nutrition final

Classical model CHO loading

• 7 day model

• depletion of glycogen w/low CHO diet and increased activity (3-4 days)

• repletion w/high CHO (3-4days)

Classical model good for

• supracompensating glycogen levels

• exercise lasting longer then 90 mins (delays fatigue 10-20%)

• Activites where a set distance must be completed as quickly as possible (2-3% improvement in performance)

Modified CHO loading

• give people a bunch of carbs after training

• takes 3 days

• can get glycogen levels very high

• no depletion phase, moderate CHO phase

updated CHO loading

Updated CHO loading involves consuming ~10–12 g/kg/day of carbohydrates for 24–48 hours combined with a reduced training load, achieving glycogen supercompensation without a prior depletion phase.

Classical CHO amount

low: <2g/kg

High: 8-12g/kg

Modified CHO amount

moderate : 5g/kg

High: 8-12 g/kg

Updated CHO loading

Training : training load decreases as CHO increases

High: 10g/kg/bm

updated CHO loading

Updated carbohydrate loading involves consuming ~10–12 g/kg/day of carbohydrates for the final 24–48 hours before an endurance event, combined with a significant reduction in training load, to achieve maximal glycogen supercompensation without a prior depletion phase

CHO loading bottom line

• don’t need to do carb loading if we don’t have more than 90 mins

• If there is a lot of muscle damage the body prioritizes muscle repair, not glycogen storage. Makes supercompensation less effective. (why taper matters)

• Supercompensation works better when done occasionally, not consistently

Ketogenic diet

a very low-carb, high fat diet designed to shift the body’s primary fuel source from CHO to fat and ketone bodies

Fat break down and ketogenic diet

Fat gets broken down in the liver but during low carb states there isn’t enough oxaloacetate for the TCA cycle, so excess acetyl coa is diverted to ketone body production

2 main ketone bodies

• acetoacetate

• b-hydroxybutate

limitations of ketones

ketones cannot support anaerobic metabolism making it inefficient for high intensity exercise

• decreases metabolic flexibility

proposed benefits of keto diet

• maximize rates of fat oxidation (spared glycogen)

• shifting fat oxidation from 45-75% of vo2 max

• increased hepatic Ketone production to provide an additional substrate for muscles and the cns

• rely more on fat = less CHO oxidation

metabolic flexibility

• the ability to pivot between the use of different fuel sources CHO/Fats/oxidation

if CHO is required for high intensity performance

reducing cho intake may decrease metabolic flexibility

Low CHO training

low CHO training is the practice of performing exercise sessions with reduced muscle glycogen availability, with the goal of enhancing fat metabolism and mitochondrial adaptations

low cho training enhances

• CHO and fat metabolic proteins

• mitochondrial biogenesis

induced vs natural Carb restriction

• elite athletes have high training and many naturally be training w/lower amounts

how to restrict CHO

• train fasted

• training 2x/day and witholding CHO between sessions

• restricting CHO post exercise

Consider CHO low

• exercise induced immunosuppression

• training load and performance

• protein intake

Train low

should be applied during typical training sessions, not during supramaximal or prolonged workouts

• high intensity or very long sessions with low glycogen can increase stress hormones and impair immunity

training load and performance (low CHO)

• performance will decrease during low-CHO sessions due to limited glycogen

• can be mitigated with ergogenic aids

Protein ingestion (low CHO)

• 20-25g before or during exercise reduces muscle protein breakdown

• this will support recovery

training low + training high

train low should be paried with training high to ensure athletes are adapted to real competition fueling strategies and don’t compromise key performance sessions

practical implications of training high

• not all athletes benefit equally

• a minimum glycogen level may be necessary to see adaptations from train low

proposed advantages of keto diet

• maximize rates of fat oxidation, sparing glycogen

• shifting fat oxidation from 45-70% of vo2 max

• increase hepatic ketone production to provide an additional substrate for muscles and CNS

Keto vs High-CHO Diets — aerobic capacity

• both ketogenic and high CHO can produce increases in vo2 max

• fat oxidation is substantially increased on keto diets

fat oxidation is substantially increased on keto diets why?

• inc intramuscular triglycerides (IMTGs)

• inc Hormone-sensitive lipase (HSL)

• inc fat/CD36 Protein (fat transport into mitcohondria)

Effects on Carbohydrate Metabolism (keto vs HCHO)

• Keto diets → reductions in CHO oxidation

• ↓ Pyruvate dehydrogenase (PDH) activity

• ↓ muscle glycogen utilization during exercise

• Glycogen content may decrease slightly if CHO intake is extremely low

Increases in performance do not (always) occur (HCHO/Keto)

u There is an increase in oxygen cost with keto diets

u CHO provide more ATP per oxygen than fat, so when oxygen becomes limiting, fat becomes a limitation

u Decreases in metabolic flexibility (even with periodization of CHO)

u Higher heart rates and perception of effort

Muscle protein breakdown and CHO/Keto

1. Muscle Protein Breakdown

• Unknown if MPS/Breakdown increases significantly to maintain glucose.

• Theoretically:

  • If CHO is extremely low → gluconeogenesis (GNG) may rely partially on amino acids from muscle.

  • Body tries to spare protein if dietary protein is adequate.

FFM and Keto/HCHO

2. Fat-Free Mass (FFM)

• Some studies show small decreases in FFM, especially if protein intake is not sufficient.

• Adequate protein helps maintain muscle mass during keto or low-CHO diets.

Suggested intake protein keto and low CHO

• 1.3–2.5 g/kg/day depending on training status and caloric intake.

• Supports:

  • Muscle maintenance

  • Gluconeogenesis (GNG)

  • Fat oxidation

Glycogen from Protein?

• Glycogen can only be replenished from CHO in the diet.

• If CHO is very low, protein-derived glucose (via GNG) may provide minimal glycogen, but not enough to support high-intensity performance.

• Glycerol from fat breakdown contributes a small amount to gluconeogenesis.

Intermittent Fasting purpose

• fat loss due to increased fat oxidations

• over a specific period of time

Protocols (intermittent fasting)

• 18:6

• Alternate day

• 5:2

All IF protocols

• all protocols seem to avoid the GNG window

18:6 protocol

18 horus of fasting, 6 hours of eating

Alternate day protocol

• ad lib eating

• followed by eating approx 25% of calories

5:2 protocol

• 5 days ab lib eating

• 2 days fasting

Data about IR

• data shows that time-restricted eating can result in weight loss (no more than other diets)

• may compromise nutrient intakes (diet quality and supplements may be required)

Iron is a

controlled substance in the body

Macronutrients and marginal deficienies

• may not be affecting sedentary individuals

• more noticable in athletes

• prolonged stress increases losses and rates of turnover

Minerals

• focus on Iron, calcium and antioxidants

• adolexcent athletes at higher risk of deficiency

Consumed iron

• hemoglobin carries o2 from lungs to tissues

• myoglobin stores and shuttles o2 within muscle for aerobic metabolism

• ETC iron participates in electron transfer for ATP production.

iron involved in

energy metabolism

antioxidant defense system

Exercise induced iron loss

1. microbleeding from the gut

2. foot strink hemolysis

3. hepcidin bursts

Microbleeding from the gut

• Exercise → blood flow is redirected from the gut → minor bleeding can occur.

• The gut is an extension of the external environment, so small losses happen naturally.

Foot-strike hemolysis

• Repetitive impact (running) → red blood cell rupture → release of iron into circulation.

• Body usually sequesters this iron for reuse.

hepcidin bursts

• Intensive exercise → increased hepcidin → limits iron release from gut and stores into the blood.

• This temporarily reduces iron availability for hemoglobin, myoglobin, and ETC.

Transferrin

look at review notes

Iron storage ferritin

• Main iron storage protein inside cells (liver, spleen, muscles).

• Stores iron safely and releases it when needed for hemoglobin synthesis, myoglobin, or enzymes.

• Low ferritin = depleted iron stores → can impair oxygen transport and performance.

ferraportin

Ferroportin transports from inside cells into the blood, allowing transferrin to carry it to the tissues

hepatin

• controls ferraportin

• bursts of hepatin decrease iron transport from the liver

Dilutional anemia

• increases in blood volume will increase with training

• blood volume increases before the red blood cells catch up

• makes it look like we have anemia even if you don’t

• especially through intense training/competition

if iron demand> absorption or absorption <losses

• ferratin decreases

• inc transferrin reporter

NOnanemic iron deficient

Cause: iron losses> absorption or iron absorption<demand

Ions

• decrease ferriting (Low iron)

• transferrin receptor increases (signal for more iron)

• Hb, MCV, MCH: normal (no anemia yet)

Iron Deficiency with Microcytosis

• Cause: Continued iron deficiency.

• Effect: RBCs become smaller (microcytic) and carry less hemoglobin (hypochromic).

• Labs:

  • MCV: ↓

  • MCH: ↓

  • Ferritin: very low

• Functional impact: Reduced oxygen-carrying capacity; fatigue may appear.

Iron Deficiency Anemia

• Cause: Chronic iron deficiency, ongoing losses, insufficient absorption.

• Labs:

  • Hb: ↓ (anemia)

  • MCV & MCH: still low

  • Ferritin: very low

• Symptoms: Fatigue, decreased performance, poor endurance.

Calcium

• cell signaling - contraction, exercise-induced GLUT-4 translocation

• highly regulated

if blood calcium levels are off

• big issue

when blood calcium levels drop

• bone stimulated to release calcium into the blood (bone density takes a hit)

• kidneys prevent us from excreting Ca (increases absorption)

• the parathyroid hormone signals kidneys to make vitD which increases ca absorption in the gut

Vitamin D

• regulated calcium metabolism

• cellular growth

• inflammation and prevention of injury

the parathyroid hormone

stimulates the kidneys to make vit D which will signal to the gut to absorb more calcium

Mahor factors of bone mass

• genetics

• mechanical factors

• endocrine factors

• nutritional factors

mechanical factors of bone mass

• body weight, physical activity (weight bearing exercise)

Endocrine factors (bone mass)

• estrogen, IGF-1

estrogen bone mass

• low estrogen decreases trabecular bone (inner, spongy bone) as it is very metabolically active, begin to get rid of bone support

Vitamin D sources

• Fatty fish

• mushrooms

• fortified foods (milk, OJ, breakfast cereal, egg yolk)

the body can absorb

500mg/sitting

ROS

• while associated w/damage to cells and DNA/cancer

• can be beneficial in exercise

REDOX reactions

• involve the loss or gain of electrons and allow for the transfer of electrons between species

• during normal metabolism : O2 is used to mitochondria for energy production but sometimes o2 intermediates are made instead

Mitochondria are the dominant source of

ROS production

Must vulnerable targets for ROS

• proteins, lipids and DNA

Oxidative stress and ROS

• exercise increases oxygen usage and ROS production

ROS play an important roll in

Hormesis

Hormesis

• positive adaptations over time

• increase in antioxidant defense system

OVertraining

High levels of repeated stress has negative effects

Positive role of ROS

• insulin sensitivity

• vasodilation

• mitochondrial biogenesis

• immune response

• growth factor signalling

• force production

When cells adapt to ros

Cells adapt to ros, becoming more resistant to the affects of oxidative stress (training>acute bout)

roles for ros in PHYSIOLOGY

• react with redox sensitive proteins

Regulate many physiological processes

• insulin sensitivity

• vasodilation

• mitochondrial biogenesis

• immune response

• growth factor signalling

• force production

Exercise adaptations to ROS

Cells adapt to ROS becoming more resistant to the adverse effects of oxidative stress

• increased antioxidant enxymes

• improved DNA repair system

• increased mitochondria

• increased heat stroke proteins

• positively affects muscle remodelling

heat shock proteins

protein that helps cells cope with stress,

• ROS and damage and stuff

types of antioxidants

• vitamin A

• vitamin C

• Vitamin E

• minerals

Vit A

• binds to free radicals

Vit C

donates electrons

VitE

donates H+ ions

Polyphenolic compounds

• biologically active componenets

• flavonoids, phenolic acids, lignana and stilbenes (coffee tea juice)

• known for antioxidant properties

Corotonoids

bind to a free radical

Antioxidant supplementation (acute)

acute supplementation before exercise many enhance performance

chronic supplementation of antioxidants

has no effect on performance and may attentuate improvements due to training

• high intensity

• dec mitochondrial biogenesis, insulin sensitivty and hypertrophy

Males supplement

• protein, amino acids, stimulants

Females

• pro/prebiotics

• enzymes

• vitamins

• minerals

Initial injury concussion

• can have increased symptoms

• less desire to eat

• need to be flexible

• promote healing

• liquid food, gatorade, gingerale

initial injury avoid

caffine (stimulant, disrupt sleep)

alcohol (inc time to sleep, red sleep quality)

eat frequently (concussion)

• brain needs a constant supply of fuel to heal

• glucose

• healthy meals and snacks

sleeping and concussion

• bedtime snack

• let them sleep

• encourage intake while they’re awake

Bedtime snack and concussion

Recommended that those experience a concussion eat a snack around 30 mins before bed

• overnight brain receive glucose from liver

• need to make sure we have adequate energy stores

• large meals may increase difficulty with sleep

Vitamins and concussion

• no strong evidence for use

• eating a cariety of foods frequently is best

• depends on length of symptoms and deficiency