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.     

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.     

Ventilatory responses to exercise and carbon dioxide in elderly and younger humans

Summary The present investigation examined the relationship between CO₂ sensitivity [at rest (S _R) and during exercise (S _E)] and the ventilatory response to exercise in ten elderly (61–79 years) and ten younger (17–26 years) subjects. The gradient of the relationship between minute ventilation and CO₂ production ( _E/ CO₂) of the elderly subjects was greater than that of the younger subjects [mean (SEM); 32.8 (1.6) vs 27.3 (0.4); P<0.01]. At rest, S _R was lower for the elderly than for the younger group [10.77 (1.72) vs 16.95 (2.13) 1 · min^–1 · kPa^–1; 1.44 (0.23) vs 2.26 (0.28) 1 · min^–1 · mmHg^–1; P<0.05], but S _E was not significantly different between the two groups [17.85 (2.49) vs 19.17 (1.62) l · min^–1 · kPa^–1; 2.38 (0.33) vs 2.56 (0.21) 1 · min^–1 · mmHg^–1]. There were significant correlations between both S _R and S _E, and _E/ CO₂ (P<0.05; P<0.001) for the younger group, bot none for the elderly. The absence of a correlation for the elderly supports the suggestion that _E/ CO₂ is not an appropriate index of the ventilatory response to exercise for elderly humans.     

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.     

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.     

Relationships between postcompetition blood lactate concentration and average running velocity over 100-m and 200-m races

The relationships between anaerobic glycolysis and average velocity () sustained during sprint running were studied in 12 national level male sprinters. A blood sample was obtained within 3 min of the completion of semi-finals and finals in the 100-m and 200-m Cameroon national championships and blood lactate concentration ([la^–]_b) was measured. The 35-m times were video-recorded. The 100-m and 200-m [la^–]_b were 8.5 (SD 0.8) and 10.3 (SD 0.8) mmol·l^–1, respectively. These were not correlated with the performances. Over 200 m [la^–]_b was correlated with the sustained over the last 165 m (r=0.65,P<0.05). In the 9 athletes who participated in both the 100-m and 200-m races, the difference between the [la^–]_b measured at the end of the two races was negatively correlated to the difference in v sustained over the two races (r=0.76,P>0.02). Energy expenditure during sprint running was estimated from the [la^–]_b values. This estimate was mainly based on the assumption that a 1 mmol·l^–1 increase in [la^–]_b corresponds to the energy produced by the utilization of 3.30 ml O₂·kg^–1. The energy cost of running was estimated at 0.275 (SD 0.02) ml O₂·kg^–1·m^–1 over 200-m and 0.433 (SD 0.03) ml O₂·kg^–1·m^–1 over 100-m races. These results would suggest that at the velocities studied anaerobic glycolysis contributes to at least 55% of the energy expenditure related to sprint running. However, the influence of both mechanical factors and the contribution of other energy processes obscure the relationship between [la^–]_b and performance.     

Effects of severe arterial hypocapnia on regional blood flow regulation,tissuePO2 and metabolism in the brain cortex of cats

The effect of a stepwise decrease inPaCO₂ from 3.9–1.6 kPa on rCBF, rCMRO₂, tissuePO₂ and concentrations of glucose, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine in the brain cortex was studied in cats lightly anaesthetized with sodium pentobarbital. 1. Moderate lowering ofPaCO₂ to 2.5 kPa induced in all animals a homogeneous decrease of rCBF in corresponding areas of the right and left hemisphere. Mean rCBF fell from 129.2 to 103.1 ml · 100 g^–1 · min^–1, while rCMRO₂ remained unchanged (12.7–12.9 ml · 100 g^–1 · min^–1). The tissuePO₂ frequency histograms showed a shift to lower values without indicating the presence of brain tissue hypoxia. 2. Severe arterial hypocapnia (PaCO₂=1.6 kPa) caused an inhomogeneous blood flow reaction. Both further decreased as well as increased rCBF values were measured simultaneously in the brain cortex of individual animals (mean rCBF=97.6 ml · 100 g^–1 · min^–1). At the same time tissuePO₂ measurements and metabolite assays indicated the presence of pronounced brain tissue hypoxia. The tissue concentrations of lactate and pyruvate and the lactate/pyruvate ratio were significantly increased, while the phosphocreatine concentration was significantly reduced. In addition, rCMRO₂ decreased to 11.3 ml · 100 g^–1 · min^–1. The results provide conclusive evidence that severe arterial hypocapnia leads to an insufficient O₂ supply of the brain cortex, which in turn seems to counteract the influence of hypocapnia on cortical blood flow regulation.Preliminary reports of these investigations were presented at the International Symposium on Oxygen Transport to Tissue, July 9–11, 1980 in Budapest and at the Second International Symposium on Pathophysiology and Pharmacotherapy of Cerebrovascular Disorders, July 22–25, 1980 in Tübingen, FRG     

Basolateral membrane chloride permeability of A6 cells: implication in cell volume regulation

The permeability to Cl^– of the basolateral membrane (blm) was investigated in renal (A6) epithelial cells, assessing their role in transepithelial ion transport under steady-state conditions (isoosmotic) and following a hypoosmotic shock (i.e. in a regulatory volume decrease, RVD). Three different complementary studies were made by measuring: (1) the Cl^– transport rates (F/F _o · s^–1 (× 10^–3)), where F is the fluorescence of N-(6-methoxyquinoyl) acetoethyl ester, MQAE, and F _o the maximal fluorescence (×10^–3) of both membranes by following the intracellular Cl^–3 activities (a _iCl^–, measured with MQAE) after extracellular Cl^– substitution (2) the blm ⁸⁶Rb and ³⁶Cl uptakes and (3) the cellular potential and Cl^– current using the wholecell patch-clamp technique to differentiate between the different Cl^– transport mechanisms. The permeability of the blm to Cl^– was found to be much greater than that of the apical membranes under resting conditions: a _iCl^– changes were 5.3±0.7 mM and 25.5±1.05 mM (n=79) when Cl^– was substituted by NO₃ ^– in the media bathing apical and basolateral membranes. The Cl^– transport rate of the blm was blocked by bumetanide (100 M) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, 50 M) but not by N-phenylanthranilic acid (DPC, 100 M). ⁸⁶Rb and ³⁶C1 uptake experiments confirmed the presence of a bumetanide- and a NPPB-sensitive Cl^– pathway, the latter being approximately three times more important than the former (Na/K/2Cl cotransporter). Application of a hypoosmotic medium to the serosal side of the cell increased F/F _o · s^–1 (×10^–3) after extracellular Cl^–3 substitution (1.03±0.10 and 2.45±0.17 arbitrary fluorescent units·s^–1 for isoosmotic and hypoosmotic conditions respectively, n=11); this F/F _o·s^–1 (×10^–3) increase was totally blocked by serosal NPPB application; on the other hand, cotransporter activity was decreased by the hypoosmotic shock. Cellular Ca²⁺ depletion had no effect on F/F _o·s^–1 (×10^–3) under isoosmotic conditions, but blocked the F/F _o·s^–1 (×10^–3) increase induced by a hypoosmotic stress. Under isotonic conditions the measured cellular potential at rest was –37.2±4.0 mV but reached a maximal and transient depolarization of –25.1±3.7 mV (n=9) under hypoosmotic conditions. The cellular current at a patch-clamping cellular potential of –85 mV (close to the Nernst equilibrium potential for K⁺) was blocked by NPPB and transiently increased by hypoosmotic shock ( 50% maximum increase). This study demonstrates that the major component of Cl^– transport through the blm of the A6 monolayer is a conductive pathway (NPPB-sensitive Cl^– channels) and not a Na/K/2Cl cotransporter. These channels could play a role in transepithelial Cl^– absorption and cell volume regulation. The increase in the blm Cl^– conductance, inducing a depolarization of these membranes, is proposed as one of the early events responsible for the stimulation of the ⁸⁶Rb efflux involved in cell volume regulation.     

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.     

Changes in acid-base status of marathon runners during an incremental field test

Summary Four top-class runners who regularly performed marathon and long-distance races participated in this study. They performed a graded field test on an artificial running track within a few weeks of a competitive marathon. The test consisted of five separate bouts of running. Each period lasted 6 min with an intervening 2-min rest bout during which arterialized capillary blood samples were taken. Blood was analysed for pH, partial pressure of oxygen and carbon dioxide (P0₂ and PCO₂) and lactate concentration ([la^–]_b). The values of base excess (BE) and bicarbonate concentration ([HCO₃ ^–]) were calculated. The exercise intensity during the test was regulated by the runners themselves. The subjects were asked to perform the first bout of running at a constant heart rate f _c which was 50 beats · min^–1 below their own maximal f _c. Every subsequent bout, each of which lasted 6 min, was performed with an increment of 10 beats · min^–1 as the target f _c. Thus the last, the fifth run, was planned to be performed with fc amounting to 10 beats · min^–1 less than their maximal f _c. The results from these runners showed that the blood pH changed very little in the bouts performed at a running speed below 100% of mean marathon velocity ( _m). However, once _mwas exceeded, there were marked changes in acid-base status. In the bouts performed at a velocity above the _mthere was a marked increase in [la^–]_b and a significant decrease in pH, [HCO₃ ^–], BE and PCO₂. The average marathon velocity ( _m) was 18.46 (SD 0.32) km·h^–1. The [la^–]_b at a mean running velocity of 97.1 (SD 0.8) % of _mwas 2.33 (SD 1.33) mmol ·l^–1 which, compared with a value at rest of 1.50 (SD 0.60) mmol·l^–1, was not significantly higher. However, when running velocity exceeded the vm by only 3.6 (SD 1.9) %, the [la^–]b increased to 6.94 (SD 2.48) mmol·l-1 (P<0.05 vs rest). We concluded from our study that the highest running velocity at which the blood pH still remained constant in relation to the value at rest and the speed of the run at which [la^–]_b began to increase significantly above the value at rest is a sensitive indicator of capacity for marathon running.     

Quantitative and sustained suppression of renal sympathetic nerve activity by left atrial distension in conscious dogs

In order to investigate the interrelations between left atrial pressure (Pla) and renal sympathetic nerve activity (RSNA) and heart rate (HR), Pla was increased by a balloon both in conscious sham-operated and cardiac-denervated dogs. RSNA was decreased and HR was increased with increasing Pla in sham-operated dogs. The reflex changes in RSNA and HR induced by the stimulation of atrial receptors persisted for at least 15 min. There was a consistent relationship between Pla and RSNA which could be described by a single exponential equation: % RSNA = 80.0(1–e^{–0.395 Pla}), or by a linear equation when Pla was less than 6 mmHg; %RSNA=-13.5Pla–2.25. The relationship between Pla and HR can be described by a single exponential equation: HR = 86.5(1–e^{–0.125 Pla}). A significant linear relationship between RSNA and HR was obtained during a graded left atrial distention (%RSNA=-1.08HR–17.7). In cardiac-denervated dogs, RSNA tended to increase and HR remained constant during the left atrial distention. These results indicate that left atrial receptors regulate RSNA and HR in both a quantitative and sustained manner in conscious sham-operated dogs.     

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

Summary These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P _a0₂) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO_2max) range = 65-77 ml·kg^–1·min^–1] performed a normoxic graded exercise test on a cycle ergometer toVO_2max at sea level. During incremental exercise atVO_2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P _A-aO₂) of above 5 kPa (range 5-5.7) and a decline from restingP _aO₂ (P _aO₂) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P _A-aO₂) of 4.0-4.3 kPa with P _aO₂ of 0.4-1.3 kPa while the remaining 3 subjects hadP _A-aO₂ of 4.3-5 kPa with P _aO₂ between 1.7 and 2.0 kPa. The correlation between P_AO₂ andP _aO₂ atVO_2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP _aO₂ and arterial partial pressure of carbon dioxide VSP _aO₂ atVO_2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

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.     

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.     

Energy cost and energy sources in karate

Energy costs and energy sources in karate (wado style) were studied in eight male practitioners (age 23.8 years, mass. 72.3 kg, maximal oxygen consumption (VO_2max) 36.8 ml · min^–1 · kg^–1) performing six katas (formal, organized movement sequences) of increasing duration (from approximately. 10 s to approximately 80 s). Oxygen consumption (VO₂) was determined during pre-exercise rest, the exercise period and the first 270 s of recovery in five consecutive expired gas collections. A blood sample for lactate (la^–) analysis was taken 5 min after the end of exercise. The overall amount of O₂ consumed during the exercise and in the following recovery increased linearly with the duration of exercise (t) from approximately 1.51 (for t equal to 10.5 s (SD 1.6)) to approximately 5.81, for t equal to 81.5 s (SD 1.0). The energy release from la^– production (VO_21a ^–) calculated assuming that an increase of 1 mmol · l^–1 la^– corresponded to a VO₂ of 3 mlO₂ · kg^–1 was negligible for t equal to or less than 20 s and increased to 17.3 ml · kg^–1 (la^– = 5.8 mmol · l^–1 above resting values) for t equal approximately to 80 s. The overall energy requirement (VO_2eq) as given by the sum of VO₂ and VO_2la ^– was described by VO_2eq = 0.87 + 0.071 · t (n = 64; r ² = 0.91), where VO_2eq is in litres and t in seconds. This equation shows that the metabolic power (VO_2eq · t ^–1) for this karate style is very high: from approximately 9.51 · min^–1 for t equal to 10 s to approximately 4.91 · min^–1 for t equal to 80 s, i.e. from 3.5 to 1.8 times the subjects' VO_2max. The fraction of VO_2eq derived from the amount of O₂ consumed during the exercise increased from 11% for t equal to 10 s to 41 % for t equal to 80 s whereas VO_21a ^– was negligible far t equal to or less than 20 s and increased to 13 % o for t equal to 80 s. The remaining fraction (from 90% for t equal to 10 s to 46% for t equal to 80 s), corresponding to the amount of O₂ consumed in the recovery after exercise, is derived from anaerobic alactic sources, i.e. from net splitting of high energy phosphates during the exercise.     

Influence of muscle fibre type and pedal rate on the V̇O2-work rate slope during ramp exercise

We hypothesised that the ratio between the increase in oxygen uptake and the increase in work rate (O₂/WR) during ramp cycle exercise would be significantly related to the percentage type II muscle fibres at work rates above the gas exchange threshold (GET) where type II fibres are presumed to be active. We further hypothesised that ramp exercise at higher pedal rates, which would be expected to increase the proportional contribution of type II fibres to the total power delivered, would increase the O₂/WR slope at work rates above the GET. Fourteen healthy subjects [four female; mean (SD): age 25 (3) years, body mass 74.3 (15.1) kg] performed a ramp exercise test to exhaustion (25 W min^–1) at a pedal rate of 75 rev min^–1, and consented to a muscle biopsy of the vastus lateralis. Eleven of the subjects also performed two further ramp tests at pedal rates of 35 and 115 rev min^–1. The O₂/WR slope for exercise <GET (S ₁) was significantly correlated with O₂ peak in ml kg^–1 min^–1 (r=0.60; P<0.05), whereas the O₂/WR slope for exercise >GET (S ₂) was significantly correlated to percentage type II fibres (r=0.54; P=0.05). The ratio between the O₂/WR slopes for exercise above and below the GET (S ₂/S ₁) was significantly greater at the pedal rate of 115 rev min^–1 [1.22 (0.09)] compared to pedal rates of 35 rev min^–1 [0.96 (0.02)] and 75 rev min^–1 [1.09 (0.05), (P<0.05)]. The greater increase in S ₂ relative to S ₁ in subjects (1) with a high percentage type II fibres, and (2) at a high pedal rate, suggests that a greater recruitment of type II fibres contributes in some manner to the xs O₂ observed during ramp exercise.     

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.     

The effect of certain phenothiazine derivatives on respiratory phosphorylation in the cardiac muscle of the rabbit

Summary Phenothiazine derivatives, mepazine and promazine, when added to homogenates of cardiac muscle of the rabbit in a concentration of 0.8·10^–3M, cause a rise in the efficacy of oxidative phosphorylation, increasing the P and the P: O coefficient. In a 1.2·10^–3M, concentration of mepazine and promazine P is reduced, though to a lesser degree than O₂, the P: O coefficient remaining slightly above the normal level.A 0.8·10^–3M phenergan concentration uniformly reduces both respiration and phosphorylation. With a further rise of the phenergan concentration phosphorylation decreases more sharply than respiration. High concentrations of mepazine, phenergan and promazine (1.6·10^–3M) sharply depress phosphocreatine formation and cause a decrease of P: O. The phenothiazine derivatives neither depress creatine kinase nor activate adenosinetriphosphatase.(Presented by Active Member AMN SSSR S. E. Severin) Translated from Byulleten Èksperimental'noi Biologii i Meditsiny Vol. 49, No. 4, pp. 60–63, April, 1960     

Gender differences in physiological reactions to thermal stress

Following an extensive anthropometric evaluation, thermoregulatory responses were studied in nine men and nine women who performed immersed exercise with post-exercise rest in 28°C water. During the post-exercise period esophageal temperature (T _es), oxygen consumption, heat flux and skin blood perfusion were monitored at 10s intervals, with average minute values used for calculations. The T _es (relative to restingT _es) at which sweating abated and shivering commenced were defined as the T _es thresholds for the cessation of sweating and onset of shivering, respectively. No significant gender differences were evident in the sweating and shivering threshold T _es values, or the magnitude of the null-zone. Usingz-tests for parallelism the rates of core cooling across the null-zone were not found to differ significantly between genders, nor were the slopes of the perfusion: T _es responses across the null-zone or the post-threshold shivering responses (ml·kg^–1·min^–1·°C^–1). The slope of the sweating response (measured from immersion until sweat cessation; g·m^–2·min^–1°C^–1) was, however, significantly lower in the female than in the male samples (z = 3.93;P < 0.01). Despite the gender-related dimorphic distribution of adipose tissue, both men and women lost equal proportions of their total heat flux from central and peripheral measurement sites. Performing a standardized regression using the rate of core cooling across the null-zone as the dependent variable and gender as a dummy variable, gender and adipose tissue mass were not found to be significant factors in determining the rate of core cooling, while mass ( = 1.73;P < 0.05) and muscle mass ( = 1.86;P < 0.05) did contribute significantly to the rate of core cooling. It was concluded that, except for the quantitative differences in the sweating response, men and women respond to deviations in core temperature in a similar manner, with mass and muscle mass modifying this response.     

Thermal characterization and transmitter analysis of single units in the preoptic and anterior hypothalamus of conscious ducks

With a multibarrel assembly combining one carbon fiber micropipette as recording electrode and 6 pipettes for microiontophoretic application of drugs, the activity of neurons in the preoptic and anterior hypothalamic (POAH) region was extracellularly recorded in situ in conscious ducks implanted chronically with a device permitting hypothalamic thermal stimulation. Among 355 neurons 17% were identified as warm-responsive (warm units) and 20% as cold-responsive (cold units). In 58 warm and 56 cold units control discharge rates at 40°C local temperature (F₄₀) and temperature coefficients (F/T) were determined and presented as means ± SEM. The F₄₀ values of warm units (35.2±2.3 Imp · s^–1) were significantly higher than of cold units (16.3±1.8 Imp · s^–1). The F/T values (+1.77±0.15 and –1.77±0.19 Imp · s^–1 · °C^–1) of warm and cold units were not different in absolute terms. In pilot experiments either activation or inhibition by lowering whole-body temperature was observed in both warm and cold units. Microiontophoretic application of one or more of the amines acetylcholine (ACh), 5-hydroxytryptamine (5-HT), and noradrenaline (NA) to warm and cold units revealed differences in their responsiveness to ACh, which more consistently stimulated cold units. NA inhibited the majority of warm units; 5-HT stimulated the majority of cold units. In both warm and cold units NA and ACh differed in their actions, with the latter amine more consistently producing activation.