The traditional methods of resistance training might not be the most effective way to increase strength
For thousands of years, athletes have used resistance training to increase their strength and performance. But as Keith Baar and Mike Gittleson explain, recent scientific advances suggest that the traditional methods of resistance training might not be the most effective way to do this.
While we have recognised the importance of the overload principle for a very long time, the exact frequency, intensity and duration of exercise to maximally increase muscle strength is still open to debate. A number of factors impact optimal training frequency, how hard to train and how long to train. These include the equipment and coaching available, individual rates of recovery after hard weight training and the individual’s ability to sustain intense exercise.
Response to training
It is easiest to view an individual’s response to resistance exercise in pictorial form (see figure 1). A training session can be separated into four phases (see figure 1A):
- The training bout itself where the muscle fatigues and strength decreases;
- The recovery phase, including both the immediate recovery from the exercise and the delayed recovery when
- amaged muscle fibres are removed and replaced;
- The adaptation or supercompensation phase;
- The return phase where any strength gains from the bout of exercise are lost.
Changing the intensity of the exercise increases or decreases the length of each of the phases (figure 1B) making it even harder for the strength coach to time the next training session.
The goal of the athlete and coach is to provide the next training session at the optimal frequency (see figure 2). If each of the sessions is optimally timed (at the peak of the adaptation phase), the athlete will increase strength at a maximal rate. If the sessions are too frequent (as is common for elite athletes – see figure 2B), the muscle doesn’t have sufficient time to adapt and strength gains are slow. Poor strength gains are also seen if the sessions are not frequent enough.
Molecular response to training
So what is it that actually causes an increase in strength? One possibility is that muscle repair results in a newer, stronger muscle. But while it is true that muscles repair themselves after a training session, there’s nothing in the repair process itself that causes the muscles to grow stronger. This can be seen by comparing muscle strength following a training session to muscle strength after a minor muscle injury. In both cases, muscle repair has occurred. However, only the training session increases muscle strength.
If not repair, then what? In every scientific model of muscle hypertrophy (growth), including mice, rats, rabbits, chickens and humans, the first response to a strength-training session is an increase in protein synthesis. If the increase in protein synthesis is more than the increase in muscle breakdown, the muscle will get bigger and stronger.
Over the past 10 years molecular exercise physiologists have identified the key regulator of muscle protein synthesis after strength-training. The technical name for this protein is the ‘mammalian target of rapamycin’, or mTOR for short. The activity of mTOR is directly related to the intensity of the training session and, over time, to the increase in muscle size and strength(1) (see figure 3).
Maximising muscle growth
If activating mTOR is the key to increasing strength, then understanding how to maximally activate this enzyme will tell us how to optimise our strength-training. To do this, we have to understand what turns mTOR on and off, and from a number of beautiful scientific studies, this is now clear.
The load on a muscle is directly related to the activation of mTOR. This means that the heavier the weight, or the greater the absolute amount of power produced by the muscle, the better the activation of mTOR(2). The only time where this relationship is not seen is when the weight-lifting is done while blood flow is restricted, but this is only really applicable to populations that can’t lift heavy weights for medical reasons. Therefore, the goal should be to lift as much weight as possible.
On the other side of the equation, mTOR activity is blocked by metabolic stress. This means that we want to use as little muscular ATP (an energy yielding molecule used in muscle contraction) as possible when we are doing our resistance training. The best way to decrease ATP consumption is to not work very long and to do exercises that use less ATP. Put together, this means that the best way to increase the activity of mTOR is to do exercise at high absolute power and low energy cost.
There are two ways to produce high power in muscle (see figure 4). The first is to perform shortening (concentric) muscle contractions with a medium amount of force, while the second is to perform lengthening (eccentric) contractions at a high force. Because of the architecture of our muscles we are able to produce about 1.8 times as much force when our muscles are lengthening than when they are shortening, resulting in much more power (even though it is negative).
Even though shortening and lengthening contractions can both result in high absolute power, they have very different energy costs. Shortening contractions are the most energy-consuming contractions, isometric contractions are the least energy-consuming (but result in the lowest amount of power) and lengthening contractions are in-between, requiring one-half of the ATP of shortening contractions(3). This information suggests activation of mTOR (and therefore strength gains) should be greatest when training with forced lengthening contractions against a very high load.
Training to maximise mTOR activation
The type of contraction is one thing that can be used to maximise mTOR activation, but are there others? The short answer is yes. Here, we will discuss one nutritional strategy and a few training programme factors that can maximise activation of mTOR.
One of the things that can activate mTOR inside muscles is an increase in circulating blood amino acids (from digested protein). Specifically, foods that are high in the branched chain amino acids (eg leucine) such as milk, can increase the response to resistance exercise. We have known for some time that adding amino acids to a strength-training programme can improve the resulting increase in strength, and now we think that we know why. When amino acids are taken into muscle, they can directly activate mTOR and improve protein synthesis and muscle growth.
There is also the suggestion that when we consume amino acids might be important in the effects on mTOR and protein synthesis, but this is still controversial. We have just finished experiments that suggest that the if amino acids are taken within one hour after training they will have a bigger effect then if they are taken later. This is because we have found that the ‘leucine transporter’ is increased in muscle between 30 and 90 minutes post-training and this might be important in mTOR activation and therefore strength gains.
It is important to remember that keeping amino acid levels high for extended periods of time can actually result in a decrease in both protein synthesis and insulin sensitivity(4). Therefore, it is unwise consume to excessive amounts of protein.
Programme features to optimise mTOR activation
Although we said we want to maximise power when we train, there is a caveat. The highest absolute power is seen when performing fast lengthening contractions with a lot of weight (high jerk), or heavy plyometric exercises. This type of exercise is very effective in activating mTOR, but unfortunately can be very bad for tendon health, and as a result can lead to injuries. Since the tendon adapts more slowly than muscle, if heavy plyometric exercises are used, providing adequate recovery time following these exercises is absolutely essential.
Another consequence of the slow recovery rate of tendon for high-jerk resistance exercise is the use of periodised training. As described in PP266, non-linear periodised programmes result in greater strength gains than traditional linear progression methods. Athough it has been demonstrated numerous times, there doesn’t seem to be a reason for this at the muscle level. Instead, this likely represents the fact that the majority of elite athletes are overtraining and periodically decreasing the load allows the required rest for muscle adaptation and tendon recovery from the high-jerk exercises.
An alternative way to promote tendon health is to use slow lengthening, or forced contractions. This type of movement has been shown to improve tendon health and recovery from injury. Further, since there is no need for prolonged tendon rest periods, linear progression programmes can be used effectively when this type of movement is included.
Second, since minimising metabolic stress is one of the keys to activation of mTOR, each set should last less than 60 seconds. This is the amount of high-energy phosphate stored in a normal muscle. Any longer and the muscle will turn on processes that shut down mTOR, decreasing the response to the training. When performing controlled repetitions this means a maximum of 10 reps per set is optimal for strength gains.
Last, in order to minimise the metabolic stress of each set, the programme should preferably consist of only one set, which should end with two to three forced repetitions. If more than one set is used, enough time must be taken between sets to allow full recovery of phosphocreatine and ATP. This takes two to three times as long as the exercise itself (around two to four minutes).
Putting together a strength programme
So how can these ideas be put together into a coherent programme to optimise strength gains? What follows is a programme built on the molecular ideas described above and the experience of 30 years of working with elite strength athletes. This programme is a linear progression system that uses one set to momentary muscular failure and push-pull methodology to maximise power and minimise metabolic stress (see box 1).
During the positive phase:
- Limit momentum: do not bounce or throw the weight upwards;
- Limit leverage: do not change the angle of any joint other than the target joint;
- Constant tension throughout the exercise: do not rest on the way down or at the bottom of the movement;
- Shortening of the target muscle should take one to two seconds; the weight should then be stopped at the top of the movement before lowering the weight with tension during the lengthening phase.
During the negative phase (forced repetitions):
When the athlete can no longer lift the weight, the coach and athlete combine for a number of forced repetitions. In this phase, the coach assists in the shortening phase and then challenges the athlete to lower as much weight as possible taking six to eight seconds. The coach can also provide extra resistance if needed.
To minimise the metabolic stress on each muscle group, athletes should progress from a pushing exercise to a pulling exercise and vice-versa. A pushing exercise is a movement away from centre of body during the shortening contraction of the target muscle (eg chest/shoulder/triceps press, leg extension, leg press). A pulling exercise is a movement toward centre of body during the shortening contraction of the target muscle (eg pulldown, row, biceps curl, leg curl). Progressing from a pushing to a pulling exercise allows full recovery and resynthesis of ATP and PCr in helper muscles between exercises, decreasing metabolic stress and allowing better activation of mTOR.
After a workout, your body begins recovery by replenishing oxygen supply, high-energy phosphate fuels and glycogen (carbohydrate) in muscle, and importantly begins to degrade and synthesise muscle proteins. This requires rest and proper nutrition. The amount of rest varies from athlete to athlete and with the intensity of exercise as discussed above, while proper nutrition can be as simple as consuming 6g of essential amino acids and 35g carbohydrate (700mls of skimmed milk is sufficient to provide these) within 30 minutes of training(5).
1. Eur J Appl Physiol. 2008, 102: 145-52
2. Am J Physiol. 1999, 276: C120-7
3. J Appl Physiol. 1997, 83: 867-74
4. J Biol Chem. 2001, 276: 38052-60
5. Clin Sports Med. 2007, 26: 17-36