Abstract: INTRODUCTION: The organism is exposed to a considerable hypoxic stress at high altitude, and the well-known polyglobulia is an effective strategy to sustain oxygen delivery to the tissue at reduced saturation of hemoglobin. In general, an increasing erythropoiesis is thought to be the reason, although this increase of red blood count can be observed after a short time of altitude exposure and the parameters are expressed as water-depending concentrations. Therefore, the influence of water distribution on hemoglobin (Hb) and hematocrit (Hct) values during a long-term exposure at high altitude was investigated. MATERIALS AND METHODS: Measurements were performed in 12 mountaineers before, during, and either 7/8 or 11/12 days after a Himalaya expedition (26-29 days at 4,850 to 7,600 m altitude). Arriving at 4,850 m an initial increase of Hb and Hct was followed by a short decrease during the first week and a continuous increase during the further stay. RESULTS: In maximum, 131.3% (Hb) and 117.4% (Hct) of the starting point were reached during the fourth week at altitude after the attempt to reach the summit of Broad Peak (8,047 m). Parallel the dehydration in the beginning turned to a hyperhydration at the end of the stay (D(2)O method). DISCUSSION: Erythropoietin rose only temporarily at altitude (max. +11 +1 mU/ml serum). Upon return, Hb and Hct normalized within a few days whereas hemoglobin mass (initially 881+ 44 g, CO-Hb method) was still increased by 13% (p < 0.01). CONCLUSION: In conclusion, a hemoconcentration effect (dehydration) is the reason of the initial peak of Hb and Hct. The further increase can only partially be explained by an absolute increase of Hb and Hct caused by stimulated erythropoiesis. A shift of intravasal fluid to the interstitial space is the other main reason of the observed changes in red blood count.
Abstract: The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Delta) in lactic acid ([La]), [HCO3-], pH and PCO2 in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (betanbi=-Delta[La]. DeltapH(-1)-Delta[HCO3-]. DeltapH(-1)) amounted to 40+/-2 (SEM) and 28+/-2 mmol l(-1) in UT and TR, respectively (P<0.01). During recovery beta (nbi) decreased to 20 (UT) and 16 (TR) mmol l(-1) (P<0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Delta[La]. betabi amounted to 37-41 mmol l(-1) being lower than at sea level. The large exercise betanbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower betanbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders betanbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO3-]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.
Abstract: Human performance, defined by mechanical resistance and distance per time, includes human, task and environmental factors, all interrelated. It requires metabolic energy provided by anaerobic and aerobic metabolic energy sources. These sources have specific limitations in the capacity and rate to provide re-phosphorylation energy, which determines individual ratios of aerobic and anaerobic metabolic power and their sustainability. In healthy athletes, limits to provide and utilize metabolic energy are multifactorial, carefully matched and include a safety margin imposed in order to protect the integrity of the human organism under maximal effort. Perception of afferent input associated with effort leads to conscious or unconscious decisions to modulate or terminate performance; however, the underlying mechanisms of cerebral control are not fully understood. The idea to move borders of performance with the help of biochemicals is two millennia old. Biochemical findings resulted in highly effective substances widely used to increase performance in daily life, during preparation for sport events and during competition, but many of them must be considered as doping and therefore illegal. Supplements and food have ergogenic potential; however, numerous concepts are controversially discussed with respect to legality and particularly evidence in terms of usefulness and risks. The effect of evidence-based nutritional strategies on adaptations in terms of gene and protein expression that occur in skeletal muscle during and after exercise training sessions is widely unknown. Biochemical research is essential for better understanding of the basic mechanisms causing fatigue and the regulation of the dynamic adaptation to physical and mental training.
Abstract: It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H+ than La- leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid-base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (-deltaABE) was 2.2 +/- 0.5 (SEM) mmol l(-1) larger than the increase of [La]blood at exhaustion, and the difference rose to 4.8 +/- 0.5 mmol l(-1) during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (delta[La](if+blood)) during exercise and only slightly larger during recovery. The discrepancy between -deltaABE and delta[La]blood mainly results from the Donnan effect hindering the rise of [La]erythrocyte to equal values like [La]plasma. The changing Donnan effect during acidosis causes that Cl- from the interstitial fluid enter plasma and erythrocytes in exchange for HCO3(-). A corresponding amount of La- remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to delta[La]blood instead to delta[La](if+blood). When performing correct comparisons and considering Cl-/HCO3(-) exchange between erythrocytes and extracellular fluid, neither the use of deltaABE nor of deltaSBE provides evidence for differences in H+ and La- transport across the tissue cell membranes.
Abstract: Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Delta) in lactic acid ([La]), [HCO(3)(-)], pH and PCO(2) in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (beta(nbi) = -Delta[La] . DeltapH(-1) - Delta[HCO(3)(-)] . DeltapH(-1)) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 +/- 2(SEM) and 20 +/- 2 mmol l(-1) in UT and TR, respectively (P < 0.02). During recovery beta(nbi) decreased to 14 (UT) and 12(TR) mmol l(-1) (both P < 0.001) corresponding to values previously found at rest by in vivo CO(2) titration. Bicarbonate buffering (beta(bi)) amounted to 44-48 mmol l(-1) during and after exercise. The large exercise beta(nbi) seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO(3)(-) or H(+) with cells and delayed HCO(3)(-) equilibration between plasma and interstitial fluid. Increase of [HCO(3)(-)] during titration by these mechanisms augments total beta and thus the calculated beta(nbi) more than beta(bi) because it reduces DeltapH and Delta[HCO(3)(-)] at constant Delta[La]. The smaller rise in exercise beta(nbi) in TR than UT may be caused by an increased extracellular volume and an improved exchange of La(-), HCO(3)(-) and H(+) between trained muscles and blood.
Abstract: A reliable and cost-effective screening test for erythropoietin (EPO) doping is still unavailable. Thus a new approach by estimating mean red blood cell (RBC) age by means of erythrocyte aspartate aminotransferase activity (eAST) was developed. We investigated 201 women and 169 men residing at low altitude for peak oxygen uptake, EPO, and eAST. Additionally, we investigated 63 women and 42 men residing at 2600 m above sea level for EPO and eAST. Furthermore, 22 female and 28 male patients with renal failure receiving recombinant human EPO (rhEPO) were investigated for eAST levels. There was no difference in eAST between trained (women, 2.9+/-0.7 U x gHb(-1); men, 2.5+/-0.4 U x gHb(-1)), moderately trained (women, 2.8+/-0.6 U x gHb(-1); men, 2.4+/-0.4 U x gHb(-1)), and untrained subjects (women, 3.0+/-0.5 U x gHb(-1); men, 2.5+/-0.4 U.gHb-1) at low altitude. Participants receiving rhEPO had a dose-dependent increase in eAST (r=0.25; P< .05). Trained high-altitude residents (women, 2.8+/-0.8 U x gHb(-1); men, 3.0+/-1.1 U x gHb(-1)) had higher eAST than untrained high-altitude residents (women, 2.5+/-0.6 U.gHb-1; men, 2.4+/-0.4 U x gHb(-1); P< .05). Since eAST was sensitive to RBC rejuvenation, eAST elevation could indicate EPO use in lowlanders. eAST values above the 95% confidence interval (>3.3 U x gHb(-1) for men; >4.1 U x gHb(-1) for women) are suspected of EPO use.
Abstract: Because of lacking ventilatory stimulation by sex hormones in postmenopausal women (PW), one might expect a lowered arterial oxygen saturation (S(O(2))) in hypoxia and therefore a stronger erythropoietic reaction than in young women (YW). Nine untrained (UTRPW) and 11 trained (TRPW) postmenopausal altitude residents (2600 m) were compared to 16 untrained (UTRYW) and 16 trained young women (TRYW) to check this hypothesis and to study the combined response to hypoxia and training. S(O(2)) was decreased in PW (89.2% +/- 2.2 vs. 93.6 +/- 0.7% in YW, p < 0.01). Hb mass, however, was similar in UT (UTRYW: 9.2 +/- 0.9 g/kg(1), UTRPW: 8.7 +/- 1.0 g/kg). But if body fat rise with age was excluded by relation to fat-free mass, Hb mass was increased in UTRPW (+1.2 g/kg, p < 0.05) compared to UTRYW. Training caused a similar rise of Hb mass in PW and YW (0.3 g/kg per mL/kg x min(1) rise in V(O(2peak))). There was no difference in erythropoietin among the groups. Ferritin was higher in PW than YW. The results show that female hormones and fitness level have to be considered in studies on erythropoiesis at altitude. The role of erythropoietin during chronic hypoxia still has to be clarified.
Abstract: PURPOSE: Since the observation that mechanical stress causes red blood cell (RBC) destruction, foot-strike hemolysis has been used to explain sports anemia and RBC rejuvenation in athletes. Recently gained knowledge questions the importance of mechanical RBC trauma on RBC hemolysis in athletes. METHODS: Male athletes (N = 90) and untrained male controls (N = 58) were investigated for aerobic performance, hematological parameters, serum erythropoietin concentration (EPO), soluble transferrin receptor concentration (sTFR), and erythrocyte aspartate aminotransferase activity (eAST). RESULTS: On hard floor running disciplines (HFR, N = 26, short- and long-distance runners, triathletes) showed a lower eAST (P < 0.001) and thus no younger RBC population than not on hard floor running athletes (NHFR, N = 64, cyclists, soccer players, others) or the untrained control group (N = 58). HFR had higher but still normal EPO (P < 0.01) and no higher sTFR. CONCLUSION: Because intravascular hemolysis occurs in swimmers, cyclists, and runners, and mean RBC age is not reduced in runners, mechanisms other than foot-strike hemolysis have to be considered as well. Possible reasons are intramuscular destruction, osmotic stress, and membrane lipid peroxidation caused by free radicals released by activated leukocytes. Intravascular hemolysis can even be regarded as physiological means to provide heme and proteins for muscle growth.
Abstract: Three methods of preparation of red blood cell concentrate for erythrocyte aspartate aminotransferase measurement were compared: (1) filtration of whole blood through a cellulose column (n = 36); (2) washing of whole blood and aspiration of buffy coat after centrifugation (n = 48); (3) optimized method with washing without aspiration of buffy coat (n = 229).
Abstract: BACKGROUND: Fatigue is a frequent and severe problem after treatment of patients with hematological malignancies. This symptom has been associated with anemia, reduced physical performance, mood, endocrine disorders and impaired nutritional status. Recently, it has been suggested that fatigue can be related to a persistent activation of the immune system with increased production of proinflammatory cytokines. However, there is no conclusive evidence regarding the role of the immune system in the origin of fatigue in cancer patients. PATIENTS AND METHODS: We evaluated the correlation of fatigue with thyroid function, markers of immune activity [interleukin (IL)-1alpha, IL-1 soluble receptor, IL-6, C-reactive protein and neopterin], liver and kidney function, mood and physical ability in 71 patients with hematological malignancies. All patients had been free of relapse and not received treatment (chemotherapy, radiotherapy or immune modulators) for at least 3 months. RESULTS: Fatigue was related to depression (r=0.84; P<0.0001) and reduced performance status (r=-0.61; P<0.0001). However, there was no correlation between fatigue and thyroid, liver and kidney function, anemia, albumin concentration or markers of immune activity (all r-values <0.20; P>0.05). CONCLUSIONS: We conclude that fatigue in relapse-free patients with hematological malignancies is associated with depressive mood and reduced physical performance, but not with impairment of thyroid function, anemia or persistent activation of the immune system.
Abstract: Total hemoglobin mass has not been systematically investigated in females at altitude. We measured this quantity (CO-rebreathing method) as well as peak oxygen uptake in 54 young women (age 22.5 +/- 0.6 SE years) with differing physical fitness living in Bogota (2600 m) and compared the results with those of 19 subjects from 964 m in Colombia and 75 subjects from 35 m in Germany. In spite of an increased hemoglobin concentration the hemoglobin mass was not changed in highlanders (means 9.0 to 9.5 g . kg (-1) in untrained subjects at all altitude levels). Endurance trained athletes, however, showed a rise in hemoglobin mass by 2 - 3 g . kg (-1) at all sites. Erythropoietin was little increased in Bogota; iron stores were within the normal range. Aerobic performance capacity was lower at high altitude than at sea level and remained so also after correction for the hypoxic deterioration in untrained and moderately trained subjects but not in athletes; possibly the cause was reduced daily physical activity in non-athletic Bogotanians compared to lowlanders. After exclusion of the factor V.O(2peak) by analysis of covariance a mean rise of 6.6 % in hemoglobin mass at 2600 m was calculated being smaller than in males (> 12 %). The attenuated increase of hemoglobin mass in female highlanders possibly results from stimulation of ventilation improving arterial oxygen saturation or from an increased hypoxia tolerance of cellular metabolism both caused by female sexual hormones.
Abstract: BACKGROUND: Physical activity has been shown to stimulate haematopoiesis in patients with anaemia due to chronic renal failure or haematological malignancies. OBJECTIVE: To evaluate the effect of moderate exercise on the production of haematopoietically active factors. METHODS: Ten patients (four men and six women, mean (SD) age 51 (10) years) with a haemoglobin concentration under 130 g/l (men) or 120 g/l (women) carried out five three minute exercise bouts at an intensity of 80% of the maximal heart rate, corresponding to a lactate concentration of 3 (0.5) mmol/l. Patients rested for three minutes between bouts. The concentrations of interleukin 6, stem cell factor, granulocyte-monocyte colony stimulating factor, granulocyte colony stimulating factor, erythropoietin, and growth hormone (GH) were evaluated before and in the eight hours after exercise. RESULTS: GH had risen significantly 15 minutes after exercise (1.1 (1.3) v 2.7 (2.8) ng/ml; p<0.05). No change in the concentration of the other cytokines and growth factors was observed in the eight hours after exercise. CONCLUSIONS: In patients with anaemia, submaximal exercise does not affect the concentration of haematopoietically active cytokines. However, it leads to an increased concentration of GH. This may be responsible for the improved haematopoiesis observed after an exercise programme in patients with chronic diseases.
Abstract: Fatigue and impaired physical performance are common and sometimes serious problems of cancer patients during and after treatment. To avoid fatigue, cancer patients are often advised to rest and downregulate their daily activities. However, these recommendations can cause paradoxical results. Since inactivity induces muscular wasting, prolonged rest can result in further loss of endurance. Recent studies suggest that exercise, as well as behavioral and some psychosocial interventions, may reduce fatigue and improve the performance status of cancer patients. In this paper, we review interventions proposed for the treatment of cancer-related fatigue and present the results of a study about the effects of exercise on the physical performance of patients with hematological malignancies. Sixty-six inpatients (34 men, 32 women) undergoing conventional ( n=45) or high-dose chemotherapy with stem cell rescue ( n=21) for the treatment of a hematological malignancy exercised daily on a treadmill. Physical performance was assessed on admission and once a week during hospitalization (30+/-10 days, range 10-49). Physical performance remained unchanged in a submaximal standard stress test (on admission: 5.5+/-1.4 km/h; midhospitalization: 5.3+/-1.3 km/h; at discharge: 5.5+/-1.3 km/h; p=0.60) despite chemotherapy and its related complications. A significant decrease in the mean hemoglobin concentration (from 10.3+/-2.0 g/dl on admission to 9.6+/-1.2 g/dl at discharge; p=0.03). We conclude that a daily endurance-training program reduces the treatment-related loss of physical performance in patients with hematological malignancies undergoing chemotherapy.
Abstract: The purpose of our study was to evaluate hematologic acclimatization during 2 weeks of intensive normoxic training with regeneration at moderate altitude (living high-training low, LHTL) and its effects on sea-level performance in well trained athletes compared to another group of equally trained athletes under control conditions (living low - training low, CONTROL). Twenty-one triathletes were ascribed either to LHTL (n = 11; age: 23.0 +/- 4.3 yrs; VO 2 max: 62.5 +/- 9.7 [ml x min -1 x kg -1]) living at 1956 m of altitude or to CONTROL (n = 10; age: 18.7 +/- 5.6 yrs; VO 2 max: 60.5 +/- 6.7 ml x min -1 x kg -1) living at 800 m. Both groups performed an equal training schedule at 800 m. VO 2 max, endurance performance, erythropoietin in serum, hemoglobin mass (Hb tot, CO-rebreathing method) and hematological quantities were measured. A tendency to improved performance in LHTL after the camp was not significant (p < 0.07). Erythropoietin concentration increased temporarily in LHTL (Delta 14.3 +/- 8.7 mU x ml -1; p < 0.012). Hb tot remained unchanged in LHTL whereas was slightly decreased from 12.5 +/- 1.3 to 11.9 +/- 1.3g x kg -1 in CONTROL (p < 0.01). As the reticulocyte number tended to higher values in LHTL than in CONTROL, it seems that a moderate stimulation of erythropoiesis during regeneration at altitude served as a compensation for an exercise-induced destruction of red cells.
Abstract: It was the aim of the study to analyse the haemostatic system during a high standardized intensive short-term (30 s) exercise (anaerobic Wingate test). Blood samples were taken from 15 male subjects before (t0 ), and within 2 (t1 ), 9 (t2 ) and 30 min (t3 ) after the test. We found that the partial thromboplastin time was markedly shortened, whereas the prothrombin time increased slightly from t0 to t1 (p < 0.002) and remained elevated (t3, p < 0.046). Factor VIII increased from t0 to t1 (p < 0.001) and remained elevated as well (t3, p < 0.001). Fibrin monomers were approximately 15 times higher immediately post-exercise (t1, p < 0.001) and continued to be elevated (t3, p < 0.004). The tissue plasminogen activator increased by 4 times after exercise (t1, p < 0.001) and remained elevated (t3, p < 0.002). The d-dimers increased from t0 to t1 (p < 0.001) as well and remained elevated (t3, p < 0.005). Thrombopoietin concentrations were unchanged, whereas the vascular endothelial growth factor increased immediately post-exercise (t0 to t1, p < 0.011 resp. at t2 p < 0.019) and returned to the control level at t3 (p < 0.878). In conclusion, it was found that prothrombotic markers and, even more pronounced, those of the fibrinolytic system were increased. The study provides evidence that due to intensive short-term exercise the balance of the haemostatic system is shifted to a higher equilibrium. Theoretically, the data show that in the case of a subject with risk factors such as impaired fibrinolysis, unfavourable conditions cannot be excluded.
Abstract: 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.
Abstract: 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.
Abstract: The use of the OSM3 oximeter for measurement of the fraction of carboxyhaemoglobin (FCOHb) in blood allows for estimation of total circulating haemoglobin mass (Hb(tot)) by using the carbon monoxide rebreathing method. To ensure high accuracy of Hb(tot) estimation, potential sources of analytical errors should be identified and adjusted for. Based on observed differences in results of measured FCOHb between simultaneously sampled, arterialized and venous blood samples we investigated the influence of haemoglobin oxygen saturation (sO2) on results of measured FCOHb. Blood from nine healthy non-smokers was tonometered with gas mixtures containing 94% N2 or air and 6% CO2. The resulting oxygenated and deoxygenated specimens were mixed in different proportions to obtain varying sO2 values in the same blood. sO2, fractions of dyshaemoglobins, pO2, pCO2 and pH were measured at each step. FCOHb was significantly (p<0.001) higher in oxygenated (median, range: 0.6%, 0.4-0.9%) compared to deoxygenated (-0.2%, -0.5-0.0%) blood. Regression analysis identified the sO2 as the most important factor explaining 86% of the variance in observed changes in FCOHb. The observed sO2 effect has important implications on calibration procedure of OSM3, accuracy of measured FCOHb, and FCOHb dependent calculations such as estimation of Hb(tot) and related quantities. If the highest accuracy of FCOHb measurement is needed, an sO2 effect on results of measured FCOHb has to be considered and adjusted for.
Abstract: Levels of alpha-tocopherol (alphaT) in plasma and red blood cells (RBC) are assumed to be modulated by exercise. The mechanisms involved remain to be established. We examined the influence of different running bouts on the content of alphaT in RBC (alphaT(RBC)), the concentration in plasma (alphaTplasma), and their relationship with lipolysis, as indicated by changes (delta) in plasma glycerol concentration ([glycerol]). Eleven healthy runners [mean (SD) age 35 (9) years, height 177.3 (7.6) cm, body mass 69.6 (9.4) kg, and peak oxygen consumption, VO2peak, 57.8 (4.8) ml.kg(-1).min(-1)] performed an incremental treadmill test [duration 17 (2) min, peak velocity, vpeak 4.8 (0.4) m.s(-1)], a training run [173 (12) min, 57 (4)% vpeak] and a marathon [197 (24) min, 75 (5)% vpeak]. Before (pre) and after (post) each run, haematological and lipid parameters, alphaT(RBC) and alphaTplasma were determined. Haemoconcentration was observed after each run. delta[glycerol] was +0.10 (0.10) mmol.l(-1), +0.40 (0.14) mmol.l(-1) and +0.51 (0.15) mmol.l(-1) in the treadmill test, training run and marathon, respectively. When corrected for haemoconcentration, values of alphaTplasma decreased [-5.4 (7.5)%, P< 0.05] in the treadmill test, were unchanged [+0.7 (8.7)%] in the training run and increased [+7.8 (8.3)%, P<0.05] in the marathon. alphaT(RBC) decreased [pre vs post: 22.7 (3.2) nmol.g haemoglobin(-1) (nmol.g Hb(-1)) vs 18.9 (3.8) nmolg Hb(-1), P < 0.05] in the treadmill test and was not significantly changed in either the training run [20.8 (1.9) nmol.g Hb(-1) vs 19.1 (3.0) nmol.g Hb(-1)] or the marathon [21.6 (2.9) nmol.g Hb(-1) vs 23.4 (2.7) nmol.g Hb(-1)]. deltaalphaT(RBC) and deltaalphaTplasma were positively related to delta[glycerol]. The reduction in alphaTRBC and alphaTplasma after short-lasting heavy exercise indicates the consumption of alphaT, whereas the association between deltaalphaT and delta[glycerol] suggests mobilisation of alphaT, especially in long-lasting exercises. However, although alphaT appears to be influenced by exercise, the results suggest a well-balanced regulation of alphaT during exercise resulting in small, and only in part, significant deltaalphaT in blood.
Abstract: Blood composition, hemoglobin mass (CO rebreathing method) and VO2peak were measured in 15 untrained (UT-Bogotá) and 14 trained males (TR-Bogotá) living at 2600 m of altitude, and in 14 untrained lowlanders (UT-Berlin). [Hb] amounted to 15.3 + 0.2(SE) g/dl in UT-Berlin, 17.4 + 0.2 g/dl in UT-Bogotá and 16.0 + 0.2 g/dl in TR-Bogotá. Hb mass was significantly higher in UT-Bogotá (13.2 + 0.4 g/kg, P < 0.01) and in TR-Bogotá (14.7 + 0.5 g/kg, P < 0.001) than in UT-Berlin (11.7 + 0.2 g/kg). In TR-Bogotá also plasma volume was expanded. Erythropoietin concentrations in UT-Bogotá and TR-Bogotá were not significantly increased. There was a positive correlation between blood volume and VO2peak for the pooled values of all subjects, if the oxygen uptake of UT-Berlin was corrected for an ascent to 2600 m. For the Hb mass - VO2peak relation two groups are indicated pointing to two types of altitude acclimatization with different Hb mass increases but similar distribution of aerobic performance capacity. We suggest that different genetic properties in a population of mixed ethnic origin might play a role.
Abstract: The aim of this paper is a critical reflection of the practice in competitive cycling to use the hematocrit value (Hct) as an indirect control measure for doping with erythropoietin. To demonstrate the individual physiological variation of Hct values, five different studies were performed: 1) Eight subjects were observed (i) during 23 h after a 1 h lasting bout of cycle exercise at 60% of maximum performance and (ii) during 24h under control conditions. 2) Seven subjects were exposed to a 20 min period of -7 head down tilt (HDT), which was followed by 15 min in sitting position. 3) From four subjects blood samples were taken in a sitting position up to 60 min after they had ingested 1 liter isotonic saline solution. 4) Ten subjects performed a vita maxima test on a cycle ergometer, starting at 100W and increasing the workload by 17W every minute. 5) Four elite cyclists participated in a 10 days competition (1,700 km). RESULTS: 1) During the 24h observation period Hct decreased during the night from 45.3+/-3.1 % to 42.9+/-1.5% and returned to the initial values in the morning. This diurnal variation was even more pronounced after submaximal exercise (-4.1 %). 2) Due to fluid shifts from the interstitial into the intravasal compartment, HDT was accompanied by a 3.1+/-0.5% lower Hct. 3) Drinking of the isotonic saline solution also reduced the hematocrit by 3.3+/-0.5% after one hour. 4) Maximum cycle exercise increased the Hct from 46.8+/-2.4 % to 51.3+/-1.9% which was due to a 15 % decrease in plasma volume. 5) Repeated bouts of cycle-exercise reduced the Hct from 46.4+/-1.5% to 41.3+/-1.6%. CONCLUSIONS: All experiments demonstrate that the Hct is not a constant value but can be considerably changed by physiological measures. Clinical studies show that brain oxygen supply decreases with increasing Hct-values, which are also associated with a higher risk of stroke accidents. We therefore recommend to use a Hct-limit solely under strongly controlled standardized conditions to protect professional cyclists from hazardous manoeuvre until more appropriate methods to detect EPO-doping are developed.
Abstract: OBJECTIVE: We investigated whether sulfoconjugation contributes to the inactivation of intravenously infused dopamine (DA) in low concentrations with a predominant action on the kidney. METHODS: Plasma DA and dopamine sulfate (DA-S) concentrations were determined during 4 h of intravenous infusion of DA (2 microg/kg/min) and up to 18 h after cessation of infusion. Twenty-seven healthy young subjects participated in the placebo controlled, randomised and double-blind study. RESULTS: Intravenously administered DA was sulfoconjugated rapidly and to a great extent. After starting the infusion, DA levels rose within minutes and reached a steady state after 30-60 min. The steady-state levels averaged 151.3 +/- 8.2 nmol/l. DA-S levels also increased markedly with infusion from 16.7 +/- 9.9 nmol/l at the start of infusion up to 261.2 +/- 24.2 nmol/l at 30 min after cessation of infusion. Plasma DA concentrations after cessation of the infusion decreased rapidly with an initial half-life of elimination of 4.8 min. Concentrations of plasma DA-S declined with a half-life of 4.5 h. Persistent elevations of free and conjugated DA compared with pre-treatment levels were observed even 18 h after cessation. Heart rate and blood pressure remained unchanged both during DA and saline infusion. CONCLUSION: Findings indicate that the sulfoconjugation pathway contributes markedly to the inactivation of intravenously infused DA and seems not to be saturable by DA infusion in low doses.
Abstract: 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.
Abstract: Before and 7-12 days after an Himalayan expedition CO2 equilibration curves were determined in the blood plasma of 12 mountaineers by in vitro and in vivo CO2 titration; in vivo osmolality changes (delta Osm x deltaPCO2(-1), deltaOsm x delta pH(-1), where PCO2 is the partial pressure of CO2) during the latter experiments yielded estimates of whole body CO2 storage. In vitro -delta[HCO3-] x delta pH(-1) [nonbicarbonate buffer capacity (beta) of blood] was increased 7 days after descent [before 31.3 (SEM 0.4) mmol x kgH2O(-1), after 38.3 (SEM 3.9) mmol x kgH2O(-1); P<0.05] resulting from an increased proportion of young erythrocytes; in additional experiments an augmented beta was found in young (low density cells) compared to old cells [<1.097 g x ml(-1): 0.216 (SEM 0.028) mmol x gHb(-1), >1.100 g x ml(-1): 0.145 (SEM 0.013) mmol x gHb(-1), where Hb is haemoglobin; P < 0.02]. In spite of increased Hb mass in vivo delta[CO2total] x deltaPCO2(-1) [0.192 (SEM 0.010) mmol x kgH2O(-1) x mmHg(-1)] and -delta[HCO3-] x delta pH(-1) [17.9 (SEM 1.0) mmol x kgH2O(-1)] as indicators of extracellular beta rose only slightly after altitude (7 days +16%, P<0.02; +7%, NS) because of haemodilution. The deltaOsm x deltaPCO2(-1) [0.230 (SEM 0.015) mosmol x kgH2O(-1) x mmHg(-1)] remained unchanged. Prealtitude differences in deltaOsm x delta pH(-1) between hypercapnia [-41 (SEM 5) mosmol x kgH2O(-1)] and hypocapnia [-20 (SEM 3) mosmol x kgH2O(-1); P<0.01] disappeared temporarily after return since the former slope was reduced. The high value during hypercapnia before ascent probably resulted from mechanisms stabilizing intracellular pH during moderate hypercapnia which were attenuated after descent.
Abstract: PURPOSE: It is well known that altitude natives differ from sea level natives in aspects of fluid and electrolyte homeostasis. METHODS: To evaluate exercise and environmental influences on the electrolyte and water status in hypoxia adapted subjects, we investigated 11 well-trained marathon runners (33.7 +/- 0.7 yr, 60.5 +/- 1.9 kg), native to an altitude above 2600 m, before and after two marathon races. One competition was held at moderate altitude (AM, 2650 m, 14 degrees C, 55% RH, running time 3 h 6 min +/- 22 min) and another under tropical conditions (HM, 470 m, 28 degrees C, 70% RH, running time 2 h 54 min +/- 30 min). Blood samples were taken 3 d before, immediately after, 1 h after, and 24 h after the races. RESULTS: The loss in body fluid was calculated to be 2.15 L during AM and 5.05 L during HM, respectively. It was compensated mostly by ingested fluids without electrolyte content and by metabolically produced water, which led to hyponatremia during AM (plasma [Na+] from 144.3 +/- 0.7 to 131.7 +/- 2.1 mmol x L(-1)). Severe dehydration without significant changes in plasma [Na+] could be detected after HM. Serum antidiuretic hormone concentrations and serum aldosterone concentrations significantly increased during both races and remained at a high level for at least 1h after both competitions. Serum atrial natriuretic peptide (ANP) concentrations were at a high level at rest, increasing during HM, and decreasing during AM. CONCLUSION: Under tropical conditions, we found a severe state of dehydration characterized by an extended ANP-response, which was not prevented by water intake during the race. Under hypoxic conditions, however, we found that hyponatremia had developed. This can be partly explained by pure water intake and metabolically produced water, and also, possibly, by a special hypoxia-induced effect.
Abstract: The aim of the study was to investigate blood alterations caused by altitude acclimatization which last more than few days after return and might play a role for exercise performance at sea level. Measurements were performed in 12 mountaineers before, during and either 7/8 or 11/12 days after a Himalaya expedition (26-29 days at 4900 to 7600 m altitude). [Erythropoietin] rose only temporarily at altitude (max. +11 +/- 1 [SE] mu/ml serum). After return hemoglobin mass (initially 881 +/- 44 g, CO-Hb method) was increased by 14% (p < 0.01); aspartate aminotransferase activity in erythrocytes (initially 682 +/- 25 U/l) was augmented (day 7: +964 +/- 152 U/l, day 11: +533 +/- 107 U/l) indicating reduced mean cell age. Calculated blood volume (+14%) was influenced by red cell formation at altitude but also by plasma expansion at sea level. The half saturation pressure for Hb-O2 (pH 7.4, 37 degrees C) as well as the 2.3-diphosphoglycerate concentration were already initially high (32.1 +/- 0.5 mmHg, 20.5 +/- 0.7 mumol/g Hb) and showed only a nonsignificant tendency to increase after return. Also Hill's n was consistently high in the mountaineers, whereas the Bohr coefficients were slightly increased only after descent. Probably the preparatory physical training, partly in the Alps, and the stay in the Himalaya influenced O2-affinity for a prolonged time. The adaptations might reduce the loss of physical performance capacity at altitude and be part of altitude training effects.
Abstract: The importance of oxygen transport and consumption in the body for endurance performance is the reason why altitude training as preparation for competitions at sea level has become popular. In hypoxia maximal O2 uptake decreases. Thus for equal work load training at altitude is harder and stimulates adaptation processes more than sea level training. A specific altitude training effect, however, can only be proven if a relative equal load (in % of VO2max) is more effective than during sea level training. In only three of 10 investigations with this design has a significant improvement of either maximal performance, VO2max or endurance been found, in two there was a nonsignificant tendency. When training in hypoxia combined with living in normoxia was investigated two of four groups improved. Living in hypoxia with training in normoxia is probably more effective but only preliminary publications are available. Summarizing, a small specific altitude effect on performance capacity seems to exist, which may be counteracted by negative influences like reduced stimulation of muscular metabolism. A series of single physiological changes at altitude might have positive or negative implications on training success: training of respiratory muscles, increase of hypoxic ventilatory stimulation, reduced heart training by vegetative "braking", increase of red cell and plasma volume (the latter after descent), right shift of the oxygen dissociation curve, increase of oxidative muscle enzymes (only after hypoxia training), shift from fat and muscle glycogen to blood glucose combustion, reduced lactic acid and ammonia production, increase in buffer capacity.
Abstract: Studies were made of pulmonary diffusion capacity and oxygen transport before and after an expedition to altitudes at and above 4900 m. Maximum power (Pmax) and maximal oxygen uptake (VO2max) were measured in 11 mountaineers in an incremental cycle ergometer test (25W.min-1) before and after return from basecamp (30 days at 4900 m or higher). In a second test, cardiac output (Qc) and lung diffusion capacity of carbon monoxide (DL,cg) were measured by acetylene and CO rebreathing at rest and during exercise at low, medium and submaximal intensities. After acclimatization, VO2max and Pmax decreased by 5.1% [from 61.0 (SD 6.2) to 57.9 (SD 10.2) ml.kg-1, n.s.] and 9.9% [from 5.13 (SD 0.66) to 4.62 (SD 0.42) W.kg-1, n.s.], respectively. The maximal cardiac index and DL,cg decreased significantly by 15.6% [14.1 (SD 1.41) 1.min-1.m-2 to 11.9 (SD 1.44)1.min-1.m-2, P < 0.05] and 14.3% [85.9 (SD 4.36) ml.mmHg-1. min-1 to 73.6 (SD 15.2) ml.mmHg-1.min-1, P < 0.05], respectively. The expedition to high altitude led to a decrease in maximal Qc, oxygen uptake and DL,cg. A decrease in muscle mass and capillarity may have been responsible for the decrease in maximal Qc which may have resulted in a decrease of DL,cg and an increase in alveolar-arterial oxygen difference. The decrease in DL,cg especially at lower exercise intensities after the expedition may have been due to a ventilation-perfusion mismatch and changes in blood capacitance. At higher exercise intensities diffusion limitation due to reduced pulmonary capillary contact time may also have occurred.
Abstract: Because of the importance of oxygen transport and consumption in the body for endurance performance altitude training as preparation for competitions at sea level has come into use. In hypoxia maximal O2 uptake decreases. Thus for equal work load training at altitude is harder and stimulates adaptation processes more than sea level training. A specific altitude training effect, however, can only be proven if a relative equal load (in % of VO2max) is more effective than during sea level training. In only 3 of 10 investigations with this design a significant improvement of either maximal performance, VO2max or endurance was found, in 2 there was a nonsignificant tendency. When training in hypoxia combined with living in normoxia was investigated two of four groups improved. Presumably there exists a small specific altitude effect on performance capacity, which may be counteracted by negative influences like reduced muscular metabolic intensity. A series of single physiological changes at altitude might have positive or negative influences on training success: training of ventilatory muscles, increase of hypoxic ventilatory stimulation, reduced heart training by vegetative 'braking', increase of red cell and plasma volume (the latter after descent), right shift of the oxygen dissociation curve, increase of oxidative muscle enzymes (only after hypoxia training), shift from carbohydrate to fat combustion, reduced lactic acid and ammonia production, improvement of buffering.
Abstract: This study was performed to investigate oxygen transport properties in whole blood (WB) of malaria-infected rats as well as in infected erythrocytes (IE) and noninfected erythrocytes (NIE) separated by density centrifugation. One week after inoculation with Plasmodium berghei, mean parasitemia was 26.5% and high correlations were found between parasitemia and hemoglobin concentration ([Hb]; r = -.902), mean cellular Hb concentration (MCHC; r = -.712), MetHb (r = .923), and base excess (r = -.922). Compared with control animals (C), the oxygen affinity was lower in WB under standard (pH 7.40) and simulated "in vivo" (pH 7.00) conditions (difference in P50, 5.7 and 5.1 mm Hg, respectively; 2P < .01, 2P < .05). In IE Hb and 2,3-biphosphoglycerate (2,3-BPG) concentrations were decreased (MCHC: IE 14.6 +/- 1.0, NIE 33.1 +/- 1.7 g/100 mL; [2,3-BPG]: IE 2.0 +/- 0.6, NIE 7.6 +/- 1.8 mmol/L), whereas [MetHb] and [ATP] were increased ([MetHb]: IE 19.0 +/- 3.7, NIE 0.7% +/- 0.8%; [ATP]: IE 33.5 +/- 2.4, NIE 6.2 +/- 1.0 mumol/g Hb). At pH 7.40, half-saturation oxygen tension (P50) was reduced in IE (29.6 +/- 2.6, NIE 39.2 +/- 5.4 mm Hg, 2P < .001), which correlates with lower [2,3-BPG], increased MetHb content, and higher intrinsic Hb-O2 affinity. However, at pH 7.00, the oxygen affinity was lower in IE when compared with NIE, which was most likely due to high [ATP] in IE. The resulting Bohr coefficients (BC) calculated for CO2 and lactic acid were extremely high in IE and low in NIE (at 50% O2-saturation BCCO2: IE -1.04 +/- 0.06, NIE -0.26 +/- 0.10, 2P < .001; BCLac: IE -0.82 +/- 0.16, NIE -0.47 +/- 0.07, 2P < .001), which was caused by different [2,3-BPG] and [ATP] as well as probably by structural changes of the Hb molecule. The O2 capacity was 14.1 mL per 100 mL erythrocytes in IE compared with 44.4 mL/100 mL in NIE. On the basis of the calculated arterio-venous O2 difference under "in vivo" conditions, the infected red blood cell fraction transports 30% of the O2 amount delivered to the tissues by the noninfected cells (IE 8.0, NIE 26.9 mL/100 mL red blood cells). We conclude that the O2 transport in malaria infected blood is not only affected by the degree of anemia but also by the percentage of infected erythrocytes.
Abstract: Aiming to evaluate the mechanisms responsible for altered O2-transporting properties in blood of Plasmodium-infected animals, stripped (cofactor-free) hemoglobin (Hb) solutions were prepared from infected erythrocytes (IE) and noninfected erythrocytes (NIE) of rats inoculated with Plasmodium berghei bergei for functional and structural characterization. At normal intraerythrocytic pH (+/- 7.2), Hb from IE showed a higher affinity, a larger Bohr effect, and lower sensitivities to 2,3-diphosphoglycerate (DPG) and to temperature than did NIE Hb. Moreover, as judged from electrophoresis, isoelectric focusing, and gel filtration experiments, Hb from IE show changes in charge and molecular assembly. The results indicate that the higher O2 affinity and greater Bohr factors observed in IE compared with those for NIE are attributable to chemical modification of the Hb that increases its intrinsic O2 affinity and decreases its sensitivity to DPG as well as to changes in the intracellular physicochemical milieu, including reduced DPG levels.
Abstract: The influence of lactic acid, hydrochloric acid, and sodium lactate addition (10 mmol/l each) on oxylabile CO2 was investigated in blood of male subjects after equilibration at 37 degrees C with 3, 6, and 10% CO2 in N2 and O2, respectively. The total CO2, pH in whole blood and erythrocytes, oxygen saturation, hemoglobin concentration, and hematocrit value were measured. With these data we calculated bicarbonate and carbamate concentrations and the corresponding differences between oxygenated and deoxygenated blood. The amount of oxylabile bicarbonate was not systematically influenced by the various experimental conditions. The carbamate content, however, was larger in deoxygenated than in oxygenated blood (up to 0.08 mol/mol hemoglobin) only in the absence of lactate. In the presence of lactic acid as well as sodium lactate, the carbamate content in oxygenated blood was higher by 0.06-0.13 mol/mol hemoglobin than in deoxygenated blood. The lactate effect even increased after 2,3-diphosphoglycerate depletion. We suggest, therefore, a competition between CO2 and the lactate ion at the NH2-terminal valine of the beta-globin chain in deoxygenated hemoglobin.
Abstract: During and after two successive incremental cycle ergometer tests (tests A and B), plasma potassium concentration ([K+]p), plasma pH (pHp), plasma partial pressure of carbon dioxide, blood lactate concentration ([Lac-]b) and ventilation (VE) were measured. While there was a good correlation between the increase in [K+]p and VE or pHp, respectively, in test A, in test B a close correlation was found only between the increase in VE and [K+]p (r greater than 0.9 for nearly all single cases; r was 0.84 and 0.89 for all (pooled) cases in tests A and B, respectively; the correlation coefficients between changes in pHp and VE in tests A and B were r = 0.74 and r = 0.28, respectively, and r = 0.89 and r = 0.10 between the changes in [Lac-]b and VE in tests A and B). The close relationship for individuals between VE and [K+]p in tests A and B supported the hypothesis that the extracellular increase in [K+] may contribute to the ventilatory drive during exercise. The comparison of the results of tests A and B further indicated that the relationship between pHp and VE was dependent on the experimental design, and that pHp and VE changes are unlikely to be cause and effect.
Abstract: Conditions simulating changes during physical exercise were induced in erythrocytes to determine the resulting Bohr effect. Lactic acid was added to red cell suspensions and whole blood with initial 25 and 60% SO2, at 42 Torr PCO2, and temperatures of 20 and 37 degrees C. Changes in pH, PO2 and SO2 were measured. CO2 liberation from buffering lactic acid in the extracellular fluid and its diffusion into erythrocytes resulted in an exaggerated Bohr shift, if the gas could not escape from the liquid phase (closed system, 'muscle' conditions). PO2 at constant SO2 increased by up to 11.7%.mmol-1.L lactic acid. After reequilibration to initial PCO2 values (open system, 'lung' conditions) the Bohr shift decreased (remaining PO2 increase 0.7-1.4%.mmol-1.L) mainly caused by the reduced acidification. In addition, the Bohr coefficients (BC) under closed conditions were larger (-0.36 to -0.50) than after reequilibration (-0.20 to -0.38). This difference is attributed to a larger CO2 BC than fixed acid BC. These effects might be enhanced in vivo by temperature differences between muscle and lung, lowered nonbicarbonate buffering of blood and counter-current blood flow in muscle.
Abstract: The physical performance of 12 anemic patients on renal dialysis was investigated following treatment of renal anemia with recombinant human erythropoietin (rhEPO; 40-120 U/kg, 3 times a week). Exercise intensity at a heart rate of 130 beats/min (PWC130) on a bicycle ergometer was assessed before rhEPO treatment, after reaching the target hematocrit (73 +/- 18 days), and in the maintenance phase (211 +/- 53 days). Hemoglobin concentrations measured at these time points were 7.3 +/- 1.2, 11.9 +/- 1.5, and 12.1 +/- 1.4 g/dl, respectively. PWC130 rose from 77 +/- 27 to 104 +/- 37 and 104 +/- 51 W, respectively. Aerobic threshold (i.e. blood lactic acid concentration of 2 mmol/l) shifted to higher workloads indicating improved muscle oxygen supply.
Abstract: Hemoglobin oxygen binding properties and acid-base status were investigated in Colombian athletes (A) and controls (C) from Cali (C-1000 m) and Bogotá (B-2600 m). [Hb] and Hct values were not influenced by altitude, but Hct was lower in the blood of athletes (in Cali 2.6%, in Bogotá 1.4%). Both training and altitude produced a right-shift of the standard oxygen dissociation curve (P50 in CC 28.5 +/- 0.9 mmHg, AC 31.0 +/- 1.4 mmHg, CB 29.6 +/- 1.5 mmHg) leading to highest P50 in blood of altitude athletes (32.3 +/- 1.1 mmHg). Opposite to the position of the ODC the slope "n" was only increased by altitude influence (delta "n" in controls 0.07, in athletes 0.28). The BCCO2 was increased in AC over the whole saturation range, whereas BCLac was neither significantly influenced by training nor by altitude. All altitude effects can be explained by higher [DPG] (delta[DPG] in controls 5.0 mumol/gHb, in athletes 3.9 mumol/gHb), but the cause for the training effects still remains unclear. The acid base status in altitude residents was characterized by low BE and pCO2, which was most pronounced in altitude athletes, the latter correcting the actual venous pH to normal values. No significant variations of the Hb-O2-binding properties could be detected in athletes one day after leaving high altitude when compared with blood samples of athletes taken at high altitude, whereas BE and venous pCO2 were already increased. It is concluded that high altitude athletes are favoured during aerobic and handicapped during anaerobic exercise after the rapid descent to low altitude.
Abstract: During resting conditions plasma hydrogen ion concentration ([H+]P) is known to influence ventilation (VE), whereas the control of plasma potassium concentration ([K+]P) at rest and of both [K+]P and VE during exercise are controversial issues. To obtain more information about these variables during muscular work, eight trained men performed two successive intense continuous cycle-ergometer tests, the first (test I) during metabolic acidosis, the second (test II) with an alkalotic pH. No correlation was found between [H+]P and [K+]P or VE in the direction of change of these variables in test I. Furthermore, no correlation between [H+]P and [K+]P in test I and II was seen. Instead [K+]P and VE changed in relation to the exercise intensity. We suggest that the results confirm [K+]P as an indicator of muscular stress. In addition, the similar behaviour of relative values of [K+]P and VE changes in test I (r = 0.9, m = 1.0, where m is the slope of the regression curve) supports the hypothesis that extracellular potassium controls VE and thereby [H+]P also.
Abstract: Correction of a base deficit with hypertonic sodium bicarbonate (NaHCO3) according to the formula 0.3 x body weight (kg) x BE may overestimate the real demands, especially during shock and cardiopulmonary resuscitation (CPR). Life threatening alkalosis and osmolal poisoning may be the consequence. As an explanation, the possibly impaired functional distribution space related to low cardiac output and volume centralization during CPR is proposed. By application of our own and outside literature, data equations are specified for an approximate precalculation of osmolality and pH changes due to infusion of hypertonic NaHCO3. Calculation of the osmotic volumes of distribution of NaHCO3 during cardiopulmonary resuscitation (CPR) from emergency literature data demonstrates a possible reduction of the functional distribution spaces of about 70 to 80% compared with normal values. This is in good agreement with the reported reduction of cardiac output to about 25% of normal during CPR. The calculated amount of sodium bicarbonate to be recommended during CPR, thus, should not exceed 50 mmol given in time intervals of at least 10 min, severe acidosis and sufficient ventilation presumed.
Abstract: Changes in blood composition, renal function, aldosterone and antidiuretic hormone (ADH) concentrations were investigated in 10 untrained male subjects when swimming (60 min at a heart rate of about 155 beats.min-1, water temperature 28 degrees C) and during the subsequent 3 h in a sitting position. Many specific effects of either exercise or immersion were abolished or attenuated; no significant changes in plasma aldosterone, [ADH], [K+], [Cl-], or of urinary volume, glomerular filtration rate, free water or osmolar clearance were observed. The urine was diluted resulting in lowered [Na+]. In blood some quantities which are only slightly influenced by immersion increased during swimming ([Na+], [Lac-], [H+], osmolality, [creatinine]). Exercise induced plasma volume loss, calculated from increasing [Hb], was small (110 ml), probably because interstitial fluid enters the vascular space during the initial phase of immersion. One might anticipate that the training effects on fluid and electrolyte metabolism and circulation are different when swimming and when performing endurance sports on land.
Abstract: The effect of three weeks ergometer training (Tr) 5 times a week for 45 min at 70% VO2max by 6 subjects on erythrocyte turnover and haemoglobin O2 affinity has been studied. Increased reticulocytosis could be observed from the second day after beginning Tr until a few days after its end, probably caused by increased erythropoietin release by the kidney. Erythrocyte destruction was most pronounced in the first and markedly reduced in the third week of Tr. Elevated glutamate oxalacetate transaminase activity and creatine as well as lowered mean corpuscular haemoglobin indicate a younger erythrocyte population in the first week of recovery. Total blood volume increased during the course of Tr by 700 ml, mainly caused by a raised plasma volume (74%). Red cell volume increased later with maximal values one week after Tr (+280 ml). In this week the standard oxygen dissociation curve was most shifted to the right (P50 increased from 3.77 +/- 0.05 kPa to 3.99 +/- 0.07 kPa) and the Bohr coefficients had their lowest values. Both effects are completely explainable by the haemoglobin O2 binding properties of young erythrocytes. After training, all parameters of physical performance (VO2max, maximal workload, heart rate during rest and exercise) were markedly improved, indicating fast adaptation mechanisms. The increased erythrocyte turnover, including higher erythropoiesis, seems to be one important part of these effects.
Abstract: Parameters characterizing the hemoglobin oxygen affinity were determined in blood of 12 male patients suffering from arterial occlusive disease (AOD) of the legs and compared with data obtained earlier from healthy human subjects (controls). Due to a COHb content of 4.8% +/- 2.2% in the cigarette-smoking AOD patients, the standard oxygen dissociation curve (ODC) was left-shifted, the half-saturation pressure (P50) amounted to 24.8 +/- 1.7 mmHg (3.30 +/- 0.23 kPa), although the 2,3-diphosphoglycerate concentration was increased to 15.3 +/- 1.7 mumol/g Hb. Correcting the effects of elevated COHb shifts the P50 to 26.3 mmHg (3.5 kPa) and increases the steepness of the ODC (Hill's "n") from 2.79 +/- 0.27 to about 2.99, which is significantly different from controls. The Bohr coefficients after acidification of blood with lactic acid (BCLac) show high values at low oxygen saturations of hemoglobin (-0.50 +/- 0.04 in AOD patients, -0.32 +/- 0.04 in controls; P less than 0.05 at 10% SO2). The cause of the alterations in hemoglobin oxygen affinity may be a reduced mean erythrocyte age, but also the influence of unknown factors generated, e.g., from anaerobic muscle metabolism in AOD.
Abstract: In blood of 21 anemic patients and 8 normal subjects (N) three oxygen dissociation curves each were measured at different pH values to calculate Bohr coefficients after acidification with CO2 (BCCO2) or fixed acid (BCFA), and other important parameters of oxygen affinity. The patients had either low hemoglobin or red cell production (L: n = 11, 7.3 g/dl Hb) or high erythrocyte production combined with high loss (H: n = 10, 7.8 g/dl Hb). The standard half saturation pressure P50 (pH 7.4, 37 degrees C) was equally elevated in both anemic groups (L: 30.5, H: 30.8, N: 26.7 mmHg), as well as the diphosphoglycerate concentration (DPG) (L: 18.7, H: 18.6, N: 12.7 mumol/g Hb). The red cell pH of the anemics was lower than for the N (approximately 0.045 units) causing part of the difference in P50. Hill's "n" tended to high values in the anemics except at low O2-saturation in the H. For BCCO2 no significant difference among the groups was observed. BCFA, however, increased in the H at low SO2 compared to the N and L. The cause for most of the changes in hemoglobin oxygen affinity in anemics was the high [DPG]. The combination of high P50 and high "n" value as in the L seems to be most advantageous for tissue oxygenation.
Abstract: Hemoglobin-oxygen-binding characteristics and essential influencing factors were investigated in human erythrocytes of different age separated by density gradient centrifugation. The most important age-dependent changes of the cell milieu are losses of K+, organic phosphates and water; the latter also leads to an increased concentration of negative charges on Hb. This augments the Donnan effect, which is only partly compensated for by a decrease of DPG-. The oxygen dissociation curve of the oldest fraction (P50 23.4 mm Hg) is shifted to the left compared to young cells (P50 29.2 mm Hg), and Hills 'n' is decreased (old cells 2.31, young cells 2.74). The Bohr effect for CO2 increases in the old population (BCCO2 at 50% SO2 -0.63 and -0.24 for old and young erythrocytes, respectively). This effect is less pronounced for the Bohr coefficients for lactic acid (delta BCLac 0.09). Most cell age-dependent alterations of Hb-O2-binding (including BCCO2) are explainable by opposite alterations of [Hb] and [DPG], causing the change of the ratio [DPG]/[Hb] from 1.3 to 0.7 during the aging process of the erythrocytes. Minor effects may result from aging of the Hb-molecule itself.
Abstract: Blood osmolality (Osm) increases with PCO2 because of CO2 absorption. The influences of NaOH addition, equilibration temperature, and hemoglobin concentration on these respiratory changes of Osm were measured by freezing-point determination in true plasma. Addition of NaOH increases Osm by 2 mosmol X kg H2O-1 X mmol base-1 X l at constant PCO2 due to the osmotic effects of Na+ and produced bicarbonate. Respiratory compensation of the pH change further increases Osm. This contrasts to the respiratory compensation of the osmolar disturbance caused by fixed acid. Raising the equilibration temperature reduces Osm by 0.5 mosmol X kg H2O-1 X degrees C-1 at constant pH mainly caused by a lower absorption coefficient for CO2 and changed pK value for H2CO3. The slope of the linear regression lines between Osm and pH during CO2 equilibration increases with hemoglobin; the value of the quotient delta Osm/delta pH depends directly on the nonbicarbonate buffer value. The use of this quotient for the estimation of the mean nonbicarbonate buffer value of the whole body is suggested. The osmotic effects of therapeutic base infusion should be regarded with caution.
Abstract: The aim of this investigation was to study how the known dependence of working efficiency on pedaling frequency is influenced by the work load as well as by physical fitness. Oxygen uptake, CO2 output, ventilation, heart rate, and lactate concentration in capillary blood from the earlobe were determined at varying combinations of work loads and pedaling rates in road-racing cyclists and medical students. Respiratory exchange ratio, consumption of energy, gross efficiency, net efficiency, and delta efficiency (delta work rate/delta metabolic rate) were calculated. All parameters showed a nonlinear dependence on pedaling frequency. The lowest oxygen uptake and the highest efficiency shifted to higher frequencies with increasing work load. Delta efficiency increased with rising pedaling frequency. Differences of VO2 and efficiencies between trained and untrained subjects were only small. Most effects can be explained by variations in leg movement frequency and recruitment of muscle fibers. There is evidence that racing cyclists chose pedaling rates yielding optimal efficiency at any load.
Abstract: Changes of osmolality (Osm) were measured by freezing-point determination in true plasma of 10 healthy subjects. This was done after equilibration with CO2 (0.5-10.0%), after the addition of lactic acid (10 and 20 mmol/l), and after deoxygenation. The graph for the dependence of Osm on CO2 partial pressure (PCO2) in oxygenated blood resembles the classical CO2 absorption curve. The increase of Osm with PCO2 (approximately 0.2 mosmol . kg H2O-1 . Torr-1) is almost as great as the increase in dissolved CO2 plus bicarbonate (HCO-3). Addition of lactic acid shifts the curve upward by only 0.6 mosmol/mmol because of displacement of HCO-3. Deoxygenation has no significant effect at constant PCO2 despite an increase in [HCO-3]. This is probably due to the binding of 2,3-diphosphoglycerate to hemoglobin. It can be seen in the Osm-pH diagram that differences between CO2 and lactic acid titration largely disappear. For each lactic acid concentration there is a linear dependence corresponding to the linear [HCO-3]-pH relation in plasma. At constant pH, Osm increases after deoxygenation. The observed in vitro relation might explain part of the osmolality increase during physical exercise.
Abstract: In 16 experiments male subjects, age 22.4 +/- 0.5 (SE) yr, inspired CO2 for 15 min (8% end-tidal CO2) or hyperventilated for 30 min (2.5% end-tidal CO2). Osmolality (Osm) and acid-base status of arterialized venous blood were determined at short intervals until 30 min after hypo- and hypercapnia, respectively. During hypocapnia [CO2 partial pressure (PCO2) -2.31 +/- 0.32 kPa (-17.4 Torr), pH + 0.19 units], Osm decreased by 3.9 +/- 0.3 mosmol/kg H2O; during hypercapnia [PCO2 + 2.10 +/- 0.28 kPa (+15.8 Torr), pH -0.12 units], Osm increased by 5.8 +/- 0.7 mosmol/kg H2O. Presentation of the data in Osm-PCO2 or Osm-pH diagrams yields hysteresis loops probably caused by exchange between blood and tissues. The dependence of Osm on PCO2 must result mainly from CO2 buffering and therefore from the formation of bicarbonate. In spite of the different buffer capacities in various body compartments, water exchange allows rapid restoration of osmotic equilibrium throughout the organism. Thus delta Osm/delta pH during a PCO2 jump largely depends on the mean buffer capacity of the whole body. The high estimated buffer value during hypercapnia (38 mmol/kg H2O) compared with hypocapnia (19 mmol/kg H2O) seems to result from very strong muscle buffering during moderate acidosis.
Abstract: Three O2 dissociation curves from venous blood [taken at rest (A), after in vitro acidification with lactic acid (B), and after exhaustive exercise (C)] were determined in eight athletes twice in a year in detrained and fully trained state. The steepness of the standard O2 dissociation curve becomes greater during the training period (increase in Hill's n from 2.68 +/- 0.10 to 2.96 +/- 0.15). There was a concomitant small rise in the intraerythrocytic organic phosphate concentrations. Bohr coefficients (BC) were calculated for blood O2 saturations ranging from 10 to 80% by comparing the dissociation curves A and B ("in vitro" BC) and curves A and C ("in vivo" BC). In detrained and trained state the in vivo BC show their maximal values at low saturation levels, in contrast the in vitro BC exhibit maximal values at middle saturations. During the training period there was an increase in the in vivo BC as well as in the in vitro BC at low saturations. These alterations may lead to augmented O2 extraction from a given volume of blood by up to 15% during heavy work in trained state. The reason for these observations could be an altered erythrocyte population.
Abstract: Aldosterone excretion (AE) and plasma renin activity (PRA) were measured in eight untrained (UT) and eight endurance-trained (TR) male subjects before and during 4 h head-out immersion to study the mechanism of reduced renal sodium excretion in athletes. AE was significantly lower before immersion, and decreased less during immersion, in TR than in UT. Fractional sodium excretion, too, was lower and increased less during immersion in TR than in UT. PRA decreased in the water bath in all subjects (p less than 0.001) with no significant difference between the groups. During immersion, plasma sodium concentration oscillated whereas potassium concentration showed a temporary rise in TR (p less than 0.001). The attenuated response of AE in TR may be due partly to this increase of plasma potassium concentration. The generally reduced aldosterone release in TR might be caused by a training induced adaptation of the adrenals to corticotropin. The lowered renal sodium excretion of TR in spite of the decreased AE suggests an intensified aldosterone effect in these subjects, diminishing the salt loss during exercise.
Abstract: To study the cause of the increased blood volume of endurance-trained athletes we assessed the renal blood volume regulating mechanisms in eight untrained (UT) and eight endurance-trained (TR) male subjects during a 4 h head-out immersion. In TR plasma volume remained constant whereas it decreased in UT by 2.4 ml/kg (p less than 0.025). Immersion diuresis of TR was only half as high as in UT (peak values: 3.22 ml/min in UT, 1.60 ml/min in TR). Free water clearance remained approximately constant in UT but temporarily decreased in TR (p less than 0.001). This points to poor or even absent inhibition of antidiuretic hormone secretion in the latter group. Osmolar clearance increased less in TR than in UT (p less than 0.02) which was partly due to a delayed increase of glomerular filtration rate. Plasma osmolality, creatinine, and protein concentrations as well as hematocrit values were reduced during immersion to a similar extent in both groups. The results indicate a reduced renal response of endurance-trained subjects to congestion of the low-pressure system resulting in an increase in blood volume.
Abstract: Oxygen dissociation curves (ODC) in whole blood and organic phosphate concentrations in red cells were determined in 10 highly trained male athletes (TR), 6 semitrained subjects (ST) who played sports regularly at low intensities and 8 untrained people (UT). In all groups standard ODCs (37 degrees C, pH 7.40, PCO2 approximately 43 Torr) at rest and after a short exhaustive exercise were nearly identical, but PO2 values measured immediately after blood sampling and corrected to standard conditions tended to fall to the right of the in vitro ODC. Elevated P50 in the physically active [28.65 +/- 1.4 Torr (3.81 +/- 0.18 kPa) in ST, 28.0 +/- 1.1 Torr (3.73 +/- 0.15 kPa) in TR, but 26.5 +/- 1.1 Torr (3.53 +/- 0.15 kPa) in UT] were partly caused by different [DPG] (11.9 +/- 1.3 mumol/GHb in UT, 13.3 +/- 1.5 mumol/GHb in TR, 13.8 +/- 2.2 mumol/gHb in ST). There were remarkable differences in the shape of the curves between the groups. The slope "n" in the Hill plot amounted to 2.65 +/- 0.12 in UT, 2.74 +/- in ST and 2.90 +/- 0.11 in the TR (2 p against UT less than 0.001), leading to an elevated oxygen pressure of about 2 Torr (0.27 kPa) at 20% saturation and an augmented oxygen extraction of 5--7 SO2 at a PO2 of about 15 Torr (2kPa), which might be favorable at high workloads. The reason for the phenomenon could be an increased amount of young red cells in the blood of TR, caused by exercise induced hemolysis.
Abstract: Eleven male sport students (age 23.3 +/- 1.7 years) exercised for 2 h on a bicycle ergometer (60 rpm), the braking force of which was regulated to yield a constant pulse rate (156 +/- 3 min-1). Before, at end of, and 3 and 6 h after exercise blood was sampled from a cubital vein and an earlobe for measurement of hemoglobin (Hb) concentration, hematocrit (Hct) value, osmolality (Osm), plasma protein (Prot), sodium (Na+), potassium (K+), inorganic phosphate (Pi), and lactate (Lac) concentrations, red cell 2,3-diphosphoglycerate (DPG) and adenosin triphosphate (ATP) concentrations, acid base status and half saturation pressure (P50) of the oxygen dissociation curve. At end of exercise [Hb], Hct, [Prot], Osm, [K+], [Pi] and [Lac] were significantly elevated, pH in ear lobe (+ 0.04) and venous blood (+ 0.08) was also increased by both respiratory and nonrespiratory effects (BE + 1.4 mmol/l). The oxygen dissociation curve showed an unexplained slight right shift (standard P50 + 0.19 kPa). During the post-exercise period most parameters approximated to control values after only 3 h. [Prot] and especially [Pi], however, remained elevated while [DPG] slightly rose during the post-exercise period. It is suggested that these changes are first signs of adaptation to exercise, perhaps caused by endocrine stimulation.
Abstract: For both sexes (7 males, 7 females) the fixed acid Bohr coefficient BCFA (delta PO2/deltapH) and the temperature coefficient TC (deltalogPO2/deltaT) were investigated in whole blood as function of oxygen saturation (SO2). BCFA which yielded maxima at midsaturation were generally lower at increased temperature (41 degrees C) and in females. Values for 50% SO2 amount to: -0.46 +/- 0.04 SD (males) and -0.37 +/- 0.06 (females) at 37 degrees C, -0.38 +/- 0.09 (MALes) and -0.31 +/- 0.04 (females) at 41 degrees C. TC, too, was generally lower in females, decreased in both sexes at falling pH, but showed no O2-saturation dependency. Mean values were 0.024 +/- 0.008 (males) and 0.017 +/- 0.003 (females) at pH 7.4, 0.019 +/- 0.008 (males) and 0.012 +/- 0.006 (females) at pH 7.2. Sex differences of both TC and BC could also be confirmed in additional experiments. While the interrelation of BC and TC and the variable saturation effect on the coefficients may be referred to known theories about ionization heats of oxylabile groups and nonuniform reactions of the single Hb4(O2)n fractions, respectively, no clear explanation was found for the sex influence.
Abstract: To evaluate to what metabolci event in contracting muscles heart rate (HR) and VE are related, time courses of femoral and cubital venous [K=], osomolality (OSM), pH, POC2, PO2, [lactate], and [orthophosphate] ([Pi]) at onset of exercise were studied in athletes (TR) and non-athletes (UT) and compared to time courses of HR and VE. During ischaemic work with the calf muscles it could be shown that most of these blood constituents were only released from contracting muscles. Thus their time courses reflected the metabolic events in working muscles being not essentially disturbed by non-working parts of the body. Ischaemic work induced, however, substantial increases of HR and VE. In the course of non-ischaemic bicycle work HR and VE rose more rapidly in TR than in UT but were lower in TR during the steady state. During non-ischaemic work only the increased of femoral venous [K=1 closely mimicked the cardiorespiratory transients in TR as well as in UT. None of the other femoral venous substances showed such a rapid change or such typical variations between TR and UT. Cubital venous [K=1 and [Pi] approached femoral venous concentrations only in second minute after start whereas pH, PCO2, and OSM increased mainly in venous outflow from contracting muscles. PO2 decreased in femoral venous blood of TR and UT, but in cubital venous blood it remained depressed only in UT. It was discussed that the cardiorespiratory adjustment during the initial stages of work was related to K+ release in working muscles and not to O2 consuming or H+ producing processes, nor to release of Pi or increase of OSM.
Abstract: The effects of 4--6 h head-out immersion on excretion of vanillylmandelic acid (VMA), blood pressure and plasma volume were estimated in 8 endurance-trained (TR) and 8 untrained (UT) subjects. In the trained only a slight increase of VMA excretion occurred (4 h value: +2.7 +/- 10.9 ng/ml GFR), but there was a highly significant increase in the UT (+29.0 +/- 17.2 ng/ml GFR). VMA values during control experiments in supine position tended to decrease in both groups. Systolic and diastolic blood pressure fell by 20 mm Hg after beginning of immersion; in the UT plasma volume was reduced while it remained constant in TR. The results indicate that orthostatic intolerance (o.i.) after immersion is not effected by decreased sympathetic innervation of vessels; in contrast it seems to be partly compensated for by an elevated sympathetic activity at least in the UT. As a main cause for the post-immersion o.i. one might suggest a decrease in renin activity.
Abstract: In healthy male subjects aldosterone excretion and plasma renin activity were reduced by a 4-6 hr head-out immersion in thermoindifferent water baths (35.5 +/- 0.1 degrees C). The red cell 2,3-diphosphoglycerate (DPG) concentration before and throughout immersion period was positively correlated both with aldosterone excretion in 2 hr pooled urine (r = +0.69; 2 p less than 0.001) and with renin activity (r = + 0.54; 2p less than 0.001) despite a concomitant increase of cubital venous pH and inorganic phosphate concentration. These findings furnish evidence for a regulatory role of aldosterone in DPG metabolism, possibily by a direct influence on red cell glycolysis.
Abstract: The relationship of femoral venous [K+], [H+], osmolality (OSM), PO2, and [inorganic phosphate] ([Pi]) with heart rate (HR), ventilation (VE), and calculated leg blood flow (Q) were investigated during bicycle exercise in endurance trained (TR) and untrained (UT) test subjects. At a given VO2 the increases of [K+], OSM, [Pi] and the decrease of PO2 were significantly lower in TR than in UT. In the same proportion the increases of HR, VE, and Q were diminished. Thus in TR and UT identical and highly significantly correlated regression lines of [K+], [H+], OSM, [Pi] and PO2 with HR, VE, and Q were obtained. These constituents changed in the same proportion as the relative VO2 in TR and UT. No relationships with [Na+], [Ca++], and [ Mg++] were found. By means of a multiple regression analysis the partial influence of K+, H+, OSM, PO2, and Pi upon the total change of HR, VE and Q was estimated to compare with data from infusion experiments. The findings were discussed in view of the hypothesis that these candidates may provide linkage between metabolic events, circulatory, and ventilatory adjustments during work.
Abstract: Red cell concentrations of hemoglobin (MCHC), H+, Na+, K+, Mg++, cl- were measured in femoral venous blood of six untrained (UT), six endurance trained (TR) and three semitrained (ST) subjects during graded increasing work (4, 8, 12, 18 and 24 mkp/s, 10-15 min on each step) on a bicycle ergometer. Before exercise no significant differences were detected for the measured variables when comparing UT and TR. During exercise MCHC, [Na+], [K+] and [Mg++] remained constant indicating lack of water shift into the erythrocytes in spite of a marked acidosis (lowest pH Blood value 7.225). This lack resulted from an elevated extracellular osmolality. [H+]Ery and [Cl-]Ery maximally increased by 2.0 X 10(-8) eq/kg H2O and 10 meq/l, respectively. The change was markedly greater in UT than in TR at equal load. However, if [H+] Ery and [Cl-] Ery were related to pH of whole blood, differences between groups, almost disappeared and the ions were distributed as predictable from in vitro experiments (Fitzsimmons and Sendroy, 1961). Behaviour of H+ and Cl- may be of importance for oxygen dissociation under in vivo conditions.
Abstract: In experiments with graded exercise of 15 men (6 untrained, 3 semitrained, 6 endurance-trained) the trained subjects showed a massive shift to the right of the in vivo O2 dissociation curve (ODC) of femoral venous blood. At a saturation of 20 to 25% (18 mkp/sec) Po2 was about 9 mm Hg higher for the trained than for the untrained group. The following factors play a role: 1. The 2,3-diphosphoglycerate [2,3-DPG] concentration was increased by 15 to 20% in the trained group which explains about 2 mm Hg of the diffenence in Po2-2. Exercise acidosis in the femoral venous blood depends to a large extent on CO2 in the trained, but on lactic acid in the untrained group. At low saturations the CO2-Bohr effect increases sharply thus having a greater importance in the trained subjects. This factor can explain about 2 mm Hg of the difference. However, influence of chloride and 2,3-DPG on the Bohr effect must be taken into consideration. 3. Since the large ODC-shift to the right of the trained group was not reproducible under in vitro conditions, it is suggested that a rapidly decaying unknown substance accounts for the remaining difference in Po2.
Abstract: The ventilatory response curve (VRC) as a function of alveolar and arterial pCO2 was recorded in 6 high-performance athletes and 6 nonathletes. The best fit to the data points could be found for an equation of the form (see article) showing that the results are strongly related to a Gaussian probability density function (PDF). After normalizing the equation to a form (see article) (M = mean value of PDF), sigma, A and M could be determined for both groups. Sigma and A are smaller in the athletic group, whereas M did not show any systematic difference. Regarding the respiratory center consisting of functional "elements" responding indirectly to variable pCO2 it can be concluded that the frequency distribution of the different active elements is greater and spread over a wider pCO2 range in the nonathletes with the same mean value in both groups. Using Loeschcke's model (1960), the open loop gain factor for different V CO2 as a function of p(A)CO2 was computed; the gain factor showed a maximum in the physiological range of pCO2.
Abstract: The 2,3-diphosphoglycerate (2,3-DPG) concentration, oxygen half saturation pressure at pH 7.4 (P50), pH in plasma and red cells, and mean corpuscular hemoglobin concentration (MCHC) of venous blood were determined during unrestricted daily activity (series I) throughout 24 hrs as well as during prolonged bed rest until noon (series II). In series I almost synchronous dirunal behavior of P50 2,3-DPG, and plasma pH as well as red cell pH became significantly apparent with highest values in the afternoon. The [2,3-DPG] yielded most pronounced alterations, which made up to 13.5% of the average day value. During prolonged recumbency the [2,3-DPG] showed a nonsignificant tendency to decline; the P50 remained unchanged throughout that period. The possible reason for the missing [2,3-DPG] increase is a reduced change of red cell pH in series II. An influence of a posture dependent aldosterone secretion either directly on the 2,3-DPG metabloism of indirectly via mediating the red cell pH and thus ruling the formation of this organic PHOSPHORIS COMPOUND IS DISCUSSED.
