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.     

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 O2 uptake of boys and girls — ages 14–17

Summary White high school girls (n = 120) and boys (n = 120) aged 14–17 years, selected from 9th, 10th, 11th and 12 grades of a northern, midwest U.S. high school performed running exercise on a motor driven treadmill for determinations of maximal O₂ uptake ( O₂ max).The mean O₂ max for all age groups was 40.8±4.0 and 54.7±5.6 ml/kg·min^–1 for girls and boys respectively. The difference in O₂ max across age groups varied only from 40.2–41.2 ml/kg·min^–1 for girls and 54.0–56.3 ml/kg·min^–1 for boys. These differences were not significant (P>0.05). The reported O₂ max data are compared with those reported in other studies for bicycle ergometer and treadmill exercise using similar age groups.     

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.     

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.     

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     

Effects of glucagon on Na+, Cl−, K+, Mg2+ and Ca2+ transports in cortical and medullary thick ascending limbs of mouse kidney

The effects of glucagon on transepithelial Na⁺, Cl^–, K⁺, Ca²⁺ and Mg²⁺ net fluxes were investigated in isolated perfused cortical (cTAL) and medullary (mTAL) thick ascending limbs of Henle's loop of the mouse nephron. Transepithelial ion 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. Simultaneously the transepithelial voltage (PD_te) and the transepithelial resistance (R _te) were recorded. In cTAL-segments (n=8), glucagon (1.2×10^–8 mol · l^–1) stimulated significantly the reabsorption of Na⁺, Cl^–, Ca²⁺ and Mg²⁺J _Na ⁺ increased from 204±20 to 228±23 pmol · min^–1 · mm^–1,J _Cl ^– from 203±18 to 234±21 pmol · min^–1 · mm^–1,J _Ca ²⁺ from 0.52±0.13 to 1.34±0.30 pmol · min^–1 · mm^–1 andJ _Mg ²⁺ from 0.51±0.08 to 0.84±0.08 pmol · min^–1 · mm^–1.J _K+ remained unchanged: 3.2±1.3 versus 4.0±1.9 pmol · min^–1 · mm^–1. Neither PD_te (16.3±1.5 versus 15.9±1.4 mV) norR _te (22.5±3.0 versus 20.3±2.6 cm²) were changed significantly by glucagon. However, in the post-experimental periods a significant decrease in PD_te and increase inR _te were noted. In mTAL-segments (n=9), Mg²⁺ and Ca²⁺ transports were close to zero and glucagon elicited no significant effect. The reabsorptions of Na⁺ and Cl^–, however, were strongly stimulated:J _Na ⁺ increased from 153±17 to 226±30 pmol · min^–1 · mm^–1 andJ _Cl ^– from 151±23 to 243±30 pmol · min^–1 · mm^–1. The rise in NaCl transport was accompanied by an increase in PD_te from 10.3±1.1 to 12.3±1.2 mV and a decrease inR _te from 19.1±2.7 to 17.8±2.0 cm². No net K⁺ movement was detectable either in the absence or in the presence of glucagon. A micropuncture study carried out in hormone-deprived rats indicated that glucagon stimulates Na⁺, Cl^–, K⁺, Mg²⁺ and Ca²⁺ reabsorptions in the loop of Henle. In conclusion our data demonstrate that glucagon stimulates NaCl reabsorption in the mTAL segment and to a lesser extent in the cTAL segment whereas it stimulates Ca²⁺ and Mg²⁺ reabsorptions only in the cortical part of the thick ascending limb of the mouse nephron. These data are in good agreement with, and extend, those obtained in vivo on the rat with the hormone-deprived model.This study was supported by the Commission des Communautés Européennes, Grant no. ST 23, 00951F (CD) and by Wissenschaftsausschuß der Nato über den DAAD     

The effect of different treadmill speeds on the variability of \dot VO_2 max 2 in children

Summary Eight boys aged 10–12 years performed three tests on each of three treadmill protocols. Each test was a continuous, progressively graded performance to exhaustion, but protocols differed in speed — (walk: 90 m·min^–1, jog: 110 m·min^–1, run: 130 m·min^–1). The walk protocol was found inappropriate for jackeO₂ max determination in children. Compared to the faster speeds, the walk test elicited a lower at exhaustion, and had lower reliability (0.56) and a high coefficient of variation (8%). For the at exhaustion on the jog and run protocols the coefficient of variation was 3–5% and the reliability coefficient averaged 0.90, comparable to values seen for repeated trials in adults. The usually accepted criterion of a plateau of with increasing work levels was inappropriate for use with children. Attempts to derive plateau criteria suitable for use with children proved unsuccessful. Plateau criteria may be difficult to achieve with children in light of their apparently weaker glycolytic energy capacity. Nevertheless, the highest measured at jog or run speeds has a consistency similar to that found for measurement in adults.Supported in part by a grant from the Ministry of Health and Welfare Canada, and in part from the Ministry of Culture and Recreation, Ontario, Canada     

Does the threshold of transcutaneous partial pressure of carbon dioxide represent the respiratory compensation point or anaerobic threshold?

On reaching the respiratory compensation point (RCP) during rapidly increasing incremental exercise, the ratio of minute ventilation (V_E) to CO₂ output (VCO₂) rises, which coincides with changes of arterial partial pressure of carbon dioxide (P _aCO₂). Since P _aCO₂ changes can be monitored by transcutaneous partial pressure of carbon dioxide (PCO_2,tc) RCP may be estimated by PCO_2,tc measurement. Few available studies, however, have dealt with comparisons between PCO_2,tc threshold (T _AT) and lactic, ventilatory or gas exchange threshold (V _AT), and the results have been conflicting. This study was designed to examine whether this threshold represents RCP rather than V _AT. A group of 11 male athletes performed incremental excercise (25 W · min^–1) on a cycle ergometer. The PCO_2,tc at (44°C) was continuously measured. Gas exchange was computed breath-by-breath, and hyperaemized capillary blood for lactate concentration ([la^–]_b) and P _aCO₂ measurements was sampled each 2 min. The T _AT was determined at the deflection point of PCO_2,tc curve where PCO_2,tc began to decrease continuously. The V _AT and RCP were evaluated with VCO₂ compared with oxygen uptake (VO₂) and V_E compared with the VCO₂ method, respectively. The PCO_2,tc correlated with P _aCO₂ and end-tidal PCO₂. At T _AT, power output [P, 294 (SD 40) W], VO₂ [4.18 (SD 0.57)l · min^–1] and [la^–] [4.40 (SD 0.64) mmol · l^–1] were significantly higher than those at V _AT[P 242 (SD 26) W, VO₂ 3.56 (SD 0.53) l · min^–1 and [la^–]_b 3.52 (SD 0.75), mmol · l^–1 respectively], but close to those at RCP [P 289 (SD 37) W; VO₂ 3.97 (SD 0.43) l · min^– and [la^–]_b 4.19 (SD 0.62) mmol · l^–1, respectively]. Accordingly, linear correlation and regression analyses showed that P, VO₂ and [la^–]_b at T _AT were closer to those at RCP than at V _AT. In conclusion, the T _AT reflected the RCP rather than V _AT during rapidly increasing incremental exercise.     

Model of bicarbonate secretion by resting frog stomach fundus mucosa I. Transepithelial measurements

In the present in vitro experiments on gastric fundus mucosa of Rana esculenta we try to define the mechanism of alkaline secretion that is observed in summer frogs in the resting stomach (blockage of HCl secretion by ranitidine, 10^–5 mol/l). The transepithelial voltage and the rate of alkalinization (ASR) of an unbuffered gastric lumen perfusate was measured as a function of serosal (and mucosal) fluid composition. ASR was high (0.88±S.E. 0.09 Eq·cm^–2·h^–1, n=11) during serosal bath perfusion with HCO₃ ^–-Ringer solution, decreased slightly to 0.50±0.07 Eq·cm^–2·h^–1 (n=6) in HCO₃ ^–-free HEPES-buffered Ringer solution of the same pH, and decreased to approximately 20% when carbonic anhydrase was inhibited by acetazolamide. While replacement of mucosal or serosal Cl^– did not — within 1 h — significantly alter ASR, replacement of serosal Na⁺ in the presence or absence of HCO₃ ^– strongly reduced ASR, and a similar reduction was observed after serosal application of the anion transport inhibitor DIDS (4,4-diisomiocyanatostilbene-2,2-disulphonate, 2·10^–4 mol/l), the metabolic poison rotenone (10^–5 mol/l), the uncoupler dinitrophenol (10^–4 mol/l), and the Na⁺ pump inhibitor ouabain (10^–4 mol/l), while serosal amiloride (10^–4 mol/l) had no effect. These data can be accounted for by a model of alkaline secretion that consists of basolateral HCO₃ ^– uptake from the serosal fluid into the cell via a DIDS-inhibitable Na⁺(HCO₃ ^–)_n-cotransporter and HCO₃ ^– secretion from the cell to the gastric lumen via an anionic conductance pathway. Microelectrode experiments on oxyntopeptic cells reported in the subsequent paper suggest that these cells may also be involved in the resting state alkaline secretion.     

Measurement of Krogh's diffusion constant of CO2 in respiring muscle at various CO2 levels: Evidence for facilitated diffusion

Summary Krogh's diffusion constant for CO₂, K_CO2, was determined in respiring muscle tissue at various levels of tissueP _CO2, between 10 and 160 torr, using a technique described previously (Kawashiro et al., 1975).With increasing mean tissueP _CO2, K_CO2 declined towards an apparently asymptotic value. The relationship between K_CO2 (10^–9 mmol·cm^–1·min^–1·torr^–1) andP _CO2 (torr) at 37° C could be approximated by the equation K_CO2=17.3 {1+1.72·exp(-0.027{P _CO2)}AtP _CO2=0 toor K_CO2 exceeded the asymptotic value, which was virtually attained atP _CO2=100 torr, by more than a factor of two. Thus CO₂ diffusion in muscle appears to be facilitated in the lowP _CO2 range.Specific CO₂ production rate of tissue, which was determined simultaneously, did not vary with CO₂ in theP _CO2 range studied.Effects of facilitated CO₂ transport on CO₂ exchange in muscle are assessed using simple models. In the presence of CO₂ facilitation muscleP _CO2 is reduced, particularly during exercise.     

APCO2 surface electrode working on the principle of electrical conductivity

APCO₂ electrode working on the principle of electrical conductivity is described. The calibration curve can be linearized according to the formula . This linearity has been tested in thePCO₂ range of 0.93–9.33 kPa (7–70 Torr). For the experiments electrodes are used which have conductivity values of about 50 nS and drifts of maximally 5%/h at aPCO₂ of 5.33 kPa (40 Torr). The response time (T ₉₀) is about 20 s. The temperature sensitivity is 2.4 nS/1 K between 298K–310K. The standard error of the measurements is =0.33 nS. With these electrodes tissuePCO₂ can be measured on the surface of various organs.     

Control of heat-induced cutaneous vasodilatation in relation to age

Summary Well matched unacclimatised older (age 55–68, 4 women, 2 men) and younger (age 19–30, 4 women, 2 men) subjects performed 75 min cycle exercise (40% ) in a hot environment (37°C, 60% rh). Rectal temperature (T _re), mean skin temperature (¯T _sk), arm blood flow (ABF, strain gauge plethysmography), and cardiac output (Q, CO₂ rebreathing) were measured to examine age-related differences in heat-induced vasodilatation.T _re and¯T _sk rose to the same extent in each group during the exposure. There was no significant intergroup difference in sweat rate (older: 332±43 ml · m^–2 · h^–1, younger: 435±49 ml · m^–2 · h^–1; mean±SEM). However, the older subjects responded to exercise in the heat with a lower ABF response which could be attributed to a lower for the same exercise intensity. The slope of the ABF-T _re relationship was attenuated in the older subjects (9.3±1.3 vs 17.9±3.3 ml · 100 ml^–1 · min^–1 · °C^–1,p <0.05), but theT _re threshold for vasodilatation was about 37.0°C for both groups. These results suggest an altered control of skin vasodilatation during exercise in the heat in older individuals. This attenuated ABF response appears to be unrelated to , and may reflect an age-related change in thermoregulatory cardiovascular function.     

O2 Uptake in hyperthyroidism during constant work rate and incremental exercise

Summary To investigate the effect of hyperthyroidism on the pattern and time course of O₂ uptake ( O₂) following the transition from rest to exercise, six patients and six healthy subjects performed cycle exercise at an average work rate (WR) of 18 and 20 W respectively. Cardiorespiratory variables were measured breath-by-breath. The patients also performed a progressively increasing WR test (1-min increments) to the limit of tolerance. Two patients repeated the studies when euthyroid. Resting and exercise steady-state (SS) O₂ (ml·kg^–1·min^–1) were higher in the patients than control (5.8, SD 0.9 vs 4.0, SD 0.3 and 12.1, SD 1.5 vs 10.2, SD 1.0 respectively). The increase in O₂ during the first 20 s exercise (phase I) was lower in the patients (mean 89 ml·min^–, SD 30) compared to the control (265 ml·min^–1, SD 90), while the difference in half time of the subsequent (phase 11) increase to the SS O₂ (patient 26 s, SD 8; controls 17 s, SD 8) were not significant (P = 0.06). The OZ cost per WR increment ( O₂/WR) in ml·min^–1·^–1, measured during the incremental period (mean 10.9; range 8.3–12.2), was always within two standard deviations of the normal value (10.3, SD 1). In the two patients who repeated the tests, both the increment of O₂ from rest to SS during constant WR exercise and the O₂/WRs during the progressive exercise were higher in the hyperthyroid state than during the euthyroid state. While both resting and exercise O₂ are increased in the hyperthyroid patients, the O₂ cost of a given increment of WR is within the normal range. However, a small reduction in the O₂ requirement to perform exercise following treatment of the hyperthyroid state suggests a subtle change O₂ cost of muscle work in this disease.     

Ventilatory response of prepubertal boys and adults to carbon dioxide at rest and during exercise

Summary The aim of this study was to determine whether the greater ventilation in children at rest and during exercise is related to a greater CO₂ ventilatory response. The CO₂ ventilatory response was measured in nine prepubertal boys [10.3 years (SD 0.1)] and in 10 adults [24.9 years (SD 0.8)] at rest and during moderate exercise ( CO₂ = 20 ml·kg^–1·min^–1) using the CO₂-rebreathing method. Three criteria were measured in all subjects to assess the ventilatory response to CO₂: the CO₂ sensitivity threshold (Th), which was defined as the value of end titalPCO₂ (P _ETCO₂) where the ventilation increased above its steady-state level; the reactivity slope expressed per unit of body mass (SBM), which was the slope of the linear relation between minute ventilation ( _E) andP _ETCO₂ above Th; and the slope of the relationship between the quotient of tidal volume (V _T) and inspiration time (t _I) andP _ETCO₂ (V _T ·t _I ^–1 ·P _ETCO₂ ^–1) values above Th. The _E,V _T, breathing frequency (f _R), oxygen uptake ( O₂), and CO₂ production ( CO₂) were also measured before the CO₂-rebreathing test. The following results were obtained. First, children had greater ventilation per unit body weight than adults at rest (P<0.001) and during exercise (P<0.01). Second, at rest, onlyV _T ·t _I ^–1 ·P _ETCO₂ ^–1 was greater in children than in adults (P<0.001). Third, during exercise, children had a higher S_BM (P < 0.02) andV _T ·t _I ^–1 ·P _ETCO₂ ^–1 (P<0.001) while Th was lower (P<0.02). Finally, no correlation was found between _E/ CO₂ and Th while a significant correlation existed between _E/ CO₂ and S_BM (adults,r=0.79,P<0.01; children,r=0.73,P<0.05). We conclude that children have, mainly during exercise, a greater sensitivity of the respiratory centres than adult. This greater CO₂ sensitivity could partly explain their higher ventilation during exercise, though greater CO₂ production probably plays a role at rest.     

Effects of acute hypoxia and CO2 inhalation on systemic and peripheral oxygen uptake and circulatory responses during moderate exercise

Summary The effect of acute hypoxia and CO₂ inhalation on leg blood flow (LBF), on leg vascular resistance (LVR) and on oxygen supply to and oxygen consumption in the exercising leg was studied in nine healthy male subjects during moderate one-leg exercise. Each subject exercised for 20 min on a cycle ergometer in four different conditions: normoxia, normoxia +2% CO₂, hypoxia corresponding to an altitude of 4000 m above sea level, and hypoxia +1.2% CO₂. Gas exchange, heart rate (HR), arterial blood pressure, and LBF were measured, and arterial and venous blood samples were analysed for , , oxygen saturation, haematocrit and haemoglobin concentration. Systemic oxygen consumption was 1.83 l · min^–1 (1.48–2.59) and was not affected by hypoxia or CO₂ inhalation in hypoxia. HR was unaffected by CO₂, but increased from 136 beat · min^–1 (111–141) in normoxia to 155 (139–169) in hypoxia. LBF was 6.5 l · min^–1 (5.4–7.6) in normoxia and increased significantly in hypoxia to 8.4 (5.9–10.1). LVR decreased significantly from 2.23 kPa · l^–1 · min (1.89–2.99) in normoxia to 1.89 (1.53–2.52) in hypoxia. The increase in LBF from normoxia to hypoxia correlated significantly with the decrease in LVR. When CO₂ was added in hypoxia a significant correlation was also found between the decrease in LBF and the increase in LVR. In normoxia, the addition of CO₂ caused a significant increase in mean blood pressure. Oxygen consumption in the exercising leg (leg ) in normoxia was 0.97 l · min^–1 (0.72–1.10), and was unaffected by hypoxia and CO₂. It is concluded that the O₂ supply to the exercising leg and its are unaffected by hypoxia and CO₂. The increase in LBF in hypoxia is caused by a decrease in LVR. These changes can be counteracted by CO₂ inhalation. It is proposed that the regulatory mechanism behind these changes is that change in brain causes change in the central regulation of vascular tonus in the muscles.     

Effect of acute sodium bicarbonate ingestion on excess C02 output during incremental exercise

Summary The effect of bicarbonate ingestion on total excess volume of CO₂ Output (CO₂ excess), due to bicaronate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g · kg^–1 body mass) of CaCO₃ (control) and NaHCO₃ (alkalosis). The resting arterialized venous blood pH (P<0.05) and bicarbonate concentration ([HCO₃ ^–]_b;P<0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO₃ ^–]_b; 29.4 (SD 1.5) mmol·1^-1] than in the control [pH, 7.39 (SD 0.03); [HCO₃ ^–]_b, 25.5 (SD 1.0) mmol·1^–1]. The blood lactate concentrations ([la^–]_b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la^–]_b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol·1^–1,P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol · l^–1,P < 0.05] were found in AMA compared with the control. The CO₂ excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml;P < 0.05]. The CO₂ excess per body mass was found to be significantly correlated with both the increase of [la^–]_b from rest to 3 min after exercise ( [la^–]_b;r=0.926,P < 0.001) and with the decrease of [HCO₃ ^–]_b from rest to 3 min after exercise ( [HCO₃ ^–]_b;_r=0.872,P<0.001), indicating that CO₂ excess per body mass increased linearly with both [la^– _b and [HCO₃ ^–]_b. As a consequence, CO₂ excess per body mass per unit increase of [la^–]_b (CO₂ excess·mass^–1· [la^–]_b) was similar for the two conditions. The present results would suggest that the relationship between CO₂ excess and blood lactate accumulation was unaffected by acute metabolic alkalosis, because the relative contribution of bicarbonate buffering of lactic acid was the same as in the control.     

Pathways of phosphate transport in chick jejunum

The effect of vitamin D₃ on intestinal phosphate (P_i) absorption was studied in everted sacs prepared from jejunum of either vitamin D-deficient (–D) or vitamin D-replete (+D) chicks. Vitamin D₃ stimulates the maximal velocity (V _max) of a mucosal active P_i transport mechanism from 125 to 314 nmol·min^–1·g^–1 tissue.K _m of this process remains virtually unchanged (–D: 0.15 mmol·l^–1; + D: 0.18 mmol·l^–1).Active P_i entry into the epithelium depends on extracellular Na⁺. Reduction of buffer Na⁺ reducesV _max in the + D group to 182 nmol·min^–1·g^–1 tissue but has no significant effect in the –D animals (V _max=105 nmol·min^–1·g^–1 tissue). In this group, the predominant effect of Na⁺ substitution is a shift ofK _m to 1.13 mmol·l^–1, whileK _m in the +D group is changed only to 0.53 mmol·l^–1.Transeptithelial P_i transport in the + D group involves the mucosal phosphate pump and hence an intracellular pathway, proceeding at a rate of 48 nmol·min^–1·g^–1 tissue. This is in contrast to –D P_i transfer (8 nmol·l^–1·g^–1 tissue) which is by a diffusional, Na⁺-insensitive, and presumably paracellular pathway.Transepithelial calcium transport (–D: 3.3 nmol·min^–1·g^–1; + D: 7.6 nmol·min^–1·g^–1 tissue) does not require the presence of extracellular Na⁺ and apparently involves pathways different from those of the P_i absorptive system.Presented in part at the Annual Meeting of the Austrian Biochemical Society, Salzburg, September 1978     

Myofibril and sarcoplasmic reticulum changes with exercise and growth

Summary The intent of this study was to observe the effects of different treadmill running programs upon selected biochemical properties of soleus muscle from young rats. Young 10 day litter-mates were assigned to endurance (E), sprint (S) and control (C) groups. Each was partitioned into either 21 or 51 day exercising groups and 10 day controls. For C the myofibril ATPase activity at 21 and 51 days were lower than 10 day activity (p0.05). In the 51 day E group ATPase activity (0.378±0.009 mol Pi·mg^–1·min^–1) was greater than at 10 and 21 days (0.307±0.006 and 0.323±0.008 mol Pi·mg^–1·min^–1) (p0.05). No change occurred in the S group from 10 to 21 and 51 days (p0.05). Both the 21 and 51 day S (0.318±0.011 and 0.399±0.010 mol Pi·mg^–1·min^–1) and E (0.323±0.008 and 0.378±0.009 mol Pi·mg^–1·min^–1) groups had higher activity compared to the C group (0.193±0.029 and 0.172±0.031 mol Pi·mg^–1·min^–1) (p0.05). Maturation (10–51 day) resulted in a lowered sarcoplasmic reticulum (SR) yield and Ca²⁺ binding (p0.05) while Ca²⁺ uptake ability did not change (p0.05). SR yield, Ca²⁺ binding and uptake were not altered with S training (p0.05). The E training resulted in greater Ca²⁺ uptake at 51 days compared to C and S (p0.05), with no change in Ca²⁺ binding (p0.05). The data suggest that E training alters the normal development pattern of young rat soleus muscle.Supported by grants A-6449 and A-0425 from the Natural Sciences and Engineering Research Council of Canada     

Limb vasodilatory capacity and venous capacitance of trained runners and untrained males

Aerobically trained athletes possess enhanced vasodilatory capacity and venous capacitance in their exercising muscles. However, whether they also possess these characteristics in their non-specific exercising muscles is undetermined. This study examined vasodilatory capacity and venous capacitance of specific (legs) and non-specific exercising muscles (arms) of ten trained runners and ten active but untrained males aged 18–35 years. Venous occlusion plethysmography determined baseline and peak blood flow after 5 min of reactive hyperaemia. Forearm and leg venous capacitance were determined as the difference between baseline and 2 min of venous occlusion at 50 mmHg. During reactive hyperaemia, trained runners had higher leg (48.4±5.3 ml·100 ml tissue^–1·min^–1) and arm (40.8±2.1 ml·100 ml tissue^–1·min^–1) vasodilatory capacity compared to the untrained (leg: 37.3±2.5 ml·100 ml tissue^–1·min^–1; arm: 34.2±2.2 ml·100 ml tissue^–1·min^–1; P<0.05), and higher calf vascular conductance (0.51±0.06 ml·100 ml tissue^–1·min^–1·mmHg^–1 versus 0.35±0.03 ml·100 ml tissue^–1·min^–1·mmHg^–1; P<0.05). The trained also had higher venous capacitance in both arms (3.5±0.2 ml 100·ml^–1) and legs (4.8±0.1 ml·100 ml^–1) compared to the untrained (3.0±0.2 ml 100·ml^–1; 4.2±0.2 ml·100 ml^–1; P<0.05). These findings show that vasculature adaptations to running occur in both specific and non-specific exercising muscles.