The Role of ROS and Calcium for the Prolonged Force Depression after Eccentric Contractions

Abstract

We recently showed that metabolically demanding high-intensity interval training results in a prolonged force depression due to increased production of reactive oxygen species (ROS) leading to defective cellular Ca2+ handling. A prolonged force depression can also be induced with mechanically demanding exercises, and we hypothesized that this deficiency also involves changes in ROS and Ca2+. To test this hypothesis, human subjects performed mechanically demanding drop jumps, which induced a prolonged force depression especially at low stimulation frequencies: 24 hours after exercise force was decreased by ∼40% at 20 Hz and ∼20% at 100 Hz. Contrary to our hypothesis, we observed no signs of ROS-induced protein modifications after the drop jumps, as judged from no significant changes in the extent of malondialdehyde or carbonyl binding to protein. There was no significant change in the expression of the two key proteins in the control of sarcoplasmic reticulum Ca2+ release (the ryanodine receptor 1 (RyR1) and the dihydropyridine receptor), but there were minor changes in the amount of FKBP12 bound to RyR1 (an early increase followed by a decrease). In conclusion, the long-lasting force depressions after mechanically demanding drop jumps is not accompanied by any obvious signs of ROS-induced damage or Ca2+ dysregulation, which is in contrast to the situation after metabolically demanding exercise.