Where does Hadd fit in the picture with Maffetone and Lydiard?

In my recent posting comparing Maffetone and Lydiard, I discussed the fact they both recommend a period of base-building in which the major component is running in the aerobic zone.  The main difference between the two is Maffetone’s recommendation that all of the training during the conditioning phase should be in the lower aerobic zone whereas Lydiard recommended several session per week at paces in the upper part of the aerobic zone.  After reviewing the evidence in support of Maffetone’s recommendations, I had concluded that there was no clear grounds for proposing that a few sessions in the upper aerobic (or even anaerobic) zones would interfere with base-building and hence, came down in support of Lydiard.  In that posting I had implicitly lumped Hadd with Maffetone, but maybe it is only fair to let Hadd speak for himself and in particular, to examine the extent to which he advises against reaching the lactate threshold, and the reasons he advances in support of his advice.

 

Hadd presents his approach in an article at:

 http://www.counterpartcoaching.com/hadd.pdf .  He argues quite strongly that the anaerobic zone should be avoided during base building.  The core of his argument is that a sound base depends on well conditioned slow twitch fibres and that these fibres can only be recruited and developed at paces in the aerobic zone.  He bases his argument largely on Gary Dudley’s observations of fibre development in rats. 

 

I will return to a discussion of this evidence later, but first it is useful to review the program that Hadd recommended for a 35 year old marathon runner whom he calls Joe.  He reported that Joe had the potential to run a marathon in 2:25, but at the beginning of the program, he was unfit and 20 lb overweight due to lack of recent training.

 

Joe’s program

Hadd’s first instruction to Joe was to get his weekly mileage up to 50 miles without concerning himself with pace.  In fact Joe achieved this rapidly.  He then recommend that Joe perform two tests: a test of maximum heart rate, which was to be recorded during a peak effort 400m that followed shortly after a peak effort 800m run  Joe posted a value of 193 bpm.  A few days later, Joe performed the ‘Hadd test’: a set of 5x2400m runs each at a predetermined target heart rate.  The target heart rate increased in steps of 10 BPM in successive runs, ranging from 140 to 180 (and hence extending from lower aerobic zone to the low part of the anaerobic zone.  Joe reported that he found the fastest pace difficult to maintain for the required 2400m, providing confirmation that 180 was above Joe’s current lactate threshold.  With the information from these two tests Hadd defined two key heart rates: a lower heart rate of  140 (approximately HRmax – 50) and an upper heart rate of 160, selected to be about 10-15 BPM below estimated current lactate threshold.  This higher heart rate was in the upper aerobic zone but comfortably below the lactate threshold.  These two heart rate levels (140 and 160)  were used to define the paces for the key workouts. 

 

Already by this stage, we can see a crucial feature of Hadd’s approach.  He sets training paces according to specific testing of the individual athlete.  Furthermore, although like Maffetone, he argues that it is important to avoid the anaerobic zone, unlike Maffetone, one of Hadd’s key training paces in the comfortable part of the upper aerobic zone.

 

In early weeks of Joe’s training, majority of sessions were at or near the lower aerobic pace but typically for two sessions per week the target pace was the comfortable upper aerobic pace.  In  week 3 when the weekly mileage was increasing, all runs were near the lower aerobic pace, but once weekly mileage had stabilized at around 100 miles per week, Hadd again introduced 2 runs at the comfortable upper aerobic pace in addition to 60 minutes at the upper pace within a 2 hour run. 

 

Thus, Hadd’s program bears a strong resemblance to Lydiard’s recommendation that most runs are at ¼ effort, with two or three faster runs at ½ or ¾ effort each week.  Although Lydiard did not define ¼ , ½ and ¾ pace precisely, the overall picture emerging from Lydiard’s writings and lectures suggests that he recommended  sessions that were a little harder than those recommended by Hadd. 

 

Molvar’s interpretation of Lydiard

John Molvar, who is one of the most thorough students of Lydiard’s writings, defines Lydiard’s paces at

http://www.bunnhill.com/BobHodge/Special/LydiardResponses.htm.  He states:

1/4 effort – easy, but still aerobic pace (not jogging), 65-70% of (Maximum minus resting heart rate). For example, with a resting of 55 and max of 195, 1/4 effort is in the range 145 to 153 beats per minute, though Molvar points out that this might increase later in the base-building phase

1/2 effort – run at a strong aerobic, but sub tempo pace, 70-75% of (Maximum minus resting heart rate). For example 153 to 160 beats per minute.

3/4 effort:  tempo pace/At Threshold (AT) pace, 75-85% of (Maximum minus resting heart rate). For example 160 to 174 beats per minute

 

Thus. Molvar’s interpretation of Lydiard’s ¼ and ¾ key paces make them a little more demanding than Hadd’s corresponding paces.  There is little doubt that the famous 22 mile Sunday hill run done by Lydiard’s protégés during base building  was more demanding than the 2 hour run with 60 minutes at HR 160 recommended by Hadd.

 

Speed work

Lydiard also recommended speed work through the conditioning phase.  In somewhat similar manner, in week 8, Hadd introduces 200/200 fartlek sessions to re-establish speed. These session consists of 25 x 200m at 5k pace with 200m recovery at an easy pace.  

 

Joe’s progress

In a little less than 20 weeks,  Joe reduced his pace at HR 180 (i.e. a little above lactate threshold) from 5:40 min per mile to 5:10 min per mile.  At this stage he entered a marathon with the plan of running with the 2:20 pace group and dropping out half-way.  He covered the half-marathon in 71:xx.  Thus, after 20 weeks his goal of a 2:25 marathon appeared plausible, if not quite within reach at that stage.  Unfortunately , Hadd does not tell us whether or not Joe achieved his marathon target.  Nonetheless, the achievements of the first 20 weeks were impressive. 

 

In summary, the program recommended by Hadd for Joe is quite different from a typical Maffetone program in which all runs in the conditioning phase are at lower aerobic pace.  In fact Hadd’s paces are only slightly less demanding than the paces recommended by Lydiard.  The major issue in following Hadd’s approach is knowing whether or not it is crucial to avoid reaching the lactate threshold.  Some of his disciples go so far as to slow to a walk when ascending hills to avoid the dreaded threshold

 

Dudley’s rats

As far as I understand Hadd’s reasoning, it is based largely on the way he interprets the findings of Dudley’s study of rats. (’Influence of Exercise Intensity and Duration on Biochemical Adaptations in Skeletal Muscle,’ Journal of Applied Physiology, vol. 53, pp. 844-850, 1982)   Dudley observed that running at relatively low speed increased mitochondria in the slow twitch fibres while running at faster speeds resulted in an increase in mitochondria in fast twitch fibres.  Hadd interprets this as reason for running at slow speeds if you want to develop the aerobic capacity of the slow twitch fibres essential for distance running  However, in Dudley’s rats, running fast produced a worthwhile increase in mitochondria even in the slow fibres, so overall, fast running is beneficial both fast and slow twitch fibres.  Dudley did not show that faster running obliterates the benefits gained from slow running.  

 

Perhaps the most striking evidence that a moderate amount of faster running does not destroy the benefits derived from the slower aerobic training is the array of Olympic gold medals won by Lydiard’s protégés, despite the demanding Sunday morning hill run.  However, it is dangerous to draw conclusions from anecdotes alone.  When in doubt, it is can be worthwhile to examine the underlying science – though if you do not feel comfortable trying to keep track of the long names of biological molecules. (or perhaps even worse, trying to keeping track of the abbreviations for the names of molecules), you can skip the next section. 

 

Some biochemistry

The core reason for advocating development of aerobic metabolism is the fact that aerobic metabolism, in which glucose is converted to carbon dioxide and water, generates 36 molecules of ATP from one molecule of glucose.  In contrast, anaerobic metabolism, in which glucose is converted to lactate (in the absence of oxygen), generates only 2 molecules of ATP.  ATP is the high energy molecule that provides the immediate fuel for muscle contraction.

 

Hadd and Maffetone imply that training the anaerobic system can damage the aerobic system.  Closer consideration of the aerobic and anaerobic metabolic pathways makes this very unlikely. 

 

The first important point is that the enzymes involved in anaerobic metabolism are mostly the same enzymes as those involved in the first stage of aerobic metabolism.  In the first stage, glucose is converted to pyruvate.  In the absence of oxygen, pyruvate is converted to lactate by an enzyme known as lactate dehydrogenase (LDH).  LDH is the only enzyme unique to anaerobic metabolism; all others are also part of the aerobic system.  However, as we shall see, LDH has very little ability to control the fate of pyruvate.  It is noteworthy that the production of lactate is also accompanied by the generation of hydrogen ions (i.e. increased acidity) and as discussed in my post on Maffetone on 5^th April, this might contribute to a decreased efficiency of fat metabolism and possibly also decreased electro-mechanical coupling within the muscle, during that training session.

 

When oxygen is available, the pyruvate enters the cycle of chemical processes delineated by Sir Hans Krebs.  Within the Krebs cycle the carbon atoms of pyruvate are converted to carbon dioxide while spare electrons are transferred to a carrier molecule called NADH.  NADH is then processed along a ‘conveyer belt’ known as the respiratory chain in which is it is oxidized by a group of enzymes known collectively as cytochrome oxidase, and in the process, a large amount of ATP is generated.  This process occurs within the organelles known as mitochondria.  One of the main goals of aerobic training is to increase the numbers of mitochondria in muscle cells, and thereby increase the amount of cytochrome oxidase.

 

Perhaps the crucial question that must be addressed in assessing the plausibility of the claims of Maffetone and Hadd is: might improvement of anaerobic metabolism interfere with aerobic metabolism?  The answer is no.  In fact the opposite is the case: aerobic metabolism switches off anaerobic metabolism.  This is known as the Pasteur effect, in honour of Louis Pasteur, who is famous for developing our understanding of germs and inventing the food sterilizing process known as pasteurization, but among other things, spent a great deal of time investigating energy metabolism in brewers yeast.  

 

When oxygen is present, and the ATP level is below the maximum required, pyruvate is voraciously sucked into the Krebs cycle and converted to carbon dioxide, meanwhile feeding electrons into the respiratory chain and generating large amounts of ATP.  The crucial question is what enzyme controls the rate of progress of glucose along the path towards pyruvate.  The main regulator is an enzyme called phosphofructokinase (PFK) which is responsible for one of the early steps along the path.  PFK is strongly controlled by the level of ATP.  When the ATP level is below full, PFK works at top speed promoting the conversion of glucose to pyruvate.  If there is any oxygen available, the pyuvate immediately enters the Krebs cycle ultimately generating 36 molecules of ATP per molecule of glucose.  If there is no oxygen available, LDH converts the pyruvate to lactate producing a net output of 2 molecules of ATP per glucose molecule.  When ATP levels are adequate, PFK slows down thereby slowing glucose metabolism.  So, the crucial regulator is an enzyme that in shared by the aerobic and anaerobic pathways.  The unique enzyme of the anaerobic system, LDH, responds passively to the level of pyruvate.  Even if it were possible to produce extra LDH by anaerobic training, this would have minimal influence on the fate of pyruvate.

 

The bigger picture

So the biochemistry suggests that training the anaerobic system does not damage the aerobic system.  Of course, the bigger picture must take account of other issues.  As Dudley’s rats showed us, if you want to maximize the development of the mitochondria in slow twitch fibres, then this can be achieved with least amount of stress by training at the relatively slow paces where slow twitch fibres are optimally recruited.  Training at higher paces will produce some development of mitochondria in slow twitch fibres, and will also develop the aerobic capacity of the type 2A (aerobic fast twitch fibres)  This is also useful and does not damage the aerobic capacity of the slow twitch fibres. 

 

The acidity produced by anaerobic metabolism does potentially have an adverse effect on fat burning and perhaps also on electro-mechanical coupling during the current session.    However, there is no evidence to suggest that this damages previously developed aerobic capacity.  Furthermore, Dudley’s rats and also studies of mixed aerobic and anaerobic training in humans (see for example the study by Ingjer, J. Physiol. vol 294, pp. 419-432, 1979) demonstrate that the aerobic capacity of slow twitch fibres is actually enhanced by training that includes moderate amounts of anaerobic running.

 

However, the even bigger picture includes the role of hormones such as cortisol.  As discussed in my recent comparisons of Lydiard and Maffetone, cortisol is a catabolic hormone that breaks down muscle protein.  Large amounts of stressful training , especially large amount of anaerobic training, will elevate cortisol, and undo the gains of the conditioning phase.

 

So in conclusion, after considering the arguments of both Maffetone and Hadd, I can see no reason for avoiding moderate amounts of running near or even above the lactate threshold during the conditioning phase, provided excess cortisol production is avoided.  The safest way to train in the conditioning phase is to spend most of the time in the lower part of the aerobic zone, but you do not need to slow to a walk up hills for fear of going anaerobic.  As far as I can see Hadd’s training program is effective, and much nearer to Lydiard than Maffetone, but I cannot find much support for his apparent concern with the need to avoid exceeding the lactate threshold.