Abstract
BackgroundCardiac troponin is the biochemical gold standard to diagnose acute myocardial infarction. Interestingly however, elevated cardiac troponin concentrations are also frequently observed during and after endurance-type exercise. Oxidative stress associated with prolonged exercise has been proposed to contribute to cardiac troponin release. Therefore, the aim of this study was to assess the effect of 4 week astaxanthin supplementation (a potent cartenoid antioxidant) on antioxidant capacity and exercise-induced cardiac troponin release in cyclists.MethodsThirty-two well-trained male cyclists (age 25±5, weight 73±7 kg, maximum O2 uptake 60±5 mL·kg−1·min−1, Wmax 5.4±0.5 W·kg−1; mean ± SD) were repeatedly subjected to a laboratory based standardized exercise protocol before and after 4 weeks of astaxanthin (20 mg/day), or placebo supplementation in a double-blind randomized manner. Blood samples were obtained at baseline, at 60 min of cycling and immediately post-exercise (≈ 120 min).ResultsThe pre-supplementation cycling trial induced a significant rise of median cardiac troponin T concentrations from 3.2 (IQR 3.0–4.2) to 4.7 ng/L (IQR 3.7–6.7), immediately post-exercise (p<0.001). Four weeks of astaxanthin supplementation significantly increased mean basal plasma astaxanthin concentrations from non-detectable values to 175±86 µg·kg−1. However, daily astaxanthin supplementation had no effect on exercise-induced cardiac troponin T release (p = 0.24), as measured by the incremental area under the curve. Furthermore, the elevation in basal plasma astaxanthin concentrations was not reflected in changes in antioxidant capacity markers (trolox equivalent antioxidant capacity, uric acid, and malondialdehyde). Markers of inflammation (high-sensitivity C-reactive protein) and exercise-induced skeletal muscle damage (creatine kinase) were equally unaffected by astaxanthin supplementation.ConclusionDespite substantial increases in plasma astaxanthin concentrations, astaxanthin supplementation did not improve antioxidant capacity in well-trained cyclists. Accordingly, exercise-induced cardiac troponin T concentrations were not affected by astaxanthin supplementation.Trial registrationClinicalTrials.gov NCT01241877
Highlights
Exercise-induced cardiac troponin T concentrations were not affected by astaxanthin supplementation
Myocardial necrosis is accompanied by the release of cardiac troponin into the bloodstream, which makes cTn the preferred biomarker for the diagnosis of acute myocardial infarction (AMI) [1]
In all these pathological settings elevated cTn concentrations are consistently associated with poor prognosis [4,5,6,7]
Summary
Myocardial necrosis is accompanied by the release of cardiac troponin (cTn) into the bloodstream, which makes cTn the preferred biomarker for the diagnosis of acute myocardial infarction (AMI) [1]. Elevated cTn concentrations are not restricted to AMI, but are observed in a wide range of cardiac and non-cardiac pathologies e.g. renal failure, pulmonary embolism, myocarditis and congestive heart failure (an extensive list has been published in [2,3]). The faster kinetics of exercise-induced cTn release, and the possible presence of a cytosolic unbound cTn fraction in the cardiomyocyte [15], triggered the postulation of a distinct release model for cTn during exercise, unrelated to myocardial cell death [16] This hypothetical model states that exercise-induced cTn release could be attributed to increased cardiomyocyte permeability (through mechanical stress or increased production of oxidative radicals) and subsequent early troponin release from a cytosolic cTn pool, possibly through membrane blebbing [16,17]. It challenges the dogma that increased cTn concentrations always reflect cell death, and unites two apparently incompatible observations: 1) the frequent occurrence of exercise-induced cTn release [18], and 2) the limited cardiomyocyte regenerative capacity [19]. The aim of this study was to assess the effect of 4 week astaxanthin supplementation (a potent cartenoid antioxidant) on antioxidant capacity and exercise-induced cardiac troponin release in cyclists
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