Detraining

Tapering, by reducing the training stimulus, can facilitate performance. What happens to highly conditioned athletes who have fine-tuned their performance abilities to peak level but then come to the end of their competitive season? Many athletes in team sports go into physical hibernation at this time. Many have been working 2 to 5h each day to perfect their skills and improve their physical condition, and they welcome the opportunity to completely relax, purposely avoiding any strenuous physical activity. But how does physical inactivity affect highly trained athletes?

Detraining is defined as the partial or complete loss of training-induced adaptations in response to either the cessation of training or a substantial decrement in the training load – in contrast to tapering, which is a gradual reduction of the peak training load over only a few days to a few weeks. Some of our knowledge about physical detraining comes from clinical research with patients who have been forced into inactivity because of injury or surgery. Athletes generally agree that suffering the pain of an injury is bad enough, but the situation is even worse when it forces them to stop training. Most fear that all they have gained through hard training will be lost during a period of inactivity. But recent studies reveal that a few days of rest or reduced training will not impair and might even enhance performance, similar to what we see with tapering. Yet at some point, training reduction or complete inactivity will decrease physiological function and performance.

Muscular strength and power

When a broken limb is immobilized in a rigid cast, changes begin almost immediately in both the bone and the surrounding muscles. Within only a few days, the cast that was applied tightly around the injured limb is loose. After several weeks, a large space separates the cast and the limb. Skeletal muscles undergo a substantial decrease in size, known as atrophy, when they remain inactive. This is accompanied by considerable loss of muscular strength and power. Total inactivity leads to rapid losses, but even prolonged periods of reduced activity lead to gradual losses that eventually can become quite significant.

Similarly, research confirms that muscular strength and power both are reduced once athletes stop training. The rate and magnitude of loss appear to vary by the level of training. Highly skilled accomplished weightlifters appear to have a rather rapid decline in strength within a few weeks of discontinuing intense training. With previously untrained people, strength gains can be maintained from several weeks up to over seven months. In a study of young(20-30 years) and older(65-75 years) men and women who trained for nine weeks, the increase in strength(1-repetition maximum) averaged 34% for the younger subjects and 28% for the older subjects, with no differences between men and women. After 12 weeks of detraining, none of the four groups had significant losses in strength from the end of the nine-week training program values. After 31 weeks of detraining, there was only an 8% loss in the younger subjects and a 13% decrease in the older subjects.

A study with collegiate swimmers revealed that even with up to four weeks of inactivity, terminating training did not affect arm or shoulder strength. No strength changes were seen in these swimmers, whether they spent four weeks at complete rest or whether they reduced their training frequency to one or three sessions per week. But swimming power was reduced by 8% to 13.5% during the four weeks of reduced activity, whether the swimmers underwent complete rest or merely reduced training frequency. Although muscular strength might not have  diminished during the four weeks of rest or reduced training, the swimmers might have lost their ability to apply force during swimming, possibly attributable to a loss of skill.

The physiological mechanisms responsible for the loss of muscular strength as a consequence of either immobilization or inactivity are not clearly understood. Muscle atrophy causes a noticeable decrease in muscle mass and water content, which could party account for a loss in the development of maximal muscle fiber tension. Changes occur in the rates of protein synthesis and degradation as well as in specific fiber type characteristics. When muscles aren’t used, the frequency of their neurological stimulation is reduced, and normal fiber recruitment  is disrupted. Thus, part of the strength loss associated with detraining could result from an inability to activate some muscle fibers.

The retention of muscular strength, power, and size is extremely important for the injured athlete. The athlete can save much time and effort during rehabilitation by performing even a low level of exercise with the injured limb, starting in the first few days of recovery. Simple isometric contractions are very effective for rehabilitation because their intensity can be graded and they do not require joint movement. Any program of rehabilitation, however, must be designed in cooperation with the supervising physician and physical therapist.

Muscular endurance

Muscular endurance performance decreases alter only two weeks of inactivity. At this time, not enough evidence is available to determine whether this performance decrement results from changes in cardiovascular capacity. In this section, we examine muscle changes that are known to accompany detraining and that could decrease muscular endurance.

The localized muscle adaptations that occur during periods of inactivity are well documented, but knowledge of the exact role that these changes play in the loss of muscular endurance still eludes us. We know that from postsurgery cases that after a week or two of cast immobilization, the activities of oxidative enzymes such as succinate dehydrogenase(SDH) and cytochrome oxidase decrease by 40% to 60%. Data collected from swimmers, shown in the figure below, indicate that the muscles’ oxidative potential decreases much more rapidly than the subjects’ maximal oxygen uptake with detraining. Reduced oxidative enzyme activity would be expected to impair muscular endurance, and this most likely relates to submaximal endurance capacity rather than to maximal aerobic capacity, or VO₂max.

In contrast, when athletes stop training, the activities of their muscles’ glycolitic enzymes, such as phosphorylase and phosphofructokinase, change little, if at all, for at least four weeks. In fact, Coyle and colleagues’ observed no change in glycolytic enzyme activities with up to 84 days of detraining compared with a nearly 60% decrease in the activities of various oxidative enzymes. This might at least partly explain why performance times in sprint events are unaffected by a month or more of inactivity, but the ability to perform longer endurance events may decrease significantly with as little as two weeks of detraining.

One notable change in the muscle during detraining is a change in its glycogen content. Endurance-trained muscle tends to increase its glycogen storage. But four weeks of detraining has been shown to decrease muscle glycogen by 40%. Figure below illustrates the decrease in muscle glycogen content after four weeks of inactivity, but the swimmers’ values decreased until they were about equal to those of the untrained people. This indicates that the trained swimmers’ improved capacity for muscle glycogen storage was reversed during detraining. 

Measurements of blood lactate and pH after a standard work bout have been used to assess the physiological changes that accompany training and detraining. For example, a group of collegiate swimmers were required to perform a standard-paced, 200 yd(183 m) swim at 90% of their seasonal best following five months of training and then to repeat this test at the same absolute pace once a week for the following four weeks of detraining. The results are shown in the table below. Blood lactate concentrations, taken immediately after this standard swim, increased from week to week during a month of inactivity. At the end of the fourth week of detraining, the swimmers’ acid-base balance was significantly disturbed. This was reflected by a significant increase in blood lactate concentrations and a significant decrease in the concentrations of bicarbonate(a buffer).

Blood lactate, pH, and bicarbonate(HCO3-) values in collegiate swimmers undergoind detraining
	Weeks of detraining
Measurement	0	1	2	4
Lactate(mmol/L)	4.2	6.3	6.8	9.7
pH	7.26	7.24	7.24	7.18
HCO3- (mmol/L)	21.1	19.5	16.1	16.3
Swim time(s)	130.6	130.1	130.5	130.0

Speed, agility, and flexibility

Training produces less improvement in speed and agility than it does in strength, power, muscular endurance, flexibility and cardiorespiratory endurance. Consequently, losses of speed and agility that occur with inactivity are relatively small. Also, peak levels of both can be maintained with a limited amount of training. But this does not imply that the track sprinter can get by with training only a few days a week. Success in actual competition relies on factors other than basic speed and agility, such as correct form, skill, and the ability to generate a strong finishing sprint. Many hours of practice are required to tune performance to its optimal level, but most of this time is spent developing performance qualities other than speed and agility.

Flexibility, on the other hand, is lost rather quickly during inactivity. Stretching exercises should be incorporated into both in-season and off-season training programs. Reduced flexibility has been proposed to increase athletes’ susceptibility to serious injury.

Cardiorespiratory endurance

The heart, like other muscles in the body, is strengthened by endurance training. Inactivity, on the other hand, can substantially decondition the heart and the cardiovascular system. The most dramatic example of this is seen in a study conducted on subjects undergoing long periods of total bed rest; they weren’t allowed to leave their beds, and physical activity was kept to an absolute minimum. Cardiovascular and metabolic function were assessed at a constant submaximal rate of work and at maximal rates of work both before and after the 20-day period of bed rest. The cardiovascular effects that accompanied bed rest included:

• A considerable increase in submaximal heart rate;
• A 25% decrease in submaximal stroke volume;
• A 25% reduction in maximal cardiac output;
• A 27% decrease in maximal oxygen consumption.

The reductions in cardiac output and VO2max appear to result from reduced stroke volume; this appears to be largely attributable to a decreased plasma volume, with reductions in heart volume and ventricular contractility playing a smaller role.

It is interesting that the two most highly conditioned subjects in the study(the two who had the highest    VO₂max values) experienced greater decrements in  VO₂max than the three less fit people, as shown in the figure below. Furthermore, the untrained subjects regained their initial conditioning levels(before bed rest) in the first 10 days of reconditioning, but the well-trained subjects needed about 40 days for full recovery. This suggests that highly trained individuals cannot afford long periods with little or no endurance training. The athlete who totally abstains from endurance training at the completion of the season will experience great difficulty getting back into top aerobic condition when the new season begins.

Inactivity can significantly reduce VO₂max. How much activity is needed to prevent such considerable losses of physical conditioning? Although a decrease in training frequency and duration reduces aerobic capacity, the losses are significant only when frequency and duration reduces aerobic capacity, thee losses are significant only when frequency and duration are reduced by two-thirds of the regular training load. However, training intensity apparently plays a more crucial role in maintaining aerobic power during periods of reduced training. Training at 70% VO₂max appears to be necessary to maintain maximal aerobic capacity.