Limited benefit of Fatmax-test to derive training prescriptions.

The intensity that elicits maximal fat oxidation (Fatmax) is recommended for training fat metabolism. However, it remains unclear whether Fatmax leads to the highest fat oxidation rates during prolonged exercise. It was hypothesized that there are no differences in fat oxidation rates among 3 different exercise intensities. Therefore, fat metabolism was compared among 1-h constant load tests at Fatmax, a higher and a lower intensity. A cohort of 16 male cyclists (28±6 yrs, BMI: 22.5±1.2 kg/m2; n=8 with maximal oxygen uptake [VO2max] of 50-60 ml/min/kg [ET]; n=8 with VO2max>60 ml/min/kg [HET]) completed a maximal incremental cycling test, a submaximal incremental Fatmax-test and, thereafter, three 1-h constant-load tests in randomized order at Fatmax, one exercise stage below (LOW) and one above (HIGH). LOW, Fatmax and HIGH were performed at 52±13, 60±13 and 70±12% VO2max. Heart rate and blood lactate were significantly different (p<0.001). However, the fat oxidation rate showed no difference (p=0.61). This was also true within each subgroup (ET: p=0.69, HET p=0.61). In conclusion, the fat oxidation rate of endurance trained cyclists shows no difference between 1-h constant load exercise bouts at about 50-70% VO2max. The precision and necessity of Fatmax-tests for controlling the training of fat oxidation are therefore debatable.

Differences in adaptations to 1 year of aerobic endurance training: individual patterns of nonresponse.

Lacking responses to endurance training (ET) have been observed for several variables. However, detailed analyses of individuals' responses are scarce. To learn more about the variability of ET adaptations, patterns of response were analyzed for each subject in a 1-year ET study. Eighteen participants [42 ± 5 years, body mass index: 24 ± 3 kg/m(2), maximal oxygen uptake (VO(2max) ): 38 ± 5 mL/min/kg] completed a 1-year jogging/walking program on 3 days/week, 45 min/session at 60% heart rate (HR) reserve. VO(2max), resting HR (rHR), exercise HR (eHR) and individual anaerobic threshold (IAT) were determined by treadmill and cycling ergometry respectively. Intraindividual coefficients of variation were extracted from the literature to distinguish random changes from training responses. Eight participants showed improvements in all variables. In 10 participants, one or two variables did not improve (VO(2max), rHR, eHR and IAT remained unchanged in four, four, three and one cases, respectively). At least one variable improved in each subject. Data indicate that ET adaptations might be detected in each individual using multiple variables of different adaptation levels and intensity domains. Nonresponse seems to occur frequently and might affect all variables. Further studies should investigate whether nonresponders improve with altered training. Furthermore, associations between patterns of nonresponse and health benefits from ET are worth considering.

Echocardiography of the right ventricle in athlete's heart and hearts of normal size compared to magnetic resonance imaging: which measurements should be applied in athletes?

Right ventricular (RV) pathologic hypertrophy and cardiomyopathy have been reported to be related to ventricular arrhythmias and sudden cardiac death in athletes. However, it is unclear which echocardiographic measurements reflect RV dimensions in athlete's heart (AH) correctly. We aimed to compare two-dimensional echocardiography of the RV in AH and normal hearts to magnetic resonance imaging (MRI), and derive recommendations for RV echocardiography in athletes. Twenty-three healthy male endurance athletes with AH (A; 28+/-4 yrs) and 26 healthy untrained males (C; 26+/-4 yrs) matched for body-dimensions were examined. In recommended echocardiographic parasternal and 4-chamber views, three enddiastolic RV free wall-thicknesses (T1,T5,T9) and RV diameters were determined (M-mode enddiastolic diameter [RV-EDD]; longitudinal [RV-LAX], sagittal, outflow-tract and tricuspid valve anulus diameters). MRI determined RV enddiastolic volumes (RV-EDV) and masses (RVM) in A and C were: 162+/-29 vs. 136+/-15 ml and 76+/-10 vs. 59+/-13 g (p<0.001). Significant correlations between RV-EDV and RV-EDD (r=0.49; p=0.001) as well as RV-LAX (r=0.38; p=0.01), and RVM and T5 (r=0.52; p=0.01) were found. For RV echocardiography, significant differences between A and C were documented for RV-EDD (medians [quartiles]: A: 26 mm [24/29 mm]; C: 22 mm [21/27 mm]; p=0.04; measurable in 49/49 subjects), and in the parasternal short axis view for T5 (A: 6.0 mm [5.4/7.8 mm]; C: 5.0 mm [4.5/5.2 mm]; p=0.04; measurable in 22/49). In conclusion, two-dimensional echocardiographic RV measurements offer only a limited potential to reflect true RV dimensions. Only RV-EDD may differentiate between normal hearts and exercise related RV adaptations in AH, and is the only recommendable parameter to be measured in athletes routinely. In unclear cases additional methods should be used to examine the RV in athletes.

Effects of one year aerobic endurance training on resting metabolic rate and exercise fat oxidation in previously untrained men and women. Metabolic endurance training adaptations.

Although metabolic training adaptations are considered to be an important aim of recreational endurance exercise, effects of aerobic endurance training on metabolism have hardly been recorded over longer training periods. The aim of the study was therefore to record changes in resting metabolic rate (RMR), substrate oxidation at rest and maximal exercise fat oxidation rate (MFO) after one year of recreational endurance training within the ACSM-recommendations. Seventeen sedentary participants (7 male symbol/10 female symbol, 42+/-5 yr, pre-training characteristics: BMI: 24.6+/-2.2 kg.m (-2), VO(2max): 37.5+/-4.7 ml.min (-1).kg (-1)) completed a 12 months jogging/walking program 3 days/week for 45 min/session at a constant heart rate (HR) prescription of 60% HR-reserve. Resting measurements and maximal incremental treadmill tests were conducted before the training program, after 6 and 12 months of training. Indirect calorimetry was used to assess metabolic parameters. After 12 months of training, body weight remained unchanged ( P=0.16), however, body fat was significantly reduced by 3.4+/-2.1% ( P<0.001). Neither RMR ( P=0.42) nor substrate oxidation at rest ( P=0.25) changed significantly. MFO increased significantly over time by 0.07+/-0.08 g.min (-1) ( P<0.01) and occurred at significantly higher exercise intensities (35+/-6 vs. 44+/-15 vs. 50+/-14%VO(2max), P<0.01). In summary one year of recreational endurance training does therefore not appear to influence RMR or substrate oxidation at rest in previously untrained non-obese participants. In contrast, a constant training stimulus within the ACSM-recommendations elicits sustained improvements in MFO over at least one year of training.

Recovery training in cyclists: ergometric, hormonal and psychometric findings.

This randomized cross-over study aimed at comparing the recovery effect of 4 days of low-intensity, discipline-specific training of 1 vs 3 h daily. Eleven athletes completed two periods of 13 days intensive cycling training (IT), followed by a recovery period consisting of 4 days of low-intensity cycling for either 1 or 3 h each day. Before IT, after IT and after the recovery period, subjects were tested in the laboratory: venous blood sampling, "profile of mood states" (POMS), graded cycling test and a 30-min time trial (TT). Maximal heart rates and lactate concentrations decreased significantly after IT. Peak power output, maximal heart rates and maximal lactate concentrations changed significantly different during the recovery periods. Whereas these parameters were similar to pre-training values after 1-h daily active recovery, 3-h recovery training (REC) led to further decreases. Power output during TT was neither affected by IT nor by both recovery periods. TT-induced increases in cortisol, adrenocorticotropic hormone and prolactin were reduced only after 3-h REC. Total POMS and subscores fatigue and vigor changed significantly different during the recovery periods, a return to pre-training levels after 1 h active recovery and a further deterioration after 3 h REC. It is concluded that low-intensity training of a 1-h duration each day is more appropriate for recovery after an IT period than 3 h.

The reliability of fat.

The exercise intensity eliciting maximal fat oxidation (Fat(max)) is typically determined during an incremental test. Its reproducibility, however, has not been thoroughly investigated so far. To address this issue, 21 healthy subjects (23.5+/-1.7 years; BMI 22.4+/-1.8 kg/m(2); VO(2peak) 47.4+/-11.3 mL/min/kg) carried out two identical cycling tests to determine Fat(max) after an initial incremental baseline test. The duration of each of five stages during the Fat(max) tests was 6 min. The first stage equalled the first increase in blood lactate during the baseline test; the highest stage corresponded to a respiratory exchange ratio of 1.00. Between these intensities the other three stages were distributed evenly. Fat(max) was 28.0+/-8.6 L/min (59.2+/-18.1% VO(2peak)) in the first test and 29.8+/-10.5 L/min (62.9+/-22.2% VO(2peak)) in the second one. There was no significant difference between both Fat(max) determinations [number of stage: P=0.31; total VO(2): P=0.20; VO(2) utilized for fat oxidation (VO(2Fat)): P=0.33]. Linear correlation coefficients between tests were r=0.84 (total VO(2); P<0.001) and r=0.83 (VO(2Fat); P<0.001). However, Bland-Altman plots revealed wide 95% limits of agreement of 0.91 L/min (total VO(2)) and 0.32 L/min (VO(2Fat)). In conclusion, spontaneous intraindividual variability in Fat(max) appears too large to recommend the use of this parameter for the prescription of training intensity.

Exercise-induced increases in NT-proBNP are not related to the exercise-induced immune response.

OBJECTIVE: To investigate if the exercise-induced immune response contributes to the exercise-induced increase in brain natriuretic peptide (BNP) in healthy athletes. This has previously been speculated, as elevated concentrations of BNP or N-terminal pro brain natriuretic peptide (NT-proBNP) in cardiovascular patients were found to be related to immune reactions and elevations in inflammatory cytokines such as interleukin 6 (IL-6). METHODS: Stored serum samples were analysed for NT-proBNP concentrations of 14 healthy endurance athletes (mean age: 25 (SD 5) years; VO(2peak) 67 (SD 6) ml/min/kg), who had been examined previously for exercise-induced immune reactions and their dependence on carbohydrate supplementation (6 or 12% carbohydrate vs placebo beverages) after three bouts of 4 h cycling at a given workload of 70% of the individual anaerobic threshold. Venous blood samples were taken before, immediately after, and 1 h and 1 day after exercise. Leucocyte subpopulations were determined immediately after blood sampling by flow cytometry. Serum samples for posterior analysis of C-reactive protein (CRP), IL-6, cortisol and NT-proBNP were stored at -80 degrees C. RESULTS: The exercise-induced increases in NT-proBNP (p<0.001) were not related to the exercise-induced immune response, although exercise induced marked (CHOS-dependent) increases in IL-6, CRP, cortisol, leucocytes, neutrophils, monocytes and natural killer cells. CONCLUSION: It is unlikely that the exercise-induced increases in NT-proBNP or BNP in healthy athletes are caused by the exercise-induced immune response. Therefore, exercise-induced increases in NT-proBNP or BNP in healthy athletes have to be differentiated from increases in cardiovascular patients with systemic inflammation.

Inhaled beta2 agonists and performance in competitive athletes.

OBJECTIVES: To provide an overview of the current literature on the use of inhaled beta2 agonists in non-asthmatic competitive athletes, and to assess the performance enhancing effect of inhaled beta2 agonists. METHODS: Review of the literature. RESULTS: Twenty randomised, placebo controlled studies (19 double blind, one single blind) were located. Only three studies reported a performance enhancing effect of inhaled beta2 agonists. However, methodological shortcomings were most likely responsible for these findings (for example, non-elite athletes, inconsistent results in different tests, subgroups with above-average responsiveness). CONCLUSIONS: This review reveals that there is no ergogenic potential of inhaled beta2 agonists in non-asthmatic athletes. In view of the epidemiology of asthma in athletes and the considerable workload involved in provision of therapeutic use exemptions the inclusion of inhaled beta2 agonists on the list of prohibited substances should be reconsidered.

Risk factors for injuries in elite female soccer players.

OBJECTIVE: To describe risk factors for injuries in elite female soccer. METHODS: A total of 143 female soccer players from the German national league participated in the study. Baseline information on player characteristics--for example, anthropometric measurements and playing position--and medical history were recorded at the start of the study. During one outdoor season, injuries and training and match exposure times were prospectively documented for each player. RESULTS: The risk of a new anterior cruciate ligament (ACL) rupture was significantly increased in players with a previous rupture (odds ratio (OR) = 5.24, p = 0.01). This was not the case for ankle sprain (OR = 1.39) or knee sprain (OR = 1.50). In addition, no significantly increased risk of new sprains or ACL ruptures was found when the injured leg was the unit of analysis. Injury incidence was considerably higher in defenders (9.4 injuries per 1000 hours exposure) and strikers (8.4/1000 hours) than goalkeepers (4.8/1000 hours) and midfielders (4.6/1000 hours). Ten per cent of all players (n = 14) sustained more than three injuries. Most of these were defenders (n = 8) or strikers (n = 4). Significantly more injuries occurred to the dominant leg (105 v 71, p = 0.01); this was particularly true for contact injuries (52 v 29, p = 0.01). CONCLUSIONS: Injury risk should be assessed on an individual basis. Therefore it seems appropriate to individualise preventive training programmes, as is recommended for other training content. Evaluating the existing rules of soccer and their appropriate application may also help to decrease injury risk, particularly in contact situations.

Cardiocirculatory and metabolic responses at different walking intensities.

OBJECTIVES: Although walking is a common physical activity, scientifically based training guidelines using standardised tests have not been established. Therefore this explorative study investigated the cardiovascular and metabolic load resulting from different walking intensities derived from maximal velocity (Vmax) during an incremental treadmill walking test. METHODS: Oxygen uptake, heart rate (HR), blood concentrations of lactate and catecholamines, and rating of perceived exertion were recorded in 16 recreational athletes (mean (SD) age 53 (9) years) during three 30 minute walking trials at 70%, 80%, and 90% of Vmax (V70, V80, and V90) attained during an incremental treadmill walking test. RESULTS: Mean (SD) oxygen uptake was 18.2 (2.3), 22.3 (3.1), and 29.3 (5.0) ml/min/kg at V70, V80, and V90 respectively (p<0.001). V70 led to a mean HR of 110 (9) beats/min (66% HRmax), V80 to 124 (9) beats/min (75% HRmax), and V90 to 152 (13) beats/min (93% HRmax) (p<0.001). Mean (SD) lactate concentrations were 1.1 (0.2), 1.8 (0.6), and 3.9 (2.0) mmol/l at V70, V80, and V90 respectively (p<0.001). There were no significant differences between catecholamine concentrations at the different intensities. Rating of perceived exertion was 10 (2) at V70, 12 (2) at V80, and 15 (2) at V90. Twelve subjects reported muscular complaints during exercise at V90 but not at V70 and V80. CONCLUSIONS: Intensity and heart rate prescriptions for walking training can be derived from an incremental treadmill walking test. The cardiovascular and metabolic reactions observed suggest that V80 is the most efficient workload for training in recreational athletes. Further studies are needed to confirm these findings.

Does prolonged cycling of moderate intensity affect immune cell function?

BACKGROUND: Prolonged exercise may induce temporary immunosuppression with a presumed increased susceptibility for infection. However, there are only few data on immune cell function after prolonged cycling at moderate intensities typical for road cycling training sessions. METHODS: The present study examined the influence on immune cell function of 4 h of cycling at a constant intensity of 70% of the individual anaerobic threshold. Interleukin-6 (IL-6) and C-reactive protein (CRP), leukocyte and lymphocyte populations, activities of natural killer (NK), neutrophils, and monocytes were examined before and after exercise, and also on a control day without exercise. RESULTS: Cycling for 4 h induced a moderate acute phase response with increases in IL-6 from 1.0 (SD 0.5) before to 9.6 (5.6) pg/ml 1 h after exercise and CRP from 0.5 (SD 0.4) before to 1.8 (1.3) mg/l 1 day after exercise. Although absolute numbers of circulating NK cells, monocytes, and neutrophils increased during exercise, on a per cell basis NK cell activity, neutrophil and monocyte phagocytosis, and monocyte oxidative burst did not significantly change after exercise. However, a minor effect over time for neutrophil oxidative burst was noted, tending to decrease after exercise. CONCLUSIONS: Prolonged cycling at moderate intensities does not seem to seriously alter the function of cells of the first line of defence. Therefore, the influence of a single typical road cycling training session on the immune system is only moderate and appears to be safe from an immunological point of view.

Toxoplasma antibodies and retinochoroiditis in the Marshall Islands and their association with exposure to radioactive fallout.

Nearly universal serologic evidence of Toxoplasma gondii infection was found to have occurred by adulthood in 517 Marshallese tested in 1981-1982. The prevalence and incidence of retinal lesions compatible with toxoplasmosis were 3.9% and 273 cases/year/100,000 seropositive persons, respectively, thus indicating a significant public health problem. Seronegativity was significantly more common in a subgroup of Marshallese that had received 110-190 rads of total-body gamma radiation as a consequence of accidental exposure to radioactive fallout in 1954. Despite this finding there was no evidence of an increase in clinically significant lesions in exposed persons.

Exercise and atherogenesis: where is the missing link?

Cardiovascular disease is the principal cause of death in Europe, the United States, and much of Asia. If sedentary people begin exercising on a regular basis, there is epidemiologal evidence of approximately 50% reduction in their risk of developing coronary heart disease. This article is an overview about epidemiology and pathogenesis of atherosclerotic lesions. It is intended to put forth the hypothesis that exercise modulates monocytes and T-lymphocytes and that this modulation is capable of guarding against atherosclerosis or inducing regression of atherosclerotic lesions. The literature does not provide sufficient data for drawing conclusions, but this article introduces a new direction of exercise immunological research. Prevention of atherosclerosis or regression of reversible forms of atherosclerotic lesions such as fatty streaks is the principal goal of preventive efforts. Sports medicine and exercise immunology may contribute significantly to the knowledge base if the cellular and molecular responses of regular exercise for atherogenesis are discovered.

Calcium antagonists and exercise performance.

Calcium antagonists lead to a relaxation of smooth vascular muscles and exert a cardiodepressive effect. They make up a heterogeneous group, with primarily substances of the nifedipine and verapamil type playing the most important role in the treatment of cardiocirculatory diseases. The principal indications include coronary heart disease and hypertension. During physical exercise, following the administration of calcium antagonists, VO2max and endurance performance are not impaired. The rate of perceived exertion does not increase to any greater extent in comparison with placebo. Nifedipine leads to an increase of noradrenaline (norepinephrine) as an expression of a reflex activation of the sympathetic system and to a slight increase in heart rate, while calcium antagonists of the verapamil type lower heart rate by 10 to 15 beats/min during physical exercise as a result of their intrinsic negative chronotropic effect. Cardiac output, in spite of the drop in heart rate, remains unchanged. Neither carbohydrate metabolism nor lipid metabolism, including lipolysis, which provide the essential energy-yielding substrates during exercise, are affected by calcium antagonists. Potassium likewise remains unchanged. The response of the hormones insulin, growth hormone and cortisol is the same with calcium antagonists both during incremental graded exercise and during prolonged exercise as with placebo. In comparison with the administration of only calcium antagonists, the combination of calcium antagonists and beta-blockers impairs physical performance. The diminishment in performance, however, is markedly less pronounced than with beta-blocker monotherapy. Unimpaired performance is crucial for physically active patients. Especially for patients performing regular physical activity who suffer from mild hypertension, calcium antagonists provide a viable therapeutic alternative to beta-blockers.

Changes in beta-endorphin levels in response to aerobic and anaerobic exercise.

Exercise-induced increases in the peripheral beta-endorphin concentration are mainly associated both with changes in pain perception and mood state and are possibly of importance in substrate metabolism. A more precise understanding of opioid function during exercise can be achieved by investigating the changes in beta-endorphin concentrations dependent upon intensity and duration of physical exercise and in comparison to other stress hormones. Published studies reveal that incremental graded and short term anaerobic exercise lead to an increase in beta-endorphin levels, the extent correlating with the lactate concentration. During incremental graded exercise beta-endorphin levels increase when the anaerobic threshold has been exceeded or at the point of an overproportionate increase in lactate. In endurance exercise performed at a steady-state between lactate production and elimination, blood beta-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. beta-Endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of cortisol. It is not yet clear whether a relationship exists between the catecholamines and beta-endorphin. These results support a possible role of beta-endorphin in changes of mood state and pain perception during endurance sports. In predominantly anaerobic exercise the behaviour of beta-endorphin depends on the degree of metabolic demand, suggesting an influence of endogenous opioids on anaerobic capacity or acidosis tolerance. Further investigations are necessary to determine the role of beta-endorphin in exercise-mediated physiological and psychological events.

Echocardiographic findings in strength- and endurance-trained athletes.

Assessment of echocardiographic measurements in athletes should take into account the specific sport and the quantity and quality of training. In addition, values corrected for body dimensions, especially the active body mass, should be used rather than absolute values. All parts of the athlete's heart are enlarged and its performance increases. Highly trained endurance athletes show the most enlarged hearts. Athlete's heart can be observed in athletes of all ages including the young. However, it is rarer than generally assumed. To differentiate between physiological and pathological myocardial changes, the relationship between heart size and ergometric performance as well as the echocardiographically measured ratio between left ventricular (LV) myocardial thickness and volume are useful; the latter remains unchanged, on the whole, in endurance- and strength-trained athletes. Concentric hypertrophy cannot be induced by strength training alone; additional factors, such as hypertension, aortic stenosis, cardiomyopathy or anabolic steroid use can play an important role. When corrected for body dimensions, non-endurance-trained, e.g. strength-trained, athletes have standard heart sizes even if considerable time is devoted to training. Findings in healthy untrained persons with large body dimensions also indicate no significant difference between the increase of echocardiographic measures caused by training and that caused by growth. An LV myocardial thickness of 13mm is seldom exceeded even in the highly endurance-trained or anabolic drug-free strength trained athletes under physiological conditions. However, the echocardiographic differentiation of cardiomyopathy can be difficult if an individual is highly trained and has large body dimensions. In such cases, LV end-diastolic diameter may be up to 66 to 70mm. The upper normal value of LV muscle mass is 170 g/m2 for a physiological heart enlargement. Future areas of investigation should include: adaptative changes; of the right ventricle; differences in the regression of the athlete's heart after cessation of training; the differentiation between echocardiographic changes; in highly endurance-trained or combined strength-endurance-trained persons and pathological changes; the importance of heart size and endurance sports performance; and finally the influence of genetic factors.

Sports-specific adaptations and differentiation of the athlete's heart.

Although the sports-specific adaptations and differentiation of an athlete's heart (AH) were first described 100 years ago, the condition is still an area of active debate. In clinical practice, there is often an obvious lack of basic knowledge concerning the prerequisites and well established extent of the structural and functional characteristics of an AH. Some misunderstandings arise from the somewhat misleading term 'athlete's heart' because not every athlete, even if he or she is training and competing at a very high level, develops an enlarged heart. Such a condition can only be expected after years of quantitative and qualitative demanding aerobic endurance training. Although the correlation with competitive performance of endurance events is rather low in trained athletes, the relationship between heart dimensions and ergometric performance represents an important criterion for differentiation between physiological and pathological cardiac enlargement. The assessment of measures exceeding the usual clinical limits, especially concerning volume-dependent echocardiographic parameters, also requires consideration of the strong influence of anthropometric data. The existence of a concentric left ventricular hypertrophy (LVH) in strength-trained athletes is still a topic of debate in the literature, but is rejected by most recent well-conducted trials. In our review. only bodybuilders using anabolic steroids exhibited a distinctly higher hypertrophic index compared with all other groups of endurance or strength athletes. Current unsolved issues in clinical sports medicine concern the early detection of myocardial complications in athletes exercising during infectious diseases, and the eligibility for competitive sport in cases of borderline LVH.

Blood hormones as markers of training stress and overtraining.

An imbalance between the overall strain experienced during exercise training and the athlete's tolerance of such effort may induce overreaching or overtraining syndrome. Overtraining syndrome is characterised by diminished sport-specific physical performance, accelerated fatiguability and subjective symptoms of stress. Overtraining is feared by athletes yet there is a lack of objective parameters suitable for its diagnosis and prevention. In addition to the determination of substrates (e.g. lactate, ammonia and urea) and enzymes (e.g. creatine kinase), the possibilities for monitoring of training by measuring hormonal levels in blood are currently being investigated. Endogenous hormones are essential for physiological reactions and adaptations during physical work and influence the recovery phase after exercise by modulating anabolic and catabolic processes. Testosterone and cortisol are playing a significant role in metabolism of protein as well as carbohydrate metabolism. Both are competitive agonists at the receptor level of muscular cells. The testosterone/cortisol ratio is used as an indication of the anabolic/catabolic balance. This ratio decreases in relation to the intensity and duration of physical exercise, as well as during periods of intense training or repetitive competition, and can be reversed by regenerative measures. Correlations have been noted with the training-induced changes of strength. However, it seems more likely that the testosterone/cortisol ratio indicates the actual physiological strain in training, rather than overtraining syndrome. The sympatho-adrenergic system might be involved in the pathogenesis of overtraining. Overtraining appears as a disturbed autonomic regulation, which in its parasympathicotonic form shows a diminished maximal secretion of catecholamines, combined with an impaired full mobilisation of anaerobic lactic reserves. This is supposed to lead to decreased maximal blood lactate levels and maximal performance. Free plasma adrenaline (epinephrine) and noradrenaline (norepinephrine) may provide additional information for the monitoring of endurance training. While prolonged aerobic exercise conducted at intensities below the individual anaerobic threshold lead to a moderate rise of sympathetic activity, workloads exceeding this threshold are characterised by a disproportionate increase in the levels of catecholamines. In addition, psychological stress during competitive events is characterised by a higher catecholamines to lactate ratio in comparison with training exercise sessions. Thus, the frequency of training sessions with higher anaerobic lactic demands or of competition, should be carefully limited in order to prevent overtraining syndrome. In the state of overtraining syndrome and overreaching, respectively, an intraindividually decreased maximum rise of pituitary hormones (corticotrophin, growth hormone), cortisol and insulin has been found after a standardised exhaustive exercise test performed with an intensity of 10% above the individual anaerobic threshold.(ABSTRACT TRUNCATED AT 400 WORDS)

Oral premedication with low dose midazolam modifies the immunological stress reaction after the setting of retrobulbar anaesthesia.

BACKGROUND/AIMS: An acute immunological stress reaction was previously reported to occur after the painful setting of retrobulbar anaesthesia before intraocular surgery. This study was conducted to find out whether an oral low dose premedication with midazolam would modify the immunological stress reaction. METHODS: 32 patients undergoing intraocular surgery using retrobulbar anaesthesia were included in a randomised, double blind trial. They received premedication with either 3.75 mg midazolam or placebo 30 minutes before the retrobulbar injection. Counts of leucocyte subpopulations, cardiovascular, and psychometric parameters were measured repetitively before and after the retrobulbar injection. RESULTS: The numbers of leucocytes increased significantly in the placebo group after the setting of retrobulbar anaesthesia (before retrobulbar injection: 6687 (SD 1025) cells x10(6)/l; after injection: 7067 (1022) cells x10(6)/l, p=0.0009) caused by rising numbers of neutrophils (before injection: 4111 (1063) cells x10(6)/l; after injection: 4352 (1147) cells x10(6)/l, p=0.0007) and natural killer cells (before injection: 290 (84) cell x10(6)/l; after injection 354 (133) cells x10(6)/l, p=0.003). There was no significant increase in total leucocytes (before injection: 5997 (1288) cells x10(6)/l; after injection: 6189 (1215) cells x10(6)/l) or in any leucocyte subpopulation in the midazolam group. A significant rise in systolic blood pressure occurred in the placebo group, but not in the midazolam group. CONCLUSION: A low dose premedication with midazolam attenuates the immunological and cardiovascular stress reactions occurring with retrobulbar anaesthesia.

Increase of serum insulin and stable c-peptide concentrations with exhaustive incremental graded exercise during acute hypoxia in sedentary subjects.

Hypoxia was shown to reduce insulin concentrations at rest and during exercise. However, some studies have also demonstrated increases in the hormone associated with arterial desaturation. This study was conducted in order to decide [1] whether acute alveolar hypoxia increased or decreased the circulating insulin levels, and [2] to elucidate whether interactions of insulin with other hormones were of relevance in this respect. Glucose (GLU), insulin (INS), c-peptide (CP), adrenaline and noradrenaline (CATs), atrial natriuretic peptide (ANP) and cortisol (CORT) as well as the capillary blood gases were determined in 15 healthy fasting male volunteers (age: 26.2 +/- 2.8 years, body mass index: 22.4 +/- 2.7 kg.m-2). On two separate test days the subjects breathed, in random order, either normal air (N) or a gas mixture with reduced oxygen content (H; FIO2: 0.14). Measurements were made at rest as well as during an incremental cycle exercise in a supine position (increments of 6 min and 50 W) at 100 W and 150 W, at volitional exhaustion (N: 227 +/- 36 W; H: 200 +/- 32 W) as well as in the 5th min of recovery. Arterial desaturation was seen throughout on H-day. At rest all hormones and GLU were normal and showed no influence of H. During exercise INS remained constant on N-day, increased on H-day and was significantly higher with H than with N, most pronounced at 150 W and at volitional exhaustion with 20%, respectively. For CP and GLU no significant exercise-induced changes were seen on either test day and no influence of H was detected.(ABSTRACT TRUNCATED AT 250 WORDS)