How often should you interval train for maximum fitness gains? Andrew Hamilton takes a look at some brand new research and comes up with surprising conclusions MORE
Strength and endurance – can you master both at once?
For hundreds of thousands of years, humans have evolved to be either as strong or as tireless as possible, but not both. As Keith Baar explains, however, recent science has provided clues as to how to legally move past the obstacles that evolution put in the way of developing both strength and endurance
The basic reason is that, within our bodies, the two processes of building strength and endurance are diametrically opposed: in other words, one tends to prevent the other. Therefore, to master both strength and endurance, we have to overcome limitations that have been laid down in our genes over hundreds of thousands of years.
It is not just decathletes that need to master both endurance and strength. All motor-endurance sports – for example, cycling, swimming and rowing – require both, as do many games, including rugby, basketball and ice hockey. Therefore, knowing how to optimise both strength and endurance is one of the keys to success for the modern sportsman.
While coaches have long been the leaders in developing strategies to maximise performance, a surprising number of advances in molecular exercise physiology mean that, for the first time, basic researchers are beginning to understand how best to train simultaneously for strength and endurance.
Enzymes and exercise training
Before we can discuss how to train for strength and endurance together, it is necessary to understand a little about the basic process of how our muscles build strength and endurance. To do this, we will have to talk about two enzymes that play an important role in the effect of training on muscle. The first is the ‘AMP-activated protein kinase’ (AMPK) and the second is the mammalian ‘target of rapamycin complex 1’ (mTORC1).
AMPK and endurance – As the name suggests, adenosine monophosphate (AMP) activates AMPK. AMP is a molecule formed in muscles when large amounts of ATP are needed to power exercise. Basically, ATP is broken down into adenosine disphosphate (ADP), inorganic phosphate, and energy. It is this energy that we use to power our bodies. In order to rapidly make new ATP, two ADP molecules can be combined by an enzyme called myokinase, to produce a new ATP plus a molecule of AMP. It is this AMP that turns on AMPK during exercise.
During exercise, this enzyme increases the rate of sugar uptake and fat oxidation, allowing us to make more energy aerobically. But AMPK also has other important roles in muscle. Along with the short-term increase in metabolism, AMPK is involved in the control of a number of genes that give muscles more endurance.
Using drugs and different models of muscle, molecular exercise physiologists have shown that repeatedly activating AMPK in muscle results in many of the adaptations that occur following endurance exercise. This includes the improved transport of fat and sugars into muscle, and the increase in mitochondrial mass, resulting in greater endurance. From these data, it is now widely believed that, within muscle, one of the primary goals of endurance training is to activate AMPK.
In an elegant study by Shin Terada, we learned that while long-duration exercise increases AMPK activity, repeated short high-intensity sprints produce a greater effect on AMPK (see figure 1). This tells us that, as far as muscle is concerned, the best type of exercise for improving endurance is repeated high-intensity sprint exercise.
However, this does not mean that purely repeated sprint training is the best way to improve whole-body endurance performance, since a number of other tissues – including the heart, the circulatory system, and the connective tissue – must also adapt in order to translate endurance training into improved performance. But as far as muscle is concerned, the higher the intensity, the higher the AMPK activity and hence the better the subsequent endurance adaptation.
mTORC1 and strength – Unlike AMPK, mTORC1 is not activated by endurance exercise. Instead, this enzyme is turned on following resistance exercise. In fact, the activity of this enzyme is the best marker for muscle growth and strength improvement discovered to date. In every animal tested, from mice to humans, mTORC1 activity following a single bout of exercise is the best predictor of muscle hypertrophy and improved strength (figure 2). Not only does the activity of mTORC1 correlate with improved strength – when this enzyme is blocked by the drug rapamycin, muscle doesn’t grow in response to a normal growth stimulus.
So, we know that mTORC1 is required for muscle growth and increased strength, but you are probably now wondering what it does. In order for our muscles to grow bigger and stronger, we need to increase how much protein we make within our muscles. This is where mTORC1 comes in. This enzyme controls muscle size and strength by regulating protein synthesis. Following resistance exercise, mTORC1 activity is increased and as a result there is an increase in protein synthesis that makes muscles bigger and stronger. From these data, strength coaches should have as their goal maximal activation of mTORC1 when looking to improve an athlete’s strength.
Many strength coaches and athletes are already doing this unwittingly, by taking amino acids. The reason that this helps increase strength is that, like resistance exercise, amino acids – especially the branched-chain amino acids, such as leucine – activate mTORC1. Consequently, coordinating amino-acid supplementation and resistance exercise results in greater mTORC1 activation and therefore greater improvements in strength.
If amino acids can increase muscle size and strength, why not take supplements to maintain high amino acids at all time? The reason that this doesn’t work is that mTORC1 has a self-braking mechanism. What this means is that if amino acids are sustained at high levels in the blood for too long, mTORC1 and protein synthesis are shut off. Therefore, it is the timing of the amino acids and not the total amount that is the key.
Another way to activate mTORC1 is through growth factors like insulin and insulin-like growth factor (IGF-1). Insulin and IGF-1 can both directly activate mTORC1 and indirectly activate mTORC1 by increasing the uptake of amino acids. This is why the IOC has banned insulin and IGF-1 as performance-enhancing drugs. However, diet can be used to legally increase insulin, simply by adding some carbohydrate to any amino-acid supplement that an athlete takes. Coordinating this supplement with resistance exercise can increase mTORC1 activation and, as a result, strength.
The concurrent training effect
Many athletes and coaches will tell you that if you train for endurance and strength together improvements in performance are slower than if you train for one alone. This phenomenon is called the ‘concurrent training effect’ (see figure 3). It is here that molecular exercise physiologists are beginning to contribute to training efficiency.
As we have already discussed, AMPK leads to improved endurance and mTORC1 increases strength. So you might be asking: if two different enzymes have evolved to enhance two different aspects of fitness, why is it difficult to increase both simultaneously? The answer lies in the fact that AMPK can block the activation of mTORC1. What this means is that, in our genes, there is a block to improving both our endurance and our muscle mass and strength at the same time. This will come as no surprise to many coaches and athletes who already know that endurance training tends to prevent strength gains.This genetic interaction almost certainly developed hundreds of thousands of years ago as we evolved to move over great distances to hunt for food. These long trips not only found the food that kept us alive, but also decreased the amount of muscle we had and, as a result, the amount of fuel we needed to consume. Today, when having enough food is not a concern, we are still fighting against the way we evolved eons ago.
Dynamics of enzyme activation
In order to overcome this genetic limitation and train for both endurance and strength, we need to understand a little more about how the two enzymes in question work. As described above, AMPK is turned on during exercise, but it is rapidly turned off when we refuel. This is because it senses the amount of glycogen in the muscle, as well as the metabolic state of the muscle. When these return to normal, AMPK turns off.
On the other hand, mTORC1 isn’t turned on during exercise, but rather during the recovery phase from resistance exercise. The maximal activation of this enzyme occurs between 30 minutes and six hours, but can be maintained a full 24 hours, after a single bout of resistance exercise. The correlation between mTORC1 and strength gains occurs both at 30 minutes and six hours after training, suggesting that it is important to have mTORC1 active for a long time, in order for it to influence muscle strength.
Training for endurance and strength
From the information above, it becomes more obvious how we can maximise both endurance and strength. The key aspects of any programme aiming to do this are the timing of the exercise and the use of diet. The basic rules are:
1. Perform endurance training first and strength training last;
2. Add intensity to your endurance;
3. Take food with your weights;
4. Keep your strength sessions short;
5. Use negative repetitions.
The whys behind the rules
1. Endurance first – strength last: AMPK is rapidly turned off after exercise, but mTORC1 needs to be high for as long as possible for maximum effect – and AMPK turns off mTORC1. Therefore, if endurance exercise is performed first, early in the day, and glycogen is reloaded, then AMPK will be low later in the day (when the strength exercises are performed) and will not interfere with mTORC1. Training for strength at the end of the day (5–6pm) allows mTORC1 to be high for the rest of the evening and while the athlete is sleeping. When the athlete wakes, they will have at least 12 hours with high mTORC1, promoting muscle growth and improved strength before their next session of endurance exercise turns on AMPK and turns off the strength signal.
2. Add intensity to your endurance: AMPK is turned on by all exercise – but, since it responds to metabolic stress, the higher the intensity, the higher the metabolic stress and, therefore, the higher the AMPK activity. The best way to add high intensity is to follow a long endurance session with some high-intensity intervals. The long, slow exercise depletes muscle glycogen and this makes the high-intensity work even more of a metabolic stress than if the high intensity is performed while the athlete is fresh. This is because, as already mentioned, AMPK senses muscle glycogen levels. Therefore, depleting muscle glycogen before high-intensity exercise is optimal for activating AMPK and improving muscle endurance.
3. Take food with your weights: Diet is the most overlooked aspect of training and, when training for both endurance and strength, diet becomes even more important. Eating a high-carbohydrate meal or snack an hour after your endurance training will help to turn off AMPK and replenish muscle glycogen. Taking a drink or snack that delivers 6-8g of protein before strength training helps deliver amino acids to the working muscles. Since blood flow is increased to these muscles, they will see more amino acids than the non-working muscles and this, together with the activation of mTORC1 by the strength training, will result in maximal strength gains. Also, adding a protein- and carbohydrate-rich meal soon after completing training (around one hour) will increase insulin and amino acids in the muscle, thus supporting the training session.
4. Keep your strength sessions short: Make sure that your strength exercises don’t last more than 60 seconds. Six to eight reps, performed properly, minimises the metabolic stress of the exercise. Energy for less than 60 seconds can be supplied from muscle stores. Stored ATP, phosphocreatine and glucose can provide all of the energy required to work hard for less than a minute. This keeps the metabolic stress of the exercise low, minimising AMPK activity and therefore maximising mTORC1. Taking twice the active time (ie, resting for around two minutes between sets) to recover those stores will also help keep the metabolic stress low.
5. Use negatives: Negatives (slow, lengthening contractions) put the maximal load on the muscle for the minimal metabolic cost. Muscle is around 1.8 times stronger when lengthening under load than when contracting. More importantly, muscle consumes much less ATP during lengthening contractions than it does during shortening contractions. This means that the body needs less ATP to lower a weight than to lift it. Besides that, we can handle a heavier weight with lengthening contractions. The result is more weight and less ATP used, and this translates into more mTORC1 activity and stronger muscles.
Most modern sports and games put a huge emphasis on developing both strength and endurance. For almost 30 years, we have known that training for both is not as efficient as training for either one individually. As molecular exercise physiologists, we are beginning to understand why this is, and that we can use diet and intensity of exercise to create training programmes that will simultaneously improve both strength and endurance. However, even when applying the rules proposed here, the genetic limitations mean that training for both strength and endurance will never be as effective as training for either individually. As a result, those of us who study concurrent training will continue to marvel at the great decathletes and always consider them the ‘World’s Greatest Athlete’!
1. Acta Physiol Scand. 2005 184: 59-65
2. Eur J Appl Physiol. 2008 102: 145-52
3. Eur J Appl Physiol Occup Physiol. 1980 45: 255-63
4. Am J Physiol. 1999 276: C120-7