The levels of superoxide dismutase,catalase, and carbonic anhydrase in erythrocytes of patients with Down's syndrome

Summary The levels of cytoplasmic superoxide dismutase (SOD₁), catalase (CAT'ase), and carbonic anhydrase isoenzymes (CA-B and CA-C) were determined in the erythrocytes from 11 male patients with Down's syndrome. The levels of SOD₁ and CAT'ase, as well as CA-B showed significant increases compared with those in normal controls, whereas the CA-C level did not change substantially. In addition, a positive correlation was noted between the levels of SOD₁ and of CAT'ase (r=0.764).Supported in part by a grant from the Japanese Ministry of Education     

Effect of benzolamide on luminal pH in proximal convoluted tubules of the rat kidney

Luminal pH in early and late proximal tubules was recorded continuously with antimony microelectrodes before and during carbonic anhydrase inhibition.Following i.v. application of benzolamide (25 mol/kg BW), luminal pH decreased almost immediately in early proximal tubules (pH –0.42±0.06 SEM), but increased in late proximal tubules (pH +0.27±0.06). Urinary pH increased (pH +1.6±0.16) after a delay of some 30 s.Similar results, i.e. decrease of pH in early and increase of pH in late proximal tubules, were obtained, when benzolamide containing solutions were microinfused into early proximal tubules or superfused on the nephron surface. In contrast, luminal pH decreased in late proximal tubules, when benzolamide was microinfused into the same nephron segment.The decrease of luminal pH indicates inhibition of luminally active carbonic anhydrase, leading to delayed buffering of secreted hydrogen ions. The increase of luminal pH in late proximal tubules may be attributed to several factors including increased delivery of bicarbonate, impaired bicarbonate exit at the antiluminal membrane and decreased hydrogen ion formation in the tubular cell due to inhibition of cellular carbonic anhydrase.     

Serum adenosine deaminase,catalase and carbonic anhydrase activities in patients with bladder cancer

OBJECTIVES:

The relationship between adenosine deaminase and various cancers has been investigated in several studies. However, serum adenosine deaminase activity and carbonic anhydrase and catalase activities in patients with bladder cancer have not previously been reported. Therefore, the aim of this study was to measure serum adenosine deaminase, carbonic anhydrase and catalase activities in patients with bladder cancer.

MATERIALS AND METHODS:

Forty patients with bladder cancer and 30 healthy controls were enrolled in the study. Serum adenosine deaminase, carbonic anhydrase and catalase activities were measured spectrophotometrically.

RESULTS:

Serum adenosine deaminase, carbonic anhydrase and catalase activities were significantly higher in patients with bladder cancer than controls (all significant, p<0.001).

CONCLUSIONS:

These markers might be a potentially important finding as an additional diagnostic biochemical tool for bladder cancer.     

Histochemische Untersuchungen über die Carboanhydrase-Aktivität der Rattenplacenta

Summary A histochemical and biochemical analysis of the distribution of carbonic anhydrase in the rat's placenta was carried out between the 12th and the 21st day of pregnancy. By this way the highest enzymic activity was found in the labyrinthine part of the placenta. The activity is not due to the presence of erythrocytes but originates from the placental tissue itself. It is suggested that carbonic anhydrase of the tissue, when in contact with fetal blood, enhances the CO₂-transport to the maternal side of the placenta by catalyzing the reaction H₂CO₃ CO₂ + + H₂O. This effect may be especially significant in pregnancy since carbonic anhydrase activity of fetal erythrocytes is much lower than it is in red blood cells of adult animals. However other possible functions of carbonic anhydrase in the placenta have to be considered as well.

---

---

Mit 3 Textabbildungen

---

Ein vorläufiger Bericht wurde bereits während der 28. Tagung der Deutschen Physiologischen Gesellschaft in Köln (4.–8. 6. 1963) gegeben [vgl. Pflügers Arch. ges. Physiol.278, 103 (1963)].     

Cardiovascular adjustments to rhythmic handgrip exercise: relationship to electromyographic activity and post-exercise hyperemia

Summary The purpose of this study was to examine the association among electromyographic (EMG) activity, recovery blood flow, and the magnitude of the autonomic adjustments to rhythmic exercise in humans. To accomplish this, 10 healthy subjects (aged 23–37 y) performed rhythmic handgrip exercise for 2 min at 5, 15, 25, 40, and 60% of maximal voluntary force. Heart rate and arterial blood pressure were measured at rest (control), during each level of exercise, and for 2 min following exercise (recovery). The rectified, filtered EMG activity of the exercising forearm was measured continuously during each level of exercise and was used as an index of the level of central command. Post-exercise hyperemia was calculated as the difference between the control and the average recovery (2 min) forearm blood flows (venous occlusion plethysmography) and was examined as a possible index of the stimulus for muscle chemoreflex activation. Heart rate, arterial pressure, forearm EMG activity, and post-exercise hyperemia all increased progressively with increasing exercise intensity. The magnitudes of the increases in heart rate and arterial pressure from control to exercise were directly related to both the level of EMG activity and the degree of post-exercise hyperemia across the five exercise intensities (heart rate vs EMG activity:r=0.99; arterial pressure vs EMG activity:r=0.99; heart rate vs hyperemia:r=0.99; and arterial pressure vs hyperemia:r=0.98; allp<0.01). Furthermore, the level of EMG activity was directly related (r=0.99) to the corresponding degree of hyperemia. These results are consistent with the hypothesis that central command is a primary mechanism by which tachycardia is mediated during submaximal, rhythmic exercise.     

Carbonic anhydrase and horseradish peroxidase: double labelling of rat dorsal root ganglion neurons innervating motor and sensory peripheral nerves

Summary Dorsal root ganglion neurons supplying peroneus longus, soleus and gastrocnemius medius muscles and the sural nerve of the rat were labelled with horseradish peroxidase and analysed for their carbonic anhydrase content. Staining of the sections was done either on the same or on alternate slides. Both methods led to the same results, despite a slight fading of the carbonic anhydrase reaction in double-stained sections. The data indicated that the musles under study were supplied by approximately the same number of horseradish peroxidase-labelled cells, irrespective of their differences in size. 74.9% of these labelled neurons had diameters exceeding 30 m and 52.4% of them also stained for carbonic anhydrase. The double-labelled cells represented 66.9% of the population of large neurons (>30 m) and comprised most of those measuring over 47.5 m. Richness in carbonic anhydrase of the large muscle afferent neurons may be linked to their innervation of the stretch receptors, as components of an active apparatus which includes the gamma motor axons which also stain positively for carbonic anhydrase. in contrast, the ganglion cells supplying the sural nerve were almost totally devoid of carbonic anhydrase, as only 6.4% showed double labelling. This contingent possibly represents the muscle afferents of the small motoneural population which supplies, through this nerve, part of the foot musculature of the rat.     

The influence of dietary carbohydrate on performance of supramaximal intermittent exercise

Summary The relative contraction force producing a reduction in exercise hyperaemia was studied by superimposing handgrip contraction at different intensities on plantar flexion of low intensity. Ten active women served as subjects. Blood flow to the forearm ( _forearm) and calf ( _calf) was measured with mercury-in-rubber strain gauges by venous occlusion plethysmography immediately after 60 s of rhythmic plantar flexion at 10% of maximum voluntary contraction (MVC), which was expressed as P₁₀H₀, or combined plantar flexion and handgrip contraction. In the combined exercise, handgrip exercise at 30%, 50% or 70% MVC was added to plantar flexion during the last 30 s of exercise (P₁₀H₃₀, P₁₀H₅₀ and P₁₀H₇₀, respectively). The _forearm increases after P₁₀H₃₀, P₁₀H₅₀ and P₁₀ were significantly larger (P<0.01) than that after P₁₀H₀, and the difference between P₁₀H₃₀and P₁₀H₇₀ was also significant (P<0.01) Immediate post-exercise _calf after P₁₀H₀ increased by 7.4 (SEM 0.9) ml·100 ml^–1·min^–1. When handgrip contraction at 70% MVC was added, the _calf increase after exercise [4.5 (SEM 0.7) ml·100 ml^–1·min^–1] was significantly lower than after plantar flexion alone (P<0.05). However, no significant change was found in _calf when the forces of added handgrip contraction were 30% and 50% MVC, although the mean value of _calf increase was lower after P₁₀H₅₀ combined exercise. Calf vascular resistance calculated as / _calf ( mean blood pressure) tended to increase after P₁₀H₇₀ to a nonsignificant extent. Heart rate and oxygen uptake in these exercises increased when handgrip contraction at 30%, 50%, or 70% MVC was added to plantar flexion at 10% MVC. However, the increases were considerably lower than the maximal ones. Thus, a reduction of _calf occurred even when the cardiac demand from the muscle was below its maximum. In conclusion, post-exercise hyperaemia in the active limb working at low intensity was inhibited by superimposition of exercise of another limb at a high contraction force. The critical force producing attenuation of exercise hyperaemia after combined exercise of short duration was found to be higher than 50% MVC in the case of handgrip contraction plus plantar flexion.     

Human renal cytoplasmic carbonic anhydrase Tissue levels and kinetic properties under near physiological conditions

The cytoplasmic form of human renal carbonic anhydrase, CA-C (carbonate dehydratase, EC 4.2.1.1), purified by affinity chromatography, was characterized kinetically at 37°C in 25 mM N-methyl imidazole buffer, 1=0.15, pH 7.1, using a pH-indicator stopped-flow technique. Under these conditions the rate constants for the uncatalyzed hydration of CO₂ and dehydration of H₂CO₃ were 0.12 s-M¹ and 0.60-s^-1, respectively. The kinetic parameters for CA-C were found to be: Hydration reaction, K_m=11.8 mM, V/[E]₀=10.6 × 10⁵ · s^-1, dehydration reaction, K_m=70 mM, V/[E]₀=5×10⁵· s^-1. In the hydration reaction CA-C was non-competitively inhibited by acetazolamide, K_i= 16 nM, sulfanilamide, K_i=8 μM, and chlorothiazide, K_il μM. The levels of immunoassayable CA-C in cortex, medulla and papilla of perfused donor kidneys were 1.3, 1.0 and 0.6 mg enzyme protein/g tissue protein respectively which corresponded well with the levels measured catalytically. The erythrocyte form, HCA-B, was also detected immunochemically (?0.1 mg/g protein) but is thought to be a contaminant. Calculations indicated that the uncatalyzed hydration of CO₂ in the tubular cells can support 17 or 0.7% of the rate of urine acidification, dependent on whether the cellular alkaline pH-disequilibrium during acid secretion is 0.1 or 0.01 pH units, respectively. CA-C accelerates the hydration rate 6800-fold which enables the cell to sustain high rates of proton generation, while maintaining near CO₂-equilibrium and maximal buffering capacity. Even at an assumed pH-disequilibrium of only 0.01 pH-unit, CA-C is present in 50-fold excess of apparent physiological needs. When the enzyme is inhibited the rate of the uncatalyzed reaction increases, which partly overcomes the effect of inhibition.     

Exercise-induced alterations in natural killer cell number and function

To study the effects of exercise on natural killer (NK) cell number and activity (NKCA) healthy male (n = 32) and female (n = 32) subjects were randomly assigned to an exercise or control condition. Exercise involved a continuous incremental protocol consisting of cycling for three periods of 6 min at work rates corresponding to 55%, 70% and 85% peak oxygen uptake ( ). Blood samples were drawn at baseline, at 6 min, 12 min and 18 min during exercise, and at 2 h following completion of exercise. Relative to both baseline and control conditions, exercise resulted in an increase in the number of circulating lymphocytes. The proportion of T cells (CD3⁺) and B cells (CD19 ⁺) significantly decreased, and NK cells (CD3^–CD16⁺CD56⁺) increased throughout exercise. NKCA increased (P < 0.001) during the initial 6 min of exercise with no further changes observed, despite increases (P < 0.001) in the number and proportion of circulating NK cells during exercise at 70% and 85% . Plasma epinephrine and norepinephrine increased (P < 0.001) above baseline at 12 min and 18 min. The changes in NK cell number and function were independent of gender. The results indicate that short-duration low-intensity exercise can significantly increase NK cell number and activity. However, alterations in NK cell number are not accompanied by changes of a similar magnitude in NKCA.     

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

Summary At a given oxygen uptake ( O₂) and exercise intensity blood lactate concentrations are lower following endurance training. While decreased production of lactate by trained skeletal muscle is the commonly accepted cause, the contribution from increased lactate removal, comprising both uptake and metabolic disposal, has been less frequently examined. In the present study the role of resting skeletal muscle in the removal of an arterial lactate load (approximately 11 mmol·-l^–1) generated during high intensity supine leg exercise (20 min at approximately 83% maximal oxygen uptake) was compared in the untrained (UT) and trained (T) forearms of five male squash players. Forearm blood flow and the venoarterial lactate concentration gradient were measured and a modified form of the Fick equation used to determine the relative contributions to lactate removal of passive uptake and metabolic disposal. Significant lactate uptake and disposal were observed in both forearms without any change in forearm O₂. Neither the quantity of lactate taken up [UT, 344.2 (SEM 118.8) mol·100 ml^–1; T, 330.3 (SEM 85.3) mol·100 ml^–1] nor the quantity disposed of [UT, 284.0 (SEM 123.3) mol·100 ml^–1, approximately 83% of lactate uptake; T, 300.8 (SEM 77.7) mol·100 ml^–1, approximately 91% of lactate uptake] differed between the two forearms. It is concluded that while significant lactate disposal occurs in resting skeletal muscle during high intensity exercise the lower blood lactate concentrations following endurance training are unlikely to result from an increase in lactate removal by resting trained skeletal muscle.     

Vascular volume changes during cycling and stepping in women at two hydration levels

Summary Five female Caucasians were studied in a hot, wet environment (32.2 C dry bulb, 30 C wet bulb) during both cycle ergometer exercise and block stepping at exercise intensities (30–40% of the subjects's O₂ max) which produced similar heart rates. During each type of exercise, the women were studied once following 24 h water deprivation and once 60 min after ingestion of an amount of water equal to 1% of their body weight. Venous blood samples were obtained before, and at 10 min intervals during each of the four 60-min exercise sessions. Hemoconcentration and osmoconcentration were observed during both types of exercise, with more rapid increases in these variables occurring during ergometer exercise compared to block stepping. While the fluid status manipulation was effective in altering the pre-exercise osmolalities by an average of 9 mosmol·kg^–1, it had little effect on vascular volume dynamics during either type of exercise. Similarly, increases in heart rate and body temperature during exercise were not altered by the water balance of the subject. The pattern of vascular volume changes during exercise in women, therefore, seems more sensitive to exercise mode than to pre-exercise water balance.Training Grant HL 07050 from the National Institutes of Health supported this project     

Roles of the Extraintestinal Pathogenic Escherichia coli ZnuACB and ZupT Zinc Transporters during Urinary Tract Infection

Roles of the ZnuACB and ZupT transporters were assessed in Escherichia coli K-12 and uropathogenic E. coli (UPEC) CFT073. K-12 and CFT073 Δznu ΔzupT mutants demonstrated decreased ⁶⁵Zn²⁺ uptake and growth in minimal medium. CFT073Δznu demonstrated an intermediate decrease of ⁶⁵Zn²⁺ uptake and growth in minimal medium, whereas the CFT073ΔzupT mutant grew as well as CFT073 and exhibited a less marked decrease in ⁶⁵Zn²⁺ uptake. CFT073 mutants grew as well as the wild type in human urine. In competitive infections in CBA/J mice, the ΔzupT mutant demonstrated no disadvantage during urinary tract infection. In contrast, the UPEC Δznu and Δznu ΔzupT strains demonstrated significantly reduced numbers in the bladders (mean 4.4- and 30-fold reductions, respectively) and kidneys (mean 41- and 48-fold reductions, respectively). In addition, in single-strain infection experiments, the Δznu and Δznu ΔzupT mutants were reduced in the kidneys (P = 0.0012 and P < 0.0001, respectively). Complementation of the CFT073 Δznu ΔzupT mutant with the znuACB genes restored growth in Zn-deficient medium and bacterial numbers in the bladder and kidneys. The loss of the zinc transport systems decreased both motility and resistance to hydrogen peroxide, which could be restored by supplementation with zinc. Overall, the results indicate that Znu and ZupT are required for growth in zinc limited-conditions, that Znu is the predominant zinc transporter, and that the loss of Znu and ZupT has a cumulative effect on fitness during UTI, which may in part be due to reduced resistance to oxidative stress and motility.Escherichia coli is a versatile bacterial species comprised of innocuous and pathogenic strains. Pathogenic E. coli cause intestinal or extraintestinal infections in humans and other animals (28). Extraintestinal pathogenic E. coli (ExPEC) cause an array of diseases, including urinary tract infections (UTIs), neonatal meningitis, and septicemia. ExPEC associated with UTI is termed uropathogenic E. coli (UPEC). Compared to E. coli K-12 and other commensal strains, ExPEC strains encode in their genomes a greater variety of characterized, as well as putative, metal transport systems (11, 54). The importance of pathogen-specific iron transport systems for ExPEC has been established (20, 21, 26). However, the importance of other metal transport systems in ExPEC is less well characterized, and in particular nothing has been reported on the potential implication of the zinc transporters for the virulence of ExPEC.Zinc (Zn²⁺) is an essential micronutrient in all living cells, since this transition metal is a component of numerous metalloproteins and serves as an enzymatic cofactor or a structural element (5). In mammals, Zn²⁺ has an important immunomodulatory function and is critical for innate and acquired immunity (45). After exposure to lipopolysaccharide (LPS), zinc levels are decreased in the serum, and zinc is accumulated in the liver (38). In addition, during bacterial infection, the host protein calprotectin is released by neutrophils and may reduce bacterial numbers by restricting the availability of metals, including zinc and manganese (16, 39, 50). Also, although zinc concentrations are estimated to be in the millimolar range within host cells, available zinc may be mostly inaccessible to bacterial pathogens (3) and/or dramatically reduced after activation of innate immune defenses (45).In bacteria, the uptake of zinc is mediated by two major types of transporters: ZnuACB, which belongs to the cluster C9 family of (TroA-like) ATP-binding cassette (ABC) transporters (15, 27), and ZupT, which is a member of the ZIP (for ZRT/IRT-like protein) family of transporters that are also present in eukaryotes (27). Thus far, the Znu transport system has been shown to be important for virulence in a number of bacterial pathogens, including Salmonella enterica, Brucella abortus, and Haemophilus ducreyi (3, 12, 35, 56). Currently, the roles of the Znu and ZupT transporters for ExPEC virulence have not been investigated.The genomes of all E. coli strains that have been sequenced thus far contain genes encoding the two described zinc transporters: ZupT and ZnuACB. In addition to the transport of zinc, ZupT can also mediate the uptake of Co²⁺, Fe²⁺, and Mn²⁺ (24). The exact mechanism by which ZupT mediates metal uptake is currently unknown, although it may involve a chemiosmotic transmembrane gradient (24). Zinc uptake mediated by the Znu system requires hydrolysis of ATP by ZnuC to transport Zn²⁺ captured by the periplasmic binding protein ZnuA through the pore in the cytoplasmic membrane formed by a ZnuB dimer (36, 44). In ExPEC strains, the SitABCD transport system represents an additional ABC transporter belonging to the C9 (TroA-like) cluster (46). Sit transporters have thus far been characterized as manganese and iron transporters (8, 29, 47), although zinc has been shown to be an effective competitive inhibitor of manganese or iron uptake by SitABCD (8, 29). The SitA periplasmic binding protein also shares similarities to the TroA periplasmic binding protein of Treponema pallidum, which has been shown to bind both zinc and manganese with essentially equal affinities (19). It remains to be determined whether in addition to Znu and ZupT transporters, SitABCD or any other undefined transport systems may contribute to zinc transport or the virulence of ExPEC.In the present study, the roles of the Znu, ZupT, and SitABCD transport systems for zinc uptake and growth in zinc-restricted medium were compared in an E. coli K-12 Δznu ΔzupT mutant. In addition, the roles of the Znu and ZupT transporters for growth of ExPEC strain CFT073 in zinc-restricted conditions and for colonization in the murine ascending UTI model were assessed.     

Metabolic and circulatory responses to the ingestion of glucose polymer and glucose/electrolyte solutions during exercise in man

Summary Six men exercised on a cycle ergometer for 60 min on two occasions one week apart, at 68±3% of . On one occasion, a dilute glucose/electrolyte solution (E: osmolality 310 mosmol · kg^–1, glucose content 200 mmol·l^–1) was given orally at a rate of 100 ml every 10 min, beginning immediately prior to exercise. On the other occasion, a glucose polymer solution (P: osmolality 630 mosmol · kg^–1, glucose content equivalent to 916 mmol · l^–1) was given at the same rate. Blood samples were obtained from a superficial forearm vein immediately prior to exercise and at 15-min intervals during exercise; further samples were obtained at 15-min intervals for 60 min at rest following exercise. Heart rate and rectal temperature were measured at 5-min intervals during exercise.Blood glucose concentration was not different between the two tests during exercise, but rose to a peak of 8.7±1.2 mmol · l^–1 (mean±SD) at 30 min post-exercise when P was drunk. Blood glucose remained unchanged during and after exercise when E was drunk. Plasma insulin levels were unchanged during exercise and were the same on both trials, but again a sharp rise in plasma insulin concentration was seen after exercise when P was drunk. The rate of carbohydrate oxidation during exercise, as calculated from and the respiratory exchange ratio, was not different between the two tests. A fall in plasma volume, calculated from changes in haematocrit and haemoglobin concentration, occurred after 15 mins of exercise: the fall was of the same magnitude (9%) at this point on both tests, but thereafter plasma volume was significantly lower with P than with E for the remainder of the exercise period and throughout recovery. Serum osmolality increased during exercise (p<0.05) on the P trial, but was unchanged on the E trial. Heart rate was higher (p<0.05) during the last 20 min of exercise on the P trial.These results suggest that the carbohydrate consumed during the P trial was not available to the working muscles during exercise, and was probably not emptied from the stomach and absorbed to any significant extent until exercise stopped. The differences in plasma volume and osmolality between the two trials are consistent with the net movement of water into the gut which is known to occur at rest when solutions of high osmolality are taken. In more prolonged exercise, this effective dehydration may impair performance.     

Delayed appearance of blood lactate with reduced frequency breathing during exercise

Summary The purpose of the present study was to investigate the blood lactate (LA^–) responses to hypoventilation induced by reduced frequency breathing (RFB) during recovery from exercise. Five male subject performed 16 4 min cycling bouts alternating with 16 min rest periods. Exercise intensities were chosen at power outputs corresponding to 30% at 2mMLA^–, at 4 mMLA^–, and 90% in each subject. Breathing frequency was voluntarily controlled starting 10 s before each 3rd min of exercise and maintained throughout the rest of the exercise period. Four different breathing patterns at each exercise intensity were used: normal breathing (NB), breathing every 4 s, breathing every 8 s, and maximal RFB. Except for the NB trials, subjects held their breath at functional residual capacity during each breathing interval. The concentration difference of LA^– between the 3rd min sample and the 4th min sample was defined as the lactate change during exercise ( LA^–ex), and that between the 4th min sample and the sample at the 3rd min after the end of the exercise as the lactate change during recovery ( LA^–rec). An ANOVA showed significant (p<0.05) differences in breathing procedures only in LA^–rec. LA^–rec seemed to increase as compared to NB only at at 4 mMLA^– and 90% , while LA^–ex remained unchanged as compared to NB in spite of reduced V _A. These results might indicate that RFB inhibited lactate removal from working muscles during exercise.     

The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption

Summary Nine males with mean maximal oxygen consumption ( ) =63.0 ml· kg^–1 · min^–1, SD 5.7 and mean body fat = 10.6%, SD 3.1 each completed nine counterbalanced treatments comprising 20, 50 and 80 min of treadmill exercise at 30, 50 and 70% . The OZ deficit, 8 h excess post-exercise oxygen consumption (EPOC) and EPOC:O₂ deficit ratio were calculated for all subjects relative to mean values obtained from 2 control days each lasting 9.3 h. The O₂ deficit, which was essentially independent of exercise duration, increased significantly (P<0.05) with intensity such that the overall mean values for the three 30%, 50% and 70% workloads were 0.83, 1.89 and 3.09 l, respectively. While there were no significant differences (P>0.05) between the three EPOCs after walking at 30% for 20 (1.01 l), 50 (1.43 l) and 80 min (1.041), respectively, the EPOC thereafter increased (P<0.05) with both intensity and duration such that the increments were much greater for the three 70% workloads (EPOC: 20 min=5.68 l; 50 min=10.04 l; 80 min= 14.59 l) than for the three 50% workload (EPOC: 20 min =3.14 l; 50 min=5.19 l; 80 min= 6.10 l). An analysis of variance indicated that exercise intensity was the major determinant of the EPOC since it explained five times more of the EPOC variance than either exercise duration or the intensity times duration interaction. The mean EPOC:O₂ deficit ratio ranged from 0.8 to 4.5 and generally increased with both exercise intensity and duration. These data imply that the EPOC is more than mere repayment of the O₂ deficit because metabolism is increasingly disturbed from resting levels as exercise intensity and duration increase due to other physiological factors occurring after the steady-state has been attained.     

Changes in blood cell response following strenuous physical exercise

Summary The generation of tumour necrosis factor (TNF) and tissue factor activity in lipopolysaccharide (LPS) stimulated blood were studied in 25 healthy subjects before and after physical exercise of different intensities. Of the subjects a group of 9 were athletes who trained once to twice every day of the week, a second group of 8 exercised 3–7 times a week, and a third group of 8 exercised 4–5 times a month. The production of TNF in freshly drawn LPS stimulated blood in heparin, drawn from top athletes at rest was significantly lower than in the other subjects. The LPS induced concentrations of TNF- of 2.73 (SEM 1.05) ng · ml^–1 in the blood of the top athletes compared to 5.08 (SEM 0.7) ng · ml^–1 and 7.6 (SEM 1.6) ng · ml^–1, respectively, in the other two groups. The group that trained the least had the highest values. Immediately after exercise, the monocytes appeared to be less responsive to LPS stimulation, as a reduction of 47%–48% was observed in the top athletes and in the other group of well-trained individuals. The group that trained the least, which was also subjected to the least stressful exercise, had a 33% reduction in TNF production. Within 6 h the TNF concentration was back to pre-exercise values. Within 6 h the TNF concentration was back to pre-exercise values. In contrast to TNF production, the LPS induced tissue factor activity of monocytes was significantly higher in the top athletes and in the group of well-trained individuals when measured immediately after 10 min of exercise compared to pre-exercise values. The increase in tissue factor activity was probably a reflection of simultaneous granulocyte- and platelet activation which is known to enhance LPS induced tissue factor activity in monocytes. Except for the period immediately after exercise, there was a significant correlation between LPS induced TNF and tissue factor activity in the whole blood of the participants. In conclusion, hard physical training appeared to suppress the availability of TNF in stimulated blood. This was even more pronounced immediately after strenuous physical exercise.     

The pattern of breathing and the ventilatory response to breathing through a tube and to physical exercise in sport divers

Summary Well-trained divers can be expected to differ from healthy controls in their ventilatory response to breathing through a tube and to physical exercise. Therefore, we measured their minute ventilation ( ) at rest and during breathing through a tube combined with two levels of physical exercise (1 or 2 W·kg body weight⁻¹). For breathing through a tube an additional dead space of 600 ml was used. All divers were trained in the breath-hold technique and in the use of the breathing apparatus. Their mean period of training as divers was 9±6 years. The approximate age of the subjects was 25 years. The pattern of breathing and the oxygen uptake were measured by spirometer, the end-tidal concentration of CO₂ was measured and all experiments were carried out above sea level. The ventilation of the divers at rest was comparable to that of the controls. During physical exercise it was smaller whether during breathing through a tube or not. The inadequate increase of during exercise in divers was associated with hypercapnia only at a higher physical work intensity (of 2 W·kg⁻¹). This finding is interpreted as a lower chemoregulatory response to the combined stimuli of hypercapnia, hypoxia and physical exercise. In some situations significant bradypnoea and higher tidal volumes were found in the divers.     

Effects of exercise detraining and deacclimation to the heat on plasma volume dynamics

Summary The effects of the discontinuation (DET) of an endurance training/heat acclimation (T/A) program on vascular volumes were studied in 16 adult males. Resting and exercise blood volume dynamics were examined prior to and during an exercise task performed after completion of T/A (CT1) and again at the end of DET (CT2). T/A consisted of cycling at 60% of peak for 90 min per day, 6 days per week, for 4 weeks. Ambient temperature was 20 C for the first 3 weeks and 40 C for the last week (rh=30–35%). Subjects were randomly assigned to one of the following DET conditions: 1) cycling one day per week at 40 C, 2) cycling one day per week at 20 C, 3) resting one day per week at 40 C, 4) control. The exercise tasks consisted of 60 min of continuous cycle ergometer exercise at 50% of peak (Ta=30 C, rh=35%). Although significant differences were found between CT1 and CT2, there were no interactions between the various DET conditions. Resting red cell volume decreased 98 ml and plasma volume decreased 248 ml following DET. A reduction in plasma protein content accounted for 97% of the decrease in plasma volume. Hemoconcentration occurred during exercise in both CT1 and CT2, while there were slight increases in plasma [Na⁺] and [Cl^–] and a rapid rise in [K⁺]. It appears that a single exercise and/or heat exposure per week was not different from complete cessation of endurance exercise in the heat with regard to maintenance of the various vascular volumes.This work was supported in part by the National Institutes of Health, under Grant H207050-09     

Catecholamines,growth hormone,cortisol, insulin,and sex hormones in anaerobic and aerobic exercise

Summary Seventeen male physical education students performed three types of treadmill exercise: (1) progressive exercise to exhaustion, (2) prolonged exercise of 50 min duration at the anaerobic threshold of 4 mmol·1^–1 blood lactate (AE), (3) a single bout of short-term high-intensity exercise at 156% of maximal exercise capacity in the progressive test, leading to exhaustion within 1.5 min (ANE).Immediately before and after ANE and before, during, and after AE adrenalin, noradrenalin, growth hormone, cortisol, insulin, testosterone, and oestradiol were determined in venous blood, and glucose and lactate were determined in arterialized blood from the earlobe. Adrenalin and noradrenalin increased 15 fold during ANE and 3–4 fold and 6–9 fold respectively during AE. The adrenalin/noradrenalin ratio was 13 during ANE and 110 during AE. Cortisol increased by 35% in ANE (12% of which appeared in the postexercise period) and 54% in AE. Insulin increased during ANE but decreased during AE. Testosterone and oestradiol increased by 14% and 16% during ANE and by 22% and 28% during AE. The results point to a markedly higher emotional stress and higher sympatho-adrenal activity in anaerobic exercise. Growth hormone and cortisol appear to be the more affected by intense prolonged exercise. Taking plasma volume changes and changes of metabolic clearance rates into consideration, neither of the exercise tests appeared to affect secretion of testosterone and oestradiol.Supported by Bundesinstitut für Sportwissenschaft, Köln-Lövenich     

Variations in serum myoglobin after a 2-min isokinetic exercise test and the effects of training

Summary Serum-myoglobin was measured after the completion of three different types of exercise i.e., dynamic, isometric, and isokinetic. The maximal rises in serum-myoglobin levels were 20%, 70%, and 300%, respectively. On the basis of this finding a 2-min isokinetic test was developed and standardized for the purpose of studying conditions in vivo that may affect myoglobin leakage from skeletal muscle cells.Fourteen healthy men performed the 2-min isokinetic test. Blood lactate increased on average eight times with maximal levels obtained 4 min after completed work. S-Myoglobin was raised approximately five times after 2 h. The rise in S-myoglobin was significantly (P<0.01) related to the loss in muscle strength (torque decline) during the test. After a training period of 3 weeks comprising 4 min of maximal isokinetic exercise three times a week the rise in S-myoglobin after a 2-min isokinetic test was reduced from on average 240 g·l^–1 to 96 g·l^–1 (P<0.001). The rise in blood lactate was not related to the variations in S-myoglobin or affected by training.The 2-min isokinetic exercise test is an easily standardized exercise test which in combination with measurements of serum-myoglobin should prove valuable in the study of conditions affecting leakage from muscle cells.