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Flashcards in Chapter 1-3 Deck (126):

what is glycogen ? origin, function

(1.3) Glycogen is the storage carbohydrate within mammalian muscle and liver.

It's a large polysaccharide polymer catalyzed by glycogen synthase. (glycogenesis)


synthesis of glycogen - how ?

by adding individual glucose units to an existing glycogen polymer.
requires energy (using 1 ATP and 1 UTP)

1) 1 ATP donates phosphate to glucose.
glucose ----(hexokinase)--> glucose-6-phosphate
2) glucose-6-phosphate glucose-1-phosphate
3) uridyl transferase reacts UTP with glucose 1-phosphate ---------> uridine diphosphate (UDP)-glucose
4) UDP-glucose attaches to existing polymer chain with glycogen synthase.


how much glycogen does the body store ?

80 kg man- 500g carbs.
400g- muscle glycogen
90-110g- liver glycogen (depending on diet)
2-3g blood glucose

(each g = 4 kcal, so 2000 kcal stored as carbs)


limits of glycogen storage

15g/ kg BM


difference between glucogenesis and gluconeogenesis

glucogenesis: creating glycogen from glucose
gluconeogenesis: creating glycogen from non-carbs (protein)


what happens when you elevate/ decrease blood glucose levels.

Elevated [gl] = beta cells of pancreas secrete insulin (feedback regulation) to facilitate glucose uptake & inhibit further insulin secretion

Falling [gl] = alpha cells secrete glucagon (insulin antagonist), stimulating glycogenolytic & gluconeogenic pathways


neural-humoral factors in exercise

E, NE, glucagon, decrease insulin release. Activates glycogen phosphorylase to facilitate glycogenolysis in liver and muscles.


homeostatic norms for plasma glucose

80-100 mg/dL blood
(4-5 mmol/L)


hypocaloric state

[gl] may decrease. but may not- there are other sources that may produce glucose (like protein)

in exercise: not enough carbs & other sources, {gl] goes down to hypoglycemic levels (


hypoglycemia effects

brain relies on glucose- without it it shuts off, CNS & PNS affected by dizziness, nausea, fainting, syncope


the relationship between RBC and glucose ?

RBC metabolize glucose (lactic-acid is a by-product). NO OTHER TISSUE IS AS EXCLUSIVE TO CARBS


what are the 2 main consumers of carbs

brains & blood


what does the heart consume?

lactic acid ( a carb), carbs, fats


what does skeletal muscle consume?

fat, carbs (glycogen & plasma glucose).


feedback regulation of glucose

[blood glucose] affects liver glucose output (increase in bl gl inhibits hepatic output)


25 % VO2max - what is going on with the carbs ?

liver furnishes glycogen. O2 meets energy demand, no especial need for blood glucose


high % VO2max- what is going on with carbs ?

(fig 1.5) intensity increases, glucose released from liver & glucose uptake increases SHARPLY. Increase in intensity leads to great demand & greater delivery & uptake.


what happens if an untrained person goes to a high exercise intensity ?

inadequate O2 provided to mitochondria. Pyruvate will only be able to go to lactic acid, since ETC, Krebs etc shuts down.
Highly trained person will produce less lactic acid.


relationship between hormonal release and binding & exercise intensity

glucagon, NE, E
as exercise intensity increases, hormonal release & binding will increase.


how much time in a strenuous workout is needed to deplete glycogen in liver & muscles ?

2 Hrs


what does the nutrient mixture for energy depend on ?

relative exercise intensity (%VO2max)


what source is prioritized for energy at different intensities ?

low intensity: FAT is main substrate.

as intensity increases: muscle glycogen decreases, so blood glucose becomes main CHO source, & fat catabolism furnishes an increasingly greater %.

even higher intensity: glucose output from liver is too little for glucose demand of muscle, plasma glucose drops (hypoglycemia). circulating fat increases dramatically.


prolonged exercise in glycogen-loaded & glycogen-depleted states - plasma glucose & fat use

(fig 1.6)
depleted: blood glucose falls with time, & circulating fat increases dramatically.
loaded: blood glucose increases, fat increases but far less dramatically.


contribution of protein ( as demonstrated by plasma 3-OHbutyrate levels (beta-Hydroxybutyric acid)) in glycogen -loaded & glycogen depleted states

(fig 1.6)
depleted: protein use increases
loaded: protein use very insignificant.


exercise intensity in glycogen loaded & glycogen depleted states

depleted: intensity on downward slope from the very beginning.
loaded: intensity can stay constant for 2 hrs.


when does fatigue occur (as related to glycogen) ?

fatigue occurs when activity continues to the point where it compromises liver & muscle glycogen content (despite O2 availability).

inactive muscles maintain full glycogen content (because skeletal muscle lacks phosphatase enzyme, which allows glucose exchange between cells)


muscle glycogen depletion = point of fatigue. why ?

1) depressed availability of CHO for CNS function.
2) muscle glycogen is a primer in fat breakdown.
3) slower rate of energy release from fat compared to CHO.


time to exhaustion with normal, high carb, and low carb (high fat) diets.

normal: 114 min.
high-fat/ low carb: 57 min. rapidly depleted liver & muscle glycogen, negatively affects anaero and aero activity.
high carb: more than 3x the low-carb diet. (+/- 170 min)

however, point of fatigue coincided with same muscle glycogen level in all three groups.


recommended amount of CHO in diet for athletes

60-70% of daily kcal


saturated vs unsaturated fatty acid

saturated: hard fat, close together.
unsaturated: double bonds inhibit close association, therefore these foods will be softer fats eg oil.



triacylglycerol formation.


when is fatty acid mobilization predominant ?

1) low-mod physical activity
2) low-cal diet
3) cold stress
4) prolonged exercise depleting glycogen reserves.


what are trans-fatty acids ?

found in junk food, vegetable shortening, etc.
decrease [HDL], increase risk of heart disease.






glycerol (3C) base with three fatty acids.


how many g of adipocytes in 80 kg individual ? implications ?

12 000. which is a lot. meaning that there is a HUGE AMOUNT OF STORED ADIPOSITY


how many g free fatty acids in plasma ?




1) HSL + water break off one fatty acid, leaving 1,2-diacylglycerol.

2) HSL + water break off another fatty acid, leaving 2-monoacylglycerol

3) HSL+ water+ MONOGLYCERIDE LIPASE break off the last fatty acid from glycerol.


where does esterification & lipolysis happen ?

usually in cytosol of adipocytes. however can also happen in small intestine (w/ lipoprotein lipase)


what are FFA bound to in blood for transport ?



what do fats need to cross membrane ?

nothing. no hormones, no energy, nothing except for a concentration gradient.


where do FFA go ?

brain, heart, liver, kidneys, muscle


distribution of fat in body

-adipose tissue mostly
- intramuscular TG
- plasma TG
- plasma FFA


hormone-sensitive lipase- what is it?

it's a lot more powerful in cleavage (lipolysis) when it is surrounded by E, NE, glucagon, GH. they excite lipase so it "does its job"


what is RQ formula ? what are the usual values ?

respiratory quotient, between 0.7 (fats) and 1 (carbs). protein is somewhere in between the two.

volume CO2 produced/ volume O2 consumed.


calculating RQ of combustion of glucose


6 mol CO2/ 6 mol O2 = 1


calculating RQ of combustion of palmitic acid


16 CO2/ 23 O2= 0.7


RQ as related to exercise duration


as exercise duration increases, RQ decreases ( more fat utilization as glycogen is depleted)


percentage of total energy as related to exercise duration

as exercise duration increases, CHO utilization decreases & fat utilization increases.


energy sources different intensities and exercise durations

(fig 1.16-1.17)

LOW-MOD: fat is the major source. (FFA released & delivered to muscle after 1) hormonal stimulation and 2) decrease in plasma insulin lvls
start of exercise demonstrates transient drop in plasma FFA due to increased FFA uptake).

MOD/MILD/HIGH: fat & carbs in equal amounts. as time goes by, fat catabolism supplies greater % of energy with progression of glycogen depletion (toward the end, may supply 80-85%).
here, carb utilization is much more noticeable than for low intensity exercise- carbs are the preferential fuel for intense aerobic exercise.


is it easier to utilize fat or carbs ?

fats use more O2 to combust (RQ= 16 CO2/23 O2), but many people are limited in their O2 consumption.
the ultimate factor in managing the proportion of energy sources is oxygen delivery.


sources of body protein

blood plasma, visceral tissue, muscle.

NO RESERVOIR of proteins, all of it contributes
between 12-15 % body mass, but protein proportion depends on different body parts (RBC and muscle cells have more, like 20%)


protein catabolism, what does it contribute to overall energy requirement ?

2-5 % in well-nourished individuals at rest


deamination (see drawing)

protein degrades into amino acids, and then loses nitrogen in liver to form urea.


what happens to the components of the amino acid in deamination ?

the NH2 group goes into the urea (kidneys and then urine / sweat glands and then sweat)

excessive protein catabolism therefore promotes fluid loss since urea requires to be dissolved in water to be excreted.

the deaminated amino acid becomes:
- another a.a
- a carb or fat
- catabolizes for energy


what happens to a deaminated amino acid in exercise?

becomes a CHO and goes to the muscle.

NH2 & urea production & excretion increases proportionally to exercise intensity.


transamination- what is it ?

amine group from a donor a.a transfers to an acceptor a.a to form a new amino acid. (enabled by transferase enzyme)


example of transamination: glutamate & pyruvate.

glutamate will donate its NH2 and go to alpha-ketoglutamic acid (alpha-ketoglutarate), which is a CHO that will go to Krebs.

pyruvate, a CHO that we get from glycolysis, will receive the NH2 and go to alanine which is an a.a


alanine- where can it be found ?

it's not in our food- we need a carbohydrate source to make it.


where do de-aminated amino acids end up ?

In the Krebs cycle (undergoes "further degradation during energy metabolism")


how are deaminated amino acids degraded in energy metabolism (eg Krebs)?

a.a like arginine, histidine, isoleucine, leucine, tryptophan

form reactive Krebs intermediates or related compounds to enter metabolic pathways.


what is nitrogen balance ?

nitrogen intake = nitrogen excretion
N(total intake from food) - N(urine) - N(feces) - N(sweat)
= 0


when is there positive nitrogen balance ?

nitrogen intake > excretion in order to synthesize new tissues from additional protein.

- pregnancy
- growing children
- in recovery
- in resistance training


where is our body's protein reserve ?

we don't have one.


where can protein content fluctuate, and where does it not ?

In neural and connective tissues, proteins remain relatively "fixed" and cannot be mobilized for energy (since they're crucial for the adequate functioning of these tissues)

In liver & muscle & energy metabolism- depends on intake.


where is there negative nitrogen balance ?

protein use for energy from a skeletal muscle usually.

EVEN if protein intake exceeds recommended amount, this can happen if body catabolizes protein when the other energy sources are lacking.

- diabetes
- fever, burns
- diet
- steroids
- recovery from illnesses


during and after exercise, what's going on with protein ?

degraded during exercise
synthesis stimulated in recovery
(fig 1.23)


when is protein used in exercise as an energy source ?

CHOs are "protein-sparers", meaning that protein will be used when glycogen stores are depleted.
Gluconeogenesis (with a.a) becomes the main source of liver glucose output (anything to maintain blood glucose)


where and from what is alanine synthesized ?

(fig 1.25) It is synthesized from muscle from glucose-derived pyruvate via trans-amination.


how does alanine help maintain blood glucose supply to muscles & NS?

accounts for 45% of liver's release of glucose in long-duration exercise.

alanine output from muscle, and enters blood.
liver then converts it into glucose and urea.
glucose is released into the blood, coincidentally with its delivery to muscle for energy

(hepatic gluconeogenesis)


how do proteins differ from carbs ?

they contain nitrogen, sulfur, phosphorus, iron


how many amino acids does the body require ?

20. (we cannot synthesize 8 of them, which we have to get from our food)


what is the recommended dietary allowance for protein?

0.83 g per kg BM


what happens to 2-5% of oxygen consumed ? why?

it forms free radicals due to electron due to electron leakage along the ETC


what is a free radical ?

a highly unstable, chemically reactive molecule that contains at least one unpaired electron in its outer orbital shell.


how are free radicals produced ?

in our metabolism, but also by external heat, ionizing radiation (cigarette smoke, pollutants, medications)


what do free radicals do ?

LIPID PEROXIDATION (damaging lipid membranes) + damaging DNA (since they're electron dense)


what is the paradox of oxidative stress ?

we can't live without oxygen, but our oxygen consumption produces small amounts of O-, putting us under constant oxidative stress.


when do we produce more O- ?

in aerobic exercise, since that's when oxygen consumption increases (that's when we open ourselves to tissue damage)
however, long-term, we lessen damage likelihood (fig 2.3)


what are anti-oxidants ?

in the form of enzymes, they reduce free radicals (that are oxidized) to eradicate them.


example of anti-oxidants dealing with free radicals.

2 O- -------superoxide dismutase----------> H2O2 + O2

H2O2 is also a free radical that we need to get rid of.

H2O2 --------catalase---------> H2O + O2


examples anti-oxidants

superoxide dismutase
vitamins A, C, E, beta-carotene


what is oxidative stress ?

potential for cellular damage by free radicals


how do we stop oxygen reduction & free-radical production ?

we can't. we can only defend ourselves against their damaging effects.


what is the oxidative-modification hypothesis of atherosclerosis ?

the mild oxidation of LDL contributes to plaque & artery clog- forming of atherosclerosis.
therefore, anti-oxidant vitamins inhibit this process.


what adaptations do we get, short term and long term, from aerobic exercise (with regards to free radicals)?

with increased oxygen consumption comes increased free radical generation from the mitochondria.

----> oxidative stress, protein oxidation, lipid peroxidation, DNA damage

HOWEVER, in the long term:
----> acute anti-oxidant response will be followed by a greater, up-regulated anti-oxidant defense.


are physically active individuals more prone to free-radical damage ?

nope. they may be under more oxidative stress, but their body also develops more effective mechanisms to cope with this stress.


for physically active individuals, do we need increasing quantities of anti-oxidants ?

not sure.
it either slows activity-induced free-radical formation, or augments body's natural defense system.

vit E would probably be the best supplement (studies have shown it reduces oxidative stress)


how are bones and teeth formed ?

calcium & phosphorus (75% of body's total mineral content)


what are the two categories of bones ?

cortical (dense, hard outer layer of bone)

trabecular (spongy, less dense, weaker)


what is osteopenia ?

midway condition where bones weaken with increased fracture risk.

BMD decreased, about 1 SD below normal distribution.


what is osteoporosis ?

when BMD is more than 2.5 SD below normal distribution.

develops progressively as bone loses calcium mass or mineral content.


how is BMD measured ?

with a DEXA, that emits mild forms of x-rays


when does BMD start to decrease ?

after 30 years old. therefore it's important to maximize BMD before then. both healthy & unhealthy people will decline at the same rate, but unhealthy people will finish in an osteoporotic state.


what category of people has a significant incidence of osteoporosis ? why ?

women 10-13 years old

the female triad


what is the female triad ?

bad diet, osteoporosis, amenorrhea


what factors contribute to bone mass ?

(fig 2.8)
- genes
- physical activity
- factors like weight & medications


what effect does weight-bearing exercise have on bone density ?

(fig 2.8)
Weight bearing exercise augments bone mass during growth above the genetic baseline. Degree of augmentation depends on amount of loading.


when are the osteogenic effects of physical activity the most effective ?

In childhood & adolescence, reduces fracture risk later in life.


what is the red-flag for female triad ?



what is the percentage of female athletes in weight-bearing sports that are affected by amenorrhea ?

25-65 % (compared to 5% in normal population)


a 5% loss in bone mass increases the risk of stress fractures by ?



how are menstruation and bone density related ?

premature cessation of menstruation (due to hormonal alterations in exercise) is correlated with the removal of the estrogen's protective effect on the bone, which makes body more vulnerable to calcium loss.


4 phases in treatment of athletic amenorrhea

1) reduce training by 10-20%
2) gradually increase total energy intake
3) increase body weight by 2-3%
4) maintain daily calcium intake at 1500 mg


what gland is exercise-related amenorrhea linked to ?

hypothalamic pituitary gland


what happens to muscle glycogen if you run on three consecutive days?

(fig 3.3) you'll experience chronic fatigue as the glycogen will be nearly depleted. by the end, it is the body's fat reserves that will supply predominantly.


what would be the recommended daily carb intake for normal people and for athletes ?

6-10 g / kg BM
10 g/ kg BM to induce protein-sparing & glycogen reserves.

a high level of carbohydrates better maintains physical performance.


what happens with carb supplementation during physical activity ?

(fig 3.10) physical and mental performance increases.
increased levels of SNS hormones (catecholamines) inhibit insulin release. since exercise increases muscle absorption of glucose, glucose will move into the cells with a lower insulin requirement.


what are the three benefits of exogenous carb intake during physical activity ?

1) spares muscle glycogen, esp in type I fibers
2) maintains a better blood glucose level.
3) better supply of glucose to muscles, especially in the later stages of prolonged exercise when glycogen reserves are depleted.


at what intensity is there the greatest benefit from carb feeding in prolonged exercise ?

75% VO2max. This is when more carbs are used for energy compared to lower intensities when fat is the main source. Therefore, it will be more helpful.


what does the glycemic index do ?

it provides a relative measure of the increase in blood glucose concentration in 2 hrs after ingestion of a food containing 50g of a carb compared to a "standard" for carbs (usually white bread/glucose) which is given an index of 100.

therefore, ingesting 50g of a food w glycemic index of 45 raises blood glucose to levels reaching 45% of the value for 50g of glucose.


relationship between glycemic index and nutritional quality

there is none.


what are the three reasons consuming food after exercise facilitates glucose transport into muscle cells ?

glycogen depletion in exercise augments the re-synthesis of glycogen in recovery.

1) enhanced hormonal milieu (high insulin, low catecholamines)
2) increased tissue sensitivity to insulin & glucose transporters GLUT 1 and GLUT 4
3) increased activity of glycogen synthase (glycogen storing)


at what rate is glycogen storage replenished ?

5-7% / hour (20 hr at least)


in what way does consuming glucose help replenish glycogen stores ?

enhances glutamine & alanine synthesis in skeletal muscles, which provide primary vehicle to transport ammonia out of muscle tissue.

removal of free ammonia facilitates glycogen replenishment


what happens when you drink something high in glucose before exercise ?

reactive hypoglycemia.

high gl -> insulin response, increase in protein synthesis.
insulin binds to protein receptor on muscle
blood glucose will drop sharply due to tremendous amount of insulin secreted.

high carb before sports is wrong because of this. affects CNS, inhibiting performance, and leading to premature fatigue.


what sort of carb snack is best before exercise ?

one with a lower GI.
glucose will be taken up by the muscle at a much slower rate, which will prevent a hypoglycemic response.


after exercise, is it better to choose a snack with high or low GI ?

depends on when the next event is.

slow replenishment with low GI is best to peak in 5-6 hrs.
fast replenishment with high GI is best if the event is sooner, and you can hope that hypoglycemia will go back to normal levels by the time of the next event.


what is the metabolic difference between glucose and fructose ?

glucose is easily metabolized. fructose can't be metabolized. it stays in the small intestine, there's no transport for it.


what happens when fructose is basically stuck in the small intestine ?

we can't use it for energy, so instead it increases the rate of osmosis. water will be absorbed into the small intestine.
this will cause GI stress (diarrhea) from excess fructose and water.
also will cause local dehydration, but if it's not corrected, it will become a full-blown dehydration.
this will be corrected by osmoreceptors that detect water leaving blood for ECF (will create thirst)


what is gastric emptying ?

basically stuff going from stomach to small intestine. we don't really want it to be decreased.


what increases gastric emptying rates ?

- increased gastric volume
low volume with high particle content (hypertonic)= bad

high volume with diluted solute = bad, particle transport would be too slow and feels awful (1L)

optimal is 250-400 mL, either a bit hypotonic, or isotonic


what decreases gastric emptying rates ?

- increased energy content
- exercise intensity > 75% (reduces blood flow to gut)
- increased solute concentration
- lower or higher pH
- dehydration


what effect does exercise intensity have on gastric emptying rate ?

higher than 75% max, blood flow to gut decreases at a rate comparable to the intensity of the exercise.
vasoconstriction in gut
less stomach content can be carried to rest of body.
(walking after meal doesn't help digest, you're taking blood away from the gut)


what will increase intestinal fluid absorption ?

low to mod level of glucose & Na (rapid co-transport of glucose)
low to mod level of Na
hypotonic / isotonic fluids containing NaCl & glucose


does fluid temperature affect gastric emptying ?