A runner who can shift most of the blood from inactive tissues to the active muscles will have a large a-v O2 difference because the active muscles will extract more oxygen from the blood than will the inactive tissues. Since the amount of oxygen in the arterial circulation is the same at rest as it is during a race (20 ml of oxygen per 100 ml of blood), any change in the a-v O2 difference is a result of a decrease in oxygen in the venous circulation—this means the muscles have extracted more oxygen.
VO2 is equal to the product of the central and peripheral factors, written as the Fick equation:
VO2 = SV x HR x (a-v O2 difference)
Since SV x HR equals cardiac output (CO), the equation can be written as:
VO2 = CO x (a-v O2 difference)
VO2 max occurs when SV, HR (and therefore CO), and the a-v O2 difference are all at their maximum.
The Limits of VO2 Max
One of the most prominent debates in exercise physiology concerns the limiting factors of VO2 max, and whether those factors are of a central (oxygen delivery) or peripheral (oxygen use) nature. Research supporting central limitations to VO2 max include findings that:
- VO2 max of the quadriceps is greater when they are isolated during exercise compared to whole-body exercise
- VO2 max decreases with beta blockers due to a decrease in cardiac output
- blood doping (removing some of your own blood, freezing it, and injecting it back in to your body at a later date) increases VO2 max by increasing hemoglobin concentration
- the capacity for VO2 max to increase is much less than that for mitochondrial and capillary volumes.
Research supporting peripheral limitations include findings that VO2 max decreases as the partial pressure of oxygen in the muscle (the driving force for diffusion from the muscle capillaries to the mitochondria) decreases, and VO2 max increases as a result of an increase in oxygen diffusing capacity when oxygen delivery is held constant.
While unfit people seem to be equally limited by central and peripheral factors (they lack both a high blood flow and abundant metabolic machinery), highly trained distance runners seem to be more centrally limited. After all, there is a structural limit to how big the left ventricle of the heart—and thus stroke volume and cardiac output—can get. Training appears to result in a shift of the limitation on the sliding scale—the more fit a runner becomes, the more he or she moves away from a metabolic limitation to VO2 max and the closer he or she moves to an oxygen supply limitation.
Progressive increases in mileage from month to month and year to year will improve VO2 max by increasing the muscles' metabolic capacity. When runners have achieved a high level of mileage (70 to 75 miles per week), the intensity of training becomes more important to increase the cardiac factors responsible for maximizing oxygen supply to the muscles.