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Purpose: This study aimed to determine whether competitive intermittent exercise in the heat affects recovery, aggravates markers of muscle fiber damage, and delays the recovery of performance and muscle glycogen stores., Methods: Plasma creatine kinase, serum myoglobin, muscle glycogen, and performance parameters (sprint, endurance, and neuromuscular testing) were evaluated in 17 semiprofessional soccer players before, immediately after, and during 48 h of recovery from a match played in 43°C (HOT) and compared with a control match (21°C with similar turf and setup)., Results: Muscle temperature was ∼1°C higher (P < 0.001) after the game in HOT compared with control and reached individual values between 39.9°C and 41.1°C. Serum myoglobin levels increased by more than threefold after the matches (P < 0.01), but values were not different in HOT compared with control, and they were similar to baseline values after 24 h of recovery. Creatine kinase was significantly elevated both immediately and 24 h after the matches, but the response after HOT was reduced compared with control. Muscle glycogen responses were similar across trials and remained depressed for more than 48 h after both matches. Sprint performance and voluntary muscle activation were impaired to a similar extent after the matches (sprint by ∼2% and voluntary activation by ∼1.5%; P < 0.05). Both of these performance parameters as well as intermittent endurance capacity (estimated by a Yo-Yo IR1 test) were fully recovered 48 h after both matches., Conclusion: Environmental heat stress does not aggravate the recovery response from competitive intermittent exercise associated with elevated muscle temperatures and markers of muscle damage, delayed resynthesis of muscle glycogen, and impaired postmatch performance.

Background: The role of the creatine kinase (CK)/phosphocreatine (PCr) energy buffer and transport system in heart remains unclear. Guanidinoacetate-N-methyltransferase-knockout (GAMT-/-) mice represent a new model of profoundly altered cardiac energetics, showing undetectable levels of PCr and creatine and accumulation of the precursor (phospho-)guanidinoacetate (P-GA). To characterize the role of a substantially impaired CK/PCr system in heart, we studied the cardiac phenotype of wild-type (WT) and GAMT-/- mice., Methods and Results: GAMT-/- mice did not show cardiac hypertrophy (myocyte cross-sectional areas, hypertrophy markers atrial natriuretic factor and beta-myosin heavy chain). Systolic and diastolic function, measured invasively (left ventricular conductance catheter) and noninvasively (MRI), were similar for WT and GAMT-/- mice. However, during inotropic stimulation with dobutamine, preload-recruitable stroke work failed to reach maximal levels of performance in GAMT-/- hearts (101+/-8 mm Hg in WT versus 59+/-7 mm Hg in GAMT-/-; P<0.05). (31)P-MR spectroscopy experiments showed that during inotropic stimulation, isolated WT hearts utilized PCr, whereas isolated GAMT-/- hearts utilized P-GA. During ischemia/reperfusion, GAMT-/- hearts showed markedly impaired recovery of systolic (24% versus 53% rate pressure product recovery; P<0.05) and diastolic function (eg, left ventricular end-diastolic pressure 23+/-9 in WT and 51+/-5 mm Hg in GAMT-/- during reperfusion; P<0.05) and incomplete resynthesis of P-GA., Conclusions: GAMT-/- mice do not develop hypertrophy and show normal cardiac function at low workload, suggesting that a fully functional CK/PCr system is not essential under resting conditions. However, when acutely stressed by inotropic stimulation or ischemia/reperfusion, GAMT-/- mice exhibit a markedly abnormal phenotype, demonstrating that an intact, high-capacity CK/PCr system is required for situations of increased cardiac work or acute stress.

To define the relation between the phosphoryl transfer via creatine kinase and the ability to recover from an ischemia-reperfusion challenge, the authors chemically inhibited creatine kinase activity with iodoacetamide (IAm) and then measured myocardial recovery after 2, 10, or 30 min of global ischemia followed by 30 min of reperfusion in the isolated, arterially perfused interventricular septa of the rabbit heart. During normoxia, IAm (0.5 M perfused for 15 min) did not by itself modify developed tension, maximal rate of tension development, or resting tension. In ischemia, IAm pretreatment increased the rate of developed tension loss and highly diminished developed tension recovery after reperfusion for all the ischemia periods tested. Moreover, IAm significantly enhanced the maximal increase in the resting tension induced by 10 or 30 min of ischemia plus reperfusion. Lactate dehydrogenase activity in reperfusion was also significantly increased over untreated septa. On the basis of the present results, the authors suggest that the aggravating effects exhibited by IAm on the ischemic myocardium are compatible with its creatine kinase inhibition properties and that creatine kinase activity is essential for full recovery from an ischemia-reperfusion challenge.

A general understanding of the pivotal role of phosphocreatine (PCr) as the principal determinant of skin flap survival is now emerging. Definitive metabolic investigations using phosphorus (31P) and proton (1H) magnetic resonance spectroscopy (MRS) have established that the inability to replenish metabolically exhausted PCr reserves predictably correlates with skin flap necrosis. Furthermore, postoperative parenteral administration of PCr has been shown to augment effectively skin flap survival. We hypothesized that creatine kinase, the enzyme controlling the utilization of the high-energy phosphate component of PCr, is a critical determinant of the tolerance of a skin flap to ischemic insult. In other words, if the rate of utilization of PCr is too rapid, PCr stores will rapidly deplete, and the flap will not be able to withstand a period of ischemia. Alternatively, if the rate of dephosphorylation of PCr is reduced, survival of skin flaps during periods of ischemia could be extended. To test this hypothesis, we investigated the metabolic distribution and fate of cyclocreatine (cCr), a competent creatine analogue with a lower affinity for the creatine kinase enzyme. When administered as 1.5 percent (w/w) of the normal diet of laboratory rats, cCr accumulates in skin as the competent phosphagen, phosphocyclocreatine (PcCr). Cutaneous flaps elevated in these animals, and studied by 31P and 1H MRS, demonstrate that once depletion of PCr has occurred, PcCr continues to sustain ATP levels. This results in significant enhancement of skin flap survival (p < 0.005). These observations confirm the importance of the creatine kinase enzyme in cutaneous flap ischemia and suggest new approaches to augment skin flap survival.

The purpose of this study was to investigate the association between elite endurance athlete (EEA) status and two restriction fragment length polymorphisms (RFLPs) at the muscle-specific creatine kinase (CKMM) gene locus. Genomic DNA was extracted from white blood cells or lymphoblastoid cell lines of 124 unrelated Caucasian male EEA (VO2max > 73 mL.kg-1.min-1) and 115 unrelated Caucasian sedentary male controls (SCON). The genetic polymorphism at the CKMM locus was detected by the polymerase chain reaction and DNA digestion with the NcoI and TaqI restriction endonucleases. The allelic frequencies for the NcoI and TaqI RFLPs were not different (P > 0.05) between EEA and SCON subjects. The three expected genotypes for CKMM-NcoI (1170/1170 bp, 1170/985 + 185 bp, and 985 + 185/985 + 185 bp) and CKMM-TaqI (1170/1170 bp, 1170/1020 + 150 bp, and 1020 + 50/1020 + 150 bp) were observed in the EEA and SCON groups. These genotype frequencies were in Hardy-Weinberg equilibrium, but they were not significantly (P > 0.05) different between the EEA and SCON. A strong (P < 0.001) linkage disequilibrium was detected among the NcoI and TaqI RFLPs in both EEA and SCON. These findings indicate that the skeletal muscle CK-NcoI and CK-TaqI gene polymorphisms are not associated with the elite endurance athlete status.

The functional development of the creatine kinase system has been studied in rabbit heart during perinatal growth. Fiber bundles were obtained from left ventricles of fetal rabbits at the 30th day of gestation, newborn rabbits aged 1, 3, 8, and 17 days, and adult rabbits. Total creatine kinase activity was constant during perinatal development, whereas myofibrillar bound creatine kinase activity increased 15-fold during the first postnatal week. Functional activity of myofibrillar creatine kinase was assayed in Triton X-100-skinned fibers by its ability to induce active tension in the absence of ATP or to relax rigor tension. It was very low in 1-day-old newborns and increased during the first 2 weeks to reach adult levels 17 days after birth. Functional activity of mitochondrial creatine kinase was determined in saponin-skinned fibers. Creatine-stimulated respiration appeared only after birth and increased gradually between 1 and 17 days after birth. The results show that, although the two creatine kinase isoforms (mitochondrial and myofibrillar) are expressed at different stages during development, their functional activities appear in parallel in mitochondria and myofibrils. Early postnatal development is characterized by binding of creatine kinase isoenzymes to intracellular organelles. Such compartmentation participates in the postnatal cardiac cellular maturation.