Inspiratory Muscle Training: Ergogenic Benefits

Inspiratory muscle training as an ergogenic aid: the story so far

Since the first reports of an ergogenic effect of specific inspiratory muscle training (IMT) in the mid-1990s, researchers have not only demonstrated its efficacy beyond reasonable doubt, but are also beginning to understand how it works. Alison McConnell takes a look at the latest thinking on IMT, its ergogenic benefits, and why serious athletes neglect it at their peril...

Background

For those readers who are unfamiliar with IMT, we should perhaps take a small step back in time to set the stage for the following discussion. In the early days of research in this area, those of us with an interest in ventilatory limitations to exercise performance were viewed with what might politely be called scepticism.
The received wisdom has always been that there is no respiratory limitation to exercise performance; after all, maximal oxygen uptake is not limited by the transfer of oxygen across the lung, but by the ability to transport and utilise it. This being the case, what possible advantage could there be to increasing the ability of the respiratory pump muscles to ventilate the lungs? Furthermore, the respiratory muscles were thought to be ‘super human’, and immune to fatigue, by virtue of their continuous activity throughout life.

The first questions about these assumptions began to surface in the early-1990s, when compelling evidence emerged that the inspiratory muscles (specifically the diaphragm) exhibit fatigue in the same way that other skeletal muscles do(1). This was followed by evidence that the work and associated metabolic demands of the inspiratory muscles during intense exercise were far greater than anyone had anticipated(2). Not only that, but the inspiratory muscle would ‘steal’ blood (and oxygen) from the exercising limbs in order to meet their own metabolic demands(2).

Any coach who was confronted with such evidence would instantly conclude that the respiratory pump muscles were a dangerous weak link and warranted specific training. However, the sport scientists were so bogged down by their preconceptions about there being no respiratory limitation to maximal oxygen uptake that it took a further five years, as well as overwhelming direct evidence, to persuade them that IMT is genuinely ergogenic(3).

How IMT works

What is now emerging from the published literature is a clearer picture of just how IMT exerts its ergogenic effect. Well-conducted studies of IMT had demonstrated consistent changes (or lack of them) in a few key physiological outcomes after four to six weeks of IMT (3). These included no change in maximal oxygen uptake, but reductions in the intensity of breathing and whole-body effort sensations, as well as a lower blood lactate concentration and heart rate at equivalent intensities of exercise. These observations provided some vital clues about how IMT actually works and sparked a series of experiments to test the resulting hypotheses.

Changes in blood lactate concentration are reminiscent of the response to whole-body training, and lead to questions about an increase in the lactate threshold. We examined this question specifically in a carefully conducted study that used the most accurate and meaningful index of lactate turnover as the main outcome variable – the maximum lactate steady state (MLSS)(4). If lactate concentration is lower after IMT because the exercise intensity corresponding to MLSS (or the lactate threshold) increases after IMT then we would expect to see a measurable change in exercise intensity at which MLSS is achieved. In short, despite a significant reduction in the lactate concentration at the cycling power output that corresponded to MLSS, we did not observe any change in MLSS power. Our study was capable of detecting changes in MLSS power of as little as 2.5% (6 Watts). Thus, we concluded that IMT cannot operate via a mechanism linked to improvements in the lactate threshold.

Changes in heart rate and effort sensations hint that the cardiovascular strain of exercise may be reduced following IMT, but this is not because the oxygen cost of exercise is measurably lower, because this does not appear to change(5). However, the evidence that inspiratory muscles can ‘steal’ blood from locomotor muscles led some researchers to examine the interaction between inspiratory muscle work and cardiovascular control during exercise.

In an elegant series of experiments, researchers at the University of Wisconsin identified that when the inspiratory muscles are subjected to fatiguing bouts of work (breathing against an added external load), they provoke a reflex change in vasoconstrictor output to the limbs(6).

In other words, in the face of fatigue, the inspiratory muscles signal the cardiovascular control centres to divert blood away from the working limbs. This has a two-fold benefit from the viewpoint of the inspiratory muscles; firstly, it ensures that they get more blood and oxygen (protecting their vital function); secondly, by restricting blood flow to the working limbs, the supply of oxygen and removal of metabolic by-products is impaired, which leads to an enforced decrease in exercise intensity, or even cessation (reducing the ventilatory demand).

The most recent study from this group went on to show that if the work of breathing is manipulated during very intense cycling exercise that the severity of leg fatigue is also changed – if inspiratory muscle work is increased, then leg fatigue is increased, and if respiratory work is reduced (by allowing a ventilator to ‘breathe’ for the subjects) leg fatigue is reduced(7). This is entirely consistent with the inspiratory muscles maintaining a high position in the ‘pecking order’ for the supply of blood flow.
What we believe occurs after IMT is that the enhanced strength, power and fatigue resistance of the inspiratory muscles leads to an abolition or delay in the triggering of the reflex vasoconstriction. This mechanism is consistent with all of the physiological changes that arise after IMT.

Practical implications

The first question that most coaches ask me is, ‘How long does IMT take?’ There are two answers to this: 1) the training itself requires about three minutes twice per day; 2) performance improvements are measurable within four weeks(8).

Until we fully understand the mechanisms (the explanation given above is our best guess at this moment in time) it will not be possible to offer specific guidance on training regimens for different sports. However, what has been identified in the laboratory is a regimen that works for time trials of between six and 60 minutes duration, in rowing(8), cycling(5) and running(9) – ie 30-repetition maximum load executed with maximal effort. The latter is important because it ensures that the muscle recruitment is maximal – ie as many muscle fibres as possible are forced to contract against the load.

Aside from the laboratory based research, my dealings with athletes in a range of sports have also led me to identify a number of postural challenges that appear to benefit from ‘posture-specific’ IMT. For example, the sport I have worked most extensively with is rowing, which is probably one of the toughest sports for the respiratory system.

Rowers normally inhale at two points in the stroke (just before the catch and just after the finish), with the largest breath being just after the finish. Both of these points in the stroke impose restrictions on breathing. At the finish, the hips are extended and the shoulders are behind the hips. This means that the muscles of the torso (including the inspiratory muscles) must work against gravity to prevent the rower from falling backwards. At the same time, the rower needs to take a large, fast breath, which means that the inspiratory muscles are subjected to competing demands for postural stability and breathing.

Once the rower reaches the catch, he or she must take another breath, but in this position the movement of the diaphragm is impeded by the crouched body position. At the catch, the thighs push the liver, stomach and gut upwards against the diaphragm, compressing the abdomen. This compression makes it harder for the diaphragm to contract, flatten and move downwards, as it must do in order to inflate the lungs.

Once again, looking at this from a pragmatic point of view, the obvious thing to do is to train the inspiratory muscles under the conditions where they experience the greatest challenge.

Summary

A very successful and knowledgeable coach friend of mine describes the inclusion of IMT in his athletes’ training as a ‘no-brainer’. In his view, there’s nothing else that he can add to their training that requires so little time and provides such a large guaranteed benefit to their performance. He coaches indoor rowers, and has taken some of them to World Championship medals, so his opinion should count for something.

Scientists have seen IMT move from being the preserve of heretics (myself included), to a credible and intensely intriguing phenomenon that is now undergoing equally intense scrutiny. The next few years should see IMT really come of age, and as more coaches and athletes gain experience of manipulating the training to suit the demands of their own sports, the greater the benefits should be for sport as whole.

Finally, for the 20% or so of athletes who have asthma, it is worth mentioning that IMT is also becoming a well-established, drug-free method of managing asthma symptoms. Indeed, one IMT device has recently been made available on prescription (POWERbreathe®), thanks to its proven efficacy in clinical trials(11). So, for athletes with asthma, or those with borderline symptoms that don’t qualify for medication in competition, IMT could provide an even greater benefit.

Alison McConnell is currently professor of applied physiology at Brunel University. Her research interests are in respiratory limitations to
exercise performance

References
1. J Physiol 1993; 460:385-405
2. J Appl Physiol 1998; 85:609-18
3. Int J Sports Med 2004; 25:284-93
4. Eur J Appl Physiol 2005; 94:277-284
5. J Sports Sci 2002; 20:547-62
6. Journal of Physiology 2001; 537:277-289
7. J Physiol (Lond) 2005
8. Med Sci Sports Exerc 2001; 33:803-9
9. Eur J Appl Physiol 2004; 93:139-44
10. Sports Med 2003; 33:407-26
11. Chest 2005; 128:3177-82

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