes

    • Thyroid hormone

      • T3 strongly affects metabolic rate

        • Lack of thyroid hormone reduces BMR

      • But how?

        • We know it’s transcriptional but exactly which genes change and how this then changes metabolic rate is not known


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