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Is there a difference in resting concentrations of ATP between fibres



how much more PCR then ATP at rest in muscle fibres

3 times more


which muscle fibre type has more PCR

Type IIb fibres- 5-15% more


aerobic contributions to a sprint

vary between people by 10-30%


Why are there different aerobic contributions to sprints

-genetic: different fibre types
-training: enzymes, lactate concentrations


Possible causes of fatigue

-Substrate depletion (ATP, PCR, Glycogen, glucose)
-metabolic byproducts (Mg 2+, H+, ADP, Pi, NH3, La-, free radicals, heat)
-lactic acid production (within exercising muscle during an all out sprint is high)
- the activity of two enzyme systems (Ca2+ ATPase (calcium reuptake) and Na+- K+- ATPase ( return electrolytes to position)- start to fail during a sprint, can't restore electrochemical gradient fast enough= slows down fibre innervations)


Wingate test

30s sprint


Lactic acid

dissociates very fast into H+ and lactate
lactate= moved into blood very quickly



can result from an accumulation in the muscle cell of H+ ions = lowered pH
may impair the activity of the key glycolytic enzyme PFK= less energy being made available for resynthesis of ATP



- protein buffers that buffer against H+ accumulation (neutralising capacity)
- reduce the rate at which the pH drops = temporary reprise during sprint
= slows the rate of fatigue


lowered pH results in

lowered activity of PFK enzyme ( this protects against a too big drop in pH)


Reduced Ca2+ ATPase activity can lead to

reduced Ca2+ re-uptake in the sarcoplasmic reticulum= incomplete relaxation
phosphate released from the breakdown of PCR during a sprint binds Ca++ in the sarcoplasmic reticulum and lowers net Ca+ release


Adaptations to sprint training

1. increase in the number of Na+ K+ ATPase pumps
2. increased activity of PFK ( better then endurance athletes)- increased ability to neutralise proteins which could delay the onset of fatigue. Also, the sprinter may be better at translocating the protons out of the active muscle cell.
3. increased CS activity
4. increased VO2 max
( no change in fibre composition)


Reduced Na+ K+ ATPase pump

With repetitive tasks, K+ is lost from the cell and the concentrations of Na++ inside the cell increase - if the pump fails to return them to their normal position a a high enough rate the ionic gradient of the cell doesn't return to normal- signifying that the cell cant depolarise


Good sprinter

1. high power output
2. high type 2 muscle fibres
3. greater hypertrophy of existing muscles
4. better synchronisation of motor units
5. increase activity of PFK = increased buffering capacity ( there are no change with resting concentrations of ATP or CrP with training)



high intensity training= repeated sessions of relatively intermittent exercise, often preformed with an all out effort.


HIT benefits

-improves markers of aerobic energy metabolism:
> maximal aerobic capacity
> mitochondrial enzymes
> improve oxidative capacity in skeletal muscle ( better performance)


Importance of improving aerobic metabolism to sprint training

1. resynthesis of PCR = aerobic process, better aerobic fitness will allow faster recovery
2. removal of lactic acid (restoration of normal pH) aerobic process
> therefore multiple sprint training increases anaerobic capacity and aerobic capacity


Davies et al. 1984

in rats, low dietary iron resulted in anemia and a 50% decrease in VO2 max and 50% reduction in endurance performance. ( (central)- low Hb and (peripheral- mitochondria capacity)
- after blood test, VO2 max increased but no change in performance.
mitochondrial function directly linked with actual performance.


VO2 max- related to

oxygen carried in the blood (central)
- not a particularly good predictor of endurance performance.
- VO2 max of elit athletes rarely changes over several months.


endurance preformance

mitochondrial function (peripheral)
- correlations with intramuscular estimates of aerobic capacity


Bishop et al. 2000

test i did- lactate threshold verse VO2 max test.


Anaerobic threshold

introduced in 1964 by wasserman
exercise intensity at which lactate produced by the muscles = the maximal rate at which it can be removed= lactate doesn't accumulates.
lactate threshold (change of lactate in blood) + vantilatery threshold ( change in ventilation)
Inflection point.



Onset of blood lactate accumulation ( assumes around 4mmol/L- shown to be wrong)



Onset of plasma lactate accumulation



Individual anaerobic threshold



ventilatory threshold


detecting AnT

1. mapping changes in blood lactate during incremental sub-maximal exercise.
2. mapping changes in ventilatory variables during incremental sub-maximal exercise



breaks glycogen down to pyruvate



turns into TCA or lactic acid.



increased ability to move lactic acid out of the muscles (increase in translacating molecules)


Carbonate amylase

breaks bicarbonate into carbonic acid ( joins a H+)
to buffer H+ during exercise.


above AnT

CO2 is being produced both through aerobic metabolism and via buffering of H+.
dispoportionate increase in CO2 Vs O2.


causes of inflection point

1. Hypoxia
2. muscle fibre recruitment (type 2)
3. lowered hepatic blood flow
( liver removes lactic acid)
4. autonomic nervous system= catacolamines * adrenaline and noedrenaline.


problems with AnT

lactic acid can be produced in aerobic conditions through 'mass action' (too much pyruvate-- gets converted into lactic acid)
(at altitude- with a high breathing rate caused by catacolamines = increase lactic acid production- accelerate glycolytic pathway--- induces mass action)


aerobic glycolysis

glucose to lactate



lactate to glucose


Cori cycle

recycling of lactate. for brain glucose levels- not producing enough for the muscles. excess
cardiac muscle= high lactate dehydrogenase.


brain and lactate

lactate maintains blood glucose levels and prevents hyperglycemia.


main route for lactate removal

oxidation by muscle with very high aerobic capacities= cardiac muscle and type 1 fibres and liver. ( type 1 fibres favour the production of pyruvate whilst type 2 the other way around)


Mcardles patients

lack enzyme glycogen phosphorylase
therefore cant produce appreciable quantities of muscle lactate. but still show a VT ( changes in plasma K+ and high recruitment of muscle mass)


endurance training and the lactate threshold

increase in PV
decrease in catacolamines
decreased glycolytic activity
delayed recruitment of type 2b fibres


endurance training

high mitochondria density and better delivery in O2- therefore more pyruvate oxidised.
increase in lactate removal.


Central and peripheral limitations to maximal exercise

1. pulmonary diffusing capacity : no, blood is fully saturated with O2. + still oxygen in venous return.
2. cardiac output and O2 carrying capacity
3.skeletal muscle: exercising muscles are capable of accepting/ extracting more oxygen when offered (davis and Sargent) = not limiting



all diseases and conditions of the heart and BV.
causes: coronary heart disease, stroke, heart failure.
leading cause of death in AUS.
2 X higher in indigenous Aus
30% higher in remote areas
43% higher in lowest socioeconomic groups
poorer health outcomes in rural and remote areas may be due to a range of factors, including a level of disadvantage related to education and employment opportunities, income and access to health services.
trends show decreased insidence in acute coronary event in women and men


Risk factors of CVD

1. high cholesterol ( high LDL): Arcloscerosis
2. not meeting active Aus guidelines and being overweight
3. High blood pressure- hypertension
4. smoking
5. type 2 diabetes or impaired glucose tolerance (1/4 have type 2 diabetes)
more risk factors= higher incidence of CVD



pain when exercising reflects low O2 delivery



deposition of Fatty plaques within the walls of arteries, resulting in thickening and hardening of the arteries, narrowing of the lumen and loss of vessel elasticity.
high LDL linked
LDL- high saturated and trans-fats in diet


coronary artery disease

angina pectoris-


angina pectoris-

temporary chest pain behind sternum. Often pain radiates from chest to the arms or shoulder, neck, teeth, jaw, abdomen or back.
follows excitement or effort
relieved by rest or sublingual glyceryl trinitrate (vasodilation).

= lack of blood supply to myocardium.


Myocardial infraction ( heart attack)

chest pain that persists for more then 20 min not relieved by GNT.
Shortness of breath
feeling of impending doom



Bleeding in the brain.
clinical syndrome characterised by the acute loss of focal brain or monocular function lasting more then 24hr or leading to death.
thought to be due to spontaneous haemorrhage or inadequate BF.


peripheral artery disease

- affects the major arteries supplying the kidneys, viscera and lower extremities.

-> hardening of the arteries- BV lose elasticity and plaque impedes BF to lower limb.
1 symptom: Claudication: cramping.
caused by walking, relieved by rest (pain doesn't occur standing or siting).
management: exercise, cessation of smoking, control of diabetes, hypertension and hyperlypidemia.
risk factors:
diabetes, smoking, c-reactive protein, hypertension, high BP, hyperlipidemia.



good cholesterol- removes cholesterol from the peripheries to liver for disposal. Exercise can increase HDL.


Cardiovascular fitness

independent risk factor for CDV and all cause mortality; it can prevent CVD independently of conventional risk factors such as HT, hyperlipedemia, obesity and smoking.

exercise that improves cardiovascular fitness will offer significant protection against CVD.


glucose and insulin- influence on CVD

high plasma glucose concentrations and insulin resistance have been associated with systemic inflammation and endothelial dysfunction.
link b/w diabetes and CVD.
thus maintaining good glycemic control is important in reducing CVD risk.



Roberts et Al. (2013) have shown that regular PA ( 1HR/ day for 7 days) decrease the magnitude of glucose excursions.
Oberlin et al. (2013) have shown that a single 60 min bout of moderate exercise lowers blood glucose for 24hrs within sedentary males with 3 meals consumed/ day.

non-insulin dependent glucose uptake by the exercising muscles both during exercise itself and following.
type 2 diabetes: insulin doesn't work.



maintained via the neural and hormonal systems- working in synch.
exercise- disrupts homeostasis- very good way to tract
blood glucose levels



fuel availability
muscle growth
fluid balance


endocrine system

9 glands ( ductless) - don't target directly a tissue
hormones (travel in blood and lymph to reach their target tissues) ( release controlled by negative feedback) ( released in small amounts and removed very quickly)
some act locally/ some globally
e.g insulin: locally acts in adipose tissue and muscles
vs nor-adrenalin synpathetic NS and the adrenal medulla. - global


Cortisol + reproductive

hormone that follows a 24hr pattern- very important role in metabolism.
monthly cycle


hormone amount used

blood concentrations of hormones cannot be used to infer production unless you know exactly how much was released.


2 types of hormones

1. steroids
2. large polypeptides or small proteins

alter membrane permeability
activate enzymes
activate protein synthesis



enter cell- smaller: lipids
initiate gene activity/ increase in enzyme activity/ increases protein synthesis


large polypeptides or small proteins (majority)

AA based- vary in size
cannot enter cell
use secondary messenger to elicit responses in cell

primary receptor -( in cell membrane with adenylase cyclase complex cyclases)-> cyclic AMP- secondary messenger )


Pancreatic hormone

Insulin and glucagon
maintain blood glucose homeostasis- glucoregulatory hormones.



Beta cells of pancreas
stimulate storage of glucose - cellular uptake into muscle and fat cells and liver
suppressed when blood glucose levels drop
1. promote glucose uptake
2. promotes glucose utilisation ( use as fuel)
3. promotes synthesis of glycogen in muscle and liver
4. promotes tri-glyceride synthesis in adipose tissue ( suppresses FFA release) (if not using glucose with be stored as fat)
* also promotes protein synthesis. -

mov of glucose from cell membrane to storage sites within the cell is achieved by specific glucose transporters.

Insulin activates GLUT4 transporters to surface of the cell.



alpha cells of pancreas
stimulate release of glucose - insulin antagonist.
promotes gluconeogenesis (liver produces glucose from AA, lactate, pyruvate) and glycogenolysis ( break down of glycogen)



Skeletal muscle cells or fibres
move to cell membrane in response to insulin and muscular contraction.


Glucose uptake during exercise

insulin not produced during exercise
(contractile action) muscular contraction promotes GLUT4to cell membrane. = non-insulin dependent absorption during exercise.
- the larger the muscle mass the greater the uptake of glucose into cells (greater the benefit for type 2 diabetic). increased permeability lasts post exercise allows for rapid resynthesis of glucose - how long depends on intensity and duration)

up regulation of GLUT4- increased receptor number - increases sensitivity


Type 1 diabetes

insulin dependent
no insulin produced


type 2 diabetes

Non insulin dependent
90% have type 2
25% of AUS adults have impaired glucose metabolism
still produces insulin- cells don't respond.

uncontrolled diabetes ( permanently high levels of insulin) = irreparable damage of nerve cells and blood vessels ( incl. blindness and kidney failure)

over eating and inactivity causes- increased concentration of hormone- down regulation of receptors. several years- chronic.
as. with insulin resistance.

when positive energy balance is combined with inactivity fat cells hypertrophy ( grow- eventually split) - can't ever reduced the number of fat cells in the body.


high concentrations of insulin

down regulation of GlUT4



produced in adrenal cortex
catabolic hormone
- breaks down protein
- increases FFA mobilisation ( release)
- increase glyconeogenesis

exercise: breaks down not exercising muscle for energy. act to maintain glucose concentrations.

cortisol + cortisone= glucocorticoids.


exercise + hromones

glucose consentrations dont change with moderate level exercise for three hours
due to actions of
- cortisol
- epinephrine
- glucagon
- norepinephrine.

the concentrations increase over duration of exercise.
- promote the increase in fuel/ the release of glucose.
- increase in HR


Adrenal hormones

catecholamines (adrenaline and nor-adrenaline- released from adrenal gland in 4:1) are secreted through the SNS and adrenal medulla .
oppose the actions of insulin

SNS- sympathetic NS

increase heart rate
increase metabolic rate
increase glyogenolysis
increase release of FFA
increase BP
increase blood redistribution
increase respiration
suppress insulin release


insulin antagonists



Changes in plasma insulin pre and post training

before training there is a huge drop in insulin concentrations.
after training there is not at all the same drop- not the same disruption

- due to more fat being burned.


Changes in glucagon pre and post training

less of an increase in glucagon
less fuel needs to be harnessed from muscles
dampening effect
more fat being burned


changes in catecholamine pre and post exercise

less disruption in homeostasis in trained state/ less of a draw on blood glucose.
initial steep dissent= increase plasma V..


Pituitary gland

controlled by the hypothalamus
releases 6 different types of polypeptide hormones


posterior pituitary

releases ADH--> increases water retention--> combat dehydration



combats dehydration


Anterior pituitary

hGH ( human growth hormone) (= somatostatin) ( very important in children)
- protein synthesis and muscle mass (children)
- stim bone growth (children)
- lipolysis ( release fat in adults)
- enhances healing after injury

increases strength and performance

- short term activity results in an increase in GH- this promotes FFA release from fat cells (lypolisis) which serves to maintain blood glucose concentration for the CNS


Thyroid hormone

largely controls metabolic rate
but no link between decrease metabolic rate ad obese



natural hormone produced by kidneys
kidney detects decreased concentrations of oxygen-> release erythropoietin --> bone marrow--> increased RBC


19. Erythropoietin is used as an ergogenic aid to…
a. increase fat-free mass and strength b. increase red blood cell mass and endurance c. increase buffering capacity and anaerobic performance d. increase agility e. increase flexibility

b. increase red blood cell mass and endurance


20. Which of the following statements regarding human growth hormone are true? a. is a potent anabolic and lipolytic agent intimately involved in the tissue building processes and human growth b. supplements may augment the increase in fat-free body mass and decrease in fat mass associated with exercise c. stimulates bone growth d. enhances fatty acid oxidation e. all of the above



The lactate threshold that occurs during incremental sub maximal exercise a. appears to coincide with the recruitment of slow twitch fibers b. appears to coincide with the recruitment of fast twitch fibres c. shifts to the left with endurance training d. means that the person is close to fatigue e. both a and c

- it shifts to the right with endurance training
- very difficult to maintain above the lactate threshold.

other potential causes:
- hypoxia
- decreased hepatic blood flow
- autonomic NS influence- (catacolamines)


21. The potential benefits of blood doping are due to… a. increased delivery of blood glucose b. increased muscle power c. increased oxygen delivery d. increased protein synthesis e. increased removal of lactic acid

Blood doping increases VO2 max by up to 14% and the VO2 max difference by 18%.
VO2 max is the maximum rate of oxygen consumption measured during incremental exercise (exercise of increasing intensity.
= when muscles are offered more oxygen they will take it.


1. Which of the following hormones inhibit/s lipolysis (i.e., fat release from adipocytes for fat oxidation)? a. Cortisol b. Growth hormone c. Epinephrine and norepinephrine d. Insulin e. Glucagon

cortisol= catabolic hormone. breaks down. increase FFA metabolism.
GH= protein synthesis, stim bone growth, lipolysis, enhances healing.
Catacholamines- fuel release- increase release of FFA.
insulin ( promotes glucose uptake, utilization, glycogen synthesis, tri-glyceride synthesis in adipose tissue= suppress release of FFA.
glucagon- insulin antagonist.



7. In the rat study by Davies et al (1984), the researchers showed a. that McArdles patients had both a lactate threshold and a ventilatory threshold. b. that blood doping improves VO2max. c. rats are actually pretty cute furry animals. d. that VO2max is a good predictor of endurance performance. e. that endurance performance is more closely related to intramuscular oxidative capacity. (i.e., mitochondrial function) compared to VO2max.

Mcardles don't have glycogen phosphorylase. therefore unable to produce appreciable quantities of muscle lactate. Still show A VT no LT.



8. The Cori Cycle describes how a. proteins can be used for energy during prolonged exercise. b. lactate can be converted to glucose during exercise. c. blood doping can improve endurance performance. d. pyruvate can be used as a fuel by type IIb muscle fibres. e. blood is redirected from the gut to the muscles and skin during exercise in the heat.



10. Anaerobic training results in which of the following changes within the muscle? a. increased muscle respiratory capacity. b. increase in oxidative enzymes. c. increase in glycolytic enzymes. d. increase in myoglobin. e. increase in capillary density.



48. During fixed intensity (eg., constant-load) submaximal exercise, endurance trained athletes (when compared to untrained individuals) a. use more muscle glycogen. b. have a higher production (and accumulation) of lactate. c. use more fat. d. use more protein. e. deplete their glycogen in the type IIb fibres first (i.e., before depletion of the type I and type IIa fibres).



50. Increases in cardiac output that occur with endurance training can be largely attributed to a. higher heart rates at a given exercise intensity. b. higher catecholamine concentrations. c. an increase in mitochondrial volume. d. an increase in stroke volume. e. a greater network of capillaries.