Why Usain Bolt Wouldn’t Run a Marathon

How sprint performance suffers from intensive endurance training, and what to do about it

Hickson, researcher as well as weightlifter, discovered in 1980 that by adding endurance exercise to resistance training, his weightlifting performance decreased significantly [4]. He called this phenomenon the interference-effect. How does the interference-effect work, and what can you do to minimize it?

Many sports require a combination of sprint and endurance performance. Cyclers of the Tour the France need to be able to cycle for more than five hours and be able to pull off a sprint to break away from the pack or to win the final sprint. This is one of many examples for athletes to see the necessity for performing sprint training next to endurance exercise. This concept is called concurrent training. As shown in Figure 1, power performance suffers when adding endurance exercise. What leads up to this effect?

Figure 1: The combination of resistance training with endurance exercise (Concurrent) will lead to weaker resistance performance (1 rep max (RM) Squat) in comparison with performing resistance training only (Strength). Adapted from Hickson[4].

The underlying mechanisms

To be able to perform a sprint, muscles need to quickly generate a lot of force. Thereby, these muscles need to have big volume and need to be able to contract quickly (power capacity). Sprint training stimulates the process in which a muscle fiber becomes bigger. This is called hypertrophy. On the other side, to be able to perform endurance exercise, muscles need to generate a sufficient amount of energy (oxidative capacity), which they make from carbohydrates and oxygen. This process takes place inside of mitochondria. A bigger density of mitochondria means that the muscle fiber has the ability to generate more energy. Next to that, oxygen doesn’t have to travel long inside the muscle fiber before reaching a mitochondrion (Figure 2 right). Endurance exercise stimulates the generation of mitochondria.

Figure 2: On the left, a muscle fiber of a sprint athlete is shown. Right is a muscle fiber of an endurance athlete.

After performing resistance training, your muscles will adapt and get bigger. Because of this process, the mitochondrial density in these muscles will decrease (Figure 2 left). Because of this, sprint athletes have big muscle fibers and endurance athletes have thin, energy-efficient muscle fibers. Put a sprint athlete next to an endurance athlete and you will quickly be able to spot the difference (Figure 3).

Figure 3: The legs of Tour du France cyclist Greipel (left) and track cyclist Förstemann (right). Sprint performance is much more important for track cycling than for cycling the Tour du France, which explain the biger muscles of Förstemann compared to Greipel.

Looking at molecular level

Right now, you know that athletes who perform concurrent training need to find a balance between big muscle fibers and a high mitochondrial density. This balance is trainable, but only till a certain height. But how is it possible that the power performance decreases after a couple of weeks of concurrent training? To answer this question, we have to dive deeper into the muscle fiber: the processes on molecular level.

Sprint training leads to adaptation of the muscles via the process of hypertrophy which is regulated by a protein called mTOR [1]. Two of the proteins activated to adapt to endurance exercise are called AMPK and PGC1α. One study has shown that AMPK inhibits activation of mTOR [3]. The intensity of endurance exercise seems to be of great significance. A more intensive endurance exercise (>70% of maximal heartrate) leads to a greater activation of AMPK [2], which will lead to a greater inhibition of hypertrophy via mTOR. The other way around, an endurance exercise of low intensity will lead to a lower increase in activation of AMPK.

In short

• Resistance training activates processes for bigger muscle fibers, which is necessary to quickly generate a lot of power. Endurance exercise activates processes for more mitochondria, which are necessary for generating energy for a prolonged time. There is a balance between these processes: an athlete cannot have the highest power capacity and the best oxidative capacity.
• Processes activated to adapt to endurance exercise decrease activity in the processes for adaptation to resistance training.
• The intensity of the endurance exercise plays a big role. A high intensive (>70% of maximal heartrate) endurance workout activates more AMPK in comparison to a low intensive endurance workout. Therefore, a high intensive endurance workout leads to a greater decrease in processes for adaptation to resistance training.

Practical advice

What could you do to minimize the interference-effect for optimal performance? Following the advice below will help you a great deal.

Training:

• When possible, perform your endurance exercise below 70% of your maximal heart rate.
• The interference-effect seems to be higher with running in comparison with cycling [5]. The various ground-impacts with running leads to a higher AMPK activity in comparison with cycling.

Recovery:

• After highly intensive endurance exercise, stick to a recovery time of 6 to 24 hours. This gives room for a decrease in AMPK-activity till baseline activity [1].

Nutrition:

• Ingesting protein after resistance training plays a significant part in the quality of hypertrophy [6]. Ingesting protein increases mTOR activity.
• Eat a good amount of carbs after every workout. A low level of carbs in the muscles causes an increase in AMPK activity [2].

Use this advice and get training!

Additional info: Muscle volume could in theory increase with an increase in muscle fiber length. This is an ideal adaptation of concurrent training, because the density of mitochondria will not change while muscle volume increases. Recent research suggests that the length of muscle fibers could be trainable with plyometric exercises.

References

1. Baar, K., Using molecular biology to maximize concurrent training. Sports Med, 2014. 44 Suppl 2: p. S117–25.

2. Chan, M.H., et al., Altering dietary nutrient intake that reduces glycogen content leads to phosphorylation of nuclear p38 MAP kinase in human skeletal muscle: association with IL-6 gene transcription during contraction. FASEB J, 2004. 18(14): p. 1785–7.

3. Fyfe, J., D.J. Bishop, and N. Stepto, Interference between Concurrent Resistance and Endurance Exercise: Molecular Bases and the Role of Individual Training Variables. Vol. 44. 2014.

4. Hickson, R.C., Interference of Strength Development by Simultaneously Training for Strength and Endurance. European Journal of Applied Physiology and Occupational Physiology, 1980. 45: p. 8.

5. Murach, K.A. and J.R. Bagley, Skeletal Muscle Hypertrophy with Concurrent Exercise Training: Contrary Evidence for an Interference Effect. Sports Med, 2016. 46(8): p. 1029–39.

6. Perez-Schindler, J., et al., Nutritional strategies to support concurrent training. Eur J Sport Sci, 2015. 15(1): p. 41–52.