Endurance but not resistance training increases intra‐myocellular lipid content and β‐hydroxyacyl coenzyme A dehydrogenase activity in active elderly men

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Endurance and resistance training (ET and RT, respectively) in older subjects have been proven beneficial against metabolic or cardiovascular disorders and against sarcopaenia respectively. Like ET, RT may also increase muscle oxidative capacities. In addition, it could be questioned whether RT, similarly to ET, is able to increase muscle energetic stores such as intra-myocellular lipids (IMCL) and glycogen contents. To evaluate a possible ET- and RT-induced parallel increase in oxidative capacity and energetic stores, active elderly men (72 ± 2 years) were submitted to a 14-week training programme (three times week(-1) ) combining lower body endurance and upper body resistance. Muscle samples were collected in ET vastus lateralis (VLat) and RT deltoid (Del) muscles before and after training. IMCL and glycogen contents were assessed by histochemistry (Oil Red O and periodic acid-Schiff staining, respectively) and by biochemical assay for glycogen. Citrate synthase (CS, marker of mitochondrial citric acid cycle), β-hydroxyacyl coenzyme A dehydrogenase (β-HAD, beta-oxidation) and phosphofructokinase (PFK, glycolytic pathway) activities were determined and so was the capillary interface index (LC/PF). Both training regimens significantly increased CS and LC/PF in ET-VLat and RT-Del. IMCL content and β-HAD activity increased (P < 0.05) only in ET-VLat, whereas PFK activity increased (P < 0.05) only in RT-Del. Glycogen content was not significantly altered in response to training in both muscles. Unlike RT, which induced an increase in PFK, ET is able to increase IMCL content and β-oxidation capacity in active elderly men, even though both training may improve CS activity and LC/PF.