Cardiac markers (BNP, NT-pro-BNP, Troponin I, Troponin T, in female amateur runners before and up until three days after a marathon.

PURPOSE: Transient cardiac ventricular dysfunction or sudden cardiac deaths have been reported for male athletes participating in marathon racing. Less is known about the myocardial response in females. We examined natriuretic peptides and cardiac troponins in female athletes after a marathon. METHODS: At the 31st real,- Berlin Marathon plasma levels of NT-pro-BNP, BNP, cTnI and cTnT were measured in 15 women (age 35+/-6 years; finishing times between 3:22 h and 5:21 h) at four different time points (before, immediately after, day one and day three). RESULTS: An increase in [NT-pro-BNP] was observed immediately after the marathon (median [NT-pro-BNP] before: 39.6 pg ml(-1), after: 138.6 pg ml(-1), p=0.003) with a further increase on day one. [BNP] did not increase immediately after the marathon but increased on day one (median [BNP] before: 15 pg ml(-1), day one: 27.35 pg ml(-1), p=0.006). On day three, [NT-pro-BNP] and [BNP] returned to initial values. [cTnI] was under the detection limit prior to the marathon in all runners. [cTnT] was under the detection limit before the marathon except in one runner who presented a concentration of 0.03 ng ml(-1). Cardiac troponins (median [cTnl] after: 0.098 ng ml(-1), p=0.028; median [cTnT] after: 0.032 ng ml(-1), p=0.012) increased immediately after the marathon and returned to initial values on day one [cTnT] and three [cTnI]. DISCUSSION: Parameters representing cardiac stress increased in females after a marathon. Different kinetics of natriuretic peptides BNP and NT-pro-BNP post-marathon could be due to their different half-lives and dependence on renal function. The increase of cTnI and cTnT may result from minor myocardial lesions.

Erythropoietin regulations in humans under different environmental and experimental conditions.

In the adult human, the kidney is the main organ for the production and release of erythropoietin (EPO). EPO is stimulating erythropoiesis by increasing the proliferation, differentiation and maturation of the erythroid precursors. In the last decades, enormous efforts were made in the purification, molecular encoding and description of the EPO gene. This led to an incredible increase in the understanding of the EPO-feedback-regulation loop at a molecular level, especially the oxygen-dependent EPO gene expression, a key function in the regulation loop. However, studies in humans at a systemic level are still very scanty. Therefore, it is the purpose of the present review to report on the main recent investigations on EPO production and release in humans under different environmental and experimental conditions, including: (i) studies on EPO circadian, monthly and even annual variations, (ii) studies in connection with short-, medium- and long-term exercise at sea-level which will be followed (iii) by studies performed at moderate and high altitude.

Observation of serum erythropoietin concentrations in female athletes for up to eight days after a marathon run.

Erythropoietin (EPO) was studied in 13 female marathon runners before and up to 8 days after a competition marathon run. The median baseline control value was 13.7 U/l. No change in EPO concentration was found immediately (15 min.) and one day after the run. However, a median increase in EPO concentration (18.1 U/l) was found on day three post-exercise (p< 0.05). On day 8 no change was found compared to pre-exercise values. This late increase in EPO concentration would seem to be responsible for the well known increase of red blood cell mass in long distance runners.

Iron-regulatory protein hepcidin is increased in female athletes after a marathon.

The propose of this study was to determine the influence of marathon race on hepcidin excretion in female athletes (age 26-45 years). Urine samples were taken before, immediately after, 1 and 3 days after the race. In the average, hepcidin transiently increased at day 1 from 32 to 85 ng/mg creatinine. We propose that the frequently observed iron deficiency of females runners is caused by elevated hepcidin levels.

Indirect evidence of CNS adrenergic pathways activation during spaceflight.

BACKGROUND: Microgravity causes cephalad fluid shift and compensatory mechanisms. Hormonal changes suggestive of peripheral sympathetic (catecholaminergic) nervous system activation have been recently found in astronauts during flight. Simulation studies showed increased perivascular sympathetic fiber density in the rat brain. HYPOTHESIS: Intracranial microcirculatory adaptations might also occur in astronauts, involving an increase in the turnover rate of catecholamines, i.e., norepinephrine (NE) and its precursor, Dopamine (DA). DA is known to inhibit prolactin (PRL) release and to enhance growth hormone (GH) secretion by the pituitary. Therefore, increased brain dopaminergic activity would result into lower circulating PRL concentrations. At the same time, plasma levels of GH and of its effector insulin-like growth factor-1 (IGF-1) would increase during flight. METHODS: Circulating cortisol (CS), PRL, GH and IGF-1 levels were measured 2 d preflight, inflight (4-5 d after launch) and on different days postflight in four astronauts involved in the Spacelab D-2 mission. RESULTS: No significant changes were found in CS concentrations. PRL decreased while GH and IGF-1 increased inflight (p < 0.05). After flight no statistically relevant hormonal changes were found with respect to preflight. CONCLUSION: The observed hormonal changes were consistent with the original hypothesis that spaceflight might activate CNS adrenergic pathways. They occurred in the absence of two typical markers of stress, namely CS and PRL increase, thus ruling out any non-specific effect of acute stress on the results. In agreement with the most recent results of real and simulated microgravity studies performed in both the experimental animal and in man, these data lend support to the hypothesis that the CNS adrenergic pathways are also activated in the human during spaceflight.

Antihypertensive and metabolic effects of diltiazem and nifedipine.

The antihypertensive effect of diltiazem (180-270 mg/day) and nifedipine (40-60 mg/day) in slow-release forms was assessed over 8 weeks in a double-blind parallel study in 40 subjects with essential hypertension at rest and during exercise. Blood pressure was comparably reduced in both groups at rest as well as during exercise. The responder rates (greater than or equal to 10% reduction in diastolic blood pressure) after 8 weeks of therapy were 53% at rest and 75% during exercise in the diltiazem group and 78% and 50%, respectively, in the nifedipine group. Diltiazem decreased heart rate by 8% (p less than 0.01), while nifedipine did not affect it. As a consequence, myocardial oxygen consumption, as judged by the pressure-rate product, was reduced by diltiazem. Resting plasma norepinephrine levels were increased significantly after 8 weeks of diltiazem therapy. Plasma epinephrine, renin, aldosterone, glucose, insulin, and lactate and routine laboratory parameters were unchanged at the end of the study. No significant changes in total cholesterol and triglyceride levels were observed after 8 weeks. Whereas therapy with diltiazem resulted in an 8% fall in low density lipoprotein cholesterol after 8 weeks (p less than 0.05), nifedipine induced a drop in very low density lipoprotein cholesterol (p less than 0.05) after 8 weeks of therapy. We conclude that both diltiazem and nifedipine are effective antihypertensive agents lacking undesirable metabolic side effect. Diltiazem, however, had the advantage of lowering heart rate and myocardial oxygen consumption.