This article is Part 3 of a 3 part series that outlines the three basic energy systems used in sport, their interactions with one another, and how to train each one.
Below the Introduction (technical explanation), we offer 7 sessions (in 3 stages) for training the Oxidative System.
The oxidative system consists of four processes to produce ATP:
- Slow glycolysis (aerobic glycolysis)
- Krebs cycle (citric acid cycle or tricarboxylic acid cycle)
- Electron transport chain
- Beta oxidation
Slow glycolysis is exactly the same series of reactions as fast glycolysis that metabolise glucose to form two ATPs. The difference, however, is that the end product pyruvic acid is converted into a substance called acetyl coenzyme A rather than lactic acid (5). Following glycolysis, further ATP can be produced by funnelling acetyl coenzyme A through the Krebs Cycle.
The Krebs cycle is a complex series of chemical reactions that continues the oxidization of glucose that was started during glycolysis. Acetyl coenzyme A enters the Krebs cycle and is broken down in to carbon dioxide and hydrogen allowing two more ATPs to be formed. However, the hydrogen produced in the Krebs cycle plus the hydrogen produced during glycolysis, left unchecked would cause cells to become too acidic (2). So hydrogen combines with two enzymes called NAD and FAD and is transported to the Electron Transport Chain.
Electron Transport Chain
Hydrogen is carried to the electron transport chain, another series of chemical reactions, and here it combines with oxygen to form water thus preventing acidification. This chain, which requires the presence of oxygen, also results in 34 ATPs being formed (2).
Unlike glycolysis, the Krebs cycle and electron transport chain can metabolise fat as well as carbohydrate to produce ATP. Lipolysis is the term used to describe the breakdown of fat (triglycerides) into the more basic units of glycerol and free fatty acids (2).
Before these free fatty acids can enter the Krebs cycle they must undergo a process of beta oxidation, a series of reactions to further reduce free fatty acids to acetyl coenzyme A and hydrogen. Acetyl coenzyme A can now enter the Krebs cycle and from this point on, fat metabolism follows the same path as carbohydrate metabolism (5).
The oxidative system can produce ATP through either fat (fatty acids) or carbohydrate (glucose). The key difference is that complete combustion of a fatty acid molecule produces significantly more acetyl coenzyme A and hydrogen (and hence ATP) compared to a glucose molecule. However, because fatty acids consist of more carbon atoms than glucose, they require more oxygen for their combustion (2).
So if your body is to use fat for fuel it must have sufficient oxygen supply to meet the demands of exercise. If exercise is intense and the cardiovascular system is unable to supply cells with oxygen quickly enough, carbohydrate must be used to produce ATP. Put another way, if you run out of carbohydrate stores (as in long duration events), exercise intensity must reduce as the body switches to fat as its primary source of fuel.
Protein is thought to make only a small contribution (usually no more than 5%) to energy production and is often overlooked. However, amino acids, the building blocks of protein, can be either converted into glucose or into other intermediates used by the Krebs cycle such as acetyl coenzyme A. Protein may make a more significant contribution during very prolonged activity, perhaps as much as 18% of total energy requirements (1).
Often it is thought that the oxidative system is predominantly active in supplying energy for rest and low intensity activity. In fact the oxidative system has been shown through numerous studies to play a significant role in determining performance in high intensity exercise (6) through both energy supply and restoration of the other energy systems. This highlights the importance the oxidative energy system plays in a high intensity intermittent sport like rugby.
With training emphasising the oxidative system there will be an improvement in an individuals’ VO2 max. This is the maximal amount of oxygen the body can take in and utilise measured in absolute terms (L/min) or relative terms (ml/kg/min). The Fick equation states that VO2 = CO x a-vO2 difference. This equation highlights the point that it is influenced by both central and peripheral physiological factors. Cardiac output = Heart rate x Stroke volume- Where stroke volume is the amount of blood pumped from the left ventricle each time the heart beats. a-vO2 difference is the arterial/venous oxygen difference which is the difference in the oxygen concentration of arterial blood and venous blood.
With training there are improvements in markers of oxygen carrying and delivery which lead to improvement in VO2 max. These include:
- Increased concentration of intra muscular mitochondria
- Increased capillary concentration
- Increase red blood cell concentration
- Increased blood volume
As with the other energy systems it is important that sessions are structured so individuals are exposed to a number of different intensities and recovery periods which will mimic those found game situations.
Training the Oxidative System – Session Examples
Long sub-maximal (65-80% VO2) – running, cycling, rowing for 60+ minutes
Fartlek – unstructured sustained efforts with increases in intensity and easier recovery periods- for example running/cycling where you sprint the hills and take it easier for 90s after each effort
Hill efforts – Find hills of differing lengths and gradients. Vary running speed and recovery periods
Gym triathlon – Choose 3 cardio machines in the gym- e.g.: rower, elliptical, arm-grind
Either choose a time spent on each (15-minutes) OR a distance to achieve on each (5km)
Record total distance at completion OR total time taken to complete- aim to beat next time.
Intervals of sub-maximal efforts (aiming for >80%) – where the work:rest is 1:1 or greater (2:1, 3:1 etc.)- so 45s work:15s recovery, 60s work:20s recovery, 20s work:10s recovery- with the shorter intervals you can sustain a higher % of max effort so will have increased benefits on other energy systems (glycolytic as well as ATP-PCr)
1. Baechle TR and Earle RW. Essentials of Strength Training and Conditioning: 2nd Edition. Champaign, IL: Human Kinetics. 2000.
2. McArdle WD, Katch FI and Katch VL. Essentials of Exercise Physiology: 2nd Edition Philadelphia, PA: Lippincott Williams & Wilkins. 2000.
3. Noakes TD. Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance. Scandinavian Journal of Medicine and Science in Sports. 10, 123-145. 2000.
4. Stager JM and Tanner DA. Swimming: 2nd Edition; An International Olympic Committee Publication. Oxford UK: Blackwell Scinece Ltd. 2005.
5. Wilmore JH and Costill DL. Physiology of Sport and Exercise: 3rd Edition. Champaign, IL: Human Kinetics. 2005.
6. Gastin PB. Energy system interaction and relative contribution during maximal exercise. Sports Med Journal. (31) 10, 725-741. 2001.
7. Ross A and Leveritt M. Long-term metabolic and skeletal muscle adaptations to short-sprint training: Implications for sprint training and tapering. Sports Med Journal. (31) 15, 1063-1082. 2001.
This is Part 3 of a 3 Part Series. Click here for Part 1 and 2.
Click here to see David Boyle’s Rugby Union Training Programs.
Click here to see John Mitchell’s Basketball Training Programs.
Cameron is the Director of Pro Training Programs