detraining

Detraining - why a change really is better than a rest

At a glance:

  • Detraining affects different aspects of fitness in different ways;
  • The extent of detraining will depend on the length of inactivity and your training background;
  • Detraining in elite athletes may produce steeper declines in fitness and require longer periods of retraining than was thought;
  • Strategies to reduce detraining during extended lay-offs should be considered.

The old adage that ‘what goes up must come down’ applies just as much to fitness as to gravity. But although athletes have come to accept detraining as a depressing but inevitable consequence of an injury or illness, few are aware of just how profound and rapid these changes are. And according to Richard Godfrey, new evidence suggests that the magnitude of these changes means that elite athletes need to plan their return to full fitness after a lay-off very carefully indeed.

Detraining (often referred to as ‘reversibility’) reflects the fact that if a training stimulus is insufficient, or removed entirely, then the aspect of physiological conditioning to which it relates begins to decline. In other words, the individual begins to lose ‘fitness’. However, ‘fitness’ is a difficult term to define because we often find ourselves asking ‘fit for what?’ Better terms are ‘conditioning’, ‘level of conditioning’ or ‘conditioned state’ and so here these terms will be used interchangeably with ‘fitness’.

In general, the removal of a training stimulus produces a significant loss in conditioning after two to six weeks. In addition, it is simply not possible to train all aspects of physiology simultaneously, hence the concept of periodisation, first introduced by the Russian, Matveyev, in the 1960s (1).

To date, the vast majority of detraining research has focused on club level athletes – hardly surprising as it’s very difficult to convince elite athletes to stop training just to allow scientists to get a feel for the consequences. For the first time, however, this article will present findings from an elite athlete – the author’s own research data on the detraining and retraining of an Olympic gold medallist rower.

Effects of detraining on the major physiological systems

Cardio-respiratory detraining

Maximal oxygen uptake (VO2max) has been shown to decline by anything from 4-20% with inactivity of two weeks or more (2-5). VO2max has two major components: maximal cardiac output (Qmax – litres per minute) and the maximal rate of oxygen uptake and consumption in the working muscles. This explains why two types of training improve VO2max. High intensity intervals (heart rate greater than 90% of max) of two to four minutes are used to improve Qmax and long slow distance (LSD) training is used to improve oxygen uptake and consumption in the muscles.

With detraining of endurance-trained athletes blood volume is reduced by 5-12% within the first two days (6). This reduction in blood volume is the primary reason for the observed rapid decline in cardiovascular function (4). As a direct result there is a decrease in cardiac output (amount of blood pumped per minute) and stroke volume (amount of blood pumped per beat) with an attendant increase in heart rate during submaximal exercise – consistent with the equation

cardiac output = heart rate x stroke volume

The dimensions of the heart have been found to decrease in parallel with stroke volume during eight weeks of inactivity, with left ventricular posterior wall thickness decreasing progressively by 25% and left ventricular mass decreasing by almost 20% in the first three weeks.

Respiratory function is also altered with inactivity. Maximal voluntary ventilation has been shown to decrease by 10-14%, while in the longer term the ventilatory response to increasing carbon dioxide levels increases after two years without training. It also appears that the energy cost of breathing is increased with detraining as increasingly more blood flow is ‘stolen’ by respiratory muscles working at more than 55% of forced vital capacity (7,8).

Metabolic detraining

Respiratory exchange ratio (RER) is calculated from the amount of oxygen consumed versus the amount of carbon dioxide produced during exercise, and gives an indication of which fuels (fat, carbohydrate and protein) predominate. After detraining has occurred, there’s a comparative increase in the amount of carbohydrate used as fuel during both maximal and submaximal exercise, with less energy derived from fat (12,14).

Whole-body insulin sensitivity is reduced with detraining and so there is a rapid reduction in glucose uptake (10,15,16). This may be as a result of a reduced muscle GLUT-4 content, which has been shown to decrease in the first 6-10 days by 1733% (15,16). GLUT-4 is a glucose transport protein that is normally found inside muscle cells. In well-conditioned individuals, however, GLUT-4 responds to muscle contraction or to blood-borne insulin by moving to the muscle cell membrane where it can enhance transport of blood glucose into the muscle cell.

As a consequence of hard training at or close to lactate threshold for a number of weeks, two main adaptations occur providing evidence of improved endurance: reduced submaximal blood lactate and a higher exercise intensity before lactate threshold is reached (see box below). However, with detraining the opposite occurs, and higher blood-lactate concentrations have been measured in swimmers and in endurance-trained runners and cyclists at a lower percentage of VO2max after just a few days of inactivity. However, when compared to sedentary individuals, those previously highly trained still have a lactate threshold at a higher percentage of their VO2max, even after detraining.

Exercise physiology concepts

Oxygen economy

The amount of oxygen used at a standardised exercise intensity. In runners this tends to be measured on the treadmill at a speed of 16kph, in rowers 330 watts is often the exercise intensity used. When testing a number of weeks after the initial testing visit to the lab, an improvement in oxygen economy is deemed to have occurred where oxygen consumption at the standardised submaximal exercise intensity is lower than it was previously.

Power at reference blood lactate values

In rowing, the power output at ‘reference’ blood lactate values of 2 and 4mM are often recorded. Where power output is improved at these same blood lactate values, it provides objective evidence of improvement.

Muscular detraining

In previously active individuals, four weeks without training results in muscle capillarisation returning to pre-training baseline but it still remains above that found in sedentary individuals (2,17). Oxygen uptake in muscles has been found to decrease by 8% and this is suggested to lead to the 9% decrease in VO2max observed after 3-12 weeks without training(2).

One effect of aerobic training on muscle is an increase in the volume of mitochondria, the organelles in cells responsible for aerobic energy production. With detraining, the volume of mitochondria is reduced. However, before that occurs, the activity of the oxidative enzymes in the mitochondria can decline by 25-45% up to 12 weeks after training cessation (2,4,9,10,13,15,20).

With high-intensity strength and power training there is increased cellular signalling that dictates many molecular changes. These cause increases in protein synthesis of the larger fast- twitch fibres and hence, several weeks after beginning training, muscle hypertrophy accompanies the observed increases in strength and power. With detraining, however, muscle cross-sectional area decreases and there is an increase in the number of oxidative fibres (slow- twitch) versus glycolytic (fast-twitch) fibres in elite power lifters and body builders (18,19).

Fast-twitch fibres are generally classified as being of two types. Fast oxidative glycolytic fibres (FOG or type IIa) have both aerobic and anaerobic metabolic capabilities and are moderately fatigable. Fast glycolytic (FG or type IIx) have only a glycolytic capacity and are highly fatigable. In endurance runners and cyclists, detraining has been shown to result in a large change from fast-twitch IIa to IIx (13).

Hormonal detraining

Twelve weeks of inactivity has been shown to lead to a less efficient catecholamine response, that is an increased adrenaline and noradrenaline concentration during submaximal exercise at the same relative intensity (13). In plain English, the same exercise is more stressful after detraining. However, some strength-trained individuals showed some positive hormonal changes after 14 days of inactivity, with increased growth hormone and testosterone and decreased cortisol concentrations in the blood (21).

Detraining effects on performance

Detraining has a number of consequences for endurance performance. We know, for example, that swimming performance decreases when time is taken off between seasons (22). In soccer players, detraining is shown to decrease the time to exhaustion by 24% in five weeks (11). With long-term inactivity there can be a large decline or even a complete reversal of training-induced performance improvements. However, a relatively short break is generally not too bad and, providing the previous training adaptations were achieved with long-term (6-12 weeks) training, two weeks without training doesn't appear to produce a significant change in time to exhaustion.

Detraining in an athlete rower

The rower was tested in the laboratory on four separate occasions:

  • Just before the Olympics;
  • Eight weeks post-Olympics (during which no activity of any kind was undertaken);
  • 16 weeks post-Olympics (back in training for eight weeks);
  • 28 weeks post-Olympics (back in training for 20 weeks).

These tests allowed a detailed examination of the effects of eight weeks of detraining followed by 20 weeks of retraining.

Body composition was determined; fat was estimated from skin-fold thickness measurement and weight and height was measured. The exercise test was of the same design that the athlete has been used to for many years. After a warm-up the athlete completes a ‘step test’ of five 4-minute efforts, each step being at 25 watts higher than the previous one (see figure 1). Between each step there was a 30-second rest during which blood lactate was measured. After the fifth step there was a 2.5-minute rest and then the athlete was asked to complete four minutes at a reasonably steady pace but to cover as much distance as possible in that time (see figure 2). Throughout the test oxygen consumption, heart rate and power output was measured.

Figure 1. Exercise protocol or ‘step test’ used with rowers

Figure 1. Exercise protocol or ‘step test’ used with rowers

Figure 2. An example of the submaximal portion of the lactate/work curve

Figure 2. An example of the submaximal portion of the lactate/work curve

Effects of detraining>

With eight weeks of complete inactivity the following changes were recorded:

  • The athlete lost 2kg in body weight;
  • Estimated percentage body fat remained the same (demonstrating a loss of muscle mass);
  • VO2max decreased by 8%;
  • Power at VO2max decreased by 20%;
  • Oxygen economy had decreased by 6%;
  • Power at reference blood lactates of 2 and 4mM (see figure 2) declined by 27% and 22% respectively;
  • Power at lactate threshold was 30 watts lower than it had been just before the Olympics.

Effects of retraining>

After eight and 12 weeks of retraining the rower had put on 2kg of muscle and body fat was unchanged. VO2max increased by 4% in the first eight weeks of retraining but this value increased only slightly during the next 12 weeks. In fact, after 20 weeks of retraining VO2max was still 4.4% less than the pre-Olympic value.

Power at VO2max increased by 15% in the first eight weeks of retraining and had returned to pre- Olympic values when retested 12 weeks later. After eight weeks of retraining, oxygen economy was back to the levels measured just before the Olympics. Power at a blood lactate reference value of 2mM was within just 4% of pre-Olympic values after 20 weeks, whilst power at 4mM was slightly better than pre-Olympic values after 20 weeks.

What does it all mean?

The decline seen in VO2max after detraining is very similar in our elite athlete when compared with sub- elite athletes. However, muscular power in our elite athlete seems to show a much larger decline (more than double). This study indicates that detraining is just as much of a problem for elite athletes as it is for the sub-elite. In fact, with respect to muscular power it may be even more of a problem.

Although it’s clear that the longer it takes to become well conditioned, the longer it takes to lose it, there’s little doubt that any prolonged period of inactivity will result in physiological and, ultimately, performance decline. Moreover, little work exists about the appropriate time-course for regaining physiological conditioning after a lay-off. Clearly though, it’s a ‘long road back’ and these findings suggest that the time-course for regaining top-level condition should not be guessed at, but rather assessed through regular monitoring and testing. Because practical realities might make this difficult, careful planning and restriction of time off may be required.

Taking time off

If your aim is to perform well over the longer term, or if you simply wish to improve your level of conditioning (‘fitness’) over a number of years then it is probably best to have no more than two weeks of complete inactivity at any one time. A better alternative would be to have a change of some kind, perhaps by performing some cross- training, or a completely different mode of activity. The old adage ‘a change is as good as a rest’ springs to mind – indeed given the detraining effects of complete inactivity, a change of activity is almost certainly better than an extended period of complete rest!

Dr Richard Godfrey is a senior research lecturer at Brunel University and has previously spent 12 years working as a chief physiologist for the British Olympic Association

References

  1. Fundamentals of sports training. Moscow: Progress, 1981
  2. J Appl Physiol 1984; 17:230-237
  3. J Am Coll Cardiol 1986; 7:982-989
  4. J Appl Physiol 1987; 63:1719-1724
  5. J Sports Cardiol 1986; 3:35-45
  6. J Appl Physiol 1986; 60:95-99
  7. Med Sci Sports 1974; 6:20-25
  8. Eur J Appl Physiol 1990; 60:353-359
  9. Int J Sports Med 1992; 13:572-576
  10. J Appl Physiol 1993; 74:776-781
  11. Res Q. 1969; 40:502-508
  12. Med Sci Sports 1972; 4:91-95
  13. J Appl Physiol 1985; 59:853-859
  14. J Sports Cardiol 1986; 3:35-45
  15. J Appl Physiol 1994; 77:1532-1536
  16. J Appl Physiol 1996; 80:240-244
  17. Acta Physiol Scand 1981; 113:9-16
  18. J Neurol Sci 1981; 51:247-257
  19. J Appl Physiol 1994; 77:1532-1536
  20. J Sports Med 1986; 26:92-100
  21. Med Sci Sports Exerc 1993; 25:923-935
  22. Can J Appl Physiol 1995; 20:395-406

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