Matthias Hütler

Maximal lactate-steady-state independent of performance.

PURPOSE The maximal lactate steady state (MLSS) corresponds to the highest workload that can be maintained over time without a continual blood lactate accumulation. MLSS and MLSS intensity have been speculated to depend on performance. Experimental proof of this hypothesis is missing. METHODS 33 male subjects (age: 23.7 +/- 5.5 yr, height: 181.2 +/- 5.3 cm, body mass: 73.4 +/- 6.4 kg) performed an exhausting incremental load test to measure peak workload and three to six 30-min constant load tests on a cycle ergometer to determine MLSS. RESULTS MLSS (4.9 +/- 1.4 mmol x L(-1)) was independent of MLSS workload (3.4 +/- 0.6 W x kg(-1)) and peak workload (4.8 +/- 0.6 W x kg(-1)). MLSS intensity (71.1 +/- 6.7%) did not correlate with peak workload or MLSS (P > 0.05). A positive correlation was found between peak workload and MLSS workload (r = 0.82, P < 0.001). CONCLUSIONS MLSS and MLSS intensity are independent of performance but subjects with higher maximum performance have higher MLSS workloads. The combination of various fitness related effects on both, the production and the disappearance of lactate during exercise, may explain that different MLSS workloads coincide with similar levels of MLSS and MLSS intensity.

Effect of Test Interruptions on Blood Lactate during Constant Workload Testing

OBJECTIVE To determine whether repetitive test interruptions (TI) during constant load testing influence blood lactate concentration (BLC), maximal lactate steady state (MLSS), MLSS workload (P-MLSS), and relative MLSS intensity (Int-MLSS). METHODS Nineteen males participated in this study. In experiment A, 10 subjects (27.5 +/- 2.9 yr; 183.7 +/- 5.2 cm; 77.4 +/- 3.7 kg) performed 30-min constant load tests: one without TI, one with TI of 30 s, and one with TI of 90 s after every 5 min of cycling at a given workload. In experiment B, nine subjects (28.0 +/- 2.7 yr; 182.9 +/- 6.8 cm; 76.2 +/- 4.5 kg) performed 30-min constant load tests at different workloads until MLSS had been determined for all three TI protocols. RESULTS In experiment A, the BLC after 30 min net working time (BLC30) was higher (P < 0.001) without TI (6.0 +/- 1.3 mmol.l(-1)) than with TI of 30 s (4.9 +/- 1.4 mmol.l(-1)) or 90 s (4.5 +/- 1.1 mmol.l(-1)). The change in BLC during the final 20 min (DeltaBLC10-30) was greater (P < 0.01) without TI (1.2 +/- 1.0 mmol.l(-1)) than with TI of 30 s (0.2 +/- 0.7 mmol.l(-1)) or 90 s (-0.3 +/- 0.7 mmol.l(-1)). In experiment B, the MLSS was not affected, but P-MLSS and Int-MLSS were lower (P < 0.01) without TI (277.8 +/- 24.4W and 73.7 +/- 7.6%) than with TI of 30 s (300.4 +/- 30.4W and 79.2 +/- 8.0%) or 90 s (310.0 +/- 31.2W and 81.5 +/- 7.1%). Approximately 35% of the variance of BLC30 and DeltaBLC10-30, and 70% of the variance of P-MLSS and Int-MLSS were explained by TI duration (P < 0.001). CONCLUSIONS TI decreased BLC30 and DeltaBLC10-30 but has no effect on MLSS. Consequently, with TI, the MLSS is achieved at higher P-MLSS and Int-MLSS.

Effect of growth hormone on exercise tolerance in children with cystic fibrosis

PURPOSE The effect of growth hormone (GH) treatment on exercise tolerance in children with cystic fibrosis was investigated. METHODS 10 prepubertal children (mean +/- SD; age: 12.1 +/- 1.7 yr; height: 137.4 +/- 9.2 cm; body mass: 27.8 +/- 4.2 kg; forced expiratory volume in 1 s (FEV1): 68 +/- 22% predicted) were randomly assigned to either control period (CON, standard therapy) or recombinant human growth hormone (GH) period (additional GH treatment, 0.11-0.14 IU.kg-1, daily, s.c.) for the first 6 months, and then assigned to the other period for the next 6 months. At study entry and after each period, anthropometric data, pulmonary function, and exercise capacity (peak exercise capacity, .VO(2peak), and isokinetic muscle strength) were measured. RESULTS Changes in height (+4.3 +/- 1.0 cm), total body mass (+2.2 +/- 0.8 kg), and lean body mass (LBM, +2.9 +/- 0.7 kg) were significantly higher (P < 0.01) after GH treatment compared with CON. Pulmonary function did not significantly change in either of the periods. In contrast to CON, GH treatment improved absolute .VO(2peak) (+19%, P < 0.01), peak ventilation (+14%, P < 0.01), and peak oxygen pulse (+18%, P < 0.01). Analysis of variance revealed that most of the changes (71%) in .VO(2peak) could be explained by those in LBM and FEV1 (P = 0.001). CONCLUSION GH treatment clearly improved exercise tolerance, presumably resulting from the combined effects of GH on the muscular, cardiovascular, and pulmonary capacity.

Determination of circulating hemoglobin mass and related quantities by using capillary blood.

PURPOSE A standardized carbon monoxide (CO) rebreathing procedure with measurements of CO-hemoglobin, hemoglobin concentration ([Hb]), and hematocrit (Hct) enables to determine total Hb mass (Hb(tot)), blood, erythrocyte, and plasma volume (BV, EV, and PV). These calculations are normally based on venous blood samples. However, micromethods also allow determinations from capillary blood. METHODS The accuracy of using capillary blood for Hb(tot), BV, EV, and PV determination was evaluated in 42 men (age: 25.1 +/- 4.0 yr, body mass: 80.3 +/- 9.6 kg) by comparison of capillary and venous data. RESULTS Capillary Hb(tot) (962 +/- 110 g) did not differ from venous values (959 +/- 106 g). Hb(tot) values were highly correlated (r = 0.987, P < 0.001, SEE 18 g). Also, capillary and venous BV, PV, and EV were highly correlated (0.94 < r < 0.98), but slightly different (-2.7 to 0.9%) because of higher capillary than venous [Hb] and Hct. Coefficients of variation of repeated Hb(tot), EV, PV, and BV measurements (3.0-5.2%) were similar in capillary and venous blood. CONCLUSION Calculation of Hb(tot) using capillary blood is as accurate and reliable as using venous blood.

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation

UNLABELLED Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. PURPOSE To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). METHODS 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. RESULTS Compared with the control condition, hyperventilation reduced (all P < .01) pCO2 (40.5 ± 2.8 vs 22.5 ± 1.6 mm Hg) and HCO3 - (25.5 ± 1.7 vs 22.7 ± 1.6 mmol/L) and increased (all P < .01) pH (7.41 ± 0.01 vs 7.61 ± 0.03) and actual base excess (1.4 ± 1.4 vs 3.2 ± 1.6 mmol/L) pre-WAnT with an ergogenic effect on WAnT average power (681 ± 41 vs 714 ± 44 W) and total metabolic energy (138 ± 12 vs. 144 ± 13 kJ) based on an increase in glycolytic energy (81 ± 13 vs 88 ± 13 kJ). CONCLUSION Hyperventilation-induced respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Hemoglobin Oxygen Affinity in Patients with Cystic Fibrosis

In patients with cystic fibrosis lung damages cause arterial hypoxia. As a typical compensatory reaction one might expect changes in oxygen affinity of hemoglobin. Therefore position (standard half saturation pressure P50st) and slope (Hill’s n) of the O2 dissociation curve as well as the Bohr coefficients (BC) for CO2 and lactic acid were determined in blood of 14 adult patients (8 males, 6 females) and 14 healthy controls (6 males, 8 females). While Hill’s n amounted to approximately 2.6 in all subjects, P50st was slightly increased by 1mmHg in both patient groups (controls male 26.7±0.2, controls female 27.0±0.1, patients male 27.7±0.5, patients female 28.0±0.3 mmHg; mean and standard error, overall p<0.01). Main cause was a rise of 1–2 µmol/g hemoglobin in erythrocytic 2,3-biphosphoglycerate concentration. One patient only, clearly identified as an outlier and with the mutation G551D, showed a reduction of both P50st (24.5 mmHg) and [2,3-biphosphoglycerate] (9.8 µmol/g hemoglobin). There were no differences in BCCO2, but small sex differences in the BC for lactic acid in the controls which were not detectable in the patients. Causes for the right shift of the O2 dissociation curve might be hypoxic stimulation of erythrocytic glycolysis and an increased red cell turnover both causing increased [2,3-biphosphoglycerate]. However, for situations with additional hypercapnia as observed in exercising patients a left shift seems to be a more favourable adaptation in cystic fibrosis. Additionally when in vivo PO2 values were corrected to the standard conditions they mostly lay left of the in vitro O2 dissociation curve in both patients and controls. This hints to unknown fugitive factors influencing oxygen affinity.