Fatigue and recovery of power and isometric torque following isotonic knee extensions

The purpose of this study was to assess fatigue and recovery of isotonic power and isometric contractile properties after a series of maximal isotonic contractions. Using a Biodex dynamometer, 13 men [26 yr (SD 3)] performed isotonic [50% of isometric maximal voluntary contraction (MVC) every 1.2 s through 75° range of motion] single-limb knee extensions at the fastest velocity they could achieve until velocity was reduced by 35%. Time to task failure was 38 s, and, compared with baseline, power declined by ∼42% [741.0 (SD 106.0) vs. 426.5 W (SD 60.3) at task failure], and MVC declined by ∼26% [267.3 (SD 42.5) vs. 198.4 N·m (SD 45.7) at task failure]. Power recovered by 5 min, whereas MVC did not recover, and at 10 min was only ∼85% of baseline. Isometric MVC motor unit activation was ∼95% at rest and was unchanged at task failure (∼96%), but a small amount of failure was apparent between 1.5 and 10 min of recovery (∼87 to ∼91%). Half relaxation time measured from a 50-Hz isometric tetanus was significantly prolonged by ∼33% immediately after task failure but recovered by 1.5 min. A decline in the 10- to 50-Hz ratio of the evoked isometric contractions was observed at 5 and 10 min of recovery, which suggests excitation-contraction coupling impairment. Changes in velocity and half relaxation time during the protocol were strongly and negatively correlated ( r = −0.85). Thus mainly peripheral mechanisms were implicated in the substantial depression but relatively fast recovery of isotonic power. Furthermore, isometric muscle contractile properties were related to some, but not all, changes in isotonic function.

Myofibrillar or mitochondrial creatine kinase deficiency alone does not impair mouse diaphragm isotonic function

Creatine kinase (CK) provides ATP buffering in skeletal muscle and is expressed as 1) cytosolic myofibrillar CK (M-CK) and 2) sarcomeric mitochondrial CK (ScCKmit) isoforms that differ in their subcellular localization. The diaphragm (Dia) expresses both M-CK and ScCKmit in abundance. We compared the power and work output of 1) control CK-sufficient (Ctl), 2) M-CK-deficient [M-CK(−/−)], 3) ScCKmit-deficient [ScCKmit(−/−)], and 4) combined M-CK/ScCKmit-deficient null mutant [CK(−/−)] Dia during repetitive isotonic activations to determine the effect of CK phenotype on Dia function. Maximum power was obtained at ∼0.4 tetanic force in all groups. M-CK(−/−) and ScCKmit(−/−) Dia were able to sustain power and work output at Ctl levels during repetitive isotonic activation (75 Hz, 330-ms duration repeated each second at 0.4 tetanic force load), and the duration of sustained Dia shortening was 67 ± 4 s in M-CK(−/−), 60 ± 4 s in ScCKmit(−/−), and 62 ± 5 s in Ctl Dia. In contrast, CK(−/−) Dia power and work declined acutely and failed to sustain shortening altogether by 40 ± 6 s. We conclude that Dia power and work output are not absolutely dependent on the presence of either M-CK or ScCKmit, whereas the complete absence of CK acutely impairs Dia shortening capacity during repetitive activation.

Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function

Watchko, Jon F., Monica J. Daood, Gary C. Sieck, John J. LaBella, Bill T. Ameredes, Alan P. Koretsky, and Be Wieringa. Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function. J. Appl. Physiol. 82(5): 1416–1423, 1997.—Creatine kinase (CK) is an enzyme central to cellular high-energy phosphate metabolism in muscle. To characterize the physiological role of CK in respiratory muscle during dynamic contractions, we compared the force-velocity relationships, power, and work output characteristics of the diaphragm (Dia) from mice with combined myofibrillar and sarcomeric mitochondrial CK deficiency (CK[−/−]) with CK-sufficient controls (Ctl). Maximum velocity of shortening was significantly lower in CK[−/−] Dia (14.1 ± 0.9 L o/s, where L o is optimal fiber length) compared with Ctl Dia (17.5 ± 1.1 L o/s) ( P < 0.01). Maximum power was obtained at 0.4–0.5 tetanic force in both groups; absolute maximum power (2,293 ± 138 W/m2) and work (201 ± 9 J/m2) were lower in CK[−/−] Dia compared with Ctl Dia (2,744 ± 146 W/m2 and 284 ± 26 J/m2, respectively) ( P < 0.05). The ability of CK[−/−] Dia to sustain shortening during repetitive isotonic activation (75 Hz, 330-ms duration repeated each second at 0.4 tetanic force load) was markedly impaired, with CK[−/−] Dia power and work declining to zero by 37 ± 4 s, compared with 61 ± 5 s in Ctl Dia. We conclude that combined myofibrillar and sarcomeric mitochondrial CK deficiency profoundly impairs Dia power and work output, underscoring the functional importance of CK during dynamic contractions in skeletal muscle.