High intensity v low intensity training for the heart

My post on 20th June looked at the evidence  that training can produce both cardiac hypertrophy and increased blood supply to the heart muscle – the combination  of features that distinguish healthy hypertrophy for the unhealthy hypertrophy seen in some cases of cardiovascular disease.  The evidence from studies of pigs on treadmills and novice runners following a moderately demanding aerobic program is that several months of aerobic training can produce a substantial increase in the mass of the left ventricle – eg a 15% increase in mass after 6 months training in Rodriguez’s study of healthy but previously untrained young men (Am J Cardiol. 97:1089-92, 2006). This increase was associated with increased ventricular diameter and increased thickness of the muscular walls of the heart.  There was an associated increase in VO2max, a direct measure of aerobic capacity and a strong predictor of performance over middle and long distances.

Naylor’s study of elite athletes also demonstrated an increased ventricular mass after 6 months training in elite athletes (J Physiol 563; 957-963, 2005), but the increase was less than in the novices studied by Rodriguez and there was a disconcerting observation that despite pre-existing hypertrophy from previous years of training, at the beginning of the study (after a 6 week lay-off) the elite athletes had evidence of slower filling of their ventricles, which would reduce the capacity to utilize the additional muscle mass effectively.

 The contrast between the studies by Rodriguez and Naylor demonstrates that the benefits of a training program vary depending on the prior training status of the athletes.  Consequently, it is difficult to provide a clear answer to a very simple question: what form of training is likely to be most beneficial for improving cardiac function.

 The alternative to examining the results of studies of training programs is to examine what we know about the mechanism of hypertrophy.  Unfortunately, rapidly growing knowledge about the mechanisms by which the body responds to training has revealed just how complex these mechanisms are.  On account of the scope for unpredictable interactions between many variables, prediction of the final outcome on the basis of simple theory is unreliable.   My own view is that the most sensible approach is to combine what we know about mechanisms with the evidence from studies of training, and test that against one’s own experience – since  no two individuals are identical in genes and experience and therefore each person has to find out what works for him or her.

 

Speculation based on theory

First we need to ask what variable is of greatest interest.  For the middle and long distance runner, the most important demand on the heart is to deliver a large volume of blood bearing oxygen – the capacity to do this is known as cardiac output – the volume of blood delivered per minute.  This is the product of heart rate and stroke volume.  From the point of view of aerobic performance, the ultimate measure  is VO2 max, the maximum rate of utilization of oxygen. This is calculated by multiplying  cardiac output by oxygen extraction fraction.  Oxygen extraction fraction is a property of the skeletal muscles determined by capillary density and density of mitochondria in the skeletal muscle.  But for the present purpose we are concerned about training the heart.  Therefore, the trainable quantity if greatest interest for our present discussion is stroke volume.

The acute effect of ventricular filling

 Stroke volume is determined largely by the diameter of the ventricles but also by the efficiency of filling of the ventricles and the power to eject blood from the ventricles.  One of the important features of the function of cardiac muscle is the fact that stretching immediately prior to contraction produces a more powerful contraction – this is the Frank-Starling principle. As heart rate and cardiac output rise in response to demand for oxygen in the muscles, the return of blood from the periphery rises, greater stretching occurs during filling, and a more powerful contraction is produced.  In a trained athlete, stroke volume normally increases as the  cardiac output, and therefore the amount of blood returned to the heart, increases, reaching its maximum when heart rate reaches its maximum. 

In the early phases of training, increase in blood volume leads to greater filling and more powerful contraction.  Incidentally, either dehydration or the forcing of fluid into body tissues that accompanies an increase in blood pressure, decreases the volume of blood returned to the heart, so stroke volume falls and heart rate needs to rise higher to compensate to maintain a given cardiac outpt. VO2 max will be truncated because maximum heart rate does not change substantially. 

 The long term effects of ventricular filling

 Not only does increased cardiac filling promote an immediate rise in force of contraction, but the stretching of the heart muscle at the end of the filling phase (diastole) acts as a trigger to hypertrophy, apparently via the Akt signaling within the heart muscle cell, which ultimately leads to both the generation of additional contractile proteins and also the parallel development of capillaries, as discussed in my blog a few days ago.  This hypertophy will lead to an increase in both the diameter  of the ventricles and also the thickness of the walls of the ventricles, as demonstrated in the study by Rodrigues et al (Am J Cardiol. 97:1089-92, 2006).

So the most efficient form of training for increasing stroke volume and for the associated development of capillaries supplying the heart muscle is likely to be fairly vigorous exercise that produces a large amount of filling of the ventricles during diastole.  It would be expected that the  greatest benefit per unit of time spent training will be gained by training near VO2 max – though of course the overall picture must take into account the risks  associated with training at this level.  We will return to that issue again in the future.

The myoglobin effect

However one additional point needs to be made. If training is to be above the lactate threshold, then each effortful interval must be relatively brief – but not too brief, because of the phenomenon of buffering by myoglobin. At the beginning of an effortful interval, oxygen attached to myoglobin in the muscles can meet the metabolic needs for a period of a minute or so, so the demand for cardiac output does not reach a peak until about two minutes after the start of the effort.  Therefore, one might expect that intervals of three or four minutes duration would proved the best value for time spent (though alternatively one might do shorter intervals if the rest period is very short (eg 10-20 sec) so that myoglobin is only partially  replenished during the rest period).

 Matching observation to theory

How does observation match theory?  There are very few studies that have directly compared the changes in stroke volume after a program of high intensity interval training compared with lower intensity aerobic training. The only one I know of is by Helgerud and colleagues from Trondheim in Norway (Med Sci Sports Exerc. 39(4):665-71; 2007). They randomly allocated 40 moderately trained male participants (with initial VO2 max around 60 ml/min/kg)  to one of four training groups for 3 sessions per week for 8 weeks:

 1) long slow distance (LSD) (70% maximal heart rate);

2) lactate threshold (85% HRmax);

 3) 15:15 interval running (15 s of running at 90-95% HRmax followed by 15 s of active resting at 70% HRmax); a session included 47 x15 s effort intervals.

4) 4 x 4 min of interval running (4 min of running at 90-95% HRmax followed by 3 min of active resting at 70%HRmax).  

The amount of work in each session was adjusted to that the total oxygen consumption was similar is all four groups. 

The two interval training programs resulted in a significantly greater improvement of VO2max (5.5% for 15:15 and 7.2% for 4 x 4 min intervals than the low intensity aerobic and lactate threshold sessions. Furthermore stroke volume increased by approximately 10%  after each of the high intensity interval programs.  Thus, it appears that compared with low intensity aerobic or lactate threshold training, high intensity interval training produces greater improvements in VO2 max  and parallel increases in stroke volume, in accord with expectation based on theoretical considerations.

 High intensity is best, but in moderation

Thus the most efficient from of training for producing an increase in stroke volume and VO2 max appears to be high intenirty interval training.   This certainly does not mean that a training program should consist entirely of high intensity sessions for two reasons.  First, it is necessary to take account of the need to train the leg muslces as well. Increasing capillaries and mitochondria in leg muscles, and also developing the ability to withstand eccentric contractions of the leg muscles for the duration of the intended race are also important aspects of optimizing racing performance.  At least for long races (half-marathon and marathon) training the leg muscles to cope with multiply repeated eccentric contractions at each footfall is crucial, and this requires a substantial training volume.  The second issue is avoiding too much stress on the heart.  The crucial issue here is maintaining heart rate variability (HRV).  HRV can be improved by training, but both excessive volume and excessive intensity of training can impair HRV.  I will examine this issue in more detail in my next posting.

 Nonetheless the simple conclusion with regard to increasing cardiac output is that both medium intensity aerobic training (as employed in the study by Rodriguez, considered in my post on 20th June) and high intensity interval training can produce benefits, but high intensity interval training is the more efficient.

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2 Responses to “High intensity v low intensity training for the heart”

  1. Ewen Says:

    Thanks Canute. Higher intensity does sound more efficient as ‘heart training’, although the body would need to be ‘mechanically’ strong enough to withstand the demands of such training.

    The short recovery intervals would seem very useful to avoid the myoglobin effect – I know sessions like ‘Mona fartlek’ and ‘Deek 400s’ use fairly fast float recoveries between hard efforts – in the case of Deek, his 200 recoveries were in 40 secs (3:20/k pace).

    Thanks for your comment on the video – it’s always interesting to see where people run. The countryside is actually a little greener than it has been! I’ll do one in drier times for comparison.

  2. Ewen Says:

    A correction, just checked the book and his 200 recoveries were in 45 secs, between 400s of 62-64 seconds, so 3:45/k pace for the recoveries.

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