Detraining and Retention of Training-Induced Adaptations

Use it or Lose it!!!

Key Points

• Improvements in VO2 max and muscle mitochondrial function produced by endurance training of mild-to-moderate intensity and duration vanish after several months of inactivity.

Key Points

• When people refrain from exercise after several years of intense and prolonged training, they display large reductions in blood volume, stroke volume, and VO2 max during the first three weeks of inactivity.

Key Points

• After two to three months of inactivity, endurance-trained athletes display no loss of muscle capillary density and only a partial loss of mitochondrial enzyme activity with values stabilizing at about 50% above values noted in untrained subjects.

Key Points

• Additionally, VO2max and the max a-vO2 difference stabilize at a point that remains 12% to 17% higher than levels found in untrained subjects.

Key Points

• It is not known whether the differences noted between experienced athletes and “novice” subjects are attributable to the influence of long-term training or by genetic differences.

Reversibility

• The principle of reversibility holds that when physical training is stopped or reduced, the body readjusts in accordance with the diminished physiological demand, and the beneficial adaptations may be lost.

VO2max

• Maximal oxygen uptake in highly trained athletes declines rapidly during the first month of inactivity, whereas a slower decline to untrained levels occurs during the second and third months of detraining.

VO2max

• Some of the factors responsible for the decline in VO2max include:

• A rapid reduction in maximal stroke volume.

• A more gradual decline in maximal a-vO2 difference.

VO2max

• There is some indication that capillary density and muscle mitochondrial activity decline to a lesser degree.

Stroke Volume

• The rapid decline in stroke volume seen with detraining is caused by a reduction in diastolic filling.

Blood Volume

• The rapid reduction in diastolic filling during upright exercise in detrained subjects is related to a decline in blood volume.

Blood Volume

• Reduction in intrinsic heart function is apparently minimal after several weeks of inactivity in people who have trained intensely for several years.

Blood Volume

• The large reduction in stroke volume during exercise in the upright position is apparently caused by a decline in blood volume and not by a deterioration of heart function.

Muscle Metabolism

• Adaptations in mitochondrial activity will be totally reversed by detraining.

Muscle Metabolism

• This will occur within 1-2 months of inactivity.

• People who have trained for longer periods experience less of a reduction.

Muscle Capillarization

• It appears that the increased capillary density observed in highly-trained people is not lost during 3 months of detraining.

Summary

• The detraining responses in skeletal muscle differ between highly-trained people and those who have trained for only a few months.

Summary

• No loss in muscle capillary density occurs with the cessation of prolonged, intense training, although a loss does occur when moderate training is stopped after a few months.

Summary

• The cessation of short-term training results in a complete reversal of the training-induced increase in mitochondrial enzyme activity, whereas only a partial decline occurs with detraining after years of intense endurance training.

Summary

• We cannot discount the possibility that the persistent elevated mitochondrial enzyme and capillary density of the detrained athletes who had undergone years of strenuous training, may be a result of genetic characteristics.

Summary

• Additionally, we do not yet know the maximal length of time that these adaptations persist following the cessation of training.

Summary

• After approximately 8 weeks of detraining, one exhibits the same capacity for exercise as those who have never trained.

Reduced Training

• Detraining produces more marked effects than reduced training.

Reduced Training

• Individuals who reduce their training levels have the potential to more effectively maintain cardiovascular and metabolic adaptations.

Reduced Training

• In fact one study demonstrated that training induced changes in VO2max and heart size can be maintained when training frequency is reduced from 6 to 2 days per week, provided that the intensity of the maintenance exercise is high (85%-100%).

Retraining

• The limiting factor in determining the time course of retraining may well be the rate of increase in mitochiondrial enzyme activity.

Retraining

• Unfortunately, we do not yet know how rapidly the decline in mitochondrial activity can be reversed with renewed training.

Retraining

• It has been estimated that it might take longer than 40 days to return mitochindrial activity levels to the trained state.

The End