CK Response Research Articles

Exertional rhabdomyolysis in quarter horses and thoroughbreds: one syndrome, multiple aetiologies.

The purpose of this study was to determine if chronic exertional rhabdomyolysis (ER) in Quarter Horses and Thoroughbreds represents one or several distinct myopathies. Eighteen Quarter Horses and 18 Thoroughbreds with ER were selected from cases presented to the Veterinary Hospital on the basis of a history of ER, assessment of muscle histopathology, and serum CK activity before and 4 h post exercise. In addition, 2 of 3 of the following parameters were evaluated: muscle glycogen concentrations, thyroid hormones (T3, T4), fractional excretion (FE) of sodium, potassium and chloride. The CK response to training, the metabolic response to a near maximal standardised exercise test (SET), blood glucose concentrations after an i.v. glucose challenge and a skeletal muscle in vitro caffeine contracture test were performed on 5 of the Quarter Horses, selected because of polysaccharide storage myopathy (PSSM), and 5 of the Thoroughbreds. Serum T3 and T4 were all within normal limits. Low FE of sodium and potassium were seen in < 20% of Quarter Horses and Thoroughbreds. Four hours post exercise, CK was increased in 77% of Quarter Horses and 72% of Thoroughbreds with ER. Muscle glycogen concentrations in Quarter Horses with ER were significantly higher than in normal Quarter Horses and Thoroughbreds with ER. No Thoroughbreds, but 15/18 Quarter Horses with ER had abnormal polysaccharide accumulation in muscle biopsies consistent with a diagnosis of PSSM. PSSM Quarter Horses had higher CK activity during training than Thoroughbreds and higher glycogen utilisation with the SET. PSSM Quarter Horses also had significantly enhanced glucose clearance compared to normal Quarter Horses and Thoroughbreds with ER. Thoroughbreds with ER had significantly lower thresholds for caffeine-induced contracture than normal horses and PSSM Quarter Horses. It was concluded that there are multiple causes for exertional rhabdomyolysis. In Quarter Horses, rhabdomyolysis is commonly due to a glycogen storage disorder, PSSM, and is readily expressed in untrained horses. In Thoroughbreds, ER is commonly due to an underlying abnormality of muscle contraction. Rhabdomyolysis in Thoroughbreds, however, is only expressed intermittently when key stressors are present.

Exercise-induced increase in serum creatine kinase is modified by subsequent bed rest.

This study was designed to find out if bed rest, which is known to markedly reduce peripheral lymph flow, immediately after strenuous exercise could affect the behaviour of creatine kinase activity (CK) in serum. Eleven endurance athletes performed an 18 km cross-country run, after which six of the subjects were placed in bed rest group (BR) for 23 hours, while a group of five control subjects maintained their normal habitual activity (C). After the bed rest all subjects performed a light jogging bout for 45 min. Seven hours after the exercise serum CK was increased threefold (p < 0.05) in both groups. During the next 16 hours serum CK increased further 30% in C (p < 0.05) but decreased (p < 0.05) in a similar magnitude in BR. Light jogging elicited a transient CK increase of 16% (p < 0.05) in C, but there was no change in BR. The fact that serum CK increased similarly in both groups during the first hours after the exercise shows that the transport of CK from muscles into circulation can be maintained for some hours despite absence of muscular activity. However, the later post-exercise serum CK response may be diminished by bed rest (effect of posture and/or lack of muscle function). The reduced response is also seen in the CK response to a repeated exercise. These observations suggest that a short-term physical inactivity (bed rest) may reduce both the lymphatic transport of CK and the release of enzyme from muscle fibres.

Pretreatment with 1,25(OH) 2 vitamin D or 24,25(OH) 2 vitamin D increases synergistically responsiveness to sex steroids in skeletal-derived cells

We demonstrated previously that vitamin D metabolites modulate the response of bone and cartilage cells to 17β-estradiol (E 2) and dihydrotestosterone (DHT) both in cell cultures and in vivo. In the present study, we investigated to what extent pretreatment with 1,25(OH) 2D 3 or 24,25(OH) 2D 3 would reduce the minimal effective dose of E 2, DHT or progesterone (P) required for stimulation of DNA synthesis and creatine kinase specific activity in cultured osteoblast-like ROS 17 2.8 cells and in rat embryo epiphyseal cartilage cells, and to what extent such pretreatment would increase the maximal response. We measured responses to sex steroids after pretreatment of the cells for 5 days with 0.02% ethanol vehicle or with the vitamin D metabolites 1,25(OH) 2D 3 (0.12 nM), or 24,25(OH) 2D 3 (1.2 nM) singly or in combination. Pretreatment of ROS 17 2.8 cells with 1,25(OH) 2D 3, but not 24,25(OH) 2D 3, increased synergistically their response to E 2 but not to P, and did not affect their lack of response to DHT. Pretreatment of epiphyseal cartilage cells with either 1,25(OH) 2D 3 or 24,25(OH) 2D 3 increased synergistically their DNA synthetic response to all three steroids, but their CK response only to E 2 or DHT. The minimal dose for causing a significant response to E 2 in ROS 17 2.8 cells or to either E 2 or DHT in epiphyseal cartilage cells was reduced 10-fold after pretreatment with vitamin D metabolites. After pretreatment, the maximal response was more than doubled in ROS 17 2.8 cells; epiphyseal cartilage cells showed a similar 10-fold decrease in the dose required for maximal response to E 2 or DHT; the improvement in the response to P was significant only for DNA synthesis. We conclude that pretreatment with the appropriate vitamin D metabolite(s) both reduces by an order of magnitude, or more, the amount of sex steroids needed to stimulate skeletal derived cells and increases synergistically the maximal response of the cells.

183 CK and PGE2 responses to repeated eccentric exercise

183 CK and PGE2 responses to repeated eccentric exercise

Myoglobin is a sensitive marker of increased muscle membrane vulnerability

Changes in muscle proteins in serum after exercise were studied to evaluate the use of such proteins as indicators of increased muscle membrane vulnerability. Seventy-one women were asked to perform bicycle exercise for 45 min at a moderate load; four proteins (creatine kinase - CK, myoglobin - Mb, aldolase - Ald and pyruvate kinase - PK) were measured in serum up to 24 h after exercise. Twenty-one women were carriers of Duchenne's muscular dystrophy (DMD); these are known to show an elevated serum CK activity at rest, as well as increased CK response after exercise. Fifty women without a family history of neuromuscular disease were tested to obtain normal values: they showed a small peak (18%) of CK activity 8 h after exercise, and an even smaller peak of Mb (9%) 1 h after exercise. The mean post-exercise increase for both CK and Mb in the 21 DMD carriers was significantly higher than in controls; the maximum of Mb, on average 70% of baseline levels, was reached 1 h after exercise and was higher than that for CK (48%), which was reached 8 h after exercise. It is concluded that myoglobin levels after exercise are a good index of increased vulnerability of the muscle membrane.