Exercise physiology:

For muscle contraction to occur:

• Action potential from a motor neuron causes a depolarisation
• Ca2+ released from the sarcoplasmic reticulum
• 4 molecules of Calcium bind to troponin C (calcium binding subunit)
o TnT binds tightly to tropomyosin
o Entire troponin protein physically moves tropomyosin exposing the myosin-
binding site
• Energised (ATP bound) myosin binds to actin
• Tension developed (power stroke) which results in shortening of muscle
• Movement occurs
• Dissociation of actin and myosin requires ATP
o If no ATP – you get rigor

Muscle contraction:
• Tight binding in the rigor state. The cross bridge is at 45° angle relative to the filaments
• ATP binds to its binding site on the myosin. Myosin then dissociates from the actin
• The ATPase activity of the myosin hydrolyses the ATP. ADP and Pi remains bound to
myosin
• The myosin head swings over and binds weakly to a new actin molecule. The cross
bridge is now at 90° relative to the filaments
• The release of Pi initiates the power strike. The myosin head rotates on its hinge, pushing
the actin filament past it
• At the end of the power stroke, the myosin head releases ADP and resumes the tightly
bound rigor state
The actin and myosin slide over each other causing the sarcomere to shorten => power stroke
– generates muscle force (myosin head polling the actin across it)
The actin and myosin do not shorten – only the sarcomere shortens

Muscle contractions:
• Isometric contraction: force is generated by the length of the muscle is unchanged
o Action but no movement
o Eg. Postural muscles, trying to move a force that is greater than the muscle force
– eg. Push a wall
• Concentric contraction: force is developed while the muscle is contracting
o Eg. Bicep curl – cross bridges are moving towards the middle
• Eccentric contraction: force is generated while the muscle is lengthening
o Eg. Lengthening the bicep, opposing gravity, walking downhill

Muscle fibers:
• Organised into motor units – smallest functional group
o Motor neuron + muscle fiber
• Motor neurons innervate different muscle fibers with common structural and functional
properties
• Different propertoes:
o Biochemical properties:
▪ Oxidative capacity:
• Number of mitochondria
 • Capillaries
• Myoglobin concentration – the more myoglobin, the more oxygen
is getting transported to the mitochondria
▪ Type of ATPase enzyme – breaks down ATP to form energy
o Contractile properties:
▪ Maximal force production
▪ Speed of contraction
▪ Muscle fiber efficiency (marathon runners vs. sprinters)

Muscle fiber types:

• Groups of muscle fibers that are used for different types of exercises
• Each group will be innervated by the same motor neuron

Fast fibres Slow fibres

Characteristic Type 2 x Type 2 a Type 1
Number of
Low High / moderate High
mitochondria
Resistance to
Low High / mod High
fatigue
Predominant
Anaerobic Combination Aerobic
energy system
Highest (makes E Low (E is available
ATPase High
fast) slowly)
Vmax (speed of
Highest Intermediate Low
shortening)
Low (cant be High (can be
Efficiency Moderate
sustained) sustained for long)
Specific tension High High Moderate
Fastest muscle Slow twitch (for
fibre (sprinter) marathon runners)

Training muscle fibres:

• If you want to be a sprinter – you have to train for sprints
• To train T2x fibers – you have to do strength activity
o A lot of force in short periods
o Amount of actin and myosin determine the force
o Change by hypertrophy
• T1 fibers:
o Don’t bulk up
▪ You can change the number of mitochondria (aerobic muscle fibers) and
you can get more blood vessels and myoglobin

Aging:
• By the age of 80, you lose 50% of muscle mass
• Some muscle fibers lose their motor innervation (mainly T2) – they will then be supplied
by the adjacent motor neuron – supplying the T1 – making them like T1 fibers

Force regulation in fibers:

1. Type of motor units
 • Fast motor units = greater force
2. Number of motor units
• More motor units = greater force
3. Nature of motor unit neural stimulation
• When the AP arrives at the muscle – it causes a cross bridge formation
• When Aps arrive at such a fast rate, the muscle cant relax between
contractions
o This causes tetanus – the force produced is bigger than a single force
• stimulation;  force produced

4. Length of the sarcomere (length tension relationship)

• Optimal overlap: amount of overlap that allows for the greatest force
production (highest)
• If the overlap is too much – it wont be able to move towards the middle – 
 force
o Occurs during shivering – feel stiff afterwards
• Same thing happens if they are too far apart
o No cross bridge interaction – occurs during static stretching
5. Speed of contraction (force velocity relationship):
• Concentric: force development decreases at higher speeds
o The faster you do an activity, the less force will be produced. The
slower you do it, the ore force is produced
• Eccentric: fast eccentric contractions allow for a max force application
o The faster you do an activity the more force is produce. The slower you
do an activity, the less force is produced
BIOENERGETICS AND EXERCISE:

Sources of energy for muscle contraction:

• High energy phosphates
• Adenosine triphosphate (ATP)
• Intramuscular stores: 5-6mmol / kg wet weight

Alactic anaerobic system:

• Also called the ATP-PC system
o PC: phosphocreatine / Creatine phosphate
▪ High energy compound stored in skeletal muscle to produce ATP
▪ There is 3 times more PC in muscles than ATP
• Only a small amount of Pc available
o Enough for 5-8 seconds of max exercise
o (Reason you slow down at the end of a sprint – because ATP-PC runs out)
• ATP-PC system does not use Oxygen and does not produce lactic acid
• Doesn’t need mitochondria or oxygen
• To make PC you need a lot of energy –  we don’t produce it during exercise but
rather when relaxing (when w don’t need creatine)

ATP can be generated in 3 ways:

• Phosphocreatine / creatine phosphate:
o ATP + PC → C + ATP
o Only supplied for 5-8 seconds of maximal exercise
o Powerlifting
• Anaerobic respiration (glycolysis)
o Used when the need for ATP s more than can be provided by the ATP-PC and
aerobic system
o Does not use oxygen and lactic acid is produced
o Needs hydrogen and electron carrier molecules (NADH and FADH)
▪ Carries the Hydrogen to the mitochondria (aerobic)
▪ Converts pyruvic acid to lactic acid (anaerobic)
▪ NAD: NAD+ + 2H+ → NADPH + H+
▪ FAD: FAD+ + 2H+ → FADH2
o NADH is shuttled into the mitochondria
▪ NADH produced in glycolysis must be converted back to NAD
• By converting pyruvic acid to lactic acid
• By shuttling H+ into the mitochondria
• Aerobic respiration:
o Takes place in the mitochondria – in the presence of oxygen
o Involves glycolysis, the krebs cycle, electron transport / oxidative phosphorylation
o Always active
o Resting conditions: provides basically all the energy that is needed
o Needs oxygen
o Takes place slowly
o In high energy exercise, you need more energy than the aerobic respiration can
provide
o Provides long duration energy
Interaction between aerobic respiration and anaerobic ATP production:
• Energy to perform exercise comes from an interaction between aerobic and
anaerobic pathways
• The contribution of each energy pathway depends on the duration and intensity of the
exercise
o Short term, high intensity activities – greater contribution of anaerobic energy
systems
o Long term, low to moderate intensity exercise – majority of ATP produced from
aerobic sources

Fuel for exercise:

• Carbohydrates are the primary source of energy during exercise:
o Stored in the liver and muscle as glycogen
o Can also use blood glucose
o Limited stores – can be depleted if the diet does not contain sufficient
carbohydrates
o The only fuel source that can provide energy in the absence of oxygen
o Supplemented by fats are fuels for energy
o Needs less oxygen for metabolism than fats
• Fats as an energy source:
o Abundant stores of fat in the body
o Fat is stored in adipose tissue as triacylglycerides (TAGs)
o Fat must first be broken down to glycerol and FFA
o Glycerol can then be converted to glucose via gluconeogenesis
o Very complicated process where fats undergo β-oxidation (acetyl-CoA and
NAHD formation from FFA in the mitochondria)
o Fats cannot be used as a fuel source in the absence of oxygen
o Thus: the rate of energy release is too low to supply the energy needs during
moderate to high intensity exercise
o Fat is only metabolised during prolonged low intensity exercise
o Fat metabolism produces more ATP than carbohydrate metabolism
o Phospholipids and steroids CANNOT be used as an energy source
• Protein as a fuel source:
o Composed of amino acids
o Amino acids must first be converted to glucose, before it can be used as an
energy source
▪ Via gluconeogenesis
▪ Amino acids join the metabolic pathways on different levels
o Proteins supply 5-10% of energy during prolonged exercise
Exercise metabolism: oxygen consumption:
• The measurement of Oxygen consumption (VO2) is an index of aerobic ATP production
• Thus, the measurement of VO2 during exercise is an indication of aerobic metabolism
during exercise
• The body’s ability to gauge the need for oxygen by the muscles at the onset of exercise
is not perfect
• So, the right amount of oxygen is not supplied immediately to the active muscle at the
beginning of exercise
• Oxygen uptake increases rapidly at the beginning of exercise but only reaches steady
state within 1-4 minutes
o Steady state = when you start feeling ok – metabolic demands are met
• During steady state, ATP is generated primarily by aerobic metabolism
• Oxygen deficit – lag in oxygen uptake at the beginning of exercise, because oxidative
phosphorylation in the mitochondria is not immediately activated (original hypothesis)
• Suggests that anaerobic pathways contribute to the total ATP production – produces
lactic acid

Oxygen deficit and excess post-exercise oxygen consumption (EPOC):

• Fast portion of EPOC: (2-3 mins)
o Resynthesis of stored PC – that was lost in the beginning
o Replacement of the oxygen stored in the muscle and blood (that was lost in the
beginning od exercise) – replacing the oxygen debt
• Slow portion of EPOC: (30 mins)
o Conversion of lactic acid to glucose (gluconeogenesis) – getting rid of Lactic
acid
o Elevated  rate and breathing, due to higher energy need
o Elevated body temperature, due to higher metabolic rate
o Elevated epinephrine and norepinephrine, due to higher metabolic rate

EPOC is greater following higher intensity exercise:

• Greater body temperature
• Greater depletion of PC
• Greater blood concentration of lactic acid
• Greater levels of epinephrine and norepinephrine

Factors contributing to EPOC:

• Elevated hormone
 • Post exercise elevation of  rate and breathing
• Elevated body temperature
• Restoration of muscle and blood oxygen stores
• Lactate conversion to glucose
• Resynthesis of PC in the muscles

Aerobic capacity:
• Aerobic capacity / cardiorespiratory endurance: the entire body’s ability to sustain
prolonged, dynamic exercise using large muscle groups
o Measure of fitness
o Good indication of endurance capacity
• VO2 – the ability to deliver O2 to the muscle (CVS) and use the oxygen (get it across the
blood to the muscle – metabolically)
• Oxygen uptake increases linearly until VO2 max is reached, thereafter no further increase
in VO2 with increasing work rate
• VO2 max – “physiological ceiling” for the delivery of O2 to muscle
o Affected by genetics and training
o Even if there is an increase in workload, the O2 input doesn’t change (plateau)
• Measure in incremental tests
o By increasing the inclination on the treadmill / increasing the workload on a bike
• After the age of 25, VO2 decreases

Oxygen consumption (Endurance capacity):

• VO2 = (HR x SV) x (a – v) O2 diff
• VO2 = CO x (a – v) O2 diff
o VO2 = HR x SV x {[Hb] x 1.34 (SaO2 – SvO2)} This is a good measure,
o VO2 = BP / TPR x {[Hb] x 1.34 (SaO2 – SvO2)} as it takes HR and SV
into account (measure
▪ CO = BP / TPR (total peripheral resistance)
of CVS health)
• The lower the TPR the better as the blood
pressure will be lower
• Oxygen transport depends on: HR, SV, BP, TPR, [Hb], SaO2 & SvO2

Lactate threshold:
• The point at which the concentration of blood lactate suddenly rises during
incremental exercise
• How fast a person can run before switching to anaerobic respiration
o If fit, the person uses fat for energy for longer before switching to anaerobic
respiration (carbohydrates)
o When lazy and unfit, you use carbs for energy, LT comes earlier
o  It is a good measure of fitness
• Mechanisms affecting LT:
o Low muscle oxygen (original theory – wrong)
o Accelerated glysolysis:
▪ The mitochondrial H+ exchanger cannot keep up with glycolysis (NADH is
produced faster than it is shuttled into the mitochondria)
▪ The excess NADH in the sarcoplasm promotes the conversion of pyruvic
acid to lactic acid
o Recruitment of fast-twitch fibers
▪ Type of lactate dehydrogenase
 • The enzyme that converts pyruvic acid to Lactic acid (can go in
any direction depending on which fibers are used)
o T2 don’t have a lot of oxidative enzymes – have lycolytic
enzymes which favour glycolysis
▪ The more T2 fibers you have the more pyruvic acid
will be converted to lactic acid (during high intensity
workout)
• LDH iso-enzyme in fibres enhances the production of lactic acid
(fast fibers are used during high – intensity exercise)
• LDH iso-enzyme in slow fibres enhances the conversion of lactic
acid to pyruvic acid
o Reduced rate of lactate removal:
▪ Rate of lactate clearance:
• Blood [lactic acid] = lactic acid production – lactic acid clearance
▪ Some muscles produce lactic acid while other tissues clear lactic acid
▪ On the graph – during aerobic respiration, where the lactate levels are
fairly constant – there is a balance between lactic acid clearance and
lactic acid production
▪ T1 clears it better:
• Increase in number and size of mitochondria
• Increased blood supply to the muscle fibres (capillarisation /
angiogenesis)

OBLA (onset of blood lactate accumulation):

• The point where the concentration of lactate in the blood reaches 4mmol / l
• Arbitory point which was allocated at 4 mmol / l
• Once you reach this point there is no turning back – you are mostly using
carbohydrates for fuel (anaerobically)
• The fitter you are, the farther and faster you can run before you reach OBLA

Lactic acid:
• Does not cause delayed onset of muscle soreness (DOMS) as t gets cleared from the
blood
o Has a half life of 30 mins
• Causes metabolic acidosis
• It stimulates nociceptors (pain) that cause the burning pain which impairs performance
• Decreases ATP production and it denatures enzymes
EXERCISE METABOLISM:

Fuel consumption during exercise:

• The percentage of carbohydrates and fat to energy metabolism during exercise can
be directly measure during exercise by measuring VCO2 and VO2
• Protein metabolism CANNOT be measured in this way
• Measurements must be made during steady state exercise (reason why we change the
workload every 3 minutes)
• Respiratory exchange ration (RER) vs. respiratory quotient (RQ):
o RQ = cellular metabolism
• RER = VCO2 / VO2
o For fat = 0.7
o For carbohydrates = 1
• After exercising (which is not long after OBLA), the person has an RER of 1.15 – this is
because he is burning lactic acid → this then dissociates into lactate and H+ → the H+ is
then buffered by HCO3- → H2CO3 → CO2 + H2O

Exercise intensity and fuel selection:

• Low intensity exercise (< 30% of VO2 max) – fats are primary fuel
• High intensity exercise (> 70% of VO2 max) – carbohydrates are primary fuel
• The cross over point:
o Describes the shift from fat to carbohydrates as exercise intensity increases
▪ Due to the recruitment of fast fibers (T2) and increased epinephrine
• The increase in intensity results in the use of carbohydrates as T2 fibers use carbs
(anaerobic respiration) and it makes Lactic acid which inhibits lipolysis

Which exercise intensity is best for burning fat?

• At low intensities (±20% of VO2 max):
o There is a high percentage of energy expenditure which is derived from fat,
however, the total energy expended is low
▪ Total fat oxidation is also low
• At higher exercise intensities (± 50% VO2 max):
o Lower percentage of energy is used from fat
o Total energy expended is higher
▪ Total fat oxidation is also higher

Exercise duration and fuel selection:

• During prolonged exercise there is a shift from carb metabolism towards fat metabolism
due to the increase rate of lipolysis
 • Lipase (breaks down fatty acids) activity is inhibited by insulin and high levels of lactic
acid but with prolonged exercise insulin levels decrease
• But: if a high carb meal or drink is taken 30 – 60 mins before exercise, blood glucose
levels rise and more insulin is secreted from the pancreas
• Usually insulin levels decrease during prolonged exercise but in this case the high insulin
levels will inhibit lipolysis and fat metabolism

Interaction between fat and carbohydrate metabolism:

• You need carbs in order to burn fat:
o “Fats burn in the carbohydrate flame”
o Glycogen is depleted during prolonged high-intensity exercise
▪ Reduced rate of glycolysis and production of pyruvate
▪ Reduced Kreb’s cycle intermediates
▪ Reduced fat oxidation
• Fats are metabolised by the Krebs cycle
• Reason why one should have a small carbohydrate meal for breakfast so it can kick
start your metabolism
o If no carbohydrates to start the metabolic pathway – no fats can join the
pathway

Fuel sources during exercise:

• Carbohydrates:
o Muscle glycogen:
▪ Primary source of carbohydrates during high intensity exercise
o Blood glucose:
▪ For liver glycogenolysis
▪ Primary source if carbohydrates during low intensity exercise
▪ Important during long-duration exercise
▪ Used as muscle glycogen declines
• Fats:
o Intramuscular triglycerides:
▪ Primary source of fat during high intensity exercise
o Plasma free fatty acids:
▪ From adipose tissue lipolysis
▪ Primary source of fat during low intensity exercise
▪ Becomes more important as muscle triglyceride levels decline in long
duration exercise

Low intensity – from plasma free fatty acids

Moderate intensity – 50 / 50 glycogen and free fatty acids
High intensity – glycogen

The longer you exercise the more free fatty acids (adipose) you use
Blood glucose also contributes after long hours of exercise

Lactate as a fuel:
• Can be used as a fuel source by skeletal muscle and the 
o Converted to acetyl-CoA and enters the Krebs cycle
 • Can be converted to glucose in the liver via the Cori cycle and goes back to the
muscle to be used
o Uses more ATP than the amount of ATP produced in the cycle
• Lactate shuttle:
o Lactate produced in one tissue and transported to another in T1 fibers

Metabolic adaptations to exercise training:

• After training OBLA shifts – can maintain a higher workload using fats
o The person has become fitter (saving carbs)

Metabolic adaptations with training (in response to Lactate threshold)

• Amount and size of mitochondria (more mitochondria - more aerobic respiration →
more fat breakdown)
• Increased intra-muscular triglycerides usage
• Increased lipolysis
o Increased blood flow to muscle (capillirization)
o Increased fat mobilisation and oxidation
o Decreased catecholamine release (inhibits lipolysis)
o Increased myoglobin
• Net effect: sparing glycogen:
o Lactate will be lower, sparing glycogen as more training will cause better
aerobic respiration
• Implications for diabetes (T2): being fit is better because they can mobilise fat instead
of carbs – this improves the sensitivity to insulin as it up regulates the GLUT 4 receptors,
which causes glucose to decrease – allowing lipolysis to occur

The ventilator system during exercise:

• Pulmonary ventilation (minute ventilation): the amount of air moved into and out of the
lungs per minute
• V = VT x f
o Product of tidal volume and breathing frequency
• PO2 shouldn’t change – should remain between 90 and 100 no matter if the person is fit
or unfit
• VT = ventilation threshold – at the break point in the V vs. work rate graph – correlates
with lactate threshold
o Happens earlier in an untrained person (need to get rid of CO2 – so  we
increase ventilation)
• pH will decrease: VT corresponds with the decrease in blood pH as with a higher
exercise intensity, the lactic acid will increase, forming H+ and lactate
Control of ventilation:
• Need to control the rate and the depth of breathing
• Respiratory control center
o Receives neural input
▪ From motor cortex or skeletal muscle
o Receives humoral input
▪ Central chemoreceptors:
• Located In the medulla
• PCO2 and H+ concentration in the cerebrospinal fluid
▪ Peripheral chemoreceptors:
• Aortic and carotid bodies
• PO2, PCO2, H+, and K+ in the blood
o There is a linear relationship between PCO2 and minute
ventilation
▪ CO2 levels in the blood
o Regulates the respiratory rate
• Hypoxic threshold – stimulates minute ventilation

Ventilatory control during exercise:

• During submaximal exercise:
o Linear increase in VE due to increased central command by the humoral
chemoreceptors and neural feedback
• During heavy exercise:
o Exponential rise above Tvent due to the increasing blood H+ (from lactic acid →
causes increased breathing)
• Oxyhaemoglobin dissociation curve:
o Rightward shift is caused by: (decreases the affinity of the Hb for O2 - will give off
O2 more easily at the tissue level)
▪  PCO2
▪  acidity (decreased in pH)
▪  temperature
▪  2-3 DPG (product of RBC cellular respiration)

Cardiovascular system and exercise:

• During exercise you have:
o  SNS activity
o  HR and contractility

Regulation of stroke volume:

• End diastolic volume (“preload”)
o Volume of the blood in the ventricles at the end of diastole
o Frank starling mechanism:
▪ Greater preload results in stretch of the ventricles and in a more powerful
contraction
▪  skeletal muscle pump
o Affected by:
▪ Venoconstriction
▪ Skeletal muscle pump
 ▪ Respiratory pump
• Average aortic blood pressure
o Indirectly proportional to SV
o Pressure the  must pump against to eject blood (“afterload”)
o High afterloads result in a decreased stroke volume – requires a greater force
generation by the myocardium to eject blood into the aorta
o Vasodilation during exercise
• Venoconstriction (veins = large storage capacity for blood)
o Decrease volume capacity of the veins-  venous return
o Skeletal muscle pump – force blood from the extremities to the 
o One way valves prevent back flow
• Respiratory pump:
o Rhythmic breathing pattern → mechanical pump
o Inspiration:  in thoracic pressure;  in abdominal pressure

Situations where venous return is inhibited:

• Prolonged exercise: sweat decreases plasma volume;  SV. To maintain the cardiac
output:  HR (=> cardiovascular drift)
• Sustained muscle contractions: causing blood to pool – if you hold a contraction there
is no pumping (static contraction)
• Valsalva manoeuvre: holding your breath ( thoracic pressure)
• Changes in body position: from horizontal to vertical – pooling

Cardiovascular changes during aerobic exercise:

• (Acute bout of exercise – the same for a person who is fit or unfit)
•  HR ( SNS activity) - this  linearly up to the age of predicted HR (220 – age)
• SV increases linearly to 40% of VO2 max – due to venous return;  afterload
o Venoconstriction
o Respiratory pump
o Skeletal muscle pump
• CO is from HR and SV – the rise is due to the increase in both and then when it
becomes less steep, it is due to the rise in HR
• Atrivenonous O2 difference – based on the extraction of O2 – beginning due to
vasodilation going to the muscles (more to pull O2 from
• BP – there is a rise in systolic until you reach your maximum - this can be seen in CO
o Diastolic – this correlates with the total peripheral resistance – dilation in the
skeletal muscle –  there is a decreased but there is constriction in the GIT –  on
a whole, the blood pressure can either increase or stay the same
▪  Diastolic doesn’t increase – if it does there is a problem
Redistribution of blood in exercise:
• In exercise CO increases from 5 to 25 l / min
• At rest 15-20% of CO goes to skeletal muscle
• During exercise: 80 – 85% of CO goes to skeletal muscle
• The brain receives a lower % of the CO during exercise but the percentage is of a larger
number –  the same volume of blood reaches the brain

Adaptation in endurance trained athletes:

•  blood volume
•  Haematocrit -  RBCs –  more haemoglobin to carry the oxygen
•  CO due to the  in SV
o  Works less hard when fit compared to unfit – same SV but the  is not pumping
so hard;  HR)
o  Increases in size => physiological hypertrophy
▪ Wall thickness and chamber size increase in size in the same ratio) –
relative wall thickness is the came as an untrained person