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J M Steinacker

Publications and source records attributed to J M Steinacker.

45 records · Page 3Linked to original sources
PubMed1993

Physiological aspects of training in rowing.

At the start of a rowing race, the boat is accelerated and the force on the oars reaches between 1000 and 1500 N. During the race, the speed is maintained at a lower level with a peak rowing force of 500-700 N for 210-230 strokes for about 6.5 min. Rowers are adapted to this effort by a large muscle mass and high metabolic capacities. The muscles of successful rowers demonstrate 70%-85% slow-twitch fibers. Both slow- and fast-twitch fibers have increased oxidative enzyme activities reflecting elevated number and density of mitochondria. Rowing force and boat velocity correlate to maximal oxygen uptake (VO2) which reaches 6.0-6.61.min-1 (65-70 ml.min-1. kg-1) and to the VO2 during a race. In turn, the VO2 during a race is related to slow-twitch fibers content of the muscles, also to the aerobic-anaerobic threshold (AAT) and inversely related to the maximal blood lactate level. The AAT is 80%-85% of maximal performance in highly trained rowers. In successful rowers training intensity is 70% -90% of the training time below the AAT. Training eliciting a blood lactate above 4.0 mmol/l, sprint training and athletics training complete the training schedule, which may reach 1000 h, or 5000-7000 km per year.

Anaerobic Threshold↗
PubMed1992

[Laparoscopic cholecystectomy versus mini-lap-cholecystectomy. Results of a prospective, randomized study].

Laparoscopic cholecystectomy (LCCE) was gaining acceptance rapidly, when several institutions could demonstrate the safety of this minimal invasive treatment modality. Nevertheless prospective randomised studies still are missing to prove the advantages of this new treatment modality in contrast to open cholecystectomy. 77 patients with symptomatic cholelithiasis were treated by LCCE (n = 40) or mini-lap CCE (n = 37) in a prospective, randomised study. As preliminary results, there were no differences in duration of anesthesia and operation time, perioperative complications or postoperative need for analgetics. Patients with LCCE had significant less postoperative pain, less restriction of total vital capacity and a shorter postoperative hospital stay as parameters of a diminished operative trauma.

Cholecystectomy↗
PubMed1988

Dependence of transcutaneous O2 partial pressure on cutaneous blood flow.

Transcutaneous PO2 was measured using a transcutaneous PO2 electrode heated to 45 degrees C on the forearm of 19 healthy volunteers. Cutaneous blood flow (CBF) was estimated indirectly from the heating power of the electrode (HP) and with an 8-MHz bidirectional ultrasonic probe by Doppler shift in a fingertip at 45 degrees C (DF). Blood flow was regulated by an upper arm cuff. Mean transcutaneous PO2 during air respiration was 86.0 +/- 6.2 Torr, and the correlation to arterial PO2 (Pao2) was 0.96 at normal blood flow. The arterial inflow was intermittently reduced in 10-15% stages of effective perfusion pressure (Peff). There was a hyperbolic decrease in PO2 when CBF was restricted in stages. A linear dependence between Peff, HP, and DF was found, which means that there is no autoregulation in the capillary bed at 45 degrees C. Transcutaneous PO2 can be also taken as an indication of CBF. The transcutaneous index, transcutaneous PO2/Pao2, is helpful for estimating local O2 availability.

Blood Gas Monitoring, Transcutaneous↗
PubMed1987

Transcutaneous monitoring of PO2 and PCO2 during running--a noninvasive determination of gas transport.

Transcutaneous pO2 and pCO2 (tcpO2 and tcpCO2) were measured during running with stepwise increased velocities and with constant speed, under both aerobic and anaerobic conditions, for the determination of blood gas transport during exercise. Arterial and transcutaneous blood gas values correlated significantly (pO2 r = 0.87, p less than 0.001, pCO2 r = 0.91, p less than 0.001 respectively). Transcutaneous pCO2 is a noninvasive method of monitoring arterial pCO2 and lactate formation during exercise. When athletes run, arterial pO2 falls to a specific limit depending on the intensity of work. This seems to be characteristic for maximum oxygen transport capacity. The aerobic endurance measured by the aerobic-anaerobic threshold may be dependent on the possibility of sustaining low arterial pO2 during high working levels at high oxygen consumption.

Blood Gas Monitoring, Transcutaneous↗
PubMed1987

Examinations on the blood flow dependence of tcPO2 using the model of the "circulatory hyperbola".

The relation of transcutaneous pO2 (tcpO2) and cutaneous blood flow (CBF) was measured on the forearm of 19 healthy volunteers by use of a tcpO2 electrode heated to 45 degrees C. CBF was estimated indirectly from the heating power of the electrode (HP) and with a 8 MHz bidirectional ultrasonic probe by Doppler shift in a fingertip warmed to 45 degrees C (DF). Arterial blood flow was regulated by a cuff on the upper arm. The arterial flow was reduced in 10-15% stages of effective perfusion pressure Peff. There was a decrease in pO2 when CBF was restricted in stages as suggested by the model of the "circulatory hyperbola" according to Lübbers. A linear dependence between Peff, HP and DF was observed. These results indicate, that there is no autoregulation in the hyperemizied capillary bed. During respiration of air mean tcpO2 was 86.0 Torr (+/- 6.2) in normal blood flow conditions and reflects well paO2. Transcutaneous pO2 may also be used as a measure of CBF. To distinguish between these two modes, the determination of paO2 in capillary blood probes is necessary for calculating the transcutaneous index tcpO2/paO2.

Blood Gas Monitoring, Transcutaneous↗
PubMed1986

Oxygen consumption and metabolic strain in rowing ergometer exercise.

Oxygen consumption (VO2) when rowing was determined on a mechanically braked rowing ergometer (RE) with an electronic measuring device. VO2 was measured by an open spirometric system. The pneumotachograph valve was fixed to the sliding seat, thus reducing movement artefacts. A multi-stage test was performed, beginning with a work load of 150 W and increasing by 50 W every 2 minutes up to exhaustion. Serum lactate concentrations were determined in a 30 s break between the work stages. 61 examinations of oarsmen performing at maximum power of 5 W X kg-1 or more were analysed VO2 and heart rate (HR) for each working stage were measured and the regression line of VO2 on the work load (P) and an estimation error (Sxy) were calculated: VO2 = 12.5 X P + 415.2 (ml X min-1) (Sxy = +/- 337 ml, r = 0.98) Good reproducibility was found in repeated examinations. Similar spiroergometry was carried out on a bicycle ergometer (BE) with 10 well trained rowers and 6 trained cyclists. VO2 of rowing was about 600 ml X min-1 higher than for bicycling in the submaximal stages for both groups. The VO2max of RE exercise was 2.6% higher than for oarsmen on BE, and the cyclists reached a greater VO2 on BE than the oarsmen. No differences were found between RE and BE exercise heart rate. The net work efficiency when rowing was 19% for both groups, experienced and inexperienced: when cycling it was 25% for cyclists and 23% for oarsmen.

Energy Metabolism↗
PubMedDate not supplied

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition.

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate concentration) in blood plasma. The difference between -delta[La].delta pH-1 and delta[HCO3-].delta pH-1 yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, delta[HCO3-].delta pH-1 can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7-8 days (group 1) or 11-12 days (group 2) after their return from a Himalayan expedition (2800-7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia -delta[La].delta pH-1 amounted to [mean (SEM)] 92 (6) mmol.l-1 before altitude, of which 19 (4), 48 (1) and 25 (3) mmol.l-1 were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude -delta[La].delta pH-1 was increased to 128 (12) mmol.l-1 (P < 0.01) in group 1 and decreased to 72 (5) mmol.l-1 in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol.l-1 in group 1 and to 10 (2) mmol.l-1 in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol.l-1]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La- and H+ across cell membranes is differently influenced by high-altitude acclimatization.

Acclimatization↗