APPLIED NUTRITION FUNDAMENTALS OF NUTRITION

CARBOHYDRATES; STRUCTURE, METABOLISM AND BIOCHEMISTRY

KEY LEARNING POINTS

Understand the structure of various carbohydrates forms

Understand the passage from ingestion through to cellular fuel.

Arguably the most hotly debated macronutrient, carbohydrate often remains the ‘accused’ when it comes to weight, fat gain and the general
health of the population.

For this reason, its inclusion, exclusion or drastic reduction from any dietary regime is commonplace. If we’re to fully understand the context
in which such strategies would be appropriate we need to get a full grasp of carbohydrates role within the diet and it’s structure.

Carbohydrates central role within the body is to provide cellular fuel for essential function. Importantly, for compositional purposes, it also
helps to facilitate the metabolism of fat.

Carbohydrates are abundant in our diets and can be found in many forms. Carbohydrates (CHO) are composed of carbon hydrogen and
oxygen in a ratio of 1:2:1 respectively. They are metabolised for energy via glycolysis and the TCA (tricarboxylic acid) cycle -also known as the
citric acid cycle (CAC) and are of vital importance to good health and optimal physical performance.

The form of CHO, timing and what it is consumed with will all impact its effectiveness. It becomes apparent that CHO consumption is not a
straightforward issue and this lesson will aim to clarify some of these issues. In many areas, the evidence is mixed or even contradictory, and
in these situations, it is often a case of working out what works with each individual. This is true not only for CHO but a lot of nutrients; the
literature can only ever be used as a guideline.

The Building Blocks of Carbohydrates

Structurally there are four major forms of carbohydrates. Monosaccharides, disaccharides, oligosaccharides and polysaccharides.

Figure 1.1 Carbohydrate Structures

Glucose

Glucose a simple monosaccharide sugar is one of the most important carbohydrates and is used as a source of energy in animals and plants.
Glucose is one of the main products of photosynthesis and starts respiration. The natural form (D-glucose) is also referred to as dextrose,
especially in the food industry and is the one the body can utilise. It's mirrored form L-glucose

Figure 1.2 Chemical Structure of Glucose

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Fructose

Fructose is more commonly found together with glucose and sucrose in honey and fruit juices. Fructose, along with glucose are the
monosaccharides found in disaccharide, sucrose.

Many processed foods use corn syrup as a sweetener, and this contains fructose. Because processed foods are so abundant in the Western
diet fructose is now one of our major dietary monosaccharides. From an exercise perspective, we will see later that fructose is mainly
metabolised in the liver and this needs to be considered when using this in energy drinks and foods.

Figure 1.3 Chemical Structure of Fructose

The main monosaccharides are joined up to form disaccharides (di = two, thus two sugars) by the removal of water. Disaccharides contain
two molecules and oligosaccharides can be anywhere between three to twenty monosaccharides in length (Although textbooks will differ on
this number).

Polysaccharides are formed majorly of starches and fibres. though more complex polysaccharides form a large molecule made up of
hundreds or thousands of molecules and form the major storage molecules in plants and animals, starch and glucose.

Irrespective of the type of saccharide (A general synonym for sugar) if the body is deficient of any particular form, it can, through various
enzymatic and molecular steps create any type of saccharide from glucose if necessary.

These specific classifications of carbohydrates allow us to understand better, the transference and passage from ingestion or consumption
through to, digestion, absorption and finally into a usable cellular fuel. The speed at which it travels from your small intestine to the blood
will dictate mainly its most effective use within a dietary regime aimed at certainly performance, for the general populous however often
these details are extraneous.

For us to make use of any these forms as a cellular fuel source, they must be digested first. In some cases, part of this process is already
accomplished, and the food is already partially broken down pre-ingestion. This is then hydrolysed (broken down by chemical reaction with
water) and further broken down into a single molecule, monosaccharides. When we consume different types of foodstuffs, the food comes
with enzymes that help break it down for us, or the body produces enzymes to act as a catalyst in the breaking down of these complex
structures into their simpler useable formats. Food that has its own enzymes rot and this is why the food industry will remove enzymes to
extend the overall shelf life of foods.

In the case of carbohydrates the ones most of note are those of starches or polysaccharides. After and to some degree before the ingestion of
starches the salivary glands, pancreas and small intestine produce amylase, the enzymatic catalyst that allows the breakdown of these more
complex forms.

The primary regulator of insulin secretion by the pancreas remains the concentration of glucose in the plasma (bloods main medium for
transportation) as if this level of glucose increases rapidly or remains high as does the synthesis of insulin. The normal concentration of
glucose in plasma is 5 mmol/l, and any level above this will cause an increase in the responsive secretory rate of insulin.
The body is in a regulatory pattern. Therefore, the level of glucose in plasma tends to stay pretty constant under healthy circumstances with
the level of insulin circulating being the larger variant of the two. Insulin is one of the critical controllers of this set point alongside the
regulatory and counter-regulatory neurohormonal system.

Any variability brought about by adverse dietary patterns and what appears to be chronically high blood glucose levels above about 11
mmol/l appear to have implications with diabetes mellitus, insulin resistance and beta-cell dysfunction.

Other fluxes in it are brought about by alterations in its uptake, retention and disposal rates, but as a general rule, if there is an increase in
exit (glucose disposal) brought about by an increase in activity, there is at the same time an increase in delivery to

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stabilise levels. 1

This supports a shift from insulin-mediated energy pathways to those that are glucagon-mediated. 2,3 The switch between these pathways
may cause short-term issues for many. Ways in which we may temporarily offset this will be discussed in the following lessons when we
consider fats in more detail, it is largely due to a simple transient adaptation period. We need time to adjust to any changes in fuel demand.
The same applies to exercise. Move from doing low reps and high weights to doing high reps and low weights it will feel very challenging
for a period until the ‘skill’ should we say of fuel use is mastered.

Within the typical Western diet, the average person consumes about 300 g of carbohydrates daily. 4 Consider that a healthy functioning
adult can store approximately 400 g as muscle glycogen, 90–110g as liver glycogen, and 25 g circulates the blood as glucose. 5

Fluctuating blood glucose, reduced insulin secretion, cellular resistance and overindulgent dietary practices (excessive hypercaloric dieting
and binge patterns of eating) all have a part to play in excess of carbohydrate being consumed, given the individual's physiological
circumstances.

If we wish to address that with further detail under normal conditions, skeletal muscle glycogen concentration is between 1.5–2 g/100 g
skeletal muscle. 6-9 This is the amount of the fuel mentioned above that has managed to make it’s way through digestion, into the
bloodstream, managed to jump on the proverbial bus (Insulin) and get a ride into the cell.
Now, if we move the body out of normal conditions and look to deplete glycogen stores the body is able to increase storage capacity by over
50%. The one caveat is that the majority of these studies are done on endurance athletes. It's speculated that the capacity for weight trained
athletes may potentially exceed this as one of the goals of ‘bodybuilding’ style training is to get good at glucose disposal by ‘wringing’ it out
of the cells through contraction and tension. Then following on from that taking the super compensated cell and packing it full of more
nutrients progressively.

Carbohydrates and Weight Loss

The vast majority of weight loss most will see from low carbohydrate diets is brought about by the alteration in cellular fluid levels alongside
the inherent reduction in calories. Remember that any “weight loss” strategy usually revolves around the omittance of a common food type
or group in which someone removes, the emphasis here is ‘remove’, not replace thus the weight loss comes from lowering the net amount
of calories consumed by foods that have commonly graced their plates in excess. People don’t know what to replace them with, or the foods
that are banned are the calorie dense or hyper-palatable foods they resonate towards. Typically a non-sustainable approach to weight loss.

Telling the average Westerner to omit carbohydrates, gluten, or such like from their diet isn’t typically a replacement thing.

They merely lower net caloric intake by taking something out of their diet that played a large role in their intake previously.

During any prolonged period of carbohydrate restriction, a decrease in plasma glucose as little as 20 mg/dl (From 90–70 mg/dl) causes a
reduction in glucose metabolism and thus signals the onset of hypoglycemia and release of the counter-regulatory hormones glucagon,
catecholamines, cortisol and growth hormone. 2

This gives support and understanding behind the methods that periodically and intentionally deplete levels of glycogen, particularly in
weight/fat loss regimes. It also outlines the necessity not to exclude carbohydrates for any sustained periods of time. The consequences to
merely energy output and response to foods is adequate alone to support this. Someone with
chronically low blood glucose is not going to be training effectively, so this offsets any benefits and the chance of any form of progression.
The consequence of dietary choices in a world where hyper-palatable glucose-raising foods are omnipresent becomes a, ‘how long can
someone stick it out for scenario’. Again, largely non-sustainable.

The period in which cells may uptake these amounts mentioned above will depend on various factors including the degree of beta-cell
function, the rate of glucose disposal, and total body mass. If we correlate with obesity, this would suggest that the total amount of carbs
required to stockpile functioning cells would be lower and the disposal of fuel to create space in these cells slower. The necessity therefore
for cellular re-feeds would be over a longer duration in more obese populations. Fundamentally, unless someone is already physically lean,
dietary re-feeds serve little more than a psychological break from the 'diet' and would be indicative of a poorly planned or unnecessarily
extreme approach.

In addition, the management of carbohydrates with a smaller molecular number of saccharides and higher GI may well be poorly managed
in such populations. The inclusion of more complex, fibrous, and lower glycemic carbs may yield better benefit in the early stages of weight
loss. However, the relevance of GI in mixed meals becomes less so.

The higher and faster the rise in glucose, the more insulin should be produced in response by the beta cells of the pancreas and at what
rate; this is referred to the glucose-sensitive insulin secretion (GSIS) which we will get into in greater detail in later lessons. A diminished

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function of GSIS is tantamount to buying your weekly shopping but only taking one carrier bag. The glucose has no carrier (insulin) to
transport it to cells, so it remains in and circulating the bloodstream. This state over time perpetuates the problem and often leads to the
various stages of insulin resistance, beta-cell dysfunction, and issues we associate with type 2 onset diabetes.

In regulating this response, low and medium GI foods are often suggested as a carbohydrate of choice. Alternatively, short term lowering of
total carbohydrate intake to rectify the insulinogenic response and bring up insulin sensitivity is also a suitable strategy. This, however,
remains to be once again superseded with the need to have a lower caloric intake and is again not as important as hypothesised.

Someone demonstrating an impaired glucose tolerance will not be able to release insulin rapidly to coincide with a rapid rise in blood
glucose. If someone is in a caloric deficit with a balanced amount of proteins, fats and carbohydrates the demand on this concurrently
lowers. Again we emphasise the need to establish energy balance beyond anything else.

Why do we need carbohydrates and is it essential?

An essential nutrient is defined by it’s requirement for survival and if it can be produced independently by the body. Carbohydrates are
therefore non-essential as a nutrient if our only intention is survival.11 We are perfectly capable of producing adequate glucose in the
absence of dietary carbohydrates and sufficient calories to fuel essential tissue on a day to day basis.

If you intend doing anything beyond that though, carbohydrates become a fundamental requirement.

Readily taking in carbohydrates to fuel our workouts and day to day activity serves multiple purposes. It allows us to keep blood glucose at a
steady state fueling the working muscles and enabling a higher work capacity , assuming that it’s delivery is fast enough and efficiently gets
into cells to do so.

Carbohydrate within the diet also allows the highly anabolic hormone, insulin to come into play. The action of insulin will help protein
synthesis and ensure that the catabolic actions of protein breakdown are kept to a minimum. Carbs for this reason are known as a ‘protein
sparing’ nutrient, a term man of you will be familiar with. This obviously limits the breakdown and usage of protein as a fuel source. 12,13

It also inhibits the catabolic effect brought about by lower blood glucose and insulin. Someone simply removing carbohydrates from their
diet, without simultaneously providing protein to pick up the 'caloric slack’ so to speak will, over time decrease the ratio of fat loss and
increase that of protein. Counterproductive if physique development, the building or maintenance of muscle tissue is the goal.

So how much carbohydrate do we require?

Glycogen is the readily mobilised stored form of glucose. When energy is needed glycogen is broken down to yield glucose. This also serves
to buffer and maintain the stable level of blood glucose concentration required between meals or in any fasted periods. 14

Glycogen is stored in two primary sites, the liver and skeletal muscle with the kidneys and intestines adding a minor storage capacity. There
is a storage capacity of approximately ∼500 g in skeletal muscle scaling upwards or downwards based largely on LBM (Lean body mass) and
the trained state of muscles. The liver stores approximately 70-100g and doesn't appear to vary greatly in individuals from this amount.

When we consider energy use, beyond the ATP-PC system and exercise that is longer in duration we move into glycolysis.

Glycolysis is the breakdown of carbohydrates and lasts roughly between 10 seconds and anywhere up to two to three minutes so when we
consider most forms of resistance training, particularly that which is focused on physique development this is the energy system that is
utilised the most.

Training that calls for the ongoing use of glycolysis as a means of fuel creates biochemical changes influencing, over time the amount of
glycogen that someone can store in muscle tissue. The time period over which this adaptation occurs is largely the reason that carb loading
protocols in novice athletes has very little impact.

Most of the data that we have on carb loading is based on endurance athletes, we actually have very little data with respect to physique
athletes or bodybuilders. Due to the training differentials between the two activities it could be hypothesised that these numbers could be
significantly larger in physique competitors or bodybuilders.

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Figure 1.4 Muscle glycogen levels across varying states.15,16

The transport of glucose into cells.

On average for every 10-15 g of carbs we consume, the body will use around 1 unit (iu) of insulin to manage and act as the substrate carrier
into cellular tissue. Most of the data regarding this is taken from diabetic populations as once again this is where the vast majority of the
research lies. The actual numbers are less of an importance, more so that we understand that there is a ratio that will be very specific to the
individual.

At basal level the amount of insulin someone produces daily would typically be divided into 24 units to reflect what is produced per hour.
Each meal ingested on top of this will classically induce a further five to six units of Insulin to be produced. This would mean an average
Westerner consuming the stereotypical three meals a day with fully functional GSIS (Glucose sensitive insulin secretion) would produce
around 42 units (relative to their basal unit amount) maximally or fundamentally, if norms are to be accepted this would correlate with the
ability to take 420-630g of glycogen into cells. This also partly explains the benefit that those with larger amounts of LBM of increased meal
frequency have.

The degree therein of insulin resistance (diminished GSIS) or sensitivity will play a role with the total capacity of cells and obviously impact
the daily amount required. This will also be related to the pancreatic function on a genetic level. Some people appear to handle
carbohydrates better than others but once again the notion that someone can't tolerate them is absurd as so many variables and influencing
factors are controllable.

A large part of the demographic we deal with as clients will be striving for weight loss and undoubtedly be in a state of diminished GSIS. The
absolute level of glycogen they are capable of storing in cells will, therefore, be compromised and the surplus would result in chronic
elevated blood glucose levels. This alongside the previously mentioned factors will impact the numbers we are considering and more than
adequate rationale to maintain a slightly lower level of carbohydrate in obese populations pursuing weight loss.

Getting leaner prior to trying to add mass will have the benefit of increased glycogen uptake, a large and important factor in growth. The
leaner someone becomes the more sensitive cells will become to the actions of insulin. If you do the math at this stage, you will realise why
frequency of meals can play a role when attempting to build more lean tissue and potentially capitalising on the benefits of insulin. This
would only play any hypothetical relevance to those that have somewhat maximised cellular saturation of glycogen and volume within their
workouts. Those already with a significant amount of tissue.

You can also see the benefit in an increased meal frequency to insulin-resistant populations.

This is a very brief overview of Insulin and it will be covered in much greater detail in the later lessons.

Carbohydrates requirements, intake, management and all of the aforementioned factors all come into play when deciding on a
carbohydrate intake for someone. Alongside this, the total caloric intake must also be taken into consideration the degree of insulin
resistance or sensitivity. The overall level of adiposity (fat mass) and the type and frequency of training. As we can see it is a hugely personal
thing with huge variability.

What is therefore low carb to one person isn’t contextually to another. Someones ability to handle carbohydrates from both the stage of
ingestion, digestion and absorption varies hugely and this, in a nutshell, is the take-home point here.

Just like any macronutrient people desire absolutes with respect to the numbers they are aiming for. To elude that there is an ‘absolute’
number or even ideal is absurd. We have guidelines and from these there is simply a baseline in which to start from.

In most cases and in the absence of in-depth laboratory testing trial and error around someone carbohydrate intake is often the best
approach. Establishing the start point of someones diet from their current intake gives us clues as to what calorically they may tolerate and
require, what they would require from protein and fats its slightly more specific (but again not absolute) and what remains we can assume

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more often than not can come from carbohydrates. From this caloric base adjusting levels of carbohydrate up and using protein and/or fats
to buffer the deficit of calories would be the general approach.

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REFERENCES

1. Wahren J., Felig P., and Hagenfeldt L. “Physical Exercise and Fuel Homeostasis in Diabetes Mellitus.” Diabetologia 14 (1978):
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2. Gerich J. “Glucose Counterregulation and Its Impact on Diabetes Mellitus.” Diabetes 37 (1988):1608–1617.

3. Rorsman P. and Braun M. “Regulation of Insulin Secretion in Human Pancreatic Islets.” Annual Review of Physiology 75
(2013):155–179.

4. Henquin J. C., Ravier M. A., Nenquin M., Jonas J. C., and Gilon P. “Hierarchy of the Beta-Cell Signals Controlling Insulin
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5. Frayn K. N. Metabolic Regulation: A Human Perspective 2nd ed. (Oxford, UK: Blackwell Publishing 2003).

6. Ørtenblad N., Westerblad H., and Nielsen J. “Muscle Glycogen Stores and Fatigue.” Journal of Physiology 591 (2013):4405–
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7. Ahlborg B., Bergstrm J., Ekelund L. G., Hultman E., and Maschio G. “Human Muscle Glycogen Content and Capacity for
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8. Burke L. “Nutrition Strategies for the Marathon” Sports Medicine 37, no. 4 (2007):344-347.

9. Fogelholm G., et al. “Carbohydrate Loading in Practice: High Muscle Glycogen Concentration Is Not Certain.” British Journal
of Sports Medicine 25, no. 1 (1991):41–44.

10. Sherman W. M., Costill D. L., Fink W. J., and Miller J. M. “Effect of Exercise-Diet Manipulation on Muscle Glycogen and Its
Subsequent Utilization During Performance. International Journal of Sports Medicine 2, no. 2 (May 1981):114–118.

11. Westman, EC (2002). "Is dietary carbohydrate essential for human nutrition?". The American Journal of Clinical Nutrition 75 (5): 951–3;
author reply 953–4. PMID 11976176.

12. Lemon PWR, Mullin JP. Effect of initial muscle glycogen levels on protein catabolism during exercise. J Appl Physiol. 48: 624-629, 1980.

13. Tarnopolsky MA, Atkinson SA, Phillips SM, MacDougall JD. Carbohydrate loading and metabolism during exercise in men and women. J
Appl Physiol. 78: 1360-1368, 1995.

14. Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Chapter 21, Glycogen Metabolism.

15. D L Costill, W M Sherman, W J Fink, C Maresh, M Witten, and J M MillerThe role of dietary carbohydrates in muscle glycogen resynthesis
after strenuous running.Am J Clin Nutr 1981 34: 9 1831-6

16. Sherman WM, Costill DL, Fink WJ, Miller JM. Effect of exercise-diet manipulation on muscle glycogen and its subsequent utilization
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