Aerobic capacity is the ability to take in, transport and utilize oxygen and is a major factor in endurance performance. So when we train, increasing our aerobic capacity is always a goal.
But how does this happen? How does the body handle oxygen? How do we measure aerobic capacity and what are the physiological effects of training on the way we handle oxygen?
Here are the notes from the talk which attempted to address a massive subject and summarise the main points.
PHYSIOLOGY OF EXERCISE 1 – AEROBIC CAPACITY
WHAT (physiological parameters) are we training and why, not HOW to train them. That comes later!
Aerobic Capacity is the ability to consume O2.
(See pdf file Doc_752043 also at the foot of the page for supporting diagrams Figure 2 – Carl’s blood lactate curve.)
Endurance athletes have superior aerobic energy transfer and so aerobic capacity is a major factor in endurance performance.
Maximum O2 consumption is referred to as VO2max.(See Figure 3 – VO2max/lactate/running speed treadmill test)
It represents the maximum amount of O2 that can be removed from the circulating blood and used by the working muscles. Elite athletes have around twice the VO2max of sedentary people. A high VO2max requires integration of pulmonary, cardiovascular and neural systems and is a good indicator of endurance performance.
However, VO2max is NOT the sole determinant of endurance performance. Other factors, mainly at the local tissue level strongly influence a muscle’s ability to utilize oxygen and hence the ability to sustain a high level of aerobic activity.
Absolute VO2max is measured in L/min. Relative VO2max is measured in ml/kg/min and takes in to account the body mass of the subject. For example:
-a huge rower 120kgs may have an absolute VO2max of 7L/min which is a relative VO2max of 7000/120=58mls/kg/min.
-a petite cyclist 50kgs may have an absolute VO2max of 4L/min which is a relative VO2 max of
So the cyclist can consume more O2 for their size.
Average relative VO2max for 35yo men in the general population is around 35mls/kg/min.
It declines with age and is lower for women.
Table of relative VO2 max scores for elite sports (mls/kg/min)
|>75||Elite runners, cross country skiers, cyclists|
|60-65||Premiership football players|
VO2 max is a good indicator of endurance performance. It will differ between sports in the same person as the exercise requirements are not the same eg running involves more all body activity than cycling, so running VO2max will be higher .
Carl: Cycling VO2max = 68mls/kg/min Carole: Cycling VO2max 58 mls/kg/min
Running VO2max= 77mls/kg/min
What are the physiological steps in the consumption of oxygen? See Figure 1
- Ventilation – LUNGS
- Circulation –CARDIOVASCULAR SYSTEM (heart, blood vessels, blood)
- Oxygen utilisation – MUSCLES
VENTILATION – LUNGS
O2 =21% of inspired air
Airways – mouth/nose/trachea/lungs/bronchi/bronchioles/alveoli
Chest cavity (thorax) – negative pressure from diaphragm contraction/other respiratory muscles causes inspiration, relaxation of diaphragm – expiration (passive at rest). Rises in CO2/H+ levels are the stimulus to breathe, not lack of O2.
FVC = Functional Vital Capacity = max inspiration – max expiration over 1 second
FVC is 4-5L in men and 3-4L in women, is mainly genetic and is NOT altered by training
FVC is NO indication of aerobic fitness or performance as long as it is within a normal range and untrained people the same size as a trained athlete may have similar FVCs.
Alveolar gaseous exchange – diffusion of O2 to the red blood cells (rbcs) and return of CO2
Gaseous exchange is NOT a limiting factor in O2 uptake except in disease
Blood flow velocity is NOT a limiting factor either (except in EIH=Exercise Induced Hypoxia in elite athletes, thought to be a ventilation/perfusion mismatch)
Women have smaller lungs, reduced lung function measures, reduced airway diameter and reduced alveolar surface area even after allowing for their smaller stature and so have reduced aerobic capacity than men.
Exercise Hyperpnoea = desperate gasping/heavy breathing at intense levels of exercise is NOT due to inability to breathe in enough O2 as alveolar O2 levels rise and CO2 levels fall in this state of hyperventilation. Stimulus for this is thought to be neural.
- Pulmonary ventilation does NOT limit maximal aerobic performance (normal FVC, no disease)
- Larger FVCs are genetic
- Untrained individuals are breathless due to a failure to regulate blood CO2/H+ levels
- Exercise Hyperpnoea (hyperventilation) at intense levels is NOT due to lack of O2
- Women have lower ventilatory capacity than men
- CIRCULATION – CARDIOVASCULAR SYSTEM (heart, blood vessels, blood)
- Heart – a pump, 4 chambers, receives deoxygenated blood from the organs and muscles, pumps it to the lungs from which oxygenated blood returns to be pumped back out to the organs and muscles again
- Arteries – a high pressure delivery system, muscular walls, pulse, systolic and diastolic pressure
- Capillaries – exchange of gases, very small, dense network, site of gaseous exchange
- Veins – low pressure return system, thin walled, no muscles, rely on muscle pump (death by crucifixion/post race collapse), flow direction controlled by valves
- Blood – cells suspended in plasma. Red blood cells carry O2 from the lungs to the muscles by binding it with haemoglobin Hb
Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)
What happens to the CV system on exercise?
Stroke Volume SV
SV is higher at rest to start with in trained athletes.
On exercise SV increases with intensity up to an exercise intensity of about 50%VO2max then plateaus. Further increases in CO are due to an increase in HR only, until max HR (and max CO) is reached.
Heart rate HR
Increases with intensity rapidly within 30 seconds to 2 minutes of a run then gradually increases further to a maximum, roughly (10% variation) 220-age
Why is HR lower in fit people? SV increases with training.
At rest, 75kg male has a CO of 5L/min.
Untrained: HR is ~70bpm, SV = 5000ml/70 = 71mls
Trained: HR is 50bpm, SV= 5000ml/50 = 100mls
Cardiac Output CO
College students increase their CO 4x to 20L/min on maximum exertion (max HR 195)
Elite athletes increase their CO 7-8x to 35-40L/min (SV = 180-200mls) (max HR 195)
Racehorse max CO = 600L/min!
The changes in SV (and hence CO) are due to increases in:
- Blood volume (increased plasma volume – increased “preload”)
- Mycocardial (heart muscle) contractility (Frank-Starling mechanism i.e. force of contraction is proportional to the initial length of the muscle fibre))
- Compliance (elasticity) of the left ventricle
and are a result of training.
Larger SV ~ larger CO ~larger VO2max ~ enhanced endurance performance
Myocardium (heart muscle)
Relies on aerobic metabolism and has 3x the oxidative capacity of skeletal muscle.
At low exercise intensities it oxidises mainly fat. At moderate intensities it oxidises both fat and glycogen. Trained heart muscles uses more fat and spares glycogen, as does skeletal muscle.At high exercise intensities it oxidises lactate as fuel (produced anaerobically by the skeletal muscle).
Normal BP 120/80mmHg, high >140/90, low 90/60 or less
Systolic BP increases rapidly with exercise at first then in proportion to intensity, reaches about 200mmHg. Increase in mean arterial pressure combined with reduced peripheral resistance as blood vessels dilate (resistance to flow is inversely proportional to radius to the power of 4 (eg if the radius doubles the resistance to flow falls by a factor of 16, so a small dilation massively reduces resistance to blood flow)
Diastolic BP remains stable or falls slightly due to blood vessel dilation.
Blood (= rbcs suspended in plasma)
Rbcs carry O2 from the lungs to the working muscles,bound to Hb
At the muscle cell, myoglobin Mb has a greater affinity (250x) for O2 than Hb and so the O2 moves from the rbc to the muscle cell. CO2 moves out from the muscle cell to the blood and is carried away dissolved in plasma (as H+ and HCO3-) to the lungs where it is breathed out (as CO2 and H2O).
Number of rbcs (haematocrit) increases with training. Normal range is 39-50% (men) 35-44% (women).
Concentration of Hb in rbcs increases with training.
Dietary Fe important – main sources of haem iron are red meat, fish seafood, poultry and other animal products, also in leafy green veg. Non haem iron is found in plants and is more difficult to absorb, hindered by phytates in some vegetables and pulses and by dairy products.
Iron deficient anaemia is common in female endurance athletes, reducing their aerobic capacity.
Women have 5-10% less Hb per L than men.
Rbc production is stimulated by lack of oxygen ( hypoxia) in the working muscles, causing release of Hypoxic Factor which stimulates release of EPO (erythropoietin) from kidneys which stimulates bone marrow to produce more rbcs.
Note – training must be of sufficient intensity ( i.e.around LT) for adequate time and repeated bouts of training for Hypoxic Factor to be released.
Blood doping – autologous blood transfusions or injecting with EPO, dangerous increases in blood viscosity result.
Plasma volume increases with training.
Untrained haematocrit 45%, plasma 55%
Trained haematocrit 38%, plasma 62%
So a trained athlete is borderline anaemic on standard blood tests with a haematocrit of 38% (normal range 38-50% for men), due to increased plasma volume. However, total rbc mass increases as well. The increased blood volume increases both SV and total rbc mass, thus increasing CO and aerobic capacity.
Only one cell thick wall (i.e. very thin), rolled up, with a diameter of 1/100th mm=one rbc wide. At rest only 1/40th of the capillaries are open.
Muscle and heart capillaries dilate massively on exercise to increase the blood flow and O2 supply (reduced “afterload”).
Controlled by autonomic nervous system (sympathetic/parasympathetic). HR and blood flow to muscles increase in anticipation of exercise as a result of training the neuromuscular pathways (148bpm before 100m sprint, 122bpm before 800m, 118bpm before 1m, 108bpm before 2m races)
“Shunting” of blood away from non-vital organs and the skin (5% blood to skin at rest, 20% during exercise in warm conditions but shunting away from the skin still occurs on maximal exercise).
In prolonged periods (>15 minutes) of submaximal exercise, SV falls and HR rises as intensity remains constant. Due to sweating and an increase in core body temperature causing a fluid shift from the plasma to the tissues, so plasma volume falls and SV falls, reducing VO2max. A trained person has reduced cardiac drift.
- OXYGEN UTILISATION – MUSCLES
Finally the oxygen laden blood arrives at the muscles. O2 uptake and utilisation at the muscle depends upon the following factors:
Density of the capillary bed – a network of tiny blood vessels throughout the muscle.
Muscle myoglobin concentration (Hb4O8 releases O2 to 4MbO2)
Oxygen exchange rate
Size of mitochondria
Number of mitochondria
Aerobic ATP production in mitochondria
ALL of these increase with training, thus increasing aerobic capacity.
Important factors which influence endurance performance are:
- Aerobic capacity – the ability to consume oxygen
- VO2max – maximum capacity to consume oxygen
- Lactate Threshold – maximum level for steady state exercise
The main variables affecting aerobic capacity, VO2max and LT are:
- CO (cardiac output) , which depends on heart rate and stroke volume
- Haemoglobin concentration
- Erythrocyte (red blood cell) production
- Capillary density in the muscles
- Oxidative enzymes in the mitochondria of muscle cells
- Running economy
Take home message:
Endurance training at different levels of intensity enhances aerobic capacity.
Training must include intensities at or around LT, for an adequate length of time per workout and workouts at this level must be repeated.
VO2max may not increase following training whilst endurance performance does improve.
As endurance is performed at LT (race pace) not at VO2max (a higher level of intensity than LT), training induced improvements in performance correlate more with training an increase in LT than with changes in VO2max.
LT increases with training due to improved aerobic capacity at lower intensity of exercise
(see figure 4 – Effect of training on LT).
Think of it a bit like HR. Training doesn’t change your max HR, but resting HR is lower if you are fit because you are physiologically more efficient. Similarly training doesn’t necessarily increase your VO2max, but your ability to consume oxygen (aerobic capacity) at submaximal exercise intensities (up to LT) does. Your LT increases, as you can utilize oxygen better and delay going anaerobic.
So you can run faster at your race pace (LT).
The diagrams to support this text can be found below:
- The Science of Running Steve Magness 2014
- Exercise Physiology – Nutrition, Energy and Human Performance MacArdle, Katch and Katch 8th edition 2015
- Daniels Running Formula Jack Daniels PhD 3rd edition 2014
- The Cyclist’s Training Bible Joe Friel 4th edition 2009
- Triathlon Science Joe Friel Jim Vance 2013