Power loss is greater following lengthening contractions in old versus young women

Compared with isometric and dynamic velocity-constrained (isokinetic) tasks, less is known regarding velocity-dependent (isotonic) muscle power and recovery in older adults following repeated fatiguing lengthening contractions. We investigated voluntary and evoked neuromuscular properties of the dorsiflexors in nine old (68.3 ± 6.1 years) and nine young women (25.1 ± 1.3 years) during and following 150 lengthening contractions for up to 30 min of recovery. At baseline, the old were ~21% weaker for maximum isometric voluntary contraction (MVC) torque (P < 0.05), ~21% slower for peak loaded shortening velocity (P < 0.05), and ~39% less powerful compared with the young (P < 0.05). Following the task, MVC torque was depressed equally (~28%) for both groups (P < 0.05), but power was reduced ~19% in the old and only ~8% in the young (P < 0.05). Both measures remained depressed during the 30-min recovery period. Peak twitch torque (P (t)) was ~50% lower in the old at task termination, whereas the young were unchanged. However, by 5 min of recovery, P (t) was reduced similarly (~50%) in both groups, and neither recovered by 30 min. The old were affected more by low-frequency torque depression than the young, as shown by the ~40% and ~20% decreases in the stimulated 10:50 Hz ratio at task termination respectively, whereas both groups were affected similarly (~50%) 5 min into recovery, and neither recovered by 30 min. Thus, the coexistence of fatigue and muscle damage induced by the repetitive lengthening contractions impaired excitation-contraction coupling and cross-bridge function to a greater extent in the old, leading to a more pronounced initial loss of power than the young for up to 10 min following the exercise However, power remained blunted in both groups during the 30-min recovery period. These results indicate that older women are more susceptible to power loss than young following lengthening contractions, likely owing to a greater impairment in calcium kinetics.