Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys

Summary To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4–12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO_2max), ventilation and the ventilatory anaerobic threshold were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% ofVO_2max and increasing it during the next run by 0.5 or 1.0 km·h^–1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. Anaerobic threshold was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol · 1^–1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional anaerobic threshold was only 2.6 mmol · 1^–1, which corresponded to 78% of theVO_2max. The correlations between the parameters of anaerobic threshold, ventilatory anaerobic threshold and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.     

Human thermoregulatory function during exercise and immersion after 35 days of horizontal bed-rest and recovery

The present study evaluated the effect of 35 days of experimental horizontal bed-rest on exercise and immersion thermoregulatory function. Fifteen healthy male volunteers were assigned to either a Control (n=5) or Bed-rest (n=10) group. Thermoregulatory function was evaluated during a 30-min bout of submaximal exercise on a cycle ergometer, followed immediately by a 100-min immersion in 28°C water. For the Bed-rest group, exercise and immersion thermoregulatory responses observed post-bed-rest were compared with those after a 5 week supervised active recovery period. In both trials, the absolute work load during the exercise portion of the test was identical. During the exercise and immersion, we recorded skin temperature, rectal temperature, the difference in temperature between the forearm and third digit of the right hand (T_{forearm-fingertip})— an index of skin blood flow, sweating rate from the forehead, oxygen uptake and heart rate at minute intervals. Subjects provided ratings of temperature perception and thermal comfort at 5-min intervals. Exercise thermoregulatory responses after bed-rest and recovery were similar. Subjective ratings of temperature perception and thermal comfort during immersion indicated that subjects perceived similar combinations of Tsk and Tre to be warmer and thermally less uncomfortable after bed-rest. The average (SD) exercise-induced increase in Tre relative to resting values was not significantly different between the Post-bed-rest (0.4 (0.2)°C) and Recovery (0.5 (0.2)°C) trials. During the post-exercise immersion, the decrease in Tre, relative to resting values, was significantly (P<0.05) greater in the Post-bed-rest trial (0.9 (0.5)°C) than after recovery (0.4 (0.3)°C). T_{forearm-fingertip} was 5.2 (0.9)°C and 5.8 (1.0)°C at the end of the post-bed-rest and recovery immersions, respectively. The gain of the shivering response (increase in O₂ relative to the decrease in Tre; O₂/Tre) was 1.19 l min^–1°C^–1 in the Recovery trial, and was significantly attenuated to 0.51 l min^–1°C^–1 in the Post-bed-rest trial. The greater cooling rate observed in the post-bed-rest trial is attributed to the greater heat loss and reduced heat production. The former is the result of attenuated cold-induced vasoconstriction and enhanced sweating rate, and the latter a result of a lower shivering O₂ response.     

Ca2+ influx induced by store release and cytosolic Ca2+ chelation in HT29 colonic carcinoma cells

Cl^– secretion in HT₂₉ cells is regulated by agonists such as carbachol, neurotensin and adenosine 5-triphosphate (ATP). These agonists induce Ca²⁺ store release as well as Ca²⁺ influx from the extracellular space. The increase in cytosolic Ca²⁺ enhances the Cl^– and K⁺ conductances of these cells. Removal of extracellular Ca²⁺ strongly attenuates the secretory response to the above-mentioned agonists. The present study utilises patch-clamp methods to characterise the Ca²⁺ influx pathway. Inhibitors which have been shown previously to inhibit non-selective cation channels, such as flufenamate (0.1 mmol·l^–1, n=6) and Gd³⁺ (10 mol·l^–1, n=6) inhibited ATP (0.1 mmol·l^–1) induced increases in whole-cell conductance (G _m). When Cl^– and K⁺ currents were inhibited by the presence of Cs₂SO₄ in the patch pipette and gluconate in the bath, ATP (0.1 mmol·l^–1) still induced a significant increase in G _m from 1.2±0.3 nS to 4.7±1 nS (n=24). This suggests that ATP induces a cation influx with a conductance of approximately 3–4 nS. This cation influx was inhibited by flufenamate (0.1 mmol·l^–1, n=6) and Gd³⁺ (10 mol·l^–1, n=9). When Ba²⁺ (5 mmol·l^–1) and 4,4-diisothiocyanatostilbene-2-2-disulphonic acid (DIDS, 0.1 mmol·l^–1) were added to the KCl/K-gluconate pipette solution to inhibit K⁺ and Cl^– currents and the cells were clamped to depolarised voltages, ATP (0.1 mmol·l^–1) reduced the membrane current (I _m) significantly from 86±14 pA to 54±11 pA (n=13), unmasking a cation inward current. In another series, the cation inward current was activated by dialysing the cell with a KCl/K-gluconate solution containing 5–10 mmol·l^–1 1,2-bis-(2-aminoethoxy)ethane-N,N,N,N-tetraacetic acid (EGTA) or 1,2-bis-(2-aminophenoxy) ethane-N,N,N,N-tetraacetic acid (BAPTA). The zero-current membrane voltage (V _m) and I _m (at a clamp voltage of +10 mV) were monitored as a function of time. A new steady-state was reached 30–120 s after membrane rupture. V _m depolarised significantly from –33±2 mV to –12±1 mV, and I _m fell significantly from 17±2 pA to 8.9±1.0 pA (n=71). This negative current, representing a cation inward current, was activated when Ca²⁺ stores were emptied and was reduced significantly (I _m) when Ca²⁺ and/or Na⁺ were removed from the bathing solution: removal of Ca²⁺ in the absence of Na⁺ caused a I _m of 5.0±1.2 pA (n=12); removal of Na⁺ in the absence of Ca²⁺ caused a I _m of 12.8±3.5 pA (n=4). The cation inward current was also reduced significantly by La³⁺, Gd³⁺, and flufenamate. We conclude that store depletion induces a Ca²⁺/Na⁺ influx current in these cells. With 145 mmol·l^–1 Na⁺ and 1 mmol·l^–1 Ca²⁺, both ions contribute to this cation inward current. This current is an important component in the agonist-regulated secretory response.     

Cutaneous blood flow and local sweating after systemic atropine administration

Localized cutaneous vasodilation (flush) is seen following systemic atropine administration. To verify calculated enhanced dry heat loss with actual changes in cutaneous blood flow, four men were studied in both control and atropine (0.025 mg·kg^–1;im) experiments (T _a=30°C,T _dp=7°C) during moderate exercise (55% O₂ peak). Esophageal temperature (T _es) and arm sweating ( ) by local dewpoint were measured continously. Skin (forearm) blood flow (FBF) was measured twice each minute by venous occlusion plethysmography. Injection of atropine (2 mg) caused an increased sensitivity (+85%,p<0.01) in FBF toT _es with no change in the vasodilator threshold. An elevatedT _es onset (0.3°C,p<0.05) for sweating occurred with no change in the sensitivity of toT _es (–27%,p<0.20). No elevation in either forearm or occurred before the onset of vasodilation, however, both mean skin ( ) and local arm temperatures were higher in the atropine experiments after 15 min of exercise. Systemic atropine resulted in higher cutaneous vasodilation at the same core temperature with the local skin temperature following passively. The effect of systemic atropine in stimulation of increased cutaneous vasodilation is suggested to result by a combination of central and local responses which may be mediated through the release of vasoactive sustances.     

Seasonal variation in sweating responses of older and younger men

Eight older (60–65 years) and six younger (20–25 years) men were exposed to a standard heat stress for 60 min in summer, autumn, winter, and spring. The test consisted of placing the lower legs and feet in a 42°C water bath while sitting in constant environmental conditions (30°C and 45% relative humidity). The increase of rectal temperature (T _re) was significantly greater (P < 0.05) in autumn, winter, and spring than in summer for the older group, but significantly greater only in winter than in summer for the younger group (P < 0.05). The T _re was greater for the older group in all seasons, but of significance only in autumn and spring (P < 0.01). There were no significant season-related differences for metabolic heat production (m) and mean skin temperature ( _sk) during the heat test in the respective groups, although the m and _sk were lower for the older group in all seasons (P < 0.01). In the older group total body sweating rate (m_sw) divided by T _re (total m_sw/T _re) decreased from summer to winter (P < 0.02) and did not differ between winter and spring, whereas total m_sw/T _re in the younger group increased in spring after decreasing from autumn to winter (P < 0.03). The variations of the value, local sweating rate on the back and thigh divided by T _re (back m_sw/T _re and thigh m_sw/T _re), were similar to those of the total m_sw/T _re in each group, except for back m_sw/T _re in the younger group, which did not increase from winter to spring. The total m_sw/T _re, back m_sw/T _re and thigh m_sw/T _re were significantly less for the older group in summer, autumn and spring (P < 0.05). The range of seasonal variations was significantly less for the older group (P < 0.001). The results indicated that, compared with younger men in older men, the enhancement of sweating function toward summer occurred later and its reduction toward winter occurred earlier despite a smaller range of seasonal variation and that older men had a somewhat lesser capability to maintainT _re when challenged by heat stress in all seasons.     

Evidence for Na+/Ca2+ exchange in isolated smooth muscle cells: a fura-2 study

Isolated smooth muscle cells (SMC) from guinea pig taenia coli were employed. Suspension of cells were externally loaded in saline with the fluorescent calcium indicators quin-2/AM or fura-2/AM at 20–40 M or 4 M respectively, resulting in an estimated intracellular concentration of 100–200 M for quin-2 or 10–20 M fura-2 (free acid). On addition of 100 M carbachol or high K _o ⁺ (80 mM) depolarization, fura-2 loaded cells contracted (104±47 m,n=121 rest: 39±13 m,n=59 contracted) identically to control (103±35 m,n=232 rest: 39±16 m,n=89 contracted) cells, whereas quin-2 loaded cells were unresponsive to these protocols and there was no significant length change. The Ca _i ²⁺ of fura-2 loaded cells was 100±18 nM (mean±SD,n=15) and was not significantly different from quin-2 loaded cells 107±26 nM (n=13). Treatment of fura-2 loaded cells with 100 M ouabain saline for 10–60 min progressively elevated the Ca _i ²⁺ to a mean of 266±83 nM (n=15). Reduction of Na _p ⁺ (96% Li⁺ replaced) significantly increased Ca _i ²⁺ to 317±77 nM (n=8). After pretreatment with ouabain (100 M), Na _o ⁺ replacement (Li⁺) increased Ca _i ²⁺ at a significantly faster rate [3.6 nM min^–1 (control) cf. 19.8 nM min^–1 (ouabain)].     

Hyperthermia and maximal oxygen uptake in men and women

To compare the effect of hyperthermia on maximal oxygen uptake (O_2max) in men and women, O_2max was measured in 11 male and 11 female runners under seven conditions involving various ambient temperatures (T_a at 50% RH) and preheating designed to manipulate the esophageal (T_es) and mean skin temperatures at O_2max. The conditions were: 25°C, no preheating (control); 25, 35, 40, and 45°C, with exercise-induced preheating by a 20-min walk at ~33% of control O_2max; 45°C, no preheating; and 45°C, with passive preheating during which T_es and were increased to the same degree as at the end of the 20-min walk at 45°C. Compared to O_2max (l·min^–1) in the control condition (4.52±0.46 in men, 3.01±0.45 in women), O_2max in men and women was reduced with exercise-induced or passive preheating and increased T_a, ~4% at 35°C, ~9% at 40°C and ~18% at 45°C. Percentage reductions (7–36%) in physical performance (treadmill test time to exhaustion) were strongly related to reductions in O_2max (r=0.82–0.84). The effects of hyperthermia on O_2max and physical performance in men and women were almost identical. We conclude that men and women do not differ in their thermal responses to maximal exercise, or in the relationship of hyperthermia to reductions in O_2max and physical performance at high temperature. Data are reported as mean (SD) unless otherwise stated.     

Thyroid function after surgery for autonomous and non-autonomous nodular endemic goitre — effect of iodide-substitution

Summary The aim of this study was to evaluate the influence of postoperative iodide-substitution on the function of thyroid remnants of different quality and quantity in order to define the appropriate prophylaxis (iodide or thyroid hormone) to prevent recurrent goitre.In a prospective, randomized clinical trial, the following patients were examined:group I: simple, non-autonomous nodular goitre, bilateral thyroidectomy (n=40);group II: simple, non-autonomous nodular goitre, selective (unilateral) thyroidectomy (n=40);group III: autonomous nodular goitre, bilateral thyroidectomy (n=40);group IV: autonomous nodular goitre, selective (unilateral) thyroidectomy (n=35). The following parameters were measured 6 and 12 weeks postoperatively. Serum-total-T₄, -T₃,-TSH, TRH-test, 99^mTc-Thyroid-Uptake (TcTU). Six weeks postoperatively the 4 groups were separately randomized into controls and treatment groups, who received 200 µg iodide/day orally. Six weeks postoperatively, patients in group I had lower T4 levels and both basal and stimulated TSH were higher than in the other groups, however no significant differences were observed in T₃, T₄/T₃ ratio and TcTU.Twelve weeks postoperatively patients from groups I, II and III, who had been treated with iodide, had lower T₃ and TcTU values but higher T₄ and T₄/T₃ than the appropriate controls. Basal and stimulated TSH showed no differences between controls and iodide-treated patients in these groups. In group IV, T₄ and T₃ showed a tendency to elevation (n.s.), and basal and stimulated TSH as well as TcTU were lower in patients with iodide.Iodide-substitution (200 µg/day) has no major influence on the pituitary-thyroid axis, except after selective surgery for autonomous nodular goitre (group IV). Generally, iodide treatment abolishes the symptoms of iodine-deficiency, improving the autoregulatory capacity of the thyroid remnant. It could replace thyroid hormone as a prophylaxis against recurrent goitre in the majority of patients after selective thyroid surgery.Abbreviations AFTT Autonomously Functioning Thyroid Tissue - TcTU 99^mTc-Thyroid-Uptake - TRH TSH-Releasing-Hormone - TSH Thyroid-Stimulating-Hormone - T₃ Triiodothyronine - T₄ Thyroxine     

Cardiac Purkinje fibres

Summary The influence of intracellular calcium concentration [Ca²⁺] _i on the steady state membrane currentsi was studied in a range of clamp potentials between –20 and –100 mV. Injection of CaCl₂ or Ca-EGTA (pCa 6) increasedi whereas injection of K-EGTA diminished it. The changes i were attributed to a change in steady state potassium conductance, g_K, by four arguments: i was restricted to potentials negative to –20 mV and depended on clamp potential in an inward rectifying manner. i displayed a reversal potential, E_rev, which followed log [K⁺]₀ with 60 mV for a tenfold change. Since E_rev obtained during Ca injection agreed with E_rev observed during EGTA injection the potassium driving force had to be constant. Wheng _K was blocked by superfusion with 20 mM Cesium neither CaCl₂ nor K-EGTA injection modifiedi .Supported by SFB 38, Membranforschung, project G2     

Cation selectivity of the isolated perfused cortical thick ascending limb of Henle's loop of rabbit kidney

The cation permeability of the cortical thick ascending limb of Henle's loop was investigated with electrophysiological methods in the isolated perfused tubule preparation of rabbit kidney. The transepithelial specific resistance (R _T) and electrical potential difference (PD) were determined in 4 experimental groups. In group 1 (n=51) the tubules were perfused with a modified Ringer's solution on both sides of the epithelium; the PD was 7±0.4 mV lumen positive, and theR _T 34±2 ·cm². In group 2 (n=12) one of both sides of the epithelium was perfused with dilute (54 mmol/l) NaCl solutions under control conditions and in the absence of active transport. Inhibition was obtained in four different ways: low temperature (22° C), zero K⁺ solutions on both sides of the epithelium, 5·10^–5 mol/l furosemide, added to lumen perfusate, or 10^–5 mol/l ouabain added to the bathing solution. In the presence and in the absence of active transport a NaCl gradient of 154 versus 54 mmol/l induced diffusion potentials across the epithelium which were symmetrical and of nearly equal magnitude: +12, –14 and +15, –14 mV respectively. In group 3 (n=51) Na⁺ was completely replaced by choline⁺, tetraethylammonium⁺, tris-hydroxymethyl-aminomethane⁺, or Li⁺ in either bath or lumen perfusate or in both perfusates. The biionic diffusion potentials were symmetric; the replacement of Na⁺ by these cations on both sides markedly increasedR _T. Both kinds of measurements yielded a permeability sequence ofP _Na ⁺>P _Li ⁺>P _{organic cation}. In group 4 (n=17) 50 mmol/l of Na⁺ was replaced by K⁺, Li⁺, Rb⁺, or Cs⁺ on one of the sides and active transport was inhibited by furosemide or ouabain. From the membrane diffusion potentials and theR _T values in group 4 as well as in group 3 the following cation permeability sequence was calculatedP _K ⁺>P _Na ⁺>P _Rb ⁺ =P _Li ⁺>P _Cs ⁺>P _{organic cation}. It is concluded that the cortical thick ascending limb of Henle's loop has a low resistance pathway which is cation selective similar to that of leaky epithelia. Since the membrane diffusion potentials are symmetric and since they are not altered by inhibition of active transport, it is likely that this low resistance pathway is formed by a paracellular shunt.This study was supported by Deutsche Forschungsgemeinschaft. Parts of this study have been presented at the following meetings: 53rd meeting of the Deutsche Physiologische Gesellschaft, Kiel 1980; 64th Federation meetings Anaheim 1980; 28th IUPS meeting Budapest 1980.     

Control of sweating during the human menstrual cycle

Summary Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4–7) phase and during the luteal (L, days 19–22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (T _es), mean skin temperature ( ), oxygen uptake and forearm sweating ( ) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at ∼80% peak during which the environmental chamber was controlled atT _a=50.0° C, rh=14% (P _w=1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at ∼85% peak atT _a=35° C and rh=25% (P _w=1.4 kPa). The normal L increase in restingT _es (≈0.3° C) occurred in all seven subjects. was higher during L than F in all experiments conducted at 50° C. During exercise and passive heat exposure, theT _es threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of toT _es between menstrual cycle phases. This rightward or upward shift inT _es threshold for initiation of sweating averaged 0.5° C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

Molecular specificity of the tubular resorption of “acidic” amino acids

Single sections of superficial proximal convolutions of rat kidney were microperfused in vivo and in situ. The perfusion fluids contained radioactively labelledl- ord-aspartate,l-glutamate,l-pyroglutamate, or N-methyl-d-aspartate.l--Carboxyglutamate as well as the other amino acids were added in the unlabelled from. Results.l- andd-Aspartate (0.073 mmol·1^–1) are quickly resorbed at about the same rate.d-Aspartate resorption was blocked byl-aspartate (5 mmol·1^–1) but not by -alanine (5 mmol·1^–1).l-Aspartate resorption was inhibited byl-glutamate (2 mmol·1^–1) but not byd-glutamate,l-asparagine,l-phenylalanine or by succinate (2 mmol·1^–1, each). The fast resorption ofl-glutamate (0.073 mmol·1^–1) was blocked byd-aspartate,l-cysteate (2 mmol·1^–1), but not by 3-mercaptopicolinic acid (0.15 mmol·1^–1),l-glutamine, 2-oxoglutarate, taurine, N-methyl-l-glutamate or kainic acid (2 mmol·1^–1, each).l--Carboxyglutamate (0.66 mmol·1^–1) and N-methyl-d-aspartate (2mol·1^–1) were found to be resorbed only at an extremely small rate.l-pyroglutamate (0.076 mmol·1^–1) resorption was not influenced byl-glutamate (1 mmol·1^–1). Fractional excretion of -carboxyglutamate was 7–25% (l-from) or 45–70% (d-form) at an artificially elevated plasma level of 12mol·1^–1.It is concluded thatl- andd-aspartate,l-glutamate,l-cysteate and, to a much smaller extent,l--carboxyglutamate, are accepted by the tubular resorption mechanism highly specific for acidic amino acids. N-Substitution, the amidation of the - or -carboxyl group, or the removal of the -amino moiety almost completely abolish the ability of such compounds to be resorbed via this carrier; N-methylated or -carboxylated derivatives of acidic amino acids are not resorbed at all from the proximal tubule. The resorption of glutamate, but not of aspartate, is highly stereospecific.Parts of this work were presented at meetings of the German Physiological Society in 1978 [28] and of the Gesellschaft für Nephrologie in 1980 [29] as well as at the VIIIth International Congress of Nephrology in Athens in 1981 [26]with technical assistance of Angelika Ascher and Gertaud Vetter     

Estimation of<Emphasis Type="Italic"> V̇</Emphasis>O<Subscript>2max</Subscript> from the ratio between HR<Subscript>max </Subscript>and HR<Subscript>rest</Subscript> – the Heart Rate Ratio Method

The effects of ̇raining and/or ageing upon maximal oxygen uptake (O_2max) and heart rate values at rest (HR_rest) and maximal exercise (HR_max), respectively, suggest a relationship between O_2max and the HR_max-to-HR_rest ratio which may be of use for indirect testing of O_2max. Fick principle calculations supplemented by literature data on maximum-to-rest ratios for stroke volume and the arterio-venous O₂ difference suggest that the conversion factor between mass-specific O_2max (ml·min^–1·kg^–1) and HR_max·HR_rest ^–1 is ~15. In the study we experimentally examined this relationship and evaluated its potential for prediction of O_2max. O_2max was measured in 46 well-trained men (age 21–51 years) during a treadmill protocol. A subgroup (n=10) demonstrated that the proportionality factor between HR_max·HR_rest ^–1 and mass-specific O_2max was 15.3 (0.7) ml·min^–1·kg^–1. Using this value, O_2max in the remaining 36 individuals could be estimated with an SEE of 0.21 l·min^–1 or 2.7 ml·min^–1·kg^–1 (~4.5%). This compares favourably with other common indirect tests. When replacing measured HR_max with an age-predicted one, SEE was 0.37 l·min^–1 and 4.7 ml·min^–1·kg^–1 (~7.8%), which is still comparable with other indirect tests. We conclude that the HR_max-to-HR_rest ratio may provide a tool for estimation of O_2max in well-trained men. The applicability of the test principle in relation to other groups will have to await direct validation. O_2max can be estimated indirectly from the measured HR_max-to-HR_rest ratio with an accuracy that compares favourably with that of other common indirect tests. The results also suggest that the test may be of use for O_2max estimation based on resting measurements alone.An erratum to this article can be found at     

Examination of a purified A′ influenza virus preparation by potentiometry

Summary The potentiometric titration of a purified influenza A virus preparation revealed 100.7×10^–4 M base and 68.8 × 10^–4 M acid-binding capacity per g. of virus protein N. The titration curve was characterized by the following fourpK values:pK ₁ = 3.37;pK ₂ = 4.50;pK ₃ = 6.37, andpK ₄ = 9.75. The isoionic point was at pH 5.43.Attempt was made to identify the dissociating groups and it was found that the carboxylic groups (pK ₁ andpK ₂) may either be glutamyl or aspartyl groups, while the cationic groups are probably the imidazolium of histidine (pK ₃) and the -amino residues of lysine (pK ₄).Inaotivation of the hemagglutinating activity of the virus preparation by mild treatment with formaldehyde at pH 8.0 resulted in a simultaneous disappearence of the -amino groups of lysine (pK ₄). The same treatment at pH 9.0 resulted in the loss of all the cationic groups previously demonstrable.The possible role of the stable positive charges on the surface of the virus at physiological pH is discussed from the point of view of the physico-chemistry of the hemagglutination.     

Recombination of yeast mitochondrial DNA does not require mitochondrial protein synthesis

Summary Mitochondrial genes recombine extensively in yeast zygotes. In heteropolar crosses (⁺ × ^–) in which the ^– allele consists of an insertion, there is preferential recovery of ⁺ and markers closely linked to it. This polarity has been postulated to be a consequence of one-way gene conversion beginning at the locus (- to ⁺). We have shown that most or all mitochondrial recombination in homopolar and heteropolar crosses, and the phenomenon of polarity itself, does not require products of protein synthesis on mitochondrial ribosomes. (i) Yeast strains were grown and mated, and the zygotes plated and grown, on glucose medium with erythromycin to inhibit and dilute out the products of mitochondrial protein synthesis. Recombination frequencies and polarity at the cap1 and oli1 loci were normal compared to controls in some homopolar (⁺ × ^–) and heteropolar crosses. Apparent changes in recombination frequencies and polarity were seen in other crosses but are attributable to locus-specific petite induction by erythromycin. (ii) Homopolar (⁺ × ⁺) and heteropolar crosses between pairs of petite mutants retaining the cap1, ery1, and oli1 loci also showed nearly normal recombination at the cap1 and oli1 loci, as determined by test-crossing the petite progeny. The petite mutants and zygotes cannot do mitochondria) protein synthesis. These results support the recombinational model of polarity.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

Summary To find out whether endurance training influences the kinetics of the increases in heart rate (f _c) during exercise driven by the sympathetic nervous system, the changes in the rate off _c adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%–70% of maximal oxygen uptake ( O_2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuousf _c recording. At the completion of the training programme, the subjects' O_2max had increased significantly(39.2 ml·min^–1·kg^–1, SD 4.7 vs 46 ml·min^–1·kg^–1, SD 5.6) and the steady-statef _c at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-statef _c was found at 150 W (146 beats·min^–1, SD 10 vs 169 beats·min^–1, SD 9) but the difference between the steady-statef _c at 150 W and that at 100 W (f _c) did not decrease significantly (26 beats·min^–1, SD 7 vs 32 beats·min^–1, SD 6). The time constant () of thef _c increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P<0.01) and the acceleration index (A=0.63·f _c·^–1) decreased from 0.20 beats·min^–1·s^–1, SD 0.05 to 0.14 beats·min^–1·s^–1, SD 0.04 (P<0.02). The major part of the changes in and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Effect of aerobic capacity on sweat rate and fluid intake during outdoor exercise in the heat

We measured the aerobic capacity, sweat rate and fluid intake of trained athletes during outdoor exercise and examined the relationship between aerobic capacity and thermoregulatory responses at high ambient temperatures. The maximal aerobic capacity ( ) of the subjects, nine male baseball players of college age, was determined by maximal exercise tests on a cycle ergometer. The subjects practised baseball regularly without drinking fluids from 1330 to 1530 hours. After 30 min rest, they played a baseball game with free access to a sports drink at 15°C from 1600 to 1830 hours. At a mean ambient temperature of 36.7 (SEM 0.2)°C, the mean percentage of body mass loss (m _b) and increase of oral temperature (T _o) from 1330 to 1530 hours was 3.47 (SEM 0.12)% and 0.81 (SEM 0.14)°C, respectively. The sweat loss from 1330 to 1830 hours was 56.53 (SEM 1.56)ml · kg^–1 of body mass (M _b) while the mean fluid consumption was 44.78 (SEM 2.39)ml · kg^–1 ofm _b, with recovery of 76.08 (SEM 2.81)% of sweat loss. The was significantly inversely correlated withm _b, fluid intake and rehydration amount, but showed no correlation withT _o. These results would suggest that at a given exercise intensity in subjects with a higher aerobic capacity body temperature is maintained with a lower sweating rate than that in subjects with a lower aerobic capacity.     

Effect of BRL-35135 on LTB4-induced guinea pig eosinophil chemotaxis

The effect of an atypical -adrenoceptor agonist, BRL-35135 on leukotriene B₄-induced-guinea pig eosinophil chemotaxis was studied. BRL-35135 and SC-41930 (leukotriene B₄-antagonist) inhibited the chemotaxis in a concentration-dependent manner (IC₅₀=9.0×10^–6 and 2.6×10^–7 M, respectively). However, isoproterenol, fenoterol and another atypical -agonist, BRL-37344 had no effects. The inhibitory effect of BRL-35135 was not affected by (±)-propranolol (10^–4 M). In contrast, the nonselective -adrenoceptor antagonist, (–)-alprenolol (10^–4 M) dextrally shifted the inhibitory curve of BRL-35135. The response to BRL-35135 was antagonized in a competitive manner by (–)-alprenolol, with the slope of the Schild plot close to unity, and a pA ₂ value of 5.62. These findings suggest that guinea pig eosinophils possess an atypical receptor, which differs from either ₁, ₂ or atypical -adrenoceptor on guinea pig ileum, and through which eosinophil chemotaxis can be modulated by BRL-35135.     

A combined study of sodium current and T-type calcium current in isolated cardiac cells

Sodium currents (I _Na) and T-type calcium currents (I _Ca,T) of isolated guinea-pig ventricular myocytes were recorded using the whole-cell voltage-clamp technique. Separation of the two currents was obtained by using the difference current method in the presence and absence of 2 mM extracellular Na (Na_o). Time to peak and the time constant of inactivation of. I_Na were about 5 times faster than that of I _Ca,T (test potential –30 mV). and I _Ca,T had an activation range positive to –50 mV, were inactivated at –50 mV, and their current/voltage relationships peaked at –22.3±1.8 mV (n=18) and –29.3±0.5 mV (n=18) respectively, with a reversal potential of +40.3±4 mV (n=18) and +30±10 mV (n=18), respectively [2 mM Na_o; 5.4 mM extracellular Ca (Ca_o)]. I _Na was blocked by 30 M tetrodotoxin (TTX), 500 M lidocaine, partly inhibited by 1 mM amiloride, but not affected by 100 M nickel (Ni). I _Ca,T was neither affected by 30 M TTX nor 500 M lidocaine, but blocked by 100 M Ni, 1 mM amiloride, 10 M R 56865 and use-dependently reduced by 5 M flunarizine. Adenosine (500 M) affected neither I _Na nor I _Ca,T, whereas 1 M isoprenaline did not affect I _Ca,T, but slightly increased I _Na. Our results demonstrate that the characteristics of I _Ca,T are not affected by the concomitant activation of I _Na, and vice versa. We conclude that I _Ca,T are not Ca currents through Na channels.     

Renal tubular reabsorption of taurine,γ-aminobutyric acid (GABA) andβ-alanine studied by continuous microperfusion

Summary Renal tubular reabsorption of taurine, -aminobutyric acid (GABA), and -alanine was studied in vivo et situ by continuous microperfusion of single proximal tubules of the rat. In each case, reabsorption was much slower than that for other amino acids that have been studied. With a concentration of 0.1 mmol/l in initial perfusate, about 60% of initial load was reabsorbed over perfusion distance of 3 mm. Taurine reabsorption saturated with only 2.17 mmol/l in initial perfusate. Assuming simple two-parameter kinetics, upper limits for K _m of 0.54 mmol/l and forV _max of 0.59 pmol·cm^–1·s^–1 for tubular reabsorption of taurine were estimated. High (20 mmol/l) concentrations of taurine or -alanine in perfusate completely inhibited GABA reabsorption, butl-phenylalanine (20 mmol/l) had no significant effect. The results indicate that the three amino acids are reabsorbed slowly from the proximal tubule by what may be a common transport system. This system appears to have a high affinity but low capacity and to be different from other known renal tubular transport systems for amino acids.Supported by National Science Foundation Research Grant No. PCM 75-09918 and by grant No. 1740 of the Austrian Fonds zur Förderung der Wissenschaftlichen Forschung.