Postcontractile force depression in humans is associated with an impairment in SR Ca2+ pump function

Abstract

To investigate the hypothesis that intrinsic changes in sarcoplasmic reticulum (SR) Ca2+-sequestration function can be implicated in postcontractile depression (PCD) of force in humans, muscle tissue was obtained from the vastus lateralis and determinations of maximal Ca2+ uptake and maximal Ca2+-ATPase activity were made on homogenates obtained before and after the induction of PCD. Eight untrained females, age 20.6 ± 0.75 yr (mean ± SE), performed a protocol consisting of 30 min of isometric exercise at 60% maximal voluntary contraction and at 50% duty cycle (5-s contraction and 5-s relaxation) to induce PCD. Muscle mechanical performance determined by evoked activation was measured before (0 min), during (15 and 30 min), and after (60 min) exercise. The fatiguing protocol resulted in a progressive reduction ( P < 0.05) in evoked force, which by 30 min amounted to 52% for low frequency (10 Hz) and 20% for high frequency (100 Hz). No force restoration occurred at either 10 or 100 Hz during a 60-min recovery period. Maximal SR Ca2+-ATPase activity (nmol ⋅ mg protein− 1 ⋅ min− 1) and maximal SR Ca2+ uptake (nmol ⋅ mg protein− 1 ⋅ min− 1) were depressed ( P < 0.05) by 15 min of exercise [192 ± 45 vs. 114 ± 8.7 and 310 ± 59 vs. 205 ± 47, respectively; mean ± SE] and remained depressed at 30 min of exercise. No recovery in either measure was observed during the 60-min recovery period. The coupling ratio between Ca2+-ATPase and Ca2+ uptake was preserved throughout exercise and during recovery. These results illustrate that during PCD, Ca2+uptake is depressed and that the reduction in Ca2+ uptake is due to intrinsic alterations in the Ca2+ pump. The role of altered Ca2+ sequestration in Ca2 release, cytosolic-free calcium, and PCD remains to be determined.