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.     

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.     

Maximal oxygen uptake in 153 elderly Dutch people (69–87 years) who participated in the 1993 Nijmegen 4-day march

There are no studies on oxygen uptake of groups of physically active subjects aged over 70. This study describes the maximal oxygen uptake ( ) of 153 elderly people who completed the Nijmegen annual 4-day march (at least 30 km · day^–1) in 1993. A total of 97 men with a mean age of 76.7 (SD 4.6) and 56 women with a mean age of 72.8 (SD 3.6) years participated in the study. The was determined using incremental cycle ergometry; 91 men and 49 women completed a maximal exercise test. Criteria for maximal performance were respiratory exchange ratio equal to or greater than 1.00, vertilatory equivalent for oxygen equal to or greater than 30.00 and maximal heart rate equal to or greater than (beats · min^–1) 210 minus age (years). Mean maximal power output was 148.2 (SD 27.2) W and 120.4 (SD 20.5) W, mean · body mass^–1 was 26.8 (SD 4.9) ml · kg^–1 · min^–1 and 24.6 (SD 4.7) ml · kg^–1 · min^–1, mean maximal heart rate was 152 (SD 18), and 157 (SD 14) beats · min^–1 in men and women respectively. The mean · body mass^–1 was about 20% higher than reported in other studies on subjects over 70 years of age. Mean maximal heart rate was about 10 beats · min^–1 higher than predicted from the equation 220 — age. The negative effect of chronic disease on · body mass^–1 was smaller than in a sedentary reference population. The mean decline in · body mass^–1 with age was 0.46 and 0.38 ml·kg^–1·min^–1 per year in the men and women respectively, which is the same rate as found in younger subjects. It was concluded that regular exercise might substantially increase aerobic power in the physically active elderly, even when they have chronic disease, and that it is unlikely that there is an accelerated loss of aerobic power in physically active elderly people aged over 70 year.     

Thermogenesis due to noradrenaline in muscles under different rates of perfusion

Vascularly isolated hind legs of cold acclimated rats were perfused with arterial blood either without noradrenaline (NA) or with a constant concentration of NA (10 ng·ml^–1) at different perfusion rates ranging from 2 to 14l·g^–1·min^–1. The oxygen consumption of the leg during perfusion both with or without NA was linearly related to the perfusion rate. The linear increase of leg oxygen consumption with respect to the perfusion was steeper after NA, which indicates that the same arterial concentration of NA may produce a greater thermogenic effect at higher blood flow rates (the difference between resting metabolic rate and the thermogenesis stimulated by NA, was 8.20 l O₂·g^–1·h^–1 at a blood flow of 3l·g^–1·min^–1, compared with 45.02 l O₂·g^–1·h^–1 at a blood flow of 14 l·g^–1·min^–1). These data confirm the important role of the extravascular influx rate of NA in the control of thermogenesis due to NA in muscles.     

Cardiovascular and metabolic responses to noradrenaline in men acclimatized to cold baths

Summary The purpose of this study was to see whether artificial acclimatization to cold would reduce the pressor response to noradrenaline (NA) as natural acclimatization has been shown to do, and whether it would induce nonshivering thermogenesis. Three white men were infused with NA at four dosage levels between 0.038 and 0.300 g·kg^–1·min^–1 (2–23 g·min^–1), before and after artificial acclimatization to cold and again 4 months later when acclimatization had decayed. Acclimatization was induced by ten daily cold (15°Q baths of 30–60 min followed by rapid rewarming in hot (38–42°C) water, and was confirmed by tests of the subjects responses to whole-body cooling in air. Three control subjects also underwent the first and third tests. Acclimatization substantially reduced the pressor response to NA at 0.150 and 0.300 g·kg^–1·min^–1, confirming earlier findings by the same technique in naturally acclimatized men, and its decay increased this response to beyond its initial levels (P<0.05 for both changes). Acclimatization did not change the response to NA of heart rate, subjective impressions, skin temperature of finger and toe, pulmonary ventilation, or plasma free fatty acids and ketone bodies. At no time did NA increase oxygen consumption, or increase skin temperature or heat flow over reported sites of brown fat. These findings would seem to show that acclimatization to cold reduces sensitivity to the pressor effect of NA but does not induce nonshivering thermogenesis, and that the reduced sensitivity is replaced by a hypersensitivity to NA when acclimatization decays.     

The metabolism of tramadol by human liver microsomes

Summary The metabolism of tramadol was investigated in vitro using microsomal fractions of human liver. The parent compound and its main metabolites were determined by a newly developed high performance liquid chromatography assay. O-demethylation of tramadol was found to be stereoselective. The V_max of the O-demethylation of (–)-tramadol was 210 pmol·mg^–·min^–1, whereas (+)-tramadol was O-demethylated with a V_max of 125 pmol·mg^–1·min^–1. The K_m for both enantiomers was determined to be 210 M. O-demethylation was inhibited competitively by quinidine (k_i=15 nM) and propafenone (k_i=34 nM). N-demethylation was also stereoselective, preferentially metabolizing the (+)-enantiomer. Whereas O-demethylation displayed monophasic Michaelis-Menten kinetics, N-demethylation was best described by a two-site model. Competitive inhibition of the O-demethylation both by quinidine and propafenone suggests that O-demethylation is carried out by P-450IID6.Abbreviations HPLC high performance liquid chromatography - k_i inhibitory constant - k_m apparent Michaelis-Menten constant - M1 O-demethylated metabolite of tramadol - M2 N-demethylated metabolite of tramadol - NADP nicotinamide-adenine dinucleotide phosphate - T tramadol - v_max maximum velocity of the reaction     

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min^–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO_{2 peak}). During exercise the subjects ingested either a 15 g · 100 ml^–1 U-¹⁴C labelled glucose solution or H₂O labelled with a U-¹⁴C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma¹⁴C glucose and¹⁴CO₂ specific activities, and respiratory gas exchange. Simultaneously, 2-³H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l^–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l^–1; infusion 5.0 (0.09) mmol · l^–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l^–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min^–1 kg fat free mass^–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min^–1 kg FFM^–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min^–1 kg FFM^–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.     

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.     

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.     

The effects of buffer ingestion on metabolic factors related to distance running performance

We examined the effects of sodium bicarbonate (BIC) and sodium citrate (CIT) ingestion on distance running performance. Seven male runners [mean = 61.7 (SEM 1.7) ml · kg^–1 · min^–1] performed three 30-min treadmill runs at the lactate threshold (LT) each followed by a run to exhaustion at 110% of LT. The runs were double-blind and randomly assigned from BIC (0.3 g · kg body mass^–1), CIT (0.5 g · kg body mass^–1) and placebo (PLC, wheat flour, 0.5 g · kg body mass^–1). Venous blood samples were collected at 5, 15 and 25 min during the run and immediately post-exhaustion (POST-EX) and analysed for pH, and the concentrations of lactate ([1a^–]_b) and bicarbonate ([HCO₃ ^– ]). Performance was measured as running time to exhaustion at 110% of LT (TIME-EX). The pH was significantly higher (P 0.05) for the BIC and CIT trials during exercise, but not POST-EX compared to PLC. The [1a^–]_b was significantly higher (P 0.05) for the CIT trial compared to PLC during exercise, and for both CIT and BIC compared to PLC at POST-EX. Blood [HCO₃ ^–] was significantly higher (P 0.05) during exercise for BIC compared to PLC. TIME-EX was not significantly different among treatments: BIC 287 (SEM 47.4) s; CIT 172.8 (SEM 29.7) s; and PLC 222.3 (SEM 39.7) s. Despite the fact that buffer ingestion produced favourable metabolic conditions during 30 min of high intensity steady-state exercise, a significant improvement in the subsequent maximal exercise run to exhaustion did not occur.     

Comparison of haemodynamic effects during venous air infusion and after decompression in pigs

We have compared haemodynamic effects of venous gas emboli during continuous air infusion into the right atrium and after rapid decompression in pigs. Eight anaesthetized and spontaneously breathing pigs received continuous air infusion at a rate of either 0.05 ml·kg^–1 · min^–1 (six pigs, air infusion group) or 0.10 ml·kg^–1 · min^–1 (two pigs). Another eight pigs (decompression group) underwent a 30-min compression to 5 bar (500 kPa, absolute pressure), followed by a rapid decompression (2 bar·min^–1). Haemodynamic variables were measured or calculated, and bubbles in the pulmonary artery were monitored using transoesophageal echocardiography. The results showed less variation in the maximal increase in mean pulmonary arterial pressure ( _{a, pulm}) during air infusion (0.05 ml·kg^–1 · min^–1) than after decompression, although the mean maximal increase did not differ between the two groups [28.0 mmHg (3.73 kPa), 95% confidence interval (CI) 23.5–32.5, vs 32.0 mmHg (4.27 kPa), 95% CI 25.3-38.7, P=0.3]. The _a,pulm stabilized or decreased very slowly after peak values were reached in the air infusion group, whereas the _a,pulm decreased rapidly during the same period in the decompression group. No significant changes in mean arterial pressure were observed during air infusion (0.05 ml· kg^–1 · min^–1), in contrast to the rapid increase and the subsequent decrease, that appeared after decompression. Finally, the maximal bubble count was much lower in the air infusion group than in most of the pigs in the decompression group. The two pigs that received 0.10 ml·kg^–1 · min^–1 stopped breathing after 5-min infusion, developed arterial hypotension and died.     

Effect of work rate increment on peak oxygen uptake during wheelchair ergometry in men with quadriplegia

Summary The purpose of this study was to determine the effect of work rate increment on peak oxygen uptake ( peak) during wheelchair ergometry (WCE) in men with quadriplegia due to cervical spinal cord injuries (CSCI). Twenty-two non-ambulatory subjects (aged 20–38 years) with CSCI were divided into two groups based on wheelchair sports classification (n = 12 for IA group and n = 10 for IB/IC group). Subjects underwent three different, continuous graded exercise tests (spaced at least 1 week apart) on an electronically braked wheelchair ergometer. Following a 3-min warm-up, the work rate was increased 2, 4, or 6 W · min^–1 for the IA group and 4, 6, or 8 W · min^–1 for the IB/IC group. Ventilation and gas exchange were measured breath-by-breath with a computerized system. Repeated-measures ANOVA showed no significant difference among the three protocols for peak in the IA group (P>0.05). The mean (SD) peak values (ml · kg^–1 · min^–1) were 9.3 (2.4), 9.4 (3.2), and 8.4 (2.6) for the 2, 4, and 6 W · min^–1 protocols, respectively. In contrast, the IB/IC group showed a significant difference among the protocols for peak (P<0.05). The mean (SD) peak values (ml · kg^–1 · min^–1) were 15.1 (4.0), 14.1 (4.4), and 12.7 (4.0) for the 4, 6, and 8 W · min^–1 protocols, respectively. Post hoc analysis revealed a difference between the 4 and 8 W · min^–1 protocols. Our results suggest that graded exercise testing of men with quadriplegia due to CSCI, using WCE, should employ work rate increments between 2 and 6 W · min^–1 and that work rate increments of 8 W · min^–1 or greater will result in an underestimate of peak.     

Differential effects of ADH on sodium,chloride, potassium,calcium and magnesium transport in cortical and medullary thick ascending limbs of mouse nephron

The effect of antidiuretic hormone (arginine vasopressin, AVP) on transepithelial Na⁺, Cl^–, K⁺, Ca²⁺ and Mg²⁺ net transports was investigated in medullary (mTAL) and cortical (cTAL) segments of the thick ascending limb (TAL) of mouse nephron, perfused in vitro. Transepithelial net fluxes (J _Na ⁺,J _Cl ^–,J _K ⁺,J _Ca ²⁺,J _Mg ²⁺) were determined by electron probe analysis of the collected tubular fluid. Transepithelial potential difference (PD_te) and transepithelial resistance (R_te) were measured simultaneously. cTAL segments were bathed and perfused with isoosmolal, HCO ₃ ^– containing Ringer solutions, mTAL segments were bathed and perfused with isoosmolal HCO ₃ ^– free Ringer solutions. In cTAL segments, AVP (10^–10 mol·l^–1) significantly increasedJ _Mg ²⁺ andJ _Ca ²⁺ from 0.39±0.08 to 0.58±0.10 and from 0.86±0.13 to 1.19±0.15 pmol·min^–1 mm^–1 respectively. NeitherJ _Na ⁺ norJ _Cl ^–, (J _Na ⁺: 213±30 versus 221±28 pmol·min^–1 mm^–1,J _Cl ^–: 206±30 versus 220±23 pmol·min^–1 mm^–1) nor PD_te (13.4±1.3 mV versus 14.1±1.9 mV) or R_te (24.6±6.5 cm² versus 22.6±6.4 cm²) were significantly changed by AVP. No significant effect of AVP on net K⁺ transport was observed. In mTAL segments, Mg²⁺ and Ca²⁺ net transports were close to zero and AVP (10^–10 mol·l^–1) elicited no effect. However NaCl net reabsorption was significantly stimulated by the hormone,J _Na ⁺ increased from 107±33 to 148±30 andJ _Cl ^– from 121±33 to 165±32 pmol·min^–1 mm^–1. The rise inJ _NaCl was accompanied by an increase in PD_te from 9.0±0.7 to 13.5±0.9 mV and a decrease in R_te from 14.4±2.0 to 11.2±1.7 cm². No K⁺ net transport was detected, either under control conditions or in the presence of AVP.To test for a possible effect of HCO ₃ ^– on transepithelial ion fluxes, mTAL segments were bathed and perfused with HCO ₃ ^– containing Ringer solutions. With the exception ofJ _Ca ²⁺ which was significantly different from zero (J _Ca ²⁺: 0.26±0.06 pmol·min^–1 mm^–1), net transepithelial fluxes of Na⁺, Cl^–, K⁺ and Mg²⁺ were unaffected by HCO ₃ ^– . In the presence of AVP,J _Mg ²⁺ andJ _Ca ²⁺ were unaltered whereasJ _NaCl was stimulated to the same extent as observed in the absence of HCO ₃ ^– . In conclusion our results indicate heterogeneity of response to AVP in cortical and medullary segments of the TAL segment, since AVP stimulates Ca²⁺ and Mg²⁺ reabsorption in the cortical part and Na⁺ and Cl^– reabsorption in the medullary part of this nephron segment.This study was supported by the Commission des communautés européennes, grant no. ST2J 00951 F(CD), and by Wissenschafts-ausschuß der Nato über den DAAD     

Effect of short-term energy intake level and exercise on oxygen consumption in men

Summary The influence of short-term energy intake and cycle exercise on oxygen consumption in response to a 1.5 MJ test meal was investigated in ten young, adult men. On the morning after a previous day's low-energy intake (LE regimen) of 4.5 MJ, the mean resting oxygen consumption increased by 0.7 ml · kg^–1 · min^–1 after the test meal (P<0.025). After a high-energy intake (HE regimen) of 18.1 MJ, the resting measurement was unchanged (+0.4 ml · kg^–1 · min^–1) after the meal (n.s.). These trends are the reverse of what would be expected if oxygen consumption in response to feeding is a factor in the acute control of body weight. The mean fasting oxygen consumption during cycle exercise at 56% of (constant work) for both LE and HE prior intakes was not different at 31.1 ml · kg^–1 · min^–1. Oxygen consumption during exercise increased after feeding by 0.5 ml · kg^–1 · min^–1 on the LE regimen (n.s.) and decreased by 1.2 ml · kg^–1 · min^–1 on the HE regimen (n.s.). These results are also the reverse of what would be expected if oxygen consumption in response to exercise is related to short-term energy intake.     

Maximal working capacity of two professional groups in North Sumatra (Indonesia)

Summary Two groups of male students from the medical school and sports academy and two groups of tricycle drivers performed maximally on two occassions on a brake type ergometer against a load sustainable between 2–6 min according to Tornvall. In the students the difference in work performance between the medical and sports academy students, maybe due to difference in their training condition, shown by the increment and decrement of pulse rate respectively on starting and stopping the test, since all their anthropometric measurements are the same. A comparison of the maximum working capacity between the tricycle drivers to study the effect of a potion called jamu showed no difference (N₁=11, X₁=1523 m·kp·min^–1, N₂=10, X₂=1,664 m·kp·min^–1, p>0.05). The maximum working capacity of the tricycle drivers was found to be the same as the students from the sports academy (N₁=21, X₁=1,587 m·kp·min^–1, N₂=9, X₂=1,524 m·kp·min^–1, p>0.05). Maximal heart rate between the medical students and the sports academy students differ significantly (N₁=22, X₁=186 min^–1, N₂=9, X₂=175 min^–1, p<0.01), but not significantly different between the sports academy students and the beca drivers (N₁=9, X₁=175 min^–1, N₂=21, X₂=180 min^–1, p>0.05).     

Verification of the heart rate threshold

Among the methods for determining anaerobic threshold (AT), the heart rate (HR) method seems to be the simplest. On the other hand, many conflicting results from comparing this method with others have been presented over the last 10 years. Therefore, the aim of this study was to compare the heart rate threshold (HRT) with the lactate turn point (LTP) —second break point of dependence of lactate (LA) to power output, ventilatory threshold (VT) and threshold determined by electromyography (EMG_AT), all determined by the same exercise test and evaluated by the same computer algorithm. A group of 24 female students [mean age 20.5 (SD 1.6) years, maximal oxygen consumption 48.8 (SD 4.7) ml · kg^–1 · min^–1 performed an incremental exercise test on a cycle ergometer (modified Conconi test) starting with an initial power output (PO) of 40 W with intensity increments of 10 W · min^–1 until the subjects were exhausted. The HRT, LTP and EMG_AT determination was done by computer-aided break-point regression analysis from dependence of functional measures on PO. The same computer algorithm was used for VT determination from the relationship between ventilation (V) and oxygen uptake ( O₂) or carbon dioxide output ( CO₂). Nonsignificant differences were found between HRT [ O₂ 35.2 (SD 4.2) ml · kg^–1 · min^–1; HR 170.8 (SD 5.5) beats min^–1; LA 4.01 (SD 1.03) mmol · l^–1; PO 2.27 (SD 0.33) W · kg^–1 VT [ O₂ 35.1 (SD 3.7) ml · kg^–1 · min^–1 HR 168.3 (SD 4.8) beats · min^–1; LA 3.87 (SD 1:17) mmol · l^–1; PO 2.22 (SD 0.27) W · kg^–1 EMG_AT [ O₂35.6 (SD 4.1) ml · kg^–1 · min^–1 HR 171.0 (SD 5.4) beats · min^–1; LA 4.11 (SD 0.98) mmol · l^–1; PO 2.30 (SD 0.31) W · kg^–1] and LTP [ O₂) 35.3 (SD 4.1) ml · kg^–1 · min^–1; HR 170.1 (SD 6.0) beats · min^–1; LA 3.99 (SD 0.76) mmol · l^–1; PO 2.27 (SD 0.29) W · kg^–1]. Highly significant correlations (P < 0.01 in all cases) were found among all measurements made at threshold level in all the thresholds investigated. Correlation coefficients ranged in selected variables at different threshold levels from 0.842 to 0.872 in O₂ measured in ml · kg^–1 · min^–1, from 0.784 to 0.912 for LA, from 0.648 to 0.857 for HR, and from 0.895 to 0.936 for PO measured in W · kg^–1. These findings have led us to conclude that HRT could be used as an alternative method of determining anaerobic threshold in untrained subjects.     

Stroke volume response to progressive exercise in athletes engaged in different types of training

Summary Using the impedance cardiography method, heart rate ( _c) matched changes on indexed stroke volume (SI) and cardiac output (CI) were compared in subjects engaged in different types of training. The subjects consisted of untrained controls (C), volleyball players (VB) who spent about half of their training time (360 min · week^–1) doing anaerobic conditioning exercises and who had a maximal oxygen uptake ( ) 41% higher than the controls, and distance runners (D) who spent all their training time (366 min·week^–1) doing aerobic conditioning exercises and who had a 26% higher than VB. The subjects performed progressive submaximal cycle ergometer exercise (10 W·min^–1) up to _c of 150 beats·min^–1. In group C, SI had increased significantly (P<0.05) at _c of 90 beats·min^–1 ( + 32%) and maintained this difference up to 110 beats·min^–1, only to return to resting values on reaching 130 beats·min^–1 with no further changes. In group VB, SI peaked (+ 54%) at _c of 110 beats·min^–1, reaching a value significantly higher than that of group C, but decreased progressively to 22010 of the resting value on reaching 150 beats·min^–1. In group D, SI peaked at _c of 130 beats·min^–1 (+ 54%), reaching a value significantly higher than that of group VB, and showed no significant reduction with respect to this peak value on reaching 150 beats·min^–1. As a consequence, the mean CI increase per _c unit was progressively higher in VB than in C (+46%) and in D than in VB (+ 105%). It was concluded that thef _c value at which SI ceased to increase during incremental exercise was closely related to the endurance component in the training programme.     

Ventilatory threshold during treadmill exercise in kindergarten children

Summary The cardiorespiratory response to graded treadmill exercise was studied in a group of kindergarten children, aged 5 to 6 years. From the non-linear change of pulmonary ventilation with increasing exercise intensity a ventilatory threshold was determined which averaged 28.1±4.9 (SD) ml O₂·min^–1·kg^–1. A significant correlation was established between this ventilatory threshold (ml O₂·min^–1) and the physical working capacity at a heart rate of 170 beats per min (PWC₁₇₀, ml O₂·min^–1):r=0.93,p<0.001. These data show that a ventilatory threshold can be obtained in young children which is an objective index of cardiorespiratory performance capacity.     

Blood metabolites during prolonged exercise in swimming and leg cycling

Summary This study was designed to compare the influence of two modes of exercise (swimming and leg cycling) on the blood concentrations of metabolic substrates and metabolites during a 45-min exercise period. Eight college students (mean age=21.6±1.2 year) exercised at 70% of O₂ max, in water using the front crawl on one occasion, and on a cycle ergometer using the legs on another. Blood samples were drawn at 0,15, 30, and 45 min and analyzed for free fatty acids, glycerol, glucose, pyruvate, and lactate concentrations. Mean oxygen uptakes (2.23 vs 2.12 l·min^–1) and heart rates (152 vs 150 b·min^–1) for cycling and swimming respectively were not significantly different. Lactate and pyruvate were significantly (p<0.01) higher during swimming as compared to cycling. Free fatty acids, glycerol, and glucose were not significantly different between the two modes of exercise (p>0.05). Assuming venous blood concentrations provide some indication of metabolic events, these data are compatible with a tendency to a higher relative carbohydrate oxidation rate during swimming as compared to cycling during prolonged exercise at the same relative work intensities.Supported by grand from C.A.F.I.R., Université de Montréal     

In vivo human myocardial metabolism during aerobic exercise by phosphorus-31 nuclear magnetic resonance spectroscopy

A few studies have been made in vivo on human myocardial energy metabolism. Hence, no discussion has taken place on metabolism during exercise or of training effects on metabolism. We examined human myocardial energy metabolism at rest and during exercise, and also training effects on the metabolism by phosphorus-31 nuclear magnetic resonance (³¹P NMR)-spectroscopy. Six sedentary male students (Cont) and six male long distance runners (Tr) were the subjects. Energy metabolism data were obtained from myocardium during rest and exercise by the region selection method using ³¹P NMR. Rotation of the legs while riding a bicycle, which was fitted with an ergometer we had made ourselves for NMR, imposed given exercise intensities. The heart rate was measured in a stationary phase during exercise. Although the heart rate at rest in the Tr group was significantly lower [Tr, 52.5 (SD 3.1) beat · min^–1; Cont, 67.1 (SD 2.9) beat · min^–1], no significant difference was observed in myocardial energy metabolism using the ³¹P NMR method [Tr, phosphocreatine/-adenosine 5-triphosphate (PCr/-ATP); 1.51 (SD 0.02); Cont, 1.51 (SD 0.01)]. When NMR measurements were investigated at two different intensities of exercise, heart rates in the Cont group were significantly higher by about 20 beat · min ^–1 than those in the Tr group at both exercise intensities, while no difference in energy metabolism was observed between the groups or between rest and exercise [Tr, 75.9 (SD 3.6), 88.3 (SD 3.7) beat · min^–; PCr/-ATP 1.51 (SD 0.03), 1.51 (SD 0.03); Cont, 95.9 (SD 2.4), 115.1 (SD 3.5) beat · min^–1 PCr/-ATP 1.51 (SD 0.01), 1.51 (SD 0.04)]. Thus, during submaximal exercise as employed in this study, it would seem that the high energy phosphate level normally observed during rest may still be maintained. From these results, the absence of change in the myocardial PCr: ATP ratio suggested that adenosine 5-diphosphate was not the primary regular of the increased metabolism needed to meet the higher cardiac workload during aerobic exercise in either group.