Detraining (or what happens when we stop training)
By Iñigo Mujika
According to the principle of training reversibility, regular physical training induces various physiological adaptations that improve sports performance, whereas cessation or a major reduction in training brings about a partial or complete loss of these adaptations, thus compromising sports performance. In other words, the principle of reversibility is the principle of detraining. The training process and competition plans of athletes are often disrupted by illness, injury, rest periods or other factors that may induce a reduction or stoppage of usual levels of physical activity. It is therefore important to identify the effects and understand the mechanisms responsible for the changes that occur in an athlete’s physiological capacities and sports performance.
Definition of detraining
Detraining is defined as the partial or complete loss of anatomical, physiological and performance adaptations induced by training, as a consequence of training reduction or cessation.
Physiological characteristics of detraining
1. Cardiorespiratory detraining
Maximal oxygen uptake falls in highly trained athletes after four weeks of insufficient training. This reduction occurs because of an almost immediate reduction in total blood volume and plasma volume, the latter caused by a reduction in the content of plasma proteins. The increase in exercise heart rate at maximal and submaximal intensities is not sufficient to counterbalance the reduction in systolic stroke volume, and maximal and submaximal cardiac output drops, whereas it may increase at rest. Cardiac dimensions, including ventricular volumes and wall thickness, are often reduced. Blood pressure and total peripheral resistance increase, and ventilatory efficiency usually diminishes after short periods of training cessation.
2. Metabolic detraining
From a metabolic point of view, one of the main consequences of insufficient training is a trend towards a higher reliance on carbohydrates as a substrate for active muscles. Even a shortlasting period of insuffcient training induces an increase in the respiratory exchange ratio at maximal and submaximal intensities. Glucose tolerance and whole-body glucose uptake are rapidly and markedly reduced, due to a decline in insulin sensitivity coupled with a reduced muscle GLUT-4 transporter protein content. Muscle lipoprotein lipase activity decreases while it increases at the adipose tissue level, thus favouring the storage of adipose tissue. In addition, the training-induced antiatherogenic lipoprotein profile is reversed. Blood lactate concentration increases at submaximal exercise intensities, and the lactate threshold is apparent at a lower percentage of maximal oxygen uptake. These changes, coupled with a base deficit, result in a higher post-exercise acidosis. Trained muscle’s glycogen concentration suffers a rapid decline, reverting to sedentary values within a few weeks of training cessation.
3. Muscular detraining
Skeletal muscle is a tissue characterised by its dynamic nature and extraordinary plasticity, which allows it to adapt to variable levels of functional demands. When these demands are not sufficient to maintain the adaptations induced by training, muscular detraining occurs. This implies alterations in both muscle structure and function. Capillary density, fiber type distribution and cross-sectional area, arterio-venous oxygen difference, and even myoglobin concentration could be reduced in athletes within a few weeks of training cessation, but this is unlikely to happen during poorly planned tapering periods. On the contrary, rapid and progressive reductions in oxidative enzime activities have been observed in swimmers.
4. Detraining and performance
The general loss in cardiorespiratory fitness, metabolic efficiency and muscular respiratory capacity induces a rapid fall in an athlete’s endurance performance. This has been shown, for example, by the loss in performance measures in maximal swim tests. Strength production diminishes slowly in parallel to a reduction in electromyographic activity, but elite athletes’ eccentric force and sport specific power can fall significantly during periods of inactivity shorter than two weeks. The negative effects of complete inactivity can be countered by reduced training strategies, cross-training and the cross-transfer effect.