Sprint training is becoming an increasingly popular form of cardio. Gone are the days when you would spend countless hours staring into space while needlessly pounding along on the treadmill or bike like your pet hamster. More and more people are starting to recognize the benefits of including sprint/interval training into their workouts.
One of the greatest things about sprint training is how it allows you to burn fat at a much higher rate after you are finished training. This process is known as EPOC (Excess Post-Exercise Oxygen Consumption), and accounts for a much greater increase in metabolism after training compared to that encountered after a steady state session.
This is your body's response in trying to recover from such an intense training session. There are many other adaptations, more physiological ones, that go along with sprint training.
In this article I will look at some of the adaptations that take place when you perform short interval sessions. Numerous studies have been done regarding sprint training that lasts from 10-60 seconds, however for this article, I will discuss what happens when we train in the < 10 sec range.
Metabolic Adaptations
The first adaptations to consider are metabolic adaptations. These are basically the muscle increasing its capacity to produce more energy. The muscle tissue does this by increasing the rate at which enzymes are working to produce energy by increasing the storage capacity of the muscle tissue for energy substrates and by increasing the muscle tissues' capability to resist fatigue (Leveritt & Ross, 2001).
Aerobic Contributions To Energy Production
- Short duration sprint exercises (< 10 sec) rely almost exclusively on anaerobic processes to produce energy. In longer duration sprints, such as those lasting 20-30 seconds, the aerobic system contributes more to the generation of energy (it should be noted that no type of training is ever purely anaerobic in nature).
In sprints less than 10 seconds, the aerobic system contributes approximately 13%, while in longer sprints; it contributes to 27% of energy produced (Leveritt & Ross, 2001). Therefore, the metabolic adaptations for the two types of sprints will differ.
Phosphate Metabolism
- One adaptation is phosphate metabolism. Phosphate creatine stores are major substrates the body uses to generate energy and a sprinter can deplete his PCr levels by more than 60% during a 60m sprint. Therefore, Myokinase, the enzyme responsible for resynthesizing energy from PCr, has been shown to increase up to 20% with sprint training.
Glycolysis
- The second adaptation is that concerned with glycolysis. This is the primary form of metabolism used during a 10-second all-out sprint and contributes between 55 and 75% toward energy production (Leveritt & Ross, 2001). Phosphofructokinase (PFK), an enzyme that catalyses the phosphorylation of the glycolytic intermediate fructose 6-phosphate) has also been shown to increase, along with the enzymes of lactate dehydrogenase and glycogen phosphorylase (other enzymes responsible for the glycolysis system).
This higher rate of enzyme production is one of the factors related to increased performance among sprint athletes compared with other athletes. Other studies have shown an increase among these enzymes with no direct increase in performance, so this remains a controversial factor related to sprint training adaptations (Leveritt & Ross, 2001).
If an athlete trains using short sprints but performs many intervals in a short time period (therefore minimizes rest periods), the aerobic system will come in to play much more, so there will be an increase in aerobic enzymes as well (succinate dehydrogenase).
Resting Metabolites
- The second aspect of metabolism adaptations to consider is that of resting metabolites. It would commonly be thought that the more stored ATP and PCr stores the athlete has in the muscles, the longer or harder they will be able work. While this is partially true, this is not an adaptation of sprint training.
What happens with sprint training is the rate of turnover for these metabolites increases, so the muscle actually decreases its stores of them. It's interesting to note that with this decreased reduction of ATP stores, there is no decrease in power output. The reason for this is that it's not so much the stores of ATP that are important in sprinting but the rate of turnover of ATP. So, since this is in fact increasing, the athlete will be better off.
Intramuscular Buffering Capacity
- The final factor to consider is intramuscular buffering capacity. During glycolysis, the process initiated shortly after intense exercise has begun, a product called lactic acid begins to accumulate. This byproduct results in a feeling of fatigue throughout the muscle tissue and is what often forces athletes to stop.
By using the chemical buffers of bicarbonate, phosphate and proteins from red blood cells, the body is able to counteract the change in pH created. When an athlete undergoes sprint training, their body becomes more accustomed to buffering this lactic acid and gets more efficient at maintaining a proper pH balance.
Summary
So, one of the big factors that occurs during sprint training is adaptations to one's metabolic system. Enzymes are a powerful factor in determining how much energy a muscle is able to produce and with a proper training protocol, we can maximize these enzymes so they favor the production of ATP to be used during short duration, intense exercise.
Other enzymes used during the process of glycolysis are also increased which raises the athletes' ability to perform. While resting enzymes in the muscle do not appear to be affected by sprint training, and in fact sometimes decrease, this does not appear to have too great of an effect on performance, as it is the rate of ATP turnover that is a more important factor to consider.
Finally, along with sprint training is the muscles increased ability to buffer fatigue byproducts. This will help athletes to resist fatigue better and keep training.
In the next part of this article, we'll look at the morphological adaptations that occur in response to short interval, high intensity training sessions.
References:
- Ausoni, S., Gorzna, L., Schiaffino, S., et al. Expression of myosin heavy chain isoforms in stimulated fast and slow rat muscles. J Neurosci 1990; 10(1):153-60.
- Bianchi, S., Rossi, B., Siciliano, G. et al. Quantitative evaluations of systemic and neuromuscular modifications induced by specific training in sedentary subjects. Med Sport: 50 (1).
- M. Leveritt & A. Ross. (2001). Long-term Metabolic and Skeletal Muscle Adaptations To Short-Sprint Training. Sports Medicine, 31(15).