Manfred Lehmann

OVERTRAINING IN ENDURANCE ATHLETES - A BRIEF REVIEW

Overtraining is an imbalance between training and recovery, exercise and exercise capacity, stress and stress tolerance. Stress is the sum of training and nontraining stress factors. Peripheral (short-term overtraining, STO) or peripheral and central fatigue may result (long-term overtraining, LTO). STO lasting a few days up to 2 wk is termed overreaching. STO is associated with fatigue, reduction, or stagnation of the 4 LT performance capacity (performance at 4 mmol lactate or comparable criterion), reduction of maximum performance capacity, and brief competitive incompetence. Recovery is achieved within days, so the prognosis is favorable. LTO lasting weeks or months causes overtraining syndrome or staleness. The symptomatology associated with overtraining syndrome has changed over the last 50 yr from excitation and restlessness (so-called sympathetic form) to phlegmatic behavior and inhibition (so-called parasympathetic form). Increased volume of training at a high-intensity level is likely the culprit. The parasympathetic form of overtraining syndrome dominates in endurance sports. Accumulation of exercise and nonexercise fatigue, stagnation, or reduction of the 4 LT performance capacity, reduction in maximum performance capacity, mood state disturbances, muscle soreness/stiffness, and long-term competitive incompetence can be expected. Complete recovery requires weeks and months, so the prognosis is unfavorable. Other optional or further confirmation requiring findings include changes in blood chemistry variables, hormone levels, and nocturnal urinary catecholamine excretion. Based on the findings reported, recommendations for training monitoring can be made, but their relevance in the practice must still be clarified.

Contrasting peripheral short-term and long-term effects of converting enzyme inhibition in patients with congestive heart failure. A double-blind, placebo-controlled trial.

To discover the underlying mechanisms involved in the beneficial long-term effects of angiotensin converting enzyme (ACE) inhibitors, we investigated the systemic and peripheral effects of short- and long-term ACE inhibition in patients with chronic heart failure. After assessing the short-term effects and dose titration with cilazapril, a new long-acting ACE inhibitor, 21 patients were randomized to receive either placebo or the ACE inhibitor. Seventeen patients completed the 3-month treatment. Central hemodynamic output, femoral blood flow (measured by thermodilution), oxygen saturation, and lactate and norepinephrine levels were determined simultaneously in the femoral vein and radial artery during treatment and after a 3-month rest and during symptom-limited bicycle exercise. Short-term ACE inhibition improved rest and exercise hemodynamic output, but it did not alter peak femoral blood flow, calculated leg oxygen consumption, or systemic oxygen uptake during exercise, despite significant reduction in femoral norepinephrine extraction and arterial angiotensin levels during exercise. In contrast, long-term ACE inhibition further improved exercise cardiac output and increased leg blood flow (from 2.3 to 2.9 l/min, p less than 0.05), leg oxygen consumption (from 277 to 403 ml/min, p less than 0.05), and systemic oxygen uptake (from 1,133 to 1,453 ml/min, p less than 0.05), whereas these variables remained unchanged with placebo treatment (p less than 0.02 between groups). Moreover, a moderate but significant increase in femoral oxygen extraction occurred after long-term therapy (ACE inhibitor: from 76% to 83%, p less than 0.05; placebo: from 75% to 74%, NS; p less than 0.01 between groups). We conclude that long-term ACE inhibition is clinically beneficial in that it improves blood flow to skeletal muscle during exercise over time. The long-term effects of ACE inhibition are, in part, probably related to peripheral (vascular) mechanisms, for example, by reversing the inability of peripheral vessels to dilate and by improving oxygen utilization.

Autonomic imbalance hypothesis and overtraining syndrome.

PURPOSEnThe parasympathetic, Addison type, overtraining syndrome represents the dominant modern type of this syndrome. Beside additional mechanisms, an autonomic or neuroendocrine imbalance is hypothesized as underlying.nnnMETHODS/RESULTSnSeveral findings support this thesis. During heavy endurance training or overreaching periods, the majority of findings give evidence of a reduced adrenal responsiveness to ACTH. This is compensated by an increased pituitary ACTH release. In an early stage of the overtraining syndrome, despite increased pituitary ACTH release, the decreased adrenal responsiveness is no longer compensated. The cortisol response decreases. In an advanced stage of overtraining syndrome, the pituitary ACTH release also decreases. In this stage, there is additionally evidence for decreased intrinsic sympathetic activity and sensitivity of target organs to catecholamines. This is indicated by decreased catecholamine excretion during night rest, decreased beta-adrenoreceptor density, decreased beta-adrenoreceptor-mediated responses, and increased resting plasma norepinephrine levels and responses to exercise. However, this complete pattern is only observed subsequent to high-volume endurance overtraining at high caloric demands.nnnCONCLUSIONnThe described functional alterations of pituitary-adrenal axis and sympathetic system can explain persistent performance incompetence in affected athletes.

Myocardial energetics in patients with dilated cardiomyopathy. Influence of nitroprusside and enoximone.

Cardiotonic agents influence myocardial energy consumption by vasodilation, which may reduce energy demand, and by inotropism, which may increase it. To distinguish between the two effects, myocardial oxygen consumption must be analyzed in relation to its hemodynamic determinants. The coupling of myocardial oxygen consumption with its determinants was investigated in 22 patients with idiopathic dilated cardiomyopathy (NYHA Class II and III). Predicted myocardial oxygen consumption by the pressure-work index, the Bretschneider index, and the pressure-volume area correlated moderately with measured myocardial oxygen consumption (r = 0.57, p less than 0.001; r = 0.52, p less than 0.005; and r = 0.63, p less than 0.001). Multiple regression analysis, including left ventricular peak systolic wall stress, systolic stress-time integral, pressure-volume work, maximum rate of left ventricular pressure rise, and mean velocity of circumferential fiber shortening indicated that systolic stress-time integral is the major determinant of myocardial oxygen consumption (r = 0.75, p less than 0.001) in these patients. Enoximone, a phosphodiesterase inhibitor, has an inotropic and a vasodilating effect. To investigate the inotropic portion of the energy cost of this phosphodiesterase inhibitor, the influence of enoximone on myocardial oxygen consumption and systolic stress-time integral was compared with the effects of nitroprusside, which is a vasodilator only. Nitroprusside (10 patients) and enoximone (12 patients) reduced left ventricular systolic stress-time integral from 109 +/- 22 to 71 +/- 21 (p less than 0.005) and from 104 +/- 23 to 42 +/- 10 (p less than 0.001) 10(3) dynes.sec/cm2, respectively. Myocardial oxygen consumption decreased from 159 +/- 44 to 112 +/- 23 (p less than 0.005) and from 134 +/- 28 to 109 +/- 21 (p less than 0.001) microliters/beat/100 g, respectively. In both groups, there was a significant correlation between the decrease in myocardial oxygen consumption and the decrease in systolic stress-time integral. The slopes of the respective linear regression lines were significantly different (1.27 for nitroprusside and 0.51 nl.cm2/100 g.dynes.sec for enoximone, p less than 0.05), indicating a smaller decrease of myocardial oxygen consumption for a given decrease of stress-time integral with enoximone. Applying the pressure-work index or the pressure-volume area instead of systolic stress-time integral yielded comparable results. Thus, vasodilation reduces myocardial oxygen consumption in proportion to the reduction of stress-time integral. With enoximone, the energy-saving effect of vasodilation is counteracted in part by the increased energy d

Plasma catecholamines, β-adrenergic receptors, and isoproterenol sensitivity in endurance trained and non-endurance trained volunteers

SummarySix male non-endurance trained subjects (S) and six marathon runners (M) underwentgraded treadmill exercise (T) andisoproterenol stimulation (I; 2 and 4 Μg·min−1),β-adrenergic receptor density was additionally determined as the amount of3H-Dihydroalprenolol (DHA) specifically bound on intact polymorphonuclear leucocytes. Heart rate,n

Age-associated changes of exercise-induced plasma catecholamine responses

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Physical training, vegetative regulation, and cardiac hypertrophy.

n uptake, lactate, plasma noradrenaline, and adrenaline were estimated during T. Heart rate, stroke volume, cardiac output, as well as lactate, glucose, free fatty acids (FFA), and glycerol levels in the blood were determined during I. M showed the known training-dependent responses during T, such as lower heart rates, lactate levels, and plasma catecholamines at identical work loads, as well as highern