Maximum Oxygen Uptake (VO2max)
Maximum Oxygen Uptake was first defined by Hill and Lupton in 1923. They postulated that
- there is an upper limit to oxygen uptake
- there are interindividual differences in VO2max
- a high VO2max is a prerequisite for success in middle- and long-distance running
- VO2max is limited by ability of the cardiorespiratory system to transport oxygen to the muscles
These principles have proved surprisingly accurate as confirmed and by further research, which has also been expanded upon these initial ideas. The following working definition has widespread acceptance.
Maximum Oxygen Uptake is the highest rate at which oxygen can be taken up and utilised by the body during severe stress
Why is VO2max important?
In short, VO2max defines the upper limit for performance in endurance events. That said, it is important to understand that VO2max is not the best predictor of athletic ability. Yes a high VO2max is important, but it is not the only determinant of performance. Other important factors include:
- The ability to work at certain percentage of VO2max (lactate threshold)
- Running economy (oxygen cost at a certain running veloctiy)
These and other factors all make up the often unpredictable results in racing.
The limiting factors for Maximum Oxygen Uptake include:
- pulmonary system
- maximal cardiac output
- oxygen carrying capacity of the blood
- skeletal muscle characteristcs
The pulmonary system in the average, healthy person works very well at sea level in saturating arterial blood with oxygen. During maximal work, the arterial oxygen saturation remains at >95% which is excellent. Elite athletes on the other hand are more likely to suffer from arterial oxygen desaturation during maximal exercise when compared to normal individuals. The elite athletes have a significantly higher maximal cardiac output than the untrained (40 vs 25 litre/min). This results in a reduced transit time of the red blood cells in the pulmonary capillary, leading to not enough time to saturate the blood with oxygen before it exits the pulmonary capillary. Saturation levels in elite athletes have been measured at around 90%. It has been shown (Powers et al 1989), that supplemental oxygen can improve oxygen saturation in elite athletes, but have no effect on the untrained. This suggests there is a pulmonary limitation to VO2max.
Maximal Cardiac Output
Cardiac Output = Heart Rate x Stroke Volume
Put another way, cardiac output is the amount of blood the heart pumps in one minute. This is a function of how many times the heart beats (heart rate) multiplied by the amount of blood pumped during each beat (stroke volume). In trained athletes there is little difference in maximal heart rate when compared to the untrained. The reason for the large difference in maximal cardiac output are mainly due to a variation in maximal stroke volume.
It is estimated that 70-85% of the limitation in VO2max is linked to maximum cardiac output. Cardiac output essentially determines the rate of blood able to be delivered to the working muscles. For example Ekblom et al (1968) showed with 16 weeks of training an increased VO2max from 3.15 to 3.68 litres/min. was related to an improvement in cardiac output from 22.4 to 24.2 litres/min. Essentially cardiac output is the main determinant of the amount of blood able to be delivered to the working muscles.
Oxygen Carrying Capacity
Oxygen is bound to haemoglobin in the blood on red blood cells. The amount of oxygen carried in the blood does affect VO2max. This is one of the main reasons athletes train at altitude. By training at altitude, or using altitude simulation, the athlete hopes to increase the body's haemoglobin concentration, and therefore the ability to carry more oxygen in the blood. This is also how blood doping works. Reinfusion of 900-1350ml of blood increases the oxygen carrying capacity of the blood and has been hown to increase VO2 by 4-9% (Gledhill 1985).
Skeletal Muscle Characteristics
It has been proposed that the number of mitochondria may have an effect on VO2max. However, it seems that if there is an effect it is only minimal. There is a lot of talk about the mitochondria being very important in endurance performance. After all, they are known as the power house of the cell. Yes, the amount of mitochondria do have a direct correlation to endurance performance, but seem to play only a very small role in determining VO2max. Only very small increases are seem in VO2max, despite a more than doubling in number of mitochondria. It appears that an increase in mitochondria have different effects including:
- oxidising fat at a higher rate and sparing muscle glycogen and blood glucose
- decreasing lactate production
Capillary density of skeletal muscles increases with training. The reason does not appear to accommodate an increased blood flow to the working muscles, but rather to lengthen the transit time of blood through the muscle. This increased transit time enhances the oxygen delivery by allowing optimal time for oxygen extraction (taking oxygen from the blood to be used by the muscle cells) even at high rates of muscle blood flow. It is generally considered that the ability of muscle to adapt to training is greater than what is observed in the pulmonary system.
In healthy, trained athletes the key limits on VO2max can be summarised as follows:
Maximum Oxygen Uptake is primarily limited by the ability of the
cardiorespiratory system (heart, lung and blood) to transport oxygen to the
muscles, not the by ability of muscle to consume oxygen.
Since it is one of the key determinants to endurance performance, it makes sense to train in a way that will lead to improve VO2max. An important focus of my next phase of training will be to achieve this. How I aim to achieve this will be the topic of my next post.
Reference / Bibliography
Bassett D R & Howley E T. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Med & Sci in Sports & Exer. 32(1): 70-84, 2000
Ekblom B, Astrand P O, Saltin B, Stenber J & Wallstrom B. Effect of training on circulatory response to exercise. J Appl Physiol. 24:518-528, 1968.
Gledhill N. The influence of altered blood volume and oxygen transport capacity on aerobic performance. Exerc. Sport Sci Rev. 13:75-93, 1985
Hill, A V, and H Lupton. Muscular exercise, lactic acid, and the supply and utilisation of oxygen. Q J Med 16:135-171, 1923
Powers S K, Lawler J, Dempsey A, Dodd S & Landry G. Effects of incomplete pulmonary gas exchange of VO2max. J Appl Physiol 66:2491-2495, 1989