Cardiovascular and muscular plasticity in an endurance‐master athlete following 12 weeks of detraining and retraining: a case study

This study examined the cardiorespiratory and muscular adaptations of a 53‐year‐old endurance master athlete following 12 weeks of detraining and retraining. Data were collected before and after detraining, and after retraining. Maximal oxygen uptake (VO2max) was evaluated during maximal cycling exercise. Proteins involved in muscle contraction, mitochondrial function and glycolysis were investigated using western blot analysis. VO2max decreased by 7% after detraining and was 5% greater than baseline after retraining. Detraining induced an important increase in the ryanodine receptor type 1 protein levels (RyR1, +44%) with a decrease in the protein levels of its stabilizer FKBP12 (−24%). We observed a 138% increase in the sarco‐endoplasmic reticulum ATPase 1 protein and a 42% increase in the myosin heavy chain fast‐twitch protein in response to detraining. This was associated with depressed levels of the mitochondrial biogenesis and oxidative phosphorylation (OXPHOS) proteins, while the expression of the mitochondrial dynamic proteins appeared stimulated. Twelve weeks of retraining reversed almost all the alterations observed in muscle proteins, but specifically increased mitochondrial biogenesis, OXPHOS and antioxidant defence proteins as well as the glucose transporter 4 (Glut‐4, +36%) and hexokinase (+100%) proteins levels above the baseline. The mitochondrial dynamic proteins were further increased with the retraining. These data provide novel information on cardiorespiratory and muscular plasticity, suggesting that highly endurance‐trained athletes might show substantial muscular adaptations while retrained after a detraining period and call for more extensive clinical trials.