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

To investigate the hypothesis that intrinsic changes in sarcoplasmic reticu lum (SR) Ca2+-sequestration function can be implicated in postcontractile d epression (PCD) of force in humans, muscle tissue was obtained from the vas tus lateralis and determinations of maximal Ca2+ uptake and maximal Ca2+-AT Pase activity were made on homogenates obtained before and after the induct ion of PCD. Eight untrained females, age 20.6 +/- 0.75 yr (mean +/- SE), pe rformed a protocol consisting of 30 min of isometric exercise at 60% maxima l voluntary contraction and at 50% duty cycle (5-s contraction and 5-s rela xation) to induce PCD. Muscle mechanical performance determined by evoked a ctivation was measured before (0 min), during (15 and 30 min), and after (6 0 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 freque ncy (10 Hz) and 20% for high frequency (100 Hz). No force restoration occur red 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 exe rcise [192 +/- 45 vs. 114 +/- 8.7 and 310 +/- 59 vs. 205 +/- 47, respective ly; mean +/- SE] and remained depressed at 30 min of exercise. No recovery in either measure was observed during the 60-min recovery period. The coupl ing ratio between Ca2+-ATPase and Ca2+ uptake was preserved throughout exer cise and during recovery. These results illustrate that during PCD, Ca2+ up take 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 Ca -2 release, cytosolic-free calcium, and PCD remains to be determined.