Wingate Sprint - Physiology

Wingate sprints cause several effects on skeletal muscles, the cardiovascular and pulmonary system.

Skeletal muscle

The fuel for anaerobic glycolysis during a Wingate sprint is muscle glycogen; as it takes too long to transport blood sugar to, and into, the working muscle. Skeletal muscle glycogenolysis (glycogen breakdown) is maximally activated soon after the start of the sprint, and remains maximally activated until approximately the halfway-mark, after which glycogenolysis starts to be inhibited. This is consistent with the ‘fight-or-flight response’ (i.e. from an evolutionary perspective the main reason for performing exercise at very high intensities).

In effect, the muscle is flooded with glucose to fuel the exercise, but this process is stopped once a large surplus of glucose is available (in order to prevent that muscle glycogen stores become fully depleted). Muscle glycogen stores are reduced by approximately 20-25% within the first 15 seconds of the first Wingate sprint.

Because of the speed at which glycogen is broken down, the effects of the rapid glycogen breakdown are quite different from those with lower intensity endurance exercise. The many glucose particles that are released into the muscle cell (together with the additional particles produced through the breakdown of phosphocreatine into creatine and inorganic phosphate) cause a hyperosmotic state. The breakdown of glucose to lactate will compound this effect (remember that 1 glucose molecule is broken down into 2 lactate molecules). The hyperosmotic state will result in rapid fluid-influx into the muscle cell, leading to muscle swelling as well as a decrease in plasma volume.

Cardiovascular system

During aerobic exercise the heart rate increases in order to deliver oxygen and fuel (glucose and free fatty acids) to the muscles. During supramaximal sprint exercise there is less of a need for this: the fuels that are used (glycogen and phosphocreatine) are already in the muscle, and aerobic metabolism takes a while to start up. However, supramaximal exercise is associated with the fight-or-flight response, and the increase in blood adrenaline levels and sympathetic nervous system activation will increase heart rate and blood flow.

This is mostly useful for transport of waste products away from the muscle. Large quantities of lactate and hydrogen ions are produced in the muscle during a Wingate sprint, and these will be released into the bloodstream. Lactate is subsequently used by the liver, active muscles and the heart during the active recovery phase following the sprint, whereas hydrogen ions (which cause a decrease in pH) are buffered by blood bicarbonate (HCO3^-). The resulting bicarbonic acid (H₂CO₃) will split into H₂O and CO₂, the latter of which will need to be exhaled. The increase in blood lactate levels can be measured in the recovery phase following a Wingate sprint.

Pulmonary system

One would expect that individuals performing a Wingate sprint need to breathe a lot harder to get enough oxygen during sprint exercise, but the main reason for the increased breathing rate with a Wingate sprint is the need to get rid of the large amount of CO₂ that is produced by buffering the decrease in pH by bicarbonate. It would be possible to perform the first 10-15 seconds of a Wingate sprint while holding ones breath, but the rapid increase in CO₂ levels will subsequently force one to hyperventilate. This becomes apparent mostly after the sprint and will take several minutes for breathing to get back to normal.

During and directly after exercise the pH will drop due to rapid anaerobic glycolysis, and buffering by bicarbonate will lead to a much larger increase in expired CO₂ than the increase in O₂ consumption required for aerobic metabolism. Therefore, [respiratory exchange ratio](wiki:/wingatcan shoot up to values that are otherwise never observed, e.g. well over 1.40.