INTRODUCTION: Strength training for heart patients seemed not to be indicated until recently. There was fear that this kind of training could lead to malignant ventricular arrhythmia and to inappropriate blood pressure increase. This opinion is changing, however, since cross-sectional strength studies with heart patients showed no increased risks, even for patients with severe heart failure. METHODS: We examined 20 patients (10 in a training group, 10 in a control group) with stable coronary heart disease, 6 or more months after acute incidence, such as myocardial infarction, PTCA or heart surgery. The left ventricular function was slightly to moderate reduced (shortening fraction minimum 0.24). All patients had an echocardiography, a bicycle ergometer test, VO2 max test, a double leg press under ECG and bloodpressure monitoring, additionally blood samples were taken. The training group underwent a normal fitness training for 3 months, twice a week. The training was performed under the supervision of a physician and an experienced physiotherapist. The training consisted of 10 different exercises for shoulder, chest, arm muscles, leg extensors and flexors and abdominal muscles. During the first 4 weeks patients trained with 10 repetitions per exercise with 50% pmax, in the following 4 weeks with 2 series each of 10 repetitions per muscle group, respectivly 3 series in the last 4 weeks. The control group participated once a week (1h) in a regular coronary sports group and trained on their own (log book). RESULTS: During the whole strength training there was no cardiovascular or orthopedic problem. The left ventricular function and the end-diastolic diameter remained unchanged in both groups. There was a clear improvement in the bicycle ergometer in the training group. Cholesterol and triglyceride level decreased slightly. The control group showed no clear improvement. CONCLUSION: Our study shows that strength-endurance training under controlled conditions could be recommended for heart patients with good to moderate decreased LV function.

We have previously reported that HSP70 in human skeletal muscle could be induced by training. However, whether HSP70 induction is dependent upon exercise volume or exercise intensity remains unknown. The aim of the present study was to investigate the relationship between HSP70 and training intensity in rowers. Fourteen well-trained male rowers were divided into two groups (group A, n = 6; group B, n = 8). Group A performed higher intensity exercise during 1st phase, whereas group B performed higher intensity exercise during 2nd training phase. Training volume in 2nd phase increased in both groups. Both training intensity and volume were reduced in 3rd phase. Muscle samples were taken from m. vastus lateralis by fine needle biopsy before training, at the end of the 1st, 2nd and 3rd training phases. HSP70 was quantitatively determined using SDS-PAGE with silver stain. In group A, HSP70 increased significantly from 38 +/- 12 etag before training to 59 +/- 16 etag at the end of the lst training phase (loaded total protein 2.5microg), and decreased afterwards. In group B, HSP70 increase (from 36 +/- 11 etag to 50 +/- 13 etag) in the 1st phase was significantly smaller, there was a further increase of HSP70 in the 2nd phase (60 +/- 14 etag). At the end of the training, HSP70 decreased in both groups. Thus, HSP70 response to training seems to be dependent upon exercise intensity.

BACKGROUND:Few data have been published on training of competitive athletes and about metabolic, hormonal and psychological reactions to overreaching (transient over-training) and tapering in successful athletes.METHODS:Training was recorded and effects on mood state and metabolic and hormonal responses were examined in 10 rowers and spares of the coxed eight during preparation for the World Championships 1995. Mood state was determined using the Recovery-Stress-Questionnaire for Athletes. Resting morning blood parameters as well as performance were measured every week over a period of five weeks.RESULTS:Very high training loads of approximately 3.2 hours per day were sustained for 18 days. Maximum performance (Pmax) and maximum lactate (Lamax) were decreased during high-load training phases (overreaching), Pmax, Lamax and endurance increased after the tapering period. There were decreases in gonadal and hypothalamic steroid hormones (fsh, 1h, prolactin, testosterone) during overreaching and increases in these hormones in tapering. Both performance and hormonal indices of training load were reflected by deterioration of recovery in the Recovery-Stress-Questionnaire for Athletes.CONCLUSIONS:Clear signs of overreaching were found after 18 days of intense training of about 3 h.d(-1) in these highly-trained athletes, i.e. decreases in performance, gonadal and hypothalamic steroid hormones and deterioration of recovery in the psychological questionnaire. After tapering values returned to baseline values before the World Championship. The findings indicate that overreaching is an integral part of successful training regimens and can be analyzed by a multi-factorial approach involving biological and psychometric data.

Previous studies have demonstrated exercise-induced heat shock protein 70 (HSP70) in animals. The purpose of this study was to investigate human skeletal muscle HSP70 response to rowing training. Ten male rowers trained for 4 wk with different forms, durations, and intensities of exercise. Biopsy was performed in the right musculus vastus lateralis before training and at the end of each week. HSP70 in 5 microg of total protein from the muscle sample was determined by using Western blot and immunodetection with chemiluminescence technique, by means of laser densitometer referring to a series of known standard HSP70. Compared with pretraining (100%), HSP70 increased during training (181, 405, 456, and 363% from the first to fourth training week, respectively) with the maximum HSP70 production at the end of second training week. Thus HSP70 is induced in highly trained human muscle by long-term training.

696 In a previous study we have reported for the first time that HSP70 could be induced in response to training in human skeletal muscle. However, it could not be differentiated whether HSP70 induction was dependent more upon exercise volume or exercise intensities. Thus, the aim of the present study was to investigate if HSP70 induction during exercise depends on training intensity. 14 well-trained male rowers, aged 18 yrs, were divided into two groups (group A, n=6; group B, n=8). Group A performed more resistance exercise during the first 2 weeks, whereas group B performed more high intensive rowing training during 3rd training week. Extensive rowing training was not different. Muscle samples were taken from right M. vastus lateralis by fine needle biopsy before training, at the end of 2nd, 3rd and 4th training week. HSP70 was quantitatively determined using SDS-PAGE with silver staining technique by referring to a series of known standard HSP70. In group A, HSP70 increased significantly from 38 ng before training to 59 ng at the end of 2nd training week (median, loaded total protein 2.5 μg), and decreased gradually afterwards. In group B, HSP70 increased from 36 ng before training to 50 ng at the end of 2nd training week, there was a further increase of HSP70 at the end of 3rd training week (60 ng). At the end of the training, HSP70 decreased in both groups. In conclusion, there was an increase of HSP70 in response to training and the response of skeletal muscular HSP70 to exercise seems to be dependent upon exercise intensity.

Definition, types, symptoms, findings, underlying mechanisms, and frequency of overtraining and overtraining syndrome have been described in an introductory article to the present volume. During the past 10 years, our increasing knowledge in this field has also been discussed in different original and review articles well as presented at the 1996 Memphis Overtraining and Overreaching in Sports Conference and summarized in a book project. Aim of this present overview, which was presented during the 1997 Reisensburg Castle workshop, is an additional up-dating of our knowledge considering mechanisms underlying overtraining-related performance incompetence in affected athletes with respect to further results obtained in this field during the past 2 years. Particular emphasis has been given to the time-course of regeneration subsequent to overtraining as far as it is known at present. From an operational standpoint, the thesis was followed that findings such as impairment of neuromuscular function depressed β-adrenergic receptor density related depressed lipolysis, glycogenolysis, glycolysis, and heart rate response as well as depressed intrinsic sympathetic activity depressed turnover in contractile proteins depressed adrenocortical and pituitary-hypothalamic responsiveness in an advanced stage or iron deficiency can explain performance incompetence in overtrained athletes, whereas appropriate regeneration should be indicated by their normalization.

807 To evaluate training-related alterations in the hypothalamo-pituitary-adrenocortical system as a possible indicator of overtraining and regeneration, we performed CRH stimulation tests in 7 junior amateur cyclists (age 17±1 yrs, height 179±2 cm, body mass 64±5 kg, VO2max 56±7 ml*kg⁁−1*min⁁−1) after a synchronisation cycle of 2 weeks (B; median 435 km*wk⁁−1, 50%ROC 226-561) following a hard and long-lasting training/competition season of 8 month, after 2 weeks of to 52 % reduced cycling volume (I), and after 3 more weeks of to 42 % reduced training (F) compared to B, respectively. Baseline resting ACTH (median 4.8 pmol × l⁁−1, 50%ROC 2.9-6.0) and cortisol levels (median 257 mmol × 1⁁−1, 50%ROC 229-441) were in the normal range with an appropriate release in the CRH stimulated pituitary-adrenal function test. After the first 2 weeks of only slight training reduction (I), cortisol release was only ∼50 % by over 70 % CRH release on an in total elevated level of these hormones. Only when the training volume was further reduced for 3 more weeks (F), ACTH and cortisol resting levels and release returned to similar values as at baseline. In conclusion, the organism seems to react to overload, which was also reflected by a reduced or stagnating performance in graded cycle ergometer tests and 10-km outdoor time trials, with hyposensitivity of target organs as a protection against possible damage. The duration necessary for recovery after prolonged and intensive training/competition periods should be rather more than 2 weeks than less with only low-intensity, low-volume activities.

1847 Heat shock protein 70 (HSP70) was reportedly induced by exercise in animals. In humans, a short exercise bout was reported to increase mRNA but not HSP70 expression, and the human muscle HSP70 response to exercise remains unclear. In rowing training, changes of body temperature, energy and metabolism may take place, which might lead to HSP70 induction in the stressed muscle. However, studies dealing with HSP70 induced in human skeletal muscle during a long-term training have not been reported, The purpose of this study was to investigate the skeletal muscle HSP70 response to rowing training with different exercise volumes. Ten male rowers trained for 4 weeks, rowed distance was 25.4, 28.5, 24.5 and 15.2 km/day from 1st to 4th week, respectively. Biopsy was performed in the right M. vastus lateralis before training and at end of each week. HSP70 amount in 5 μg total protein from muscle sample was determined using western blot and immunodetection with chemiluminescence technique, by means of laser densitometer referring to a series of known standard HSP70 amounts. Compared to baseline (0.043 μg) HSP70 increased significantly during whole training (0.078, 0.174, 0.194 and 0.156 μg from the 1 st to 4th training week, respectively). The increase of HSP70 was associated with the exercise volumes in training, but the peak level of HSP70 appeared later than the maximum exercise volume during the whole training. It can be concluded that HSP70 can be induced in human muscle by exercise, and the HSP70 response to exercise is related to training volume.

1289 It is important in rowing training to improve force and endurance capacity. The endurance capacity was traditionally considered to be more dependent on muscle fiber type I while force development more on type II. However, muscle fibers have been currently proven to contain heterogeneous contractile proteins which may determine force or endurance capacity. This study was designed to investigate muscular adaptation to a 4-week-training on the protein level (myosin heavy chain I and II, i.e. MHC I and II, and actin). Ten well trained rowers were enrolled in the study. The training program was divided into 4 phases with emphasis on force development, high intensive endurance and rowing specifically endurance training, and World Championships, respectively. Muscle samples were taken from M. vastus lateralis before training and at end of each training phase by fine needle biopsy. Protein analysis was performed by standard Western blot with specific antibodies, and followed by densitometry. Actin increased during training and decreased after the Championship. MHC II increased clearly and reached its peak level after the force training phase and decreased gradually during the endurance training. During endurance (including sports specific) training, MHC I increased progressively and reached its maximum level. In conclusion, force training leads to increase of MHC II while endurance training to MHC I increment. The dynamic changes of contractile proteins can be observed during a relative short training period, which may provide useful information for evaluation of training strategies.

The management of intermittent claudication involves diagnostic evaluation of the extent of arteriosclerosis in different vascular areas, cardiac risk, other important diseases and indications for interventional procedures in diseased vessels.Nonmedical therapeutic measures involve control of major contributing risk factors, e.g. smoking, arterial hypertonia, hypercholesteremia and metabolic syndrome. Resting blood now to skeletal muscles is low. Therefore, exercise is important in addition to all therapeutic measures because it increases blood Bow and thereby causes endogenous vasodilatation and improves performance, Medical therapy should be focused on underlying diseases, risk factors and on peripheral blood now, Vasodilators are generally useful, however, arteriolar vasodilation seems to be more beneficious than a more venous site of action like in nitrates or alpha-blockers. Increased sympathetic activity may impair collateral blood now despite effective vasodilatation like in nifedipine, Data on calcium-antagonists are not consistent, however, selective dihydropyridines like felodipine increase collateral blood now, Ace-inhibitors are beneficial after at least 10 weeks of therapy, possibly by cardiac action and effects on (collateral) endothelic function, Peripheral vasodilatators like pentoxifylline or i.v. prostaglandins are only useful if severe peripheral now problems exist, Cardiac function is important for maintaining blood now to the stenosis and is improved by ace-inhibitors, beta-blockers and antihypertensive medication, Beta-adrenergic blockers have no negative effects on performance and decrease cardiac risk, Transstenotic blood now is dependent on blood fluidity which is influenced by hematocrit, pentoxifylline, felodipine and exercise. Diuretics should be used cautiously, Patients should receive low dose aspirin. LDL-cholesterol should be lowered to 100 mg/dl, this improves endothelic function, decreases complaints and may cause regression of arteriosclerosis.

Overtraining can be defined as "training-competition > > recovery imbalance", that is assumed to result in glycogen deficit, catabolic > anabolic imbalance, neuroendocrine imbalance, amino acid imbalance, and autonomic imbalance. Additional non-training stress factors and monotony of training exacerbate the risk of a resulting overtraining syndrome. Short-term overtraining called overreaching which can be seen as a normal part of athletic training, must be distinguished from long-term overtraining that can lead to a state described as burnout, staleness or overtraining syndrome. Persistent performance incompetence, persistent high fatigue ratings, altered mood state, increased rate of infections, and suppressed reproductive function have been described as key findings in overtraining syndrome. An increased risk of overtraining syndrome may be expected around 3 weeks of intensified/prolonged endurance training at a high training load level. Heavy training loads may apparently be tolerated for extensive periods of time if athletes take a rest day every week and use alternating hard and easy days of training. Persistent performance incompetence and high fatigue ratings may depend on impaired or inhibited transmission of ergotropic (catabolic) signals to target organs, such as: (I) decreased neuromuscular excitability, (II) inhibition of alpha-motoneuron activity (hypothetic), (III) decreased adrenal sensitivity to ACTH (cortisol release) and increased pituitary sensitivity to GHRH (GH release) resulting in a counter-regulatory shift to a more anabolic endocrine responsibility, (IV) decreased beta-adrenoreceptor density (sensitivity to catecholamines), (V) decreased intrinsic sympathetic activity, and (VI) intracellular protective mechanisms such as increased synthesis of heat-shock proteins (HSP 70) represent a complex strategy against an overload-dependent cellular damage.

This double-blinded, randomized, placebo-controlled study was designed to investigate the acute effect of felodipine on regional blood supply and collateral vascular resistance in patients with peripheral arterial occlusive disease (PAOD). Thirty men with PAOD were treated with a single dose of 5 mg felodipine or placebo. Systolic blood pressure (SBP), Doppler ankle pressure (DAP), calf blood flow (CBF) by venous occlusion plethysmography and calf transcutaneous oxygen tension (tc pO2) were measured during a cycle ergometry. Felodipine reduced SBP significantly (from 149 to 136 mmHg, p < 0.05), while placebo did not. DAP increased slightly but not significantly in both groups. The pressure gradient between SBP and DAP fell significantly in the felodipine group (60 vs 39 mmHg, p < 0.01) but not in the placebo group (59 vs 56 mmHg). There was a trend for lower velocity in tc pO2 decrease during the stress test and higher velocity of tc pO2 increase during recovery from exercise in the felodipine group although the differences between both groups were not significant. In the felodipine group, CBF increased by 35.6% ( p < 0.05) whereas it did not change in the placebo group. In conclusion, while lowering SBP, felodipine increased slightly, or at least maintained, the blood supply to the calves in PAOD patients, which probably results from reducing collateral vascular resistance.

This study was designed to test the hypothesis that the arm muscles are fatigued prior to the leg muscles in rowing exercise. 13 well-trained male rowers performed 2.5 min rowing ergometry with maximal voluntary effort at a frequency of 20 strokes/min. The surface electromyographic (EMG) activity was measured from the dominant M. biceps brachii (BB) and M. vastus lateralis (VL) with silver chloride electrodes 8 cm apart and a sampling frequency of 1000 Hz. The values taken from the 1st and last 30 seconds (30s) were averaged for median frequency (MF), mean power frequency (MPF) and root mean square (RMS) of the EMG amplitude and maximal power output (Pmax). The results show that between the 1st and last 30s of rowing, Pmax decreased significantly by 27 Watts (from 417 to 390 Watts, P=0.01). While MF and MPF of BB decreased significantly from 1st to last 30s (7.2%, P<0.03 and 6.7%, P<0.01, respectively), MF and MPF of VL kept constant (1.3% and 1.0%, respectively, NS). Additionally, RMS of BB showed a trend of an increase by 9.8% (P=0.08) while it of VL remained unchanged (0.7%, P=0.5). Since a decrease of MF and MPF and an increase of RMS are the electromyographic phenomena of muscular fatigue and these were found in BB but not in VL in the present study, it can be concluded that the decrease of Pmax in the last 30s can be contributed to fatigue in arm muscles prior to leg muscles in rowing exercise.

Since we failed to induce an overtraining syndrome in distance runners by 150%*4wks-1 increase in intens. training (ratio ext./intens. training:5.8,3.2,3.1,2.7, wk 1 - 4), we tried it again in 6 less experienced athletes (26.1±1 ys; VO2max 51.5±4.5 ml) by 6 wk bic.erg.training (average ext./ intens.train.ratio:0.17). Results: During graded exercise, performance was increased in wk 3 (+36%) at 2 mmol lactate(P2), decreased in wk 6 (-9% vs wk 3), and after 2 wks of recovery (-11% vs wk 3); P4 was increased in wk 3 (+8%, stagnated in wk 6, and after recovery; total work (summed time*watt) was increased in wk 3 (+8%), stagnated in wk 6, and decreased after recovery (-8% vs baseline). Since glucose-exercise curce in wk 6, after recovery, and glucose response to iv-noradrenaline were suppressed, P2, P4 may have been overestimated (decreased glycogen stores). Suppressed performance and neuromusc. excitab., lack of supercompensation, may indicate an early overtraining stage. The only significant haemotological or blood-chemical change was a decrease in ferritin (-26% in wk 6, -67% vs baseline after recovery). Conclusion: Less adapted athletes may be at risk to get overtrained during monotonous, intensive, non-cyclic training of more than 3 wks with ext./intens.train.ratio << 1. Haematological, blood-chemical parameters, or basal catechol.excr. were not suitable to monitore such a training at a daily caloric demand of 2815±647kcal.

Quantitatively estimating functional reserve of blood supply to the legs in patients with peripheral arterial occlusive disease (PAOD) remains a clinical issue. This study was designed to investigate the regional blood supply to the legs in PAOD patients during exercise by use of thallium 201 (201Tl) whole-body imaging in comparison with transcutaneous PO2 (tcPO2) measurement. Thirty-three patients with PAOD and 10 subjects without PAOD (control) performed an incremental cycle ergometry (CE), while tcPO2 was continuously registered on the involved calf. In the last minute of exercise, 2 mCi of 201Tl was injected intravenously and the 201Tl whole-body images were taken immediately (stress) and four hours (redistribution) following stress with a dual-head camera system. Regional blood supply (RBS) (%) was calculated from the geometric mean counts of the region of interest divided by the total counts of the whole body. The performance of PAOD patients was reduced in doing CE, and tcPO2 fell distinctly in PAOD patients (from 51 to 19 mmHg) whereas it increased in controls (from 57 to 67 mmHg). The RBS in PAOD patients was obviously reduced in comparison with that of controls. While in controls the RBS of the calf (3.1%) at stress did not differ from that at redistribution (3.4%), in PAOD patients the redistribution RBS (2.8%) increased as compared with that of stress (1.5%). There was a hyperbolic relationship between stress RBS of the calf and the velocity of tcPO2 fall in PAOD patients during exercise test (velocity of tcPO2 fall = -0.032 + 0.39/RBS, r2 = 0.54, P < 0.05). In conclusion, the RBS determined by 201Tl whole-body imaging is comparable to the tcPO2 measurement in differentiating patients with PAOD from subjects without PAOD during exercise. Regional 201Tl uptake reflects regional blood supply in PAOD patients. There is a hyperbolic relationship between the RBS derived from 201Tl whole-body imaging and tcPO2 in PAOD patients during exercise, implying that in a critical ischemia the lower the RBS is, the more steeply the tcPO2 decreases.