orderly flow of blood throughout the heart
maintained by valves
the cardiac cycle refers to what is happening in the ventricles
diastole - passive ventricular filling during relaxation
systole - AV valves close, semilunar valves open, ventricles eject blood
contraction produced by the QRS complex as seen on ECG
amount of blood pumped by the heart (L/min)
Q = HR x SV
around 5L/min at rest, increases with exercise until it eventually plateaus at Qmax - differs depending on individual fitness
in a sedentary person, Q increases to 20-22L/min during exercise. in an athlete, Q increases to 35-40L/min during exercise. This is to match the need for increased oxygen supply to the working muscles
SV = EDV - ESV
Stroke volume is the amount of blood ejected with each contraction of the left ventricle
Preload determines SV
during exercise, stroke volume can increase by up to 1.8 times at rest
in untrained individuals, SV may go from 70-110 mL, while in trained individuals, from 100-180mL
athletes achieve a higher Q solely through enhanced SV
to increase SV during exercise, you need to increase venous return (blood back to the heart). this can be done by:
increasing ventricular filling during diastole (frank starling law)
Normal ventricular filling, followed by a forceful contraction
training adaptations - increase blood volume
Exercise has an effect on ventricular contractility - ventricular contraction as a given preload
positive inotropic effect: increase contractility
negative inotropic effect: decrease contractility
Factors causing inotropic effects:
autonomic NS activity
hormones
changes in ion concentrations
the total amount of blood filling the left ventricle
EDV is affected by filling time
as heart rate decreases, filling time increases
Filling amount (venous return)
this is dependent on cardiac output, blood volume, peripheral blood distribution and skeletal muscle activity
this is the amount of blood at the end of ventricular filling, i.e. the amount of blood that flows from the atrium into the ventricle
preload is directly proportional to EDV, the greater the volume in the ventricle at end diastole, the greater the stretching of the ventricle
the frank starling curve can be used to represent stroke volume (y) vs EDV/pre load (x)
sarcomeres lengthen and contract to pump blood
in athletes a larger EDV results in increased SV due to training
the amount of blood left following contraction
this is affected by
ventricular preload
how much fills the ventricles (EDV)
ventricular contractility
ventricular afterload
the pressure which the ventricle has to overcome to eject blood (BP)
maximal oxygen consumption (VO2 max) reflects the bodies ability to transport and utilise oxygen. this is dependent on:
ventilatory responses to exercise
external respiration: transfer of O2 in the lungs
transport of O2 in the blood
dependent on cardiac output, peripheral resistance and O2 carrying capacity
peripheral utilisation of O2: extraction at the tissue level as reflected by the a-vO2 diff
VO2 = (Q x a-vO2diff) / 100
in an untrained individual at rest, the VO2 is around 300, and at maximal exercise 3100
in an endurance athlete, VO2 at maximal exercise is around 5570
during exercise VO2 increases ~10x in untrained individuals due to:
increase in cardiac output via increase in SV (1.5x) and HR (2.5x)
increase in a-vO2 diff (the utilisation of O2 increases around 3x)
increases directly in proportion to workload
max heart rate = 220 - age
heart rate and oxygen uptake are linearly related but HRmax is lower in trained athletes despite increased oxygen consumption
heart rate at submaximal exercise intensities is lower after training despite similar submaximal cardiac outputs
due to increased sympathetic tone, the SA node is accelerated, increasing heart rate
due to decreased parasympathetic tone and less parasympathetic innervation, heart rate decreases
this inhibits acetylcholine and stops brachycardia
initially (until ~120bpm) during exercise there is a decrease in parasympathetic activity, followed by an increase in sympathetic activity
HR response i rapid initially partly due to feed-forward anticipatory increase stimulated by central command
as exercise continues, HR is increasingly controlled by catecholamine release
this is a slower, hormonal response
the largest increase in HR occurs during anticipation for an event to occur, increasing from ~60bpm - 130bpm
Heart transplant patients have no neural control of heart rate, so the peak HR occurs after the event has finished as hormones take a while to circulate
during a heart transplant, nerves are cut so HR can only be adjusted during exercise via catecholamine release
Cardiac tissue has a large blood supply, myocardium has to be fed from the coronary arteries, blood does not diffuse through
as the heart rate increases, time to fill decreases, decreasing stroke volume
the heart has its own internal rhythm regulated by the SA node
heart rate is also regulated by the medulla
the medulla receives signals from various receptors/detectors in the body
parasympathetic nerve endings concentrate in the atria, including the SA and AV nodes
sympathetic fibers supply the SA and AV nodes and the muscle of the atria and ventricles
In athletes, cardiac muscle may be up to 1.5 times thicker to allow increased cardiac output
not all exercise increases the left ventricular mass equally. while swimming, running, and wrestling all increase ventricular mass, wrestling shows the biggest increase
cardiac muscle grows due to the relationship between the pressure in the ventricles and adaptation, constant stretching causes an increase in size
cardiac muscle grows to match the workload imposed on the ventricle
a volume overload of the left ventricle leads to eccentric hypertrophy (dilation of the cavity and some thickening of the walls)
a pressure overload (increased afterload) of the left ventricle leads to concentric hypertrophy (thickening of the walls).
LV mass increases more in endurance athletes compared to resistance athletes. In fact, more resistance athletes experienced a decrease in ventricular mass
medulla oblongata of the brainstem contains the control centre for the cardiovascular system
Control centre receives input (afferent signals) from receptors (e.g. baroreceptors which are sensitive to blood pressure changes)
corrective signals are sent via the nervous system and via hormone release
neural influences flow through the sympathetic and parasympathetic components of the autonomic nervous system
impulses from aortic and carotid arterial mechanoreceptors, cardiac mechanoreceptors, skeletal muscle ergoreceptors (afferent) travel to the ventrolateral medulla. the medulla then sends signals to the effectors (heart, skeletal muscles, kidneys, etc)
sympathetic nerves stimulate the SA node to induce tachycardia through noradrenaline
parasympathetic nerves (via vagus nerves) induce brachycardia through acetylcholine
during steady state prolonged exercise, particularly in the heat, SV gradually decreases while HR gradually increases
this is due to blood flow being redirected to the skin to dissipate heat, as well as decreased plasma volume due to movement into interstitial fluid (sweating)
these changes decrease venous return, decrease EDV, and decrease SV
Heart rate increases to compensate for decreased stroke volume, i.e. to maintain cardiac output
the increase in HR that occurs when exercising at the same pace over time to maintain Q is known as cardiovascular drift
increased stroke volume increases performance
when fully dilated, the body’s blood vessels can hold ~20L of blood (4x total blood volume)
smaller arterial branches = arterioles
arterioles can alter their internal diameter = regulates blood flow
vasoconstriction and vasodilation
the ability to redistribute blood is important during exercise where blood is diverted to the active muscles
arteries form smaller vessels ~0.01mm in diameter called capillaries
usually contain ~5% of total blood volume
some capillaries are so narrow that only one blood cell can squeeze through
capillary density of human skeletal muscle averages 2000-3000 capillaries per mm^2 of tissue
around each capillary is a pre-capillary sphincter (not skeletal muscle)
the pre-capillary sphincter is a ring of smooth muscle that encircles the capillary and controls the diameter of the capillary. The capillary cannot constrict or dilate on its own.
constriction and relaxation of the sphincter provides an important local means for blood flow regulation within a specific tissue
deoxygenated blood moves from the tissue into the capillary into small veins - venules
the venules empty into the body’s largest veins - inferior vena cava and superior vena cava
this large vessel returns mixed venous blood to the right atria
since humans stand upright, ~70% of blood volume lies below heart level
the driving force for venous return (post capillary) is 15mmHg (0-30mmHg)
downwards hydrostatic pressure on the blood is 100mmHg. the veins lack this pressure to return blood from the extremities into the right atrium
venous return determines preload and therefore cardiac output and BP
regional differences in venous structure - lower limb veins are stiffer as the compression allows more blood to be sent upwards
muscle pump generates ~90mmHg of pressure. decreased volume increases pressure and forces the blood upwards
active “cool-down” prevents peripheral pooling
athletes who collapse at the end of a long race can be revived by lying down and elevating legs (this aids venous return)
valves prevent the backflow of blood and break the continuous column into smaller supported sections. varicose veins cause circulatory failure
increased heart rate increases pulsatility, increasing the contribution of the counter flow mechanism
during inhalation, blood is forced from the abdomen to the heart
pressure in the inferior vena cava increases → blood back to the heart
increase in venous return, augmenting stroke volume and cardiac output
during exhalation, semilunar vales prevent blood backflow. Blood is forced from the abdomen to the heart
pressure in the inferior vena cava decreases
normal systolic blood pressure in an adult is 110-120mmHg
normal diastolic blood pressure in an adult is 70-80mmHg
Hypotension is classified as a SBP of less than 100 and DBP of less than 60
blood flow and pressure vary considerably in systemic circulation
during the cardiac cycle, BP varies from 120-80mmHg in the aorta/large vessels
pressure decreases in proportion to the resistance of the vascular circuit
30mmHg in arterioles, ~0mmHg at the right atrium
Blood pressure is regulated by the medulla oblongata and responds to afferent messages from baroreceptors located in the aortic and carotid bodies
Blood pressure is also regulated via hormones
adrenaline, atrial natriuretic peptide, anti-diuretic hormone, angiotensin II
with a drop in blood pressure, a pressure error is registered by the control centres and autonomic nervous system activity is modified
pressure = (HRxSV) x TPR
Parasympathetic nervous system inhibition → HR and SV decreases
Sympathetic nervous system activation increases HR and SV and thereby Q, increasing TPR
average force exerted by the blood against the arterial walls during the entire cardiac cycle
the heart remains in diastole longer than systole
MAP = DBP + (1/3 x (SBP-DBP)
SBP-DBP = pulse pressure
an elevated systolic or diastolic blood pressure is referred to as hypertension
hypertension is classified as a SBP of 140mmHg or higher and DSP of 90mmHg or higher
systolic BP at rest can exceed 200mmHg in individuals with atherosclerosis (plaque) or thickening of the connective tissue of the artery
plaque can cause blood clots → stroke
diastolic blood pressure can also exceed 100mmHg under these conditions
hypertension causes chronic strain on the cardiovascular system
untreated chronic hypertension can lead to:
heart disease
stroke
kidney failure
eye problems
Hypertension can be prevented by:
regular physical activity
weight loss
stress management
smoking cessation
reduced sodium and alcohol consumption
adequate potassium, calcium and magnesium intake
medications such as beta blockers, alpha blockers, Ca channel blockers, diuretics, ACE inhibitors, ARBs
Response
Regular aerobic exercise reduces blood pressure by ~6-10mmHB
reduced sympathetic nervous system (decreased peripheral resistance)
increased renal function (removal of sodium = decreased fluid)
Generally, blood pressure during exercise is affected by:
Cardiac output (Q)
Increased during exercise → increased blood pressure
Blood Viscosity
increases during exercise → increased blood pressure
Resistance to flow
as a result of changes in the vascular system
BP = Q x total peripheral resistance
During Exercise
during the initial stage of exercise, there is an increase in systolic blood pressure during the first few mins of steady state exercise
SBP usually levels off at around 140-160mmHg
DBP remains relatively unchanged
for every 3ml/Kg you would expect SBP to go up by 10mmHg
this is most likely due to increased cardiac output due to increased venous return
During maximal graded exercise there is a linear increase in SBP proportional to workload
BP can be 200mmHg or higher during max exercise, most likely due to large cardiac output (increased venous return = increased cardiac output = increased blood flow)
DBP remains relatively stable during exercise
During steady state exercise, there is rhythmic muscle activity → vasodilation to active muscles → decreased total peripheral resistance → increased blood flow
venous valves prevent backflow
muscle pump increases pressure
indirect index of myocardial oxygen consumption (VO2 of the myocardium)
associated significantly with both morbidity and mortality
RPP = SBP x HR
in healthy individuals, RPP will be higher than 20,000mmHg per minute
Anything below 16,000mmHg per minute is considered insufficient
extra strain on the heart or kidneys
RPP increases faster in arm exercises than leg exercises
blood flow to tissues varies depending on the immediate needs of specific tissue (oxygen supply = blood flow x arterial oxygen content)
Liver and kidneys ~50%
Skeletal muscle ~15-20%
Volume of flow in any vessel is directly proportional to the pressure gradient between the 2 ends of the vessel (not absolute pressure in the vessel)
inversely related to the resistance against the flow (caused by friction between the vessel wall and red blood cells)
poiseuille’s law relates resistance and radius of the vessel. Radius of the vessel and resistance to flow are the most important factors
arterioles control blood flow by either constricting or dilating
if blood vessels were all fully dilated, they could hole ~20L of blood (4x more than normal volume)
this is done through smooth muscle contraction and relaxation
blood flow in the arterioles is governed by two factors:
Autoregulation
local metabolites act on arterial wall (detected by arterial wall → dilate, constrict, relax)
refers to the arterioles ability to self regulate their own blood flow
sensitive to local tissue environment
local control of blood distribution
in response to changes in the tissue’s local chemical (metabolites) and gas environment
decreased PO2, increased PCO2, increased temperature, decrease in pH, increase in nitric oxide (potent vasodilator), increased adenosine, ATP, K+
the above occur during exercise and result in vasodilation and increased blood flow to the local area
Extrinsic neural control
stiffen veins
Sympathetic nervous system stimulation = release of hormones (adrenaline and noradrenaline) that cause a generalised vasoconstriction (except coronary arteries and skeletal muscle)
increased stimulation of nerves by the medulla causes the arterioles to constrict thus reducing blood flow
reduced stimulation allows arterioles to stay dilated - more blood flow to the area
in theory, in areas that need extra blood, sympathetic stimulation decreases and arterioles stay dilated, allowing blood flow to the area
Functional sympatholysis
sympathetic nervous system activity also increases to skeletal muscles, but the action of it is modulated/inhibited by the local metabolites to blunt the constriction
during exercise, blood is redirected to the areas where it is needed
blood flow is restricted to non-active areas (kidney, liver, pancreas) and redirected to working muscles
during heavy exercise, muscles receive 80-85% of blood flow
redirection of blood flow during exercise is also accompanied by an increase in Q
cardiac output increases from 5L/min to 25-30L/min
this increase delivers more blood (oxygen) to the working muscles
During exercise, sympathetic output to the non active tissues increases, resulting in increased vascular constriction and reducing blood flow to those areas
resistance to flow is dependent upon the radius of the blood vessel. this alters resistance to flow (total peripheral resistance)
doubling the radius increases volume and flow
halving the diameter increases resistance by 16x
humans maintain a constant core body temperature in the range 36.1 - 37.8˚C
homeotherms - maintain constant temperature
the role of the thermoregulatory system is to maintain stable core temp
Brain death begins at 41˚C, at 45˚C death is nearly certain
during exercise the body gains heat faster than it can lose heat
Internal temperature can exceed 40˚C - adversely affecting the nervous system
muscle temperature can exceed 42˚C
The body attempts to regulate its internal temperature vi
heat is lost through
conduction
the rate of conductive heat loss depends on two factors:
the temperature gradient between the skin and surrounding surfaces
thermal qualities of surrounding surfaces - water absorbs heat faster than air. the body loses heat ~25 times faster in water than it does in air of the same temperature
Conduction alone cannot provide enough cooling
convection
the transfer of heat from one place to another by the motion of a gas or liquid across a heated surface - wind chill factor
Combined, the heat loss through convection and conduction mechanisms only accounts for about 10-20% of heat loss to the surrounding air (provided the air is cooler than the skin)
radiation
transfer of hear in the form of infra-red rays (electromagnetic)
primary heat loss mechanism at room temperature without sweating (~60% of heat loss at rest)
evaporation
heat loss during the “phase-shift” of a liquid to a gas
accounts for 20% of heat loss at rest (insensible perspiration)
primary avenue of heat loss during exercise (~80%)
very dependent on the environment
sweat must evaporate to allow for heat transfer
1L of sweat evaporation = 580kcal heat loss
heat is gained by the body through:
metabolism - basal metabolic rate
Can increase 20 times above resting levels during intense exercise
theoretically can increase core temp by 1˚C every 5-7 mins
environment
solar radiation from objects in the environment that are warmer than the body
muscular activity
hormones
thermic effect of food
postural changes
thermoregulatory centre of the body is in the brain (hypothalamus/thermostat)
Thermal receptors in the skin and changes in blood temperature activate the hypothalamus
Increased blood and internal temperature
impulses go go the hypothalamus
vasodilation occurs in skin blood vessels so more heat is lost across the skin
sweat glands become more active, increasing evaporative heat loss (2-4million sweat glands)
body temperature decreases
heat flows down a temperature gradient to cooler areas
if the body is hotter than the environment, then:
heat in the body moves (via the blood) from the core to the skin and cools
evaporation of sweat also cools the skin which then cools the blood and then the core
cooled blood returns to the core
during exercise, metabolism can increase 15 fold - heat production increases 15x from rest + heat gained from the environment
heat loss is critical during exercise
heat flows down temperature gradient from muscle to core and then to skin
some heat is directly conducted to the skin from the muscle underlying it
heat transfer from the core to the skin is dependent upon skin blood flow
the transfer of heat from the skin to the environment depends upon:
the temperature gradient
the rate of evaporation
If ambient temperature exceeds core temperature, conduction, convection, and radiation cause heat gain
therefore at high ambient temps, evaporation is the only effective means of heat loss
the rate of heat loss by evaporation depends on:
surface area exposed to air - higher surface area = increased convection = increased evaporation
temperature of ambient air - higher temp = increased sweating
convective air movement around the body - convection improves evaporation
relative humidity of air - high RH impedes evaporation (most important)
the amount of water in ambient air compared to the total quantity of moisture that air can hold
for evaporation to occur effectively, RH must be lower than that of moist skin - 40mmHg → 40%
sweat beads represent useless water loss and can produce dehydration and overheating
individuals can tolerate reasonably high temps provided that the relative humidity is low
during exercise in the heat, there is competition for cardiac output between the working muscles and the skin
muscles require delivery of blood (oxygen) to sustain energy metabolism
as core temperature rises, blood diverts to the skin for cooling
This means less blood to the working muscles, resulting in:
less fuel (O2)
greater dependence on anaerobic metabolism
earlier accumulation of H+
greater use of glycogen stores
reduced ventilation
impaired exercise performance
premature fatigue
the amount of blood that muscles can receive is ~30L/min
peak cardiac output of the heart in an untrained person is ~25L/min
the body’s need for blood surpasses the supply
during heat stress, 15-25% of cardiac output passes through the skin → blood vessels near the skin vasodilate → flushed appearance → increase in cutaneous blood flow
sweating leads to plasma loss → increased viscosity → lower stroke volume and higher heart rate (cardiovascular drift)
this decreases venous return, and end diastolic volume
heart rate increases to compensate for decreased stroke volume, i.e. to maintain cardiac output → increased strain on the thermoregulatory and cardiovascular system
the increase in heart rate that occurs when exercising at the same pace over time to maintain cardiac output is known as cardiovascular drift
bench rotations
cool rooms during breaks
spray players during breaks
ice slushies
ice jackets
play games during cooler times of the day
do not rely on thirst. the thirst centre is easily switched off by sensory receptors during exercise, this can lead to voluntary dehydration during exercise
pre-exercise: 400-600mL water in the 60 mins prior
150mL every 15-20mins during
1.5x sweat loss post exercise, consume beyond thirst, drink salty drinks
sports drinks replace electrolytes lost during exercise
during long events, excess water intake can cause hyponatraemia
some CHO ingestion post exercise is critical for glycogen repletion
several days of activity in a hot environment will lead to improved heat tolerance and performance
adaptations such as:
increase in plasma volume
decrease in resting core temp
increase in sweat rate
NaCl content of sweat decreases
reduced heart rate (compared to unacclimatised)
once acclimatisation occurs, effects last several weeks