KIN 4433 - Midterm 1 & 2

General Adaptation Syndrome

response of the body:

- alarm reaction

- resistance development

- exhaustion

stress & response

- appropriate stress (stimuli/response to exercise) to initiate a response (strain)

- if you give an appropriate amount of time to heal after appropriate stress, you will come back stronger

*stress could also include sickness

not enough time to recuperate + too much of a stress =

a LOT of damage

T or F: changing osmolarity of cell can change size of cell

True --> nuclei will start lying down more protein to fill empty space (actin & myosin)

training principles (4)

- overload

- specificity

- individual differences

- reversibility

overload principle

- must stress the body more than normal activities --> can be detrimental to the individual

- overload must be progressive

- must manipulate frequency, intensity, volume & rest

specificity principle

- adaptations depend on the type of overload

- exercise specific

- muscle specific

- test specific

reversibility principle

- physiologic / performance adaptations rapidly lost if exercise is discontinued

- rate of loss (days, weeks, months) depends on parameter

- w/out stress, everything will drop back down to baseline

skeletal muscle fibres

- Lots of mitochondria in muscle cell (more in slower twitch fibres)

- Myofibrils contain the sarcomeres

- Contains numerous nuclei (myonuclei) which are dispersed along the inner surface of the plasmalemma (sarcolemma)

where are myonuclei located in skeletal muscle fibres?

under basement membrane and the sarcolemma/plasmalemma

embryonic stem cells

can make bone cells, epithelial cells, etc. → not destined for a specific type of cell

calcium-mediated contraction (steps)

- AP - sarcolemma

- AP - TT

- Calcium release - SR

- Calcium binding to troponin

- Binding site on tropomyosin exposed to myosin

- ATP-mediated contraction

T or F: you produce more mitochondria with aerobic training

true

What makes a muscle cell unique?

many nuclei within a given fibre (not just one nucleus)

--> some of these are stem cells --> can change with training

what determines the makeup of a muscle cell?

Transcription & translation of genetic material within myonucleus

T or F: cardiac muscle does not have striations

False

adult stem cells (satellite cells)

*Not embryonic

- Destined for a certain grouping

--> Pre-destined to be a certain type of cell

- Muscle stem cells can vary in it’s type & can also become muscle-like factors (e.g. collagen)

myonuclei vs satellite cell

- myonuclei of muscle fibre are almost undistinguishable from satellite (stem) cells

--> myonuclei are a little further within muscle cell

- myonuclei are very numerous (1000s per fibre); found under the basement membrane & the plasmalemma

- satellite cells are relatively rare (1-20 per muscle fibre); found under the basement membrane but outside the plasmalemma (has its own plasmalemma)

skeletal muscle contractile properties

Each thick filament is surrounded by 6 thin filaments in a precise geometrical formation

individual differences principle

- training response to same exercise is highly variable

- depends on genetics, age, sex, initial level of fitness

- disease vs healthy

types of training

- aerobic, resistance and HIIT

- the overload can be varied by manipulating volume and the frequency of training (use cycles to further vary volume of exercise)

- need to allow enough time for adaptation to occur

training methods of evaluation

- HR

- lactate

- molecular

how can we adapt the ability of the body to use lactate with training?

liver becomes better at taking up lactate

modality of exercise: training variables

- frequency

- intensity

- duration

modality of exercise: training format

- MICT

- HIIT

- SIT

modality of exercise: physiological adaptations to skeletal muscle

- cellular stress

- molecular responses

- mitochondria content

- capillary density

modality of exercise: physiological adaptations to cardiovascular & integrative

- maximum cardiac output

- maximum stroke volume

- blood volume

- VO2max

is exercise always beneficial?

not necessarily... exercise is a stressor

*e.g. certain activities are NOT beneficial for T1DM population

general adaptation syndrome: alarm phase

initial phase of training when stimulus is first recognized & performance generally decreases in response to fatigue

general adaptation syndrome: resistance phase

the second phase in which adaptation occurs & the system is returned to baseline or in most instances elevated above baseline

general adaptation syndrome: supercompensation phase

new level of performance capacity that occurs in response to the adaptive response found in step 2 --> higher than baseline

general adaptation syndrome: overtraining phase

if stressors are too high, performance can be further suppressed & overtraining syndrome can result --> below level prior to training

type 1 diabetes

autoimmune disorder --> immune system attacks beta cells of pancreas (secrete insulin)

- difficulty regulating blood sugar

exercise-mediated hypoglycemia

- in young T1DM patients, exercise is the most frequent cause of known hypoglycemia events --> very concerning

- the primary barrier to exercise is the fear of hypoglycemia onset

- higher glycemia values than non-EX T1DM

insulin

rest & digest hormone --> causes glucose to be taken up by tissues & stored as glycogen

why do we need glucose in the blood?

glucose is favourable

- main energy source for brain

- not stored in the brain

why do blood glucose levels increase prior to exercise?

anticipatory response

insulin-independent mechanism of glucose uptake

- relies purely on muscle contraction

- only working muscles are taking up glucose

T or F: blood sugar levels do not fluctuate much in healthy individuals

True

what is dizziness caused by?

not getting enough glucose to the brain

what occurs when glucose below 3 mmol?

you will pass out --> laying horizontal allows more blood to get to brain

what occurs when glucose below 4 mmol?

has major complications

*hypoglycemic symptoms

is insulin used during exercise?

no --> rest & digest hormone

*plummets in non-diabetics

HBA1C

sugary RBC

T or F: diabetics who exercise have higher BG levels

True --> moving away from the #1 treatment strategy

exogenous

produced outside of the body

endogenous

produced within the body

diabetics & insulin

diabetic take exogenous insulin but cannot regulate it --> potentiates glucose uptake

T or F: diabetics do not experience large fluctuations in BG levels during exercise

False --> HUGE drops occur in blood glucose levels

*not uncommon to see a drop of ~8 mmol

"dead in bed" syndrome

BG levels can become so depleted following activity that T1DM patients can enter into a coma & pass while they are asleep

antecedent exercise & BG levels in diabetics

prior exercise will cause a bigger drop in BG levels

T or F: overcorrecting with insulin after exercise is worse for a T1DM patient than not exercising at all

True --> & the more they exercise, the worse it gets

Lactate is a by-product of ______ ________

anaerobic respiration

Which organ LOVES lactate?

Liver

BG levels need to be maintained in __-__ mmol range

4-7

Gluconeogenesis

- Make new glucose

- Occurs in liver

- Can be made from anything with a CHO skeleton

Male vs Female BG Levels

- Females have a smaller drop in BG during exercise in comparison to males

--> Females are better able to utilize fat stores → better fat utilization at a given exercise intensity relative to males

--> Might be estrogen, might be progesterone

- Higher intensity you go = less reliance on fat

--> Could be detrimental to performance in females

Arteries

- Arteries are more elastic & better able to deal with pressure

- Muscular and/or elastic walls

- High pressure

- Blood flow away from heart

Veins

- Thin walls

- Low pressure

- Blood flow toward heart

- At a given time, about 75% of the blood is contained within the veins

Vein Valves

Valves capture blood & with assistance from muscles can push blood back to heart

Varicose Veins

- Dysfunctional valves → usually in a certain area & often in lower limbs

- Blood can pool in these

- When you have a faulty valve it puts 2x as much pressure on the valve below it

- Superficial veins* more visible → do not have muscle wrapped around them to help push blood back up to heart

- Not allowing sufficient blood to return to the heart

Capillaries

- Smallest form networks → capillary beds ensure that all cells receive oxygen & nutrients & remove waste

- We rapidly change how many capillaries we have around muscles

CV Adaptations to Aerobic Exercise: SV

- Hit a plateau eventually

- Stroke volume increases with training

- LEDV increases

- Ejection fraction increases → how much blood is being expelled for every beat

- Maximal Q increased at same HR (or lower)

- Submaximal Q output decreased/maintained at lower HR

- Elevation in Q must be due to SV since you see a decrease in HR

- At a given absolute work rate, SV is higher and the plateau should happen later but is higher

- In terms of % of VO2, untrained working at 60% VO2 max this work rate is going to be lower than in a trained individual - trained individuals work rate at 60% VO2max will be much higher so SV is much higher

CV Adaptations to Aerobic Exercise: HR

- Resting HR decreases slightly

- Submaximal exercise HR decreases significantly

- Maximal HR may decrease slightly (will not change much)

- Increased parasympathetic activity → endurance training

--> More PSNS fibres going to heart → becomes dominating NS at rest

--> Remove innervation to heart → it will beat at ~100 bpm, PSNS lowers this

- Decreased sympathetic activity

- Rate of a trained individual will be lower than that of an untrained individual

- Having a slower HR is more efficient ⇒ more time for it to fill → delaying time it takes to reach maximal HR

- At a given absolute intensity, HR is going to be lower in trained - likely getting more blood back to heart and requirement of beats per minute is lower since they can pump out more blood, even at rest trained individuals have a lower HR

CV Adaptations to Aerobic Exercise: CO

- Q does not change much at rest or submaximal exercise

- Q increases dramatically at maximal exertion due to increases in SV

- HRmax does not change much with training (220 - age) → not responsible for change in cardiac output (SV is)

--> Heart is able to expel more blood

- For a given workload, Q is the same between unTr & Tr

- ATP requirement for a given weight will be exactly the same between an unTr & Tr individual

- Work at 50% VO2 max = same intensity but two different workloads between Tr & unTr

- Absolute workload → they are the same at submaximal levels & different with relative workload

--> trained individual will be able to go to higher speeds and can go to higher demanding exercise protocol since they can match an elevation in CO (since their plateau in SV much greater)

Cardiovascular Fick Equation

- The Fick equation represents the relationship of the body’s oxygen consumption (VO2) to cardiac output (Q) & the arterial-mixed venous oxygen difference (a-vO2 difference):

VO2 = Q x a-vO2 diff

OR

VO2 = HR x SV x a-vO2 diff

--> During maximal exercise: VO2max = HRmax x SVmax x a-vO2 diff (max)

***Measuring VO2 with exercise is a good way of determining training improvements

***Resistance training drastically improves your ability to extract oxygen from the blood → change in a-vO2 diff = change in VO2

What is the number one predictor of mortality & morbidity?

VO2 --> higher VO2 = decreased risk of developing life-threatening diseases

GK

glucokinase → traps glucose into a cell (muscle)

HK

hexokinase → traps glucose into a cell (liver)

GS

glycogen synthase - stores & makes glycogen

Hepatic Glycogen & Enzymes: Following 10 weeks of training

- Adaptations with training

- Elevation in receptors → muscles trying to be more sensitive to insulin

- Liver is adapting in a favourable manner to try to store more glycogen

- Heighten our catecholamine response to exercise

- Patients with T1D do not store sufficient amounts of glycogen within the liver

- Resistance exercise increases liver glycogen

--> Resistance exercise prior to aerobic gives you the benefits of both types of exercise → however, if you reverse these two, it will be more challenging to normalize BG levels

What is the most common way insulin is used as a treatment for T1D individuals?

injection

Exercise with near normal BG

- Greatest drop in BG occurs during aerobic exercise

- In control patients, there is a drop in insulin during exercise

--> At end of exercise (post-exercise period) there is a small & quick increase in insulin to inhibit release of glucagon & for the liver to store excess glucose as glycogen

- Increase in epi during exercise → returns to pre-exercise levels afterwards

- Glucagon starts to rise in post-exercise period to normalize BG levels

--> However, there is no glucagon response in people with T1D

--> There is a sufficient catecholamine response

- Takes about 48-72 hours to replenish glucose stores

Glycogen Stores

- Liver has highest concentration of glycogen

- Muscle has largest store of glycogen

- Brain has a VERY small amount of glycogen stored

- Glycogen stores can be completely depleted from all of these places during exercise

Where are GLUT-4 Transported Located?

Muscle

Increases length of exercise = increased use of ______

Glucose

Glucose Counter-regulatory response (GCR response)

- Liver, pancreas & adrenal gland will normalize any fluctuations in BG (blood glucose) response

- BG levels need to be maintained in 4-7 mmol range

- Glucose receptors exist in brain

—> Brain conc. of glucose causes an increase or decrease in the liver's output of glucose

- Anticipation of intensity of exercise → liver will pump out a bit of extra glucose

- Right at start of exercise, muscle will be taking in glucose

- We rely most on glucose → primary energy source

Boyle's Law

for a constant volume, if you decrease area, you will increase pressure

Boyle's Law: Cardiac Cycle

Area in ventricles is decreasing, pressure is going up steadily → the second the pressure in the ventricle goes above the pressure in the periphery (mainly the aorta-left or pulmonary-right artery) the aortic valve will open

Exercise with Elevated BG

- With training, we now have glucagon response back in patients with T1D that mimics what we see in controls

- Can respond back to BG levels quicker with training

Contraction-mediated glucose uptake (insulin independent)

Only muscles that are contracting will take up glucose

*more specific than insulin

Why is high BP bad?

Forces the heart to work harder, BP is higher in the periphery, heart has to contract stronger to overcome this increase in pressure so that blood can leave (60-100 times per minute at rest depending on the individual)

Pathological cardiac hypertrophy

changes to one side of heart causing an imbalance

Exercise-mediated cardiac hypertrophy

better balanced growth of heart → improvements on left side are accompanied by improvements on right side

—> aerobic exercise and resistance exercise improves heart in different ways (volume vs pressure)

Factors Influencing SV

- preload

- contractility

- afterload

Preload: SV

the amount of sarcomere stretch experienced by cardiomyocytes at the end of ventricular filling during diastole --> directly related to ventricular filling

Contractility: SV

ability of heart to contract

Afterload: SV

pressure outside of the heart that the heart has to work against, however, afterload is a negative on the heart in terms of its ability to expel blood

--> BP in periphery

isovolumic contraction

no change in left ventricular volume

Fight or flight response (SNS): adrenal gland

- Brain stimulates release of glucose through the liver during flight or fight response

- SNS stimulates adrenal gland to release catecholamines: epi and norepi

--> Adrenal gland located in lower trunk above kidneys

- Can increase these hormones into circulation

Fight or flight response (SNS): pancreas

- SNS stimulates pancreas

--> Pancreas can release insulin &/or glucagon

- Glucagon also stimulates the liver to release glucose

--> Glucagon's release from pancreas inhibits the release of insulin → these hormones have opposite effects

T1D & Exercise

- See a decrease in the regulation of the glucose response

- Do not have a sufficient release of insulin from the pancreas and must take exogenous insulin

--> During exercise insulin is exposed to muscle

- We want insulin to decrease during exercise → it is nonspecific & will cause any tissue to take up glucose that can

- Higher amounts of insulin than glucagon released in patients with T1D

Liver & Pancreas Response to Exercise

- Liver is controlled by brain to release sufficient amounts of glucose to normalize BG levels

- We want insulin to decrease during exercise → it is nonspecific & will cause any tissue to take up glucose that can

--> Higher levels of insulin may be advantageous in muscle, however, there will also be an uptake of glucose in muscles that are not working

--> Liver (which should be releasing glucose) will be taking up glucose

--> Also want insulin levels to go down during exercise because we want glucagon levels to increase

--> Insulin levels inhibit the gluconeogenesis response → hindered

insulin vs glucagon: ANS

Insulin is part of rest & digest system whereas glucagon is fight or flight

T or F: right & left ventricular hypertrophy will have the same prognosis

False

CV Adaptations to Aerobic Exercise: Blood Flow

- Increased blood flow to working muscles

- Redistribution of blood to active muscle fibres

- Increased capillary density

- Increased vasoactive properties

- Decreased splanchnic and renal flow

T or F: the number of capillaries we have decrease with age, but we can mitigate this loss by engaging in training

True

Capillary domain area

measure of how far vessel is from muscle

Does the ability to vasodilate change with training?

- As you age, vessels lose the ability to vasodilate

- Despite aging impacting the ability to vasodilate, if you train, you will be able to vasodilate significantly more

Vessel vasodilation

- Nitric oxide is important for vessels to vasodilate

- Acetylcholine binds the endothelial cell inside the vessel → cascade of events leads to release of NO

- Smooth muscle & its tension determines the constriction of the vessel