Identification of histamine H1- and H2-receptors by means of mepyramine,cimetidine and theophylline in the cardiovascular system of the dog

The haemodynamic effects of histamine infusions (0.5 to 8 g kg^–1 min^–1) were studied in anaesthetized dogs previously instrumented for measurements of left ventricular pressure (LVP),dP/dt _max, aortic and femoral blood pressure (P _AO;P _AF) and femoral blood flow (F _AF). Blockage of H₁- or H₂-receptors alone with either mepyramine (1 mg kg^–1 min^–1) or cimetidine (2 mg kg^–1 min^–1) did not prevent the dose-dependent decrease in contractility and blood pressure responses to histamine. Since, however, both antihistamines administered in combination competitively antagonized responses to histamine, it is concluded that peripheral and cardiac effects of histamine involve interaction with both H₁- and H₂-receptors. The potentiation ofdP/dt _max,P _AO andF _AF responses to histamine as produced by theophylline (4 mg kg^–1 min^–1) was completely reversed by cimetidine, which thus may be taken as an indication that also under in vivo conditions cyclic AMP serves as a mediator only for histamine H₂-responses. However, since these results do not allow clearly to separate between primary cardiac and peripheral responses in a further set of experiments blood pressure was held constant during histamine infusions. When peripheral mechanisms were excluded as responsible for cardiac actions of histamine by this procedure histamine evoked small positive inotropic responses which were prevented by cimetidine. These findings suggest that on ventricular muscle of dogs there exists a small fraction of H₂-receptors mediating positive inotropic effects which, however, were masked on intact animals by negative inotropic responses due to a pronounced fall in blood pressure.     

Neuromuscular characteristics and fatigue in endurance and sprint athletes during a new anaerobic power test

The purpose of this study was to investigate neuromuscular and energy performance characteristics of anaerobic power and capacity and the development of fatigue. Ten endurance and ten sprint athletes performed a new maximal anaerobic running power test (MARP), which consisted ofn x 20-s runs on a treadmill with 100-s recovery between the runs. Blood lactate concentration [la^–]_b was measured after each run to determine submaximal and maximal indices of anaerobic power (P _3mmol·1 ^–1,P_5mmol·1 ^–1,P_10mmol·1 ^–1andP _max) which was expressed as the oxygen demand of the runs according to the American College of Sports Medicine equation: the oxygen uptake (ml·kg^–1·min^–1)=0.2·velocity (m·min^–1) +0.9·slope of treadmill (frac)·velocity (m·min^–1)+3.5. The height of rise of the centre of gravity of the counter movement jumps before (CMJ_rest) and during (CMJ) the MARP test, as well as the time of force production (t _F) and electromyographic (EMG) activity of the leg muscles of CMJ performed after each run were used to describe the neuromuscular performance characteristics. The maximal oxygen uptake ( _max), anaerobic and aerobic thresholds were determined in the _max test, which consisted ofn x 3-min runs on the treadmill. In the MARP-testP _max did not differ significantly between the endurance [116 (SD 6) ml·kg^–1·min^–1] and sprint [120 (SD 4) ml·kg^–1·min^–1] groups, even though CMJ_rest and peak [la^–]_b were significantly higher and _max was significantly lower in the sprint group than in the endurance group and CMJ_rest height correlated withP _max (r=0.50,P<0.05). The endurance athletes had significantly higher mean values ofP _3mmol·1 ^–1andP _5mmol·1 ^–1[89 (SD 7) vs 76 (SD 8) ml·kg^–1·min^–,P<0.001 and 101 (SD 5) vs 90 (SD 8) ml·kg^–1·min^–1,P<0.01. Significant positive correlations were observed between theP _3mmol·l ^–1and _max, anaerobic and aerobic thresholds. In the sprint group CMJ and the averaged integrated iEMG decreased andt _F increased significantly during the MARP test, while no significant changes occurred in the endurance group. The present findings would suggest thatP _max reflected in the main the lactacid power and capacity and to a smaller extent alactacid power and capacity. The duration of the MARP test and the large number of CMJ may have induced considerable energy and neuromuscular fatigue in the sprint athletes preventing them from producing their highest alactacidP _max at the end of the MARP test. Due to lower submaximal [la^–]_b (anaerobic sprinting economy) the endurance athletes were able to reach almost the sameP _max as the sprint athletes.     

Bio-energetic profile in 144 boys aged from 6 to 15 years with special reference to sexual maturation

Summary The effects of growth and pubertal development on bio-energetic characteristics were studied in boys aged 6–15 years (n = 144; transverse study). Maximal oxygen consumption (VO_2max, direct method), mechanical power at (VO_2max ( ), maximal anaerobic power (P_max; force-velocity test), mean power in 30-s sprint (P _30s; Wingate test) were evaluated and the ratios between P_max,P _30s and were calculated. Sexual maturation was determined using salivary testosterone as an objective indicator. Normalized for body massVO_2max remained constant from 6 to 15 years (49 ml· min^–1 · kg^–1, SD 6), whilst P_max andP _30s increased from 6–8 to 14–15 years, from 6.2 W · kg^–1, SD 1.1 to 10.8 W · kg^–1, SD 1.4 and from 4.7 W · kg^–1, SD 1.0 to 7.6 W · kg^–1, SD 1.0, respectively, (P < 0.001). The ratio P_max: was 1.7 SD 3.0 at 6–8 years and reached 2.8 SD 0.5 at 14–15 years and the ratioP _30s: changed similarly from 1.3 SD 0.3 to 1.9 SD 0.3. In contrast, the ratio P_max:P _30s remained unchanged (1.4 SD 0.2). Significant relationships (P < 0.001) were observed between P_max (W · kg^–1),P _30s (W · kg^–1), blood lactate concentrations after the Wingate test, and age, height, mass and salivary testosterone concentration. This indicates that growth and maturation have together an important role in the development of anaerobic metabolism.     

Role of aspirin in modulating myocardial ischemic reperfusion injury

The role of low-dose aspirin (3 mg/kg, i.v.) in attenuating ischemic reperfusion injury was studied in a canine model. Regional ischemia for 40 min was produced by temporary occlusion of the left anterior descending coronary artery and thereafter reperfusion instituted for 3 h. Mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), positive (+) LV dP/dt _max and negative (–) LV dP/dt _max were monitored alongwith myocardial adenosine triphosphate (ATP), creatine phosphate (CP), glycogen and lactate. Following reperfusion, there was a significant fall in (i) MAP, (ii) (+) LV dP/dt _max and (iii) (–) LV dP/dt _max. LVEDP was corrected after about 2h of reperfusion. Replenishment of only myocardial CP occurred, without any change in ATP and glycogen, although lactate accumulation was corrected.Aspirin administered 15 min before reperfusion (posttreatment) caused normalisation of LVEDP within 15 min and prevented any deterioration in (–) LV dP/dt _max, although it had no effect on MAP and (+) LV dP/dt _max. After 3h of reperfusion (post-treatment), myocardial ATP, CP, glycogen and lactate contents became normal. The number of premature ventricular complexes was significantly reduced after aspirin treatment. The present study indicates that low-dose aspirin post-treatment can ameliorate at least some of the deleterious consequences of reperfusion injury of the myocardium.     

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     

Scaling or normalising maximum oxygen uptake to predict 1-mile run time in boys

There is still considerable debate and some confusion as to the most appropriate method of scaling or normalizing maximum oxygen uptake (O_2max) for differences in body mass (m) in both adults and children. Previous studies on adult populations have demonstrated that although the traditional ratio standard O_2max (ml kg^–1 min^–1) fails to render O_2max independent of body mass, the ratio standard is still the best predictor of running performance. However, no such evidence exists in children. Hence, the purpose of the present study was to investigate whether the ratio standard is still the most appropriate method of normalising O_2max to predict 1-mile run speed in a group of 12-year-old children (n=36). Using a power function model and log-linear regression, the best predictor of 1-mile run speed was given by: speed (m s^–1)=55.1O_2max^0.986m^–0.96. With both the O_2max and body mass exponents being close to unity but with opposite signs, the model suggest the best predictor of 1-mile run speed is almost exactly the traditional ratio standard recorded in the units (ml kg^–1 min^–1). Clearly, reporting the traditional ratio standard O_2max, recorded in the units (ml kg^–1 min^–1), still has an important place in publishing the results of studies investigating cardiovascular fitness of both children and adults.     

Effect of atrial natriuretic factor and cyclic guanosine monophosphate on water and urea transport in the inner medullary collecting duct

We examined the action of high (2×10^–8M) and low (6×10^–9M) concentrations of atrial natriuretic factor (ANF) on water and urea transport in the rat inner medullary collecting duct (IMCD) using the in vitro microperfusion technique. We measured the hydraulic conductivity (Lp ×10^–6 cm/atm per second) and both lumen-to-bath (P _u(lb)) and bath-to-lumen (P _u(bl)) ¹⁴C-urea permeabilities (P _u× 10^–5 cm/s) in the absence and in the presence of vasopressin (VP). High concentrations of ANF were able to inhibit the maximum activity of (50 U/ml) VP-stimulated L _p but physiological concentration of ANF inhibit only submaximum activity (10 U/ml) of VP-stimulated L _p. The hydrosmotic effect of dibutyryl-cyclic 3,5 adenosine monophosphate (cAMP) (10^–4M) was unchanged by high concentrations of ANF (2×10^–8M). Also we found that high (10^–4M) and low (10^–6M) concentrations of exogenous cyclic 3,5-guanosine monophosphate (GMP) while unable to change the Lp in the absence of VP, decreased the maximum activity of VP-stimulated Lp significantly. We also found that ANF inhibits partially and in a reversible manner the VP-stimulated P _u(lb) but not the VP-stimulated P _u(bl). These results demonstrated that plasma concentrations of ANF observed during volume expansion (10^–10M) are able to inhibit submaximum activity of VP-stimulated (10 U/ml) L _p in the rat IMCD, this effect seems to occur before cAMP formation and it appears to be mediated by cGMP. ANF (6× 10^–9M) also reduced the VP-stimulated urea outflux. Therefore, the increase in water excretion produced by ANF could be explained, at least in part, by the inhibition by ANF of vasopressin effects on water and urea transport in the IMCD.This study was presented in part at the VI Latin American Congress of Nephrology, Brazil, October 1985 and at the X^th International Congress of Nephrology, London, July 1987.     

Noninvasive assessment of cardiac contractility by using (dP/dt)/P of carotid artery pulses during exercise

In earlier studies we have shown that both the pressure (P) of the carotid artery pulse (CAP) and its first derivative (CAP dP/dt) could be recorded during moderate exercise. To establish that the CAP (dP/dt)/P is a noninvasive substitute for the left ventricular (LV) value, LV (dP/dt)/P, an index of cardiac contractility, we studied CAP (dP/dt)/P under various states of activity in the autonomic nervous system in 12 healthy male subjects. Increased sympathetic nerve activities yielded by passive tilting, emotional load, or cold stress increased CAP (dP/dt)/P significantly (P< 0.05). Increased parasympathetic nerve activity by ocular compression, however, did not significantly affect the value. Moderate exercise at a heart rate of approximately 150 beats·min^–1 increased it significantly from 16.7 to 25.2·s^–1 in a supine position (P<0.001) and from 16.6 to 24.8·s^–1 in an upright position (P<0.001). It increased monotonically as heart rate increased, but the slope was steeper when the heart rate was greater than approximately 100 beats·min^–1 than it was when the rate was less than 100 beats·min^–1. In conclusion, the present study indicated that CAP (dP/dt)/P can be used as a noninvasive index of cardiac contractility even in moderate exercise.     

Effect of physical training on the responses of serum adrenocorticotropic hormone during prolonged exhausting exercise

Summary The purpose of this study was to investigate the effects of physical training on the responses of serum adrenocorticotropic hormone (ACTH) and cortisol concentration during low-intensity prolonged exercise. Five subjects who had fasted for 12 h cycled at the same absolute intensity that elicited 50% of pre-training maximal oxygen uptake ( O_2max), either until exhaustion or for up to 3 h, before and after 7 weeks of vigorous physical training [mean daily energy consumption during training exercise, 531 kcal (2230 kJ)]. In the pre-training test, serum ACTH and cortisol concentrations did not increase during the early part of the exercise. Increases in concentrations of both hormones occurred in all subjects when blood glucose concentration decreased during the later phase of the exercise. The mean values and SEM of serum ACTH and cortisol concentrations at the end of the exercise were 356 ng · l^–1, SEM 79 and 438 g · l^–1, SEM 36, respectively. After the physical training, O_2max of the subjects improved significantly from the mean value of 50.2 ml · kg^–1 · min^–1, SEM 2.5 to 57.3 ml · kg^–1 · min^–1, SEM 2.0 (P < 0.05). In the post-training test, exercise time to exhaustion was prolonged in three subjects. Comparing the pre- and post training values observed after the same length of time that the subjects had exercised in the pre-training test, the post-training values of serum ACTH (44 ng · l^–1, SEM 3) and cortisol (167 g · l^–1, SEM 30) concentration were less than the pre-training value (P < 0.05). However, after the subjects stopped exercising in the post-training test, the serum ACTH (214 ng · l^–1, SEM 49) and cortisol (275 g · l^–1, SEM 50) concentrations were not significantly different from those measured after the subjects stopped exercising in the pre-training test (P > 0.10). In conclusion, high-intensity physical training reduced the responses of both hormones during prolonged exercise, propbably because of a delayed decrease of blood glucose concentration after physical training, while the level of the blood glucose concentration which induces ACTH and cortisol secretion did not change.     

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

Summary We attempted to determine the change in total excess volume of CO₂ Output (CO₂ excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO₂ excess and distance-running performance. Six male endurance runners, aged 19–22 years, were subjects. Maximal oxygen uptake (VO_2max), oxygen uptake (VO₂) at anaerobic threshold (AT), CO₂ excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for C02 excess per unit of body mass per unit of blood lactate accumulation (Ala^–) in exercise (CO₂ excess·mass^–1·la^–), 12-min ERP, VO₂ at AT (AT-VO₂) and VO_2max on average were 0.8 ml·kg^–1·l^–1·mmol^–1, 97.8m, 4.4 ml·kg^–1· min^–1 and 7.3 ml·kg^–1·min^–1, respectively. The percentage change in CO₂ excess·mass^–1·la^– (15.7%) was almost same as those of VO_2max (13.7%) and AT-VO₂ (13.2%). It was found to be a high correlation between the absolute amount of change in CO₂ excess·mass^–1·la^– and the absolute amount of change in AT-VO₂ (r=0.94, P<0.01). Furthermore, the absolute amount of change in C02 excess·mass^–1·la^–, as well as that in AT-VO₂ (r=0.92, P<0.01), was significantly related to the absolute amount of change in 12-min ERP (r=0.81, P<0.05). It was concluded that a large CO₂ excess·mass^–1·la^–1 of endurance runners could be an important factor for success in performance related to comparatively intense endurance exercise such as 3000–4000 m races.     

Cardiac output during exercise in paraplegic subjects

Summary The purpose of this study was to measure the cardiac output using the CO₂ rebreathing method during submaximal and maximal arm cranking exercise in six male paraplegic subjects with a high level of spinal cord injury (HP). They were compared with eight able bodied subjects (AB) who were not trained in arm exercise. Maximal O₂ consumption ( O_2max) was lower in HP (1.1 1·min^–1, SD 0.1; 17.5 ml·min^–·kg, SD 4) than in AB (2.5 1·min^–1, SD 0.6; 36.7 ml·min^–1·kg, SD 10.7). Maximal cardiac output was similar in the groups (HP, 141·min^–1 SD 2.6; AB, 16.81·min^–1 SD 4). The same result was obtained for maximal heart rate (f _c,max (HP, 175 beats·min^–1, SD 18; AB, 187 beats·min^–, SD 16) and the maximal stroke volume (HP, 82 ml, SD 13; AB, 91 ml, SD 27). The slopes of the relationshipf _c/ O₂ were higher in HP than AB (P<0.025) but when expressed as a % O_2max there were no differences. The results suggests a major alteration of oxygen transport capacity to active muscle mass in paraplegics due to changes in vasomotor regulation below the level of the lesion.     

An improved isolated, left ventricular ejecting, murine heart model

 An improved, isolated, left ventricular-ejecting, murine heart model is described and evaluated. Special attention was paid to the design and impedance characteristics of the artificial aortic outflow tract and perfusate composition, which contained glucose (10 mM plus insulin) and pyruvate (1.5 mM) as substrates. Temperature of the isolated perfused hearts was maintained at 38.5 °C. During antegrade perfusion (preload 10 mm Hg, afterload 50 mm Hg, 2.5 mM Ca²⁺) proper design of the aortic outflow tract provided baseline values for cardiac output (CO), left ventricular developed pressure (LVDP) and the maximum first derivative of left ventricular pressure (LV dP/dt _max) of 11.1±1.7 ml min^–1, 83±5 mm Hg and 6283±552 mm Hg s^–1, respectively, resembling findings in the intact mouse. During 100 min normoxic antegrade perfusion CO declined non-significantly by less than 10%. Varying pre- and afterloads resulted in typical Frank-Starling relationships with maximal CO values of 18.6±1.8 ml min^–1 at pre- and afterload pressures of 25 and 50 mm Hg, respectively. Left ventricular function curves were constructed at free [Ca²⁺] of 1.5 and 2.5 mM in the perfusion medium. Significantly higher values for CO, LVDP and LV dP/dt _max and LV dP/dt _min were obtained at 2.5 mM Ca²⁺ at all loading conditions investigated. Phosphocreatine and creatine levels remained stable throughout the perfusion period. Despite a small but significant decline in tissue ATP content, the sum of adenine nucleotides did not change during the normoxic perfusion period. The tissue content of glycogen increased significantly. Received: 28 April 1998 / Received after revision and accepted: 10 September 1998     

The continuous measurement of tubular volume changes in response to step changes in contraluminal osmolality

A new method to measure time dependent (t) volume (V) changes in proximal straight tubules (PST) is described.V is calculated from diameter (d) measurements for which a video camera and an integrating circuit are used. A tubular image of high optical contrast is recorded with the TV camera such that the scan lines run crosswise to the tubule. The video signal is analyzed by a special processor which adds 225 tubular diameters of each TV frame and feeds this analog signal to a pen recorder. The fractional error ind measurements is 10^–3. Diameter changes of less than 0.05 m can be detected, as compared to the usual error of a single measurement of about 0.4 m.P _os ^cb , the osmotic water permeability of the contraluminal cell membrane was measured by setting up osmotic steps across it in less than 0.1 s and following the ensuing d/t. the time delay between solution change and the linear part of the osmotic response was 0.51±0.05 s.P _os ^cb was found to be 50.4 (±8.7)×10^–4 cm³·cm^–2 of basement membrane area ·s^–1·osmolar^–1.     

Regulation of phosphatidylinositol kinases by arachidonic acid in rat submandibular gland cells

Phosphoinositide kinases were characterized in membrane extracts of rat submandibular gland cells. Both phosphatidylinositol (PI) 4-kinase and phosphatidylinositol-4-phosphate (PI(4)P) 5-kinase phosphorylated endogenous substrates in reactions that were linear for up to 5 min, were activated by Mg²⁺ and showed maximal activity around neutral pH. PI 4-kinase was stimulated by Triton X-100 at an optimal concentration of 0.22%, but the detergent had an inhibitory effect on PI(4)P 5-kinase. Arachidonic acid (AA), at concentrations greater than 100 M, inhibited the activity of both enzymes in a dose-dependent manner. The inhibitory effect was replicated by other unsaturated fatty acids, but not by a saturated fatty acid of the sn-20 series. The nature of AA inhibition of the kinases was examined in enzyme kinetic studies with exogenous phosphoinositide and adenosine 5-triphosphate (ATP) substrates. Lineweaver-Burk plots of PI 4-kinase activity showed that AA had no effect on the apparent K _m for either PI or ATP, but that the fatty acid significantly reduced V _max (PI) from 331 to 177 pmol.mg^–1.min^–1 and V _max (ATP) from 173 to 59 pmol.mg^–1.min^–1. This inhibitory action was consistent for PI(4)P 5-kinase kinetics, where again, AA did not alter apparent K _m values, but lowered V _max for both PI(4)P and ATP by around 50%. Since the combination of a reduced V _max and an unchanged K _m value indicates noncompetitive enzyme inhibition, it is proposed that AA regulates phosphoinositide cycle activity in submandibular gland cells by acting as a noncompetitive inhibitor of PI 4-kinase and PI(4)P 5-kinase.     

Lactate kinetics during passive and partially active recovery in endurance and sprint athletes

We investigated the effects of passive and partially active recovery on lactate removal after exhausting cycle ergometer exercise in endurance and sprint athletes. A group of 14 men, 7 endurance-trained (ET) and 7 sprint-trained (ST), performed two maximal incremental exercise tests followed by either passive recovery (20 min seated on cycle ergometer followed by 40 min more of seated rest) or partially active recovery [20 min of pedalling at 40% maximal oxygen uptake ( O_2max) followed by 40 min of seated rest]. Venous blood samples were drawn at 5 min and 1 min prior to exercise, at the end of exercise, and during recovery at 1, 2, 3, 4, 5, 6, 8, 10, 15, 20, 30, 40, 50, 60 min post-exercise. The time course of changes in lactate concentration during the recovery phases were fitted by a bi-exponential time function to assess the velocity constant of the slowly decreasing component (₂) expressing the rate of blood lactate removal. The results showed that at the end of maximal exercise and during the 1st min of recovery, ET showed higher blood lactate concentrations than ST. Furthermore, ET reached significantly higher maximal exercise intensities [5.1 (SEM 0.5) W · kg^–1 vs 4.0 (SEM 0.3) W · kg^–1,P < 0.05] and O_2max [68.4 (SEM 1.1) ml · kg^–1 · min^–1 vs 55.5 (SEM 5.1) ml · kg^–1 · min^–1,P < 0.01]. There was no significant difference between the two groups during passive recovery for ₂ During partially active recovery, ₂ was higher than during passive recovery for both groups (P < 0.001), but ET recovered faster and sooner than ST (P < 0.05). Compared to passive recovery, the ₂ measured during partially active recovery was increased threefold in ET and only 1.5-fold in ST. We concluded that partially active recovery potentiates the enhanced ability to remove blood lactate induced by endurance training.     

Oxygen uptake during running as related to body mass in circumpubertal boys: a longitudinal study

Summary To investigate the effect of endurance training on physiological characteristics during circumpubertal growth, eight young runners (mean starting age 12 years) were studied every 6 months for 8 years. Four other boys served as untrained controls. Oxygen uptake ( O ₂) and blood lactate concentrations were measured during submaximal and maximal treadmill running. The data were aligned with each individual's age of peak height velocity. The maximal oxygen uptake ( O _2max; ml · kg^–1 · min^–1) decreased with growth in the untrained group but remained almost constant in the training group. The oxygen cost of running at 15 km · h^–1 ( O ₂₁₅, ml · kg^–1 · min^–1) was persistently lower in the trained group but decreased similarly with age in both groups. The development of O _2max and O ₂₁₅ (1 · min^–1) was related to each individual's increase in body mass so that power functions were obtained. The mean body mass scaling factor was 0.78 (SEM 0.07) and 1.01 (SEM 0.04) for O _2max and 0.75 (SEM 0.09) and 0.75 (SEM 0.02) for O ₂₁₅ in the untrained and trained groups, respectively. Therefore, expressed as ml · kg^–0.75 · min^–1, O ₂₁₅ was unchanged in both groups and O _2max increased only in the trained group. The running velocity corresponding to 4 mmol · 1^–1 of blood lactate ( _la4) increased only in the trained group. Blood lactate concentration at exhaustion remained constant in both groups over the years studied. In conclusion, recent and the present findings would suggest that changes in the oxygen cost of running and O _2max (ml · kg^–1 · min^–1) during growth may mainly be due to an overestimation of the body mass dependency of O ₀₂ during running. The O ₂ determined during treadmill running may be better related to kg^0.75 than to kg¹.     

A new approach to rowing ergometry: establishing exercise intensity relative to maximum force output

Summary The present experiment evaluated a new approach to establish exercise intensity during hydraulic rowing ergometry. In contrast to the traditional approach where exercise intensity is augmented by systematically increasing workload, the new procedure increments the intensity of exercise while maintaining a constant percentage of maximum force output. Ten college females exercised on a hydraulic rower that allowed for control of rowing speed and resistance. The new method to establish work intensity was to row at a cadence of 30 c·min^–1 at a force output equal to 50% of maximum rowing force at each setting determined dynamically prior to testing. Two protocols were used for the maximum tests on the hydraulic rower. Row 1 was a 17-min, six-stage, incremental continuous row test performed at increasingly difficult settings from easy (setting 1; 603 N) to difficult (setting 6; 893 N). Row 2 was identical to row 1 until 15 min when resistance was reduced to setting 2 (658 N) for allout effort during the last 2 min. During this time, cadence declined from 30 c·min^–1 to 19.4 c·min^–1 at dial setting 6 and increased to 35.4 c·min^–1 at dial setting 2. Both rowing protocols were compared to maximal physiological responses during treadmill running (TM). Compared to TM, both rowing protocols elicited. significantly lower maximum oxygen uptake (VO_2max;P<0.05; row 1=29.0% and row 2=12.9%) and maximum heart rate (HR_max;P<0.05; row 1=12.9% and row 2=6.7%). Maximum ventilation (V _Emax) during row 1 was also lower by 30.4% than TM (P<0.05). In addition, row 1 was significantly lower (P<0.05) than row 2 forVO_2max (2.23 vs 2.60 l·min^–1), HR_max (165.5 vs 177.3 beats·min^–1), andV _Emax (62.7 vs 86.3 1·min^–1). These results demonstrate thatVO_2max, HR_max, andV _Emax are depressed when rowing exercise is performed at a high intensity relative to maximum strength. We conclude that the new approach to establish exercise intensity relative to maximum force production is more effective for eliciting near maximum values ofVO₂, HR, andV _E than the conventional method that increases the workload by set increments without consideration of maximal strength.     

Effects of muscarinic blockade on the thermic effect of oral or intravenous carbohydrate

Summary Muscarinic blockade by atropine has been shown to decrease the thermic effect of a mixed meal, but not of intravenous glucose. To further delineate the mechanisms involved in the atropine-induced inhibition of thermogenesis after a meal, plasma substrate and hormone concentrations, energy expenditure (EE) and substrate oxidation rates were measured before and during a continuous glucose infusion (44.4 mol·kg^–1·min^–1) with or without atropine. After 2 h of glucose infusion, a 20-g oral fructose load was administered while the glucose infusion was continued. Plasma insulin concentrations attained a plateau at 596 (SEM 100) pmol·l^–1 after 120 min of glucose infusion and were not affected by muscarinic blockade; plasma glucose concentrations peaked at 13.3 (SEM 0.5) mmol·l^–1 at 90 min and decreased progressively thereafter; no difference was observed with or without atropine. Plasma free fatty acid and glucagon concentrations, with or without atropine, were both decreased to 201 (SEM 18) mol·l^–1 and 74 (SEM 4) ng·l^–1, respectively, after 2 h of glucose infusion, and were not further suppressed after oral fructose. Carbohydrate oxidation rates (CHO_ox) increased to 20.8 (SEM 1.4) mol·kg^–1·min^–1 and lipid oxidation rates (L_ox) decreased to 1.5 (SEM 0.3) mol·kg^–1·min^–1 between 90 and 120 min after the beginning of glucose infusion and were not affected by atropine. Glucose-induced thermogenesis was similar with [6.5% (SEM 1.4%) of basal EE] or without [6.0% (SEM 1.0%), NS) muscarinic blockade during the 30 min preceding fructose ingestion. During the second half-hour after fructose ingestion, atropine infusion inhibited markedly the stimulation of CHO_ox [+2.8 (SEM 1.0) mol·kg^–1·min^–1 vs +6.9 (SEM 1.0) mol·kg^–1·min^–1, saline, P<0.02] and the suppression of L_ox [–0.8 (SEM 0.2) mol·kg^–1·min^–1 vs –1.4 (SEM 0.2) mol·kg^–1·min^–1, saline, P<0.05]. Carbohydrate-induced thermogenesis during the second half-hour after fructose ingestion, increased to 13.0% (SEM 2.0%) without atropine and was suppressed to 7.7% (SEM 1.9%) (P< 0.05, vs saline) with atropine. It was concluded that muscarinic blockade suppressed the increase of thermogenesis observed after oral fructose, but not during intravenous glucose infusion and that this suppression occurred independently of alterations of plasma insulin concentrations.     

Energetics of locomotion in African pygmies

Summary The energy cost of walking (C _w). and running (C _r), and the maximal O₂ consumption (VO_2max) were determined in a field study on 17 Pygmies (age 24 years, SD 6; height 160 cm, SD 5; body mass 57.2 kg, SD 4.8) living in the region of Bipindi, Cameroon. TheC _w varied from 112 ml·kg^–1·km^–1, SD 25 [velocity (), 4 km·h^–1] to 143 ml·kg^–1·km^–1, SD 16 (, 7 km·h^–1). Optimal walking was 5 km·h^–1. TheC _r was 156 ml·kg^–1·km^–1, SD 14 (, 10 km·h^–1) and was constant in the 8–11 km·h^–1 speed range. TheVO_2max was 33.7 ml·kg^–1· min^–1, i.e. lower than in other African populations of the same age. TheC _r andC _w were lower than in taller Caucasian endurance runners. These findings, which challenge the theory of physical similarity as applied to animal locomotion, may depend either on the mechanics of locomotion which in Pygmies may be different from that observed in Caucasians, or on a greater mechanical efficiency in Pygmies than in Caucasians. The lowC _r values observed enable Pygmies to reach higher running speeds than would be expected on the basis of theirVO_2max.     

Lung diffusion capacity,oxygen uptake,cardiac output and oxygen transport during exercise before and after an Himalayan expedition

Studies were made of pulmonary diffusion capacity and oxygen transport before and after an expedition to altitudes at and above 4900 m. Maximum power (P _max) and maximal oxygen uptake (VO _2max) 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 (Q _c) and lung diffusion capacity of carbon monoxide (D _L,CO) were measured by acetylene and CO rebreathing at rest and during exercise at low, medium and submaximal intensities. After acclimatization, VO_2max and P _max 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,co 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^–t 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 Q _c, oxygen uptake and D_L,CO. A decrease in muscle mass and capillarity may have been responsible for the decrease in maximal Q_c which may have resulted in a decrease of D _L,CO and an increase in alveolar-arterial oxygen difference. The decrease in D _L,CO 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.