These data (1) provide the first evidence for ongoing myofibrillar degradation and increased cardiac troponin I levels in patients with advanced heart failure and (2) show potential usefulness of cardiac troponin I as a specific and sensitive new serum marker molecule in severe congestive heart failure.

The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2 uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running (median peaks: 309 U/l CK concentration (-CK-)), 466 microgram/l Mb concentration (-Mb-), 1,021 microU/l MHC concentration (-MHC-), and 27.3 microgram/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l -CK-, 98 microgram/l -Mb-, 501 microU/l -MHC-, and 6.6 microgram/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 microgram/l) for at least 1-2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).

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This study examined eccentric exercise-induced muscle damage and rapid adaptation. Twenty-two male subjects performed 70 eccentric actions with the knee extensors. Group A (n = 11) and group B (n = 11) repeated the same exercise 4 and 13 days after the initial bout, respectively. Criterion measures included muscle soreness, muscle force generation (vertical jump height on a Kistler platform), and plasma levels of creatine kinase (CK), slow-twitch skeletal (cardiac beta-type) myosin heavy chains (MHC), and cardiac troponin I. Subjects were tested pre-exercise and up to day 4 following each bout. The initial exercise resulted in an increase in CK and MHC, a decrement in muscle force, and delayed onset muscle soreness in all participants. CK and MHC release correlated closely (rho = 0.73, p = 0.0001), both did not correlate with the decrement in muscle force generation after exercise. Because cardiac troponin I could not be detected in all samples, which excluded a protein release from the heart (cardiac beta-type MHC), this finding provides evidence for a injury of slow-twitch skeletal muscle fibers in response to eccentric contractions. Repetition of the initial eccentric exercise bout after 13 days (group B) did not cause muscle soreness, a decrement in muscle reaction force with vertical jump or significant changes in plasma MHC and CK concentrations, whereas in case of repetition after 4 days (group A) only the significant increases in CK and MHC were abolished. The decrement in reaction force with vertical jump did not differ significantly from that after the initial exercise session, but perceived muscle soreness was less pronounced.(ABSTRACT TRUNCATED AT 250 WORDS)

The screening by immunoenzymometric assay (IEMA) of 784 monoclonal antibody (MAb) combinations resulted in the selection of an optimal pair of MAbs for measuring human cardiac troponin I (TnI). Using a one-step IEMA described here, we were able to detect TnI within the range of 0.2-20 micrograms/L in 30 min at room temperature. No cross-reactivity was observed with the skeletal isoforms of troponin up to a concentration of 500 micrograms/L. This assay was used to measure cardiac TnI in the plasma of 43 patients with acute myocardial infarction (AMI). TnI was detected relatively early after the onset of chest pain (4.3 +/- 2.1 h, mean +/- SD); the peak occurred after 12.2 +/- 4.6 h in a population that had undergone fibrinolysis. TnI disappearance was generally observed between 5 and 9 days after the onset of chest pain. No cardiac TnI could be detected in 145 healthy donors or in a control group of 6 patients (with skeletal damage or rhabdomyolysis). This assay allows a specific diagnosis of AMI in its early acute phase, with a high diagnostic specificity and sensitivity.