Early Studies on Strength and Endurance Training
This story concerning the potential molecular conflicts associated with synchronous strength and endurance training goes back to the 1970s when Robert Hickson, then a post-doctoral researcher at Washington University in St. Louis, discovered that the running workouts he was completing with his mentor, John Holloszy, seemed to be producing a sharp decrease in his muscle mass. Hickson went on to complete a study in which he demonstrated that endurance training had a negative impact on the gains in strength associated with concurrent resistance training.1 The lesson from this research was consequently adopted by the running community. Runners began to believe that it made little sense to carry out strength training since endurance-running activities would throttle the possible emergence of greater strength. Furthermore, the two activities seemed to be too disparate—aerobic (running) versus anaerobic (strength training) in the parlance of the day—to be joined together in any serious runner’s training log.
What is often forgotten is that Hickson’s own follow-up study found that strength training was extremely beneficial to runners. In that inquiry, runners who took part in a 10-week resistance program primarily geared toward upgrading the strength of the quadriceps muscles increased their endurance time while running at an intensity of O2max by a solid 12 percent.2 In additional research conducted several years later by Hickson and colleagues at the University of Chicago, runners who had reached a “steady-state level of performance” carried out strength training three times a week for 10 weeks, with their regular endurance training remaining constant during this period.3 This research, far from revealing problems associated with synchronizing strength training with endurance work, revealed that the addition of strength training was linked with a 13 percent enhancement of endurance during intense running.
Other studies were not able to demonstrate that endurance training harmed the development of strength. In one of the most ingenious of these investigations, some subjects performed endurance training on one leg and a combination of endurance and strength training with the other leg. A second group of athletes carried out strength training on one leg and the combination of endurance and strength training with the other. The endurance training was composed of five 3-minute intervals of cycling per workout at an intensity of 90 to 100 percent of O2max; the strength training centered on six sets of 15 to 22 repetitions of leg presses with challenging resistance.4
After 22 weeks, the legs that engaged in both endurance and strength training were just as strong as the legs that performed strength training only, indicating that endurance training did not interfere with the development of force production. An interesting aspect of this research was that the same leg muscles were used for both the endurance and strength training, and the movements involved (pushing on a bike pedal and pressing a leg-press platform) were similar mechanically. This contradicted one common view that endurance-training’s depressing effect on strength would be particularly strong if the same muscles were engaged in both types of training.
From the molecular standpoint, it had been thought that individual muscles could never go in two directions at once. It was believed that when asked to do so, muscles would abandon gains in strength and size in favor of endurance-related changes just as Hickson’s quads had lost mass when he became a serious runner. In this 22-week study, however, muscles engaged in endurance training had no problem at all with the task of building up strength when they were asked to do so. Since the movements involved in the research (pedaling and pressing) overlapped biomechanically, there was a strong indication that the development of running-specific strength would not be retarded at all by using high-quality running workouts.
Why, then, did Hickson’s original study detect a negative effect of endurance training on strengthening? It is possible that the strength-endurance subjects in that research simply became overtrained. The strength-endurance subjects were working out at least 70 minutes per day (40 minutes of endurance running and 30 minutes of strengthening) five times per week, whereas the strength-only athletes were training just 30 minutes per day. As strength increased, additional weight was added to maintain maximal resistance for the required numbers of repetitions. In fact, the strength-endurance participants did gain strength, as measured during the parallel squat, at the same rate as the strength-only athletes over the first 6 to 7 weeks of the study before stabilizing and then losing strength over the last 2 weeks. If the study had ended after 6 weeks, the conclusion would have been that endurance training does not hurt the development of strength at all!
An important point to note, too, is that Hickson’s strength-endurance athletes did gain strength over the 10 weeks of the study; their gains over 10 weeks were simply not as great as those achieved by the strength-only subjects. From the beginning of the study to the end of the sixth week, the strength-endurance participants upgraded their squat strength by about 35 percent, which is considerable. This makes it unlikely that some powerful molecular mechanism existed that blocked gains in strength as a result of the simultaneous endurance training.
Balancing Strength and Endurance Training
When an athlete engages in resistance exercise, it is clear that hypertrophy occurs when the stimulus originating the adaptation is one of short-duration effort at high intensity (e.g., with increased muscle tension). Research suggests that this kind of strength training produces a cascade of biochemical changes (the signals described in chapter 30) inside muscle cells, alterations that are quite different from those occurring in response to endurance training; however, these internal alerts don’t necessarily block the processes that lead to endurance-related adaptations. Although the possible pathways toward greater strength are quite complex, much of the intramuscular makeover seems to hinge on a critically important protein called mTOR; chemicals that block the actions of mTOR make it impossible for muscles to increase their size in response to resistance exercise.5
The protein mTOR is activated when resistance training is performed, probably in response to growth factors released by muscles in response to strength training; to make matters more complicated, it can exist in two different protein complexes. TOR complex 1 is composed of mTor, G-protein beta-like protein, and a unique compound called raptor; this complex is responsible for augmentations of muscle size. TOR complex 2, on the other hand, is made up of mTOR, G-protein beta-like protein, and a different chemical called rictor; TOR complex 2 appears to be essential for remodeling the internal structure, or cytoskeleton, of muscle fibers. The overall process by which workouts initiate dramatic changes in muscle size and architecture is often referred to as exercise signaling. Once this signaling is completely understood, scientists could check to see which kinds of strength training do the best job of enhancing the two types of mTOR.
If endurance exercise really disrupts gains in muscle strength, it merely needs to interfere with the mTOR complexes, especially TOR complex 1. There is, in fact, a potential mechanism for this. When sustained endurance training is carried out, there is usually an increase in the activity of a chemical called AMP-activated protein kinase (AMPK) that is found inside muscle cells.6 Heightened AMPK activity leads to a variety of chemical transformations that increase mitochondrial production and augment aerobic enzyme concentrations. However, greater AMPK action also activates a chemical called TSC2, which in turn can at least partially inactivate mTOR, leading to a decreased rate of protein synthesis. The AMPK-TSC2 mechanism solves the muscle fibers’ potential problem of trying to do too many things at once (i.e., augmenting strength while at the same time improving aerobic characteristics) and pushes adaptation in the direction of endurance development.
Note, though, that AMPK’s potential inactivation of mTOR does not mean that muscle growth cannot occur; it suggests rather that it might take place at a slower rate compared with when endurance exercise is not being carried out. It is important to note that athletes in Hickson’s study who trained for strength and endurance still manag
ed to boost squatting strength by 35 percent after 6 weeks. Furthermore, there are some kinds of strength training that lead to improvements in strength without hypertrophy; these forms of resistance training would not be harmed by AMPK’s blocking effect on mTOR. For example, changes in the way the nervous system recruits and coordinates key collections of muscle cells, or motor units, can greatly improve strength without involving gains in muscle size, and such changes should not be thwarted to any degree by AMPK’s inactivation of mTOR.
Although there is debate about whether endurance training slows down gains in strength, there is now a consensus that strength training can boost endurance performances. A variety of studies have shown that appropriately conducted strength training can enhance running economy, decrease foot-contact times, improve leg-muscle stiffness during running, and—the ultimate bottom line—upgrade race performances.
The molecular biology approach has produced interesting insights concerning the merits of concurrent strength and endurance training, and it also suggests that training balance is important. If a runner is completing large amounts of weekly running and carrying out small amounts of strength training, for example, this runner is probably covering his or her muscular mTOR with a thick blanket of AMPK and thus will achieve no change, small positive changes, or negative changes in running-specific strength. If training is in balance, however, and moderate-volume, high-quality running training is blended with regular doses of running-relevant strength training, mTOR levels should be adequate and activated, and running-specific strength, speed, and endurance should all improve at the same time. Running-relevant strength training is described in Chapters 14 and 28.
Training Twice Per Day
An understanding of how training produces responses at the molecular level can also help answer questions about training frequency. For example, many experienced runners train two times a day, often known as the daily double; the basic argument supporting such training has been that it is a practical way to boost total training volume. The extra volume is then supposed to lead to upswings in aerobic capacity, strength, and endurance. Some physiologists also contend that there is a unique benefit associated with training more frequently; their hypothesis suggests that two 5-mile workouts would be better than a single session of 10 miles because the body has been physiologically jolted by being provided with an adaptation-creating stimulus twice instead of once. From the viewpoint of molecular biology, two instances of cell signaling have been initiated instead of one.
What does molecular biology have to say about this controversy? As it turns out, a recent molecular approach has linked a unique form of the daily double with significant gains in endurance capability. The innovative research suggests that the strategy of conducting two workouts per day can activate special genes in an athlete’s muscles that cause the production of protein molecules that fight fatigue and prolong endurance during high-quality exertions. As the investigation reveals, higher performances are the end result.
Training With Low Glycogen Levels
The intriguing story about molecular adaptations to the daily double emerged from the Department of Infectious Diseases and the Copenhagen Muscle Research Centre at the University of Copenhagen in Denmark.7 There, researchers Anne K. Hansen, Christian Fischer, Peter Plomgard, Jesper Lovind Andersen, Bente Klarlund Pedersen, and Bengt Saltin began exploring the molecular mechanisms responsible for improvements in fitness. They noted that low muscle glycogen levels had been linked with the transcription of a number of genes involved in adaptations to training. (As explained in chapter 30, transcription means that the genes are read; this process leads to the production of proteins, which may have a positive effect on physical capacity.) The scientists began to wonder whether consistent training with low glycogen levels in the muscles might enhance a runner’s adaptations to training by stimulating the expression of key genes associated with endurance performance.
At first glance, the idea of training with low glycogen levels might seem bizarre. After all, why would athletes want to train with very little carbohydrate fuel in their legs? Wouldn’t that be a sure recipe for fatigue and consistently slow training speeds, plus a heightened probability of injury? However, there is a logical underlying principle supporting low-glycogen training. The general principle is that deficiencies in a substrate or in a process are what actually lead to major physiological adjustments and thus improvements in performance. From the molecular biology perspective, deficiencies lead to remedial cell signaling, followed by gene expression and the production of proteins that decrease the risk of future deficiencies.
For example, for experienced runners, training at an intensity above O2max—a level of effort at which the cardiovascular and muscular system fail to meet the aerobic energy production requirements of the exercise and thus must rely on anaerobic pathways to provide the needed energy—provides a much more potent stimulus for O2max improvement compared with training at piddling intensities below O2max. During the latter efforts, the cardiovascular, nervous, and muscular systems think that everything is in order and may fail to change and adapt because they are able to handle the aerobic energy production requirements of the exercise. Thus, little or no change in O2max is ultimately produced. When intensity soars above O2max, however, the circulatory, nervous, and muscular systems think they are deficient and create adaptations that increase O2max. (The word think is employed here to simplify the discussion of the actual triggers that the circulatory, muscular, and nervous systems use to fire up their adaptation processes).
Along similar lines, high-intensity training can create a great problem for muscle cells because the cells often lack the buffering proteins that soak up the excess quantity of fatigue-inducing hydrogen ions produced during such scorching training. This deficiency in buffering proteins eventually leads to an expression of buffering-related genes and an increased production of buffers within the muscles; endurance at high intensities can improve considerably as a result. If the training had not exposed the deficiency in the buffer system (e.g., if it had been conducted at moderate intensities with little accumulation of hydrogen ions), there would have been no stimulus for the buffering system to upgrade itself, and performance at high-quality speeds would have been less likely to improve.
Testing the Low-Glycogen Theory
To test the glycogen-deficiency theory, the Danish researchers in the aforementioned study recruited seven healthy young men, average age 26. These subjects took part in a rigorous 10-week training program that involved both one- and two-leg exercise. As part of the design of the investigation, the right and left legs of each participant trained quite differently. One leg, chosen at random, carried out two workouts during a day, the second of which was completed under low-glycogen conditions. This two-workout day was then followed by a rest day for that leg during which no training sessions were conducted. In contrast, the other high-glycogen leg trained once per day, every day.
Here’s how it worked in actual practice for a sample subject. On the first day of the investigation, the subject exercised both legs simultaneously for one hour at an intensity of 75 percent of the maximal possible work rate, or Wmax. Two hours later on that same day, he exercised his left leg, which had been chosen at random to be the low-glycogen leg, for another hour at 75 percent of Wmax for that leg. During this left-leg effort, the right leg did absolutely nothing. The left leg was almost out of fuel because its glycogen had been exhausted in the workout that had occurred 2 hours earlier. Furthermore, the continuous hour of effort plunged the left leg into full glycogen desperation. No carb loading or eating of any kind was permitted during the 2-hour period between workouts.
Following the second workout of the day, the subject began eating normally and thus began restocking glycogen. On the second day of the study, he exercised his right leg only. The left leg took the day off since it had worked twice on the first day. The right-leg exertion was carried out at 75 percent of the right leg’s Wmax. The right leg was in good gl
ycogen shape on both days. On the first day, it had exercised simultaneously with the left leg; the right leg had an adequate supply of glycogen at that time because the subject had been following a healthy diet. On the second day, the right leg worked by itself for one hour 24 hours after the two-leg work, which was enough time for glycogen reloading.
On the third day, this basic pattern started over. There was a 1-hour workout with both legs training at the same time. Two hours later, the left leg worked alone on low glycogen. On the fourth day, the right leg worked by itself with plenty of glycogen on board. This regimen was then repeated over and over, which meant that each leg performed exactly the same amount of exercise, at the same intensity, over the course of the study.
Throughout the study, the workouts began in the morning after an overnight fast, making things even tougher for the low-glycogen leg. On the days with two workouts, no food or sports drink was permitted until the second workout was done, but water consumption was ad libitum, or at whatever quantity was wanted. Over the course of 10 weeks, the study participants became stronger; workload gradually increased but was exactly the same for the two legs. The subjects consumed a typical athlete’s diet during the investigation, with 70 percent of calories coming from carbohydrate, 15 percent from protein, and 15 percent from fat. Two-day rest periods from training were provided approximately every week.
Results of the Low-Glycogen Theory Study
After 10 weeks of this training, one-leg Wmax had improved considerably in both legs and was absolutely equivalent between the limbs. The Wmax, possible work rate, in this case was the topmost intensity that could be reached during a one-leg test that began with a 10-minute warm-up at an intensity of 20 Watts and continued with a step-wise increase in intensity of 10 Watts every 2 minutes until complete exhaustion was reached.
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