An Analysis of Hadd’s Approach to Distance Training
Part 2 – Mitochondria
In part 1 of this analysis of Hadd’s approach to distance training we examined in detail Hadd’s training prescription. Our examination revealed that the two primary components of Hadd’s training method are a recommended training intensity known to cause performance improvements (80% VO2peak) and a significant increase in weekly training mileage (increase from 50 miles per week to 116 miles per week).
In addition to the detailed training recommendations that he makes, Hadd also spends a considerable amount of time in his article articulating a physiological explanation for his training method. In fact, his training method is clearly presented as a method to improve those physiological factors that he believes limit endurance performance.
Therefore, in this section we will examine a core physiological belief presented by Hadd and review the research he cites in support of this belief.
Hadd begins his physiological explanation with a discussion of VO2peak, lactate threshold (LT), and aerobic and anaerobic metabolism. Following are his explanations of these physiological factors.
“Sooooo. Let’s sum all this up, it’s very simple.
1. Better trained runners can maintain a higher percentage of their VO2peak (85% or higher) in a marathon than lesser trained runners.
2. They can do so because their blood lactate AT ANY PACE or any percentage of VO2peak is lower than the blood lactate of less well-trained runners.”
“As I repeatedly stressed in my long earlier thread, the training to improve your VO2peak (essentially the stroke volume of your heart) is NOT the same training as that required to raise your LT (increase capillaries, mitochondria and aerobic enzymes in your muscles). The speeds required are totally different. LT training is one case in which faster is NOT better.”
“Final summation: if you cannot maintain a good relationship across race performances it is because your LT is not good enough (not a high enough percentage of your personal VO2peak). Your LT is dependent on adaptations in your leg muscles caused by training. If you have a poor LT, your adaptations have not occurred well enough (despite even years of training). As will be better explained later, these adaptations are intensity dependent (train too fast, they won’t happen).”
“Let’s look at some major negative effects of “borrowing” from your anaerobic ability in a distance event (anything from 5k upwards). (For those of you who do not think you are doing this, just note that if you have a poor(er) pace relationship as the distances increase, you are.)”
“1. When the muscle cells in your legs build up too much acidity (caused by running anaerobically), those cells shut down since the acidity inhibits enzymatic action and contractibility in the cell and energy breakdown can no longer continue…This is not so if you use those self-same cells/fibers aerobically.”
Hadd is promoting standard cardiovascular/anaerobic theory. He believes that at a certain level of work the energy needs of the muscle cannot be met via aerobic metabolism. When this occurs, anaerobic metabolism is increasingly called upon to meet the energy needs of the working muscles. He further believes that the by-products of anaerobic metabolism, lactate in particular, cause muscle acidity to increase. This increased muscle acidity interferes with muscle contractility and causes muscle fatigue.
As a solution to the problem of inadequate aerobic metabolism, Hadd provides a training prescription supported by two research studies – a 1960s study by John Holloszy and a 1982 study by Gary Dudley. Using these studies, especially the study by Dudley, Hadd promotes the idea that training at very specific intensity levels will cause an increase in mitochondria density and an increase in aerobic metabolism.
“Way back in the late 1960s a professor called John Holloszy got some rats to run on a treadmill for various lengths of time up to 2hrs per day at around 50-75% of the rats’ VO2peak (easy running, therefore). After 12 weeks, he found that the rats had increased the mitochondria (vital for aerobic energy production) in their running muscles (compared to control rats that did no training). This was a seminal piece of work, because it explained why runners get better with training.”
“The next question was logical. How long should people run for to optimally cause this effect?
Back to Holloszy and his fellow researchers who formed 4 groups of rats to train: one group running 10mins/day, a second running 30mins/day, a third running 60mins and a fourth running 2hrs/day. All at the same easy 50-60% VO2peak, and for 5 days/week for 13 weeks.
Perhaps logically, the 2hr-group had the greatest increase in mitochondria at the end of the training period.”
“But what about intensity? Were mitochondria only created while running long and slow?
In 1982, a guy called Gary Dudley decided to explore this question. He had several groups of rats training five days/week (but only for 8 weeks). Like Holloszy, he also used a range of different training durations, from 5-90 mins per day. However UNLIKE Holloszy (whose rats all trained at the same pace) he also used a range of training intensities. Dudley’s rats trained at either 100%, 85%, 70%, 50% or 40% VO2peak. He also examined how different intensities and different durations affected different muscle types (fast twitch white, fast twitch red or “intermediate”, and slow twitch).”
“…the best way to cause improvements in slow-twitch fibers was to run long and slow at 70% VO2peak (adaptation began from as low as 50% VO2peak pace). Faster was not better. Although Dudley found that 90 mins was not better than 60 mins, Holloszy had shown that 2hrs was definitely better than one…”
“So, to sum up:
To improve your LT (which will have a direct impact on your race performances), you must increase the mitochondria in your running muscles (in a neat move, the optimal training to improve mitochondria is also the optimal training to improve capillary density).”
“The more mitochondria, the less lactate at every running pace. But mitochondrial adaptation in each fiber type is training-intensity dependent. If you want to maximize the number of mitochondria in each fiber type, you must train at the correct pace for that type. (remember; the more mitochondria, the less lactate; the less lactate, the faster the racing pace and the more economical you are at any pace, meaning you can keep that pace up for longer.)”
In summary, based on the research work of Holloszy and Dudley, Hadd promotes the belief that training for long durations of up to 2 hours at 70% VO2peak is the best method for increasing slow twitch muscle fiber mitochondrial density. He further believes that training at intensities of about 80% VO2peak and above will not cause these same adaptations in the slow twitch fibers. He states that an increase in mitochondrial density results in the runner being able to run at increasingly faster paces all the while meeting his muscles’ energy needs via aerobic metabolism.
It is important to note that Hadd’s views are quite consistent with modern training theory. Certainly there are unique aspects to his training approach, but in general there are more similarities than differences.
A significant point in Hadd’s theory is that training of too high intensity will not produce the same improvements in slow twitch fibers as training at lower intensities. In fact, Hadd believes that only the lower intensity training will produce the desired changes in slow twitch muscle fiber aerobic energy metabolism. As noted above, this evidence is based on the research data from Dudley. It is appropriate then to review in detail the research study by Dudley for a complete understanding of the data Hadd’s logic is based upon.
Dudley and his fellow researchers wanted to specifically characterize the influence of exercise intensity and duration on the adaptive changes in oxidative capacity in the working muscles (1). They took a large number of rats and divided them into 19 distinct training groups. These exercising animals were assigned to one of six different training intensities (10, 20, 30, 40, 50, & 60 meters/minute). As the researchers stated, “These running speeds represent a progression in exercise intensity requiring a moderate submaximal oxygen consumption (VO2) to a supramaximal exercise effort that surpasses the rat’s maximal aerobic capacity.” The relationship between the six different training intensities and percentage of VO2peak is presented in table 3.
Table 3: Relationship between training speed and percent of VO2peak
The animals were then further divided into three or four exercise durations for each intensity in an attempt to characterize the influence of exercise duration. All animals ran 5 days per week and the training program lasted a total of 8 weeks. All animals running 10, 20, 30, & 40 m/min ran continuously during their workouts. Due to the high intensity associate with running 50 & 60 m/min, these animals were exercised via intervals, with the number of intervals matched to the desired total daily run time. The summary of the training program is found in Table 1 (all table and figure data in this article, with the exception of table 3, are re-printed from Dudley’s original study thanks to permission from the copyright holder).
At the end of the training program muscle samples were taken from each animal and measured for cytochrome c concentration. Cytochrome c was used as an index of training induced changes in oxidative capacity because “cytochrome c is an integral part of the mitochondrial electron transport assembly, its level varies directly with mitochondrial content in the different skeletal muscles fiber types, and its level changes in proportion to the coordinated changes in a wide variety of enzyme markers of oxidative metabolism.”
Based upon their observed changes in cytochrome c concentration the researchers concluded that “running longer times per day tended to increase the magnitude of the adaptive changes in cytochrome c in a nonlinear manner.” Additionally, they also noted that intensity of exercise played an important role in causing changes, with a general increase in peak adaptive response as exercise intensity increased. Summing up these two findings the researchers stated, “Thus it is possible to induce the same increase in cytochrome c at the faster run speeds using shorter run times as that found at the lower intensities but at longer run times.”
There were distinct differences in cytochrome c concentrations in the three types of muscle fibers (slow twitch red, fast twitch red, and fast twitch white). These changes are summed in figures 1, 2, and 3. Red vastus data in fig. 1 is fast twitch red fiber. White vastus data in fig. 2 is fast twitch white fiber. Soleus data in fig. 3 is slow twitch red fiber. Table 2 provides the best estimate of the peak cytochrome c concentrations for each exercise intensity.
An examination of the data provided in figures 3 & 4 and table 2 emphasizes several points. First, recall the relation between exercise pace and intensity levels. The corresponding intensity level is provided for each of the 6 different training paces in fig. 4. Intensity began at 63% of VO2peak and peaked at 116% VO2peak.
Slow Twitch Fiber: In contrast to Hadd’s comments that “the best way to cause improvements in slow-twitch fibers was to run long and slow at 70% VO2peak” the data provided shows that training intensities above 70% VO2peak caused greater increases in cytochrome c concentrations of slow twitch fibers than did intensities of 70% VO2peak and below. Peak adaptations in slow twitch fiber occurred at an intensity of about 90% VO2peak (fig.4). Furthermore, the adaptations at 105% VO2peak were greater than those occurring at 73% VO2peak (15.92 vs. 15.65 respectively).
For a training duration of 30 minutes an intensity of 83% VO2peak caused the largest adaptation in slow twitch cytochrome c concentration with 105% VO2peak causing the second largest adaptation (approx. 17 and 15.92 respectively).
For a training duration of 60 minutes an intensity of 83% VO2peak caused the largest adaptation in slow twitch cytochrome c concentrations with 93% intensity causing the second largest adaptation (approx. 17.9 and 16.5 respectively).
For a training duration of 90 minutes an intensity of 93% VO2peak caused the largest adaptation in slow twitch cytochrome c concentration with 83% intensity causing the second largest adaptation (approx. 17.89 and 16 respectively).
Based on these data it is clear that a training intensities higher than 70% VO2peak cause greater adaptations within slow twitch fiber than does training at or below 70% VO2peak. The data also shows that peak adaptations occur at a much higher intensity than is suggested by Hadd (90% vs. 70% respectively).
Hadd made the point that “these adaptations are intensity dependent “(train too fast, they won’t happen).” The data from this study clearly contradicts this belief. Adaptations not only continue to increase in slow twitch fibers at intensities above 70% VO2peak, but peak adaptations within the slow twitch fibers occurred at an intensity fully 20% greater than Hadd states is the upper limit for adaptations. Additionally, intensity levels from 90% to 105% VO2peak produced greater adaptations than did training below 70% VO2peak.
Hadd seems to have made 3 primary errors in his reference to this particular study.
First, he stated that “Dudley’s rats trained at either 100%, 85%, 70%, 50% or 40% VO2peak.” Instead, Dudley’s rats trained at exercise intensities between 116% – 63% VO2peak, considerably above the intensities Hadd suggested.
Hadd then went on to draw the conclusion that “…the best way to cause improvements in slow-twitch fibers was to run long and slow at 70% VO2peak…” Instead, the data shows that training at an intensity of about 85% – 95% for 60 minutes caused the greatest changes in slow twitch fibers.
And finally, Hadd stated that with respect to intensities above 70% VO2peak that “Faster was not better.” Again this statement by Hadd is disputed by the facts. Though the adaptation to the slow twitch fibers decreased after reaching a peak, the decline was not as precipitous as is implied by Hadd. Adaptations did decrease after peak but it was not until intensity levels beyond 105% VO2peak that adaptations decreased to a lower level than did training at 70% VO2peak. Clearly, training at a pace faster than optimal for causing peak changes in slow twitch fiber do not result in no changes in slow twitch fibers. Faster training, while not optimal for developing the slow twitch fibers, still produces significant adaptations in those fibers and in some cases faster training produced more adaptations than slow training.
In conclusion, though the argument could be made that other adaptations may occur from training long and slow it is clear that the adaptations in the oxidative capacity of slow twitch fibers are not maximized at these lower intensities.
The research data provided by Dudley shows that mitochondrial adaptations in slow twitch fibers reach a peak at about 85% – 95% VO2peak. The oxidative capacity improvements that occur in slow twitch fibers from training intensities of 90% – 105% VO2peak are greater than those adaptations that occur at 70% VO2peak and below. In contrast to the training recommendation of Hadd that the best way to improve the aerobic capacity of slow twitch fibers is to exercise at an intensity of 70% VO2peak and below, the data provided indicates that a training intensity of 85% – 95% produced the greatest improvements in the oxidative capacity of slow twitch fibers.
Dudley G., Abraham W., Terjung R., Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle J. Appl. Phsiol 1982, 53(4), 844-850