The effects of intensity of exercise on excess postexercise oxygen consumption and energy expenditure in moderately trained men and women

Summary This experiment investigated the effects of intensity of exercise on excess postexercise oxygen consumption (EPOC) in eight trained men and eight women. Three exercise intensities were employed 40%, 50%, and 70% of the predetermined maximal oxygen consumption (VO_2max). All ventilation measured was undertaken with a standard, calibrated, open circuit spirometry system. No differences in the 40%, 50% and 70% VO_2max trials were observed among resting levels of oxygen consumption (V0₂) for either the men or the women. The men had significantly higher resting VO₂ values being 0.31 (SEM 0.01) 1·min^–1 than did the women, 0.26 (SEM 0.01) 1·min^–1 (P < 0.05). The results indicated that there were highly significant EPOC for both the men and the women during the 3-h postexercise period when compared with resting levels and that these were dependent upon the exercise intensity employed. The duration of EPOC differed between the men and the women but increased with exercise intensity: for the men 40% – 31.2 min; 50% – 42.1 min; and 70% – 47.6 min and for the women, 40% – 26.9 min; 50% – 35.6 min; and 70% – 39.1 min. The highest EPOC, in terms of both time and energy utilised was at 70% VO_2max. The regression equation for the men, where y=O₂ in litres, and x=exercise intensity as a percentage of maximum was y=0.380x + 1.9 (r ²=0.968) and for the women is y=0.374x–0.857 (r ²=0.825). These findings would indicate that the men and the women had to exercise at the same percentage of their VO_2max to achieve the maximal benefits in terms of energy expenditure and hence body mass loss. However, it was shown that a significant EPOC can be achieved at moderate to low exercise intensities but without the same body mass loss and energy expenditure.     

The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption

Summary Nine males with mean maximal oxygen consumption ( ) =63.0 ml· kg^–1 · min^–1, SD 5.7 and mean body fat = 10.6%, SD 3.1 each completed nine counterbalanced treatments comprising 20, 50 and 80 min of treadmill exercise at 30, 50 and 70% . The OZ deficit, 8 h excess post-exercise oxygen consumption (EPOC) and EPOC:O₂ deficit ratio were calculated for all subjects relative to mean values obtained from 2 control days each lasting 9.3 h. The O₂ deficit, which was essentially independent of exercise duration, increased significantly (P<0.05) with intensity such that the overall mean values for the three 30%, 50% and 70% workloads were 0.83, 1.89 and 3.09 l, respectively. While there were no significant differences (P>0.05) between the three EPOCs after walking at 30% for 20 (1.01 l), 50 (1.43 l) and 80 min (1.041), respectively, the EPOC thereafter increased (P<0.05) with both intensity and duration such that the increments were much greater for the three 70% workloads (EPOC: 20 min=5.68 l; 50 min=10.04 l; 80 min= 14.59 l) than for the three 50% workload (EPOC: 20 min =3.14 l; 50 min=5.19 l; 80 min= 6.10 l). An analysis of variance indicated that exercise intensity was the major determinant of the EPOC since it explained five times more of the EPOC variance than either exercise duration or the intensity times duration interaction. The mean EPOC:O₂ deficit ratio ranged from 0.8 to 4.5 and generally increased with both exercise intensity and duration. These data imply that the EPOC is more than mere repayment of the O₂ deficit because metabolism is increasingly disturbed from resting levels as exercise intensity and duration increase due to other physiological factors occurring after the steady-state has been attained.     

Muscle triacylglycerol and hormone-sensitive lipase activity in untrained and trained human muscles

During exercise, triacylglycerol (TG) is recruited in skeletal muscles. We hypothesized that both muscle hormone-sensitive lipase (HSL) activity and TG recruitment would be higher in trained than in untrained subjects in response to prolonged exercise. Healthy male subjects (26 ± 1 years, body moss index 23.3 ± 0.5 kg m⁻²), either untrained (N = 8, VO_2max 3.8 ± 0.2 l min⁻¹) or trained (N = 8, VO_2max 5.1 ± 0.1 l min⁻¹), were studied. Before and after 3-h exercise (58 ± 1% VO_2max), a biopsy was taken. Muscle citrate synthase (32 ± 2 vs. 47 ± 6 μmol g⁻¹ min⁻¹ d.w.) and β-hydroxy-acyl-CoA-dehydrogenase (38 ± 3 vs. 52 ± 5 μmol g⁻¹ min⁻¹ d.w.) activities were lower in untrained than in trained subjects (p < 0.05). Throughout the exercise, fat oxidation was higher in trained than in untrained subjects (p < 0.05). Muscle HSL activity was similar at rest (0.72 ± 0.08 and 0.74 ± 0.03 mU mg⁻¹ protein) and after exercise (0.71 ± 0.1 and 0.68 ± 0.03 mU mg⁻¹ protein) in untrained and trained subjects. At rest, the chemically determined muscle TG content (37 ± 8 and 26 ± 5 mmol g⁻¹ d.w.) was similar (p > 0.05), and after exercise it was unchanged in untrained and lower (p < 0.05) in trained subjects (41 ± 9 and 10 ± 2 mmol g⁽¹ d.w.). Determined histochemically, TG was decreased (p < 0.05) after exercise in type I and II fibres. Depletion of TG was not different between fibre types in untrained, but tended to be higher (p = 0.07) in type I compared with type II fibres in trained muscles. In conclusion, HSL activity is similar in untrained and trained skeletal muscles both before and after prolonged exercise. However, the tendency to higher muscle TG recruitment during exercise in the trained subjects suggests a difference in the regulation of HSL or other lipases during exercise in trained compared with untrained subjects.     

Pituitary–adrenal responses to arm versus leg exercise in untrained man

The purpose of this study was to examine pituitary–adrenal (PA) hormone responses [beta-endorphin (β-END), adrenocorticotropic hormone (ACTH) and cortisol] to arm exercise (AE) and leg exercise (LE) at 60 and 80% of the muscle-group specific VO₂ peak. Eight healthy untrained men (AE VO₂ peak=32.4±3.0 ml kg⁻¹ min⁻¹, LE VO₂ peak=46.9±5.3 ml kg⁻¹ min⁻¹) performed two sub-maximal AE and LE tests in random order. Plasma β-END, ACTH and cortisol were not different (P>0.05) between AE and LE at either exercise intensity; the 60% testing elicited no changes from pre-exercise (PRE) values. For 80% testing, plasma β-END, ACTH and cortisol were consistently, but not significantly, greater during LE than AE. In general, plasma β-END and ACTH were higher (P<0.05) during 80% exercise, than PRE, for both AE and LE. Plasma cortisol was elevated (P<0.05) above PRE during 80% LE, and following 80% for both AE and LE. Plasma ACTH was higher (P<0.05) during 80% LE and AE versus 60% LE and AE, respectively. Plasma β-END and cortisol were significantly higher during and immediately after 80% LE than 60% LE. Thus, plasma β-END, ACTH and cortisol responses were similar for AE and LE at the two relative exercise intensities, with the intensity threshold occurring somewhere between 60 and 80% of VO₂ peak. It appears that the smaller muscle mass associated with AE was sufficient to stimulate these PA axis hormones in a manner similar to LE, despite the higher metabolic stress (i.e., plasma La^-) associated with LE.     

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.     

Is the balance between skeletal muscular metabolic capacity and oxygen supply capacity the same in endurance trained and untrained subjects?

We attempted to test whether the balance between muscular metabolic capacity and oxygen supply capacity in endurance-trained athletes (ET) differs from that in a control group of normal physically active subjects by using exercises with different muscle masses. We compared maximal exercise in nine ET subjects [Maximal oxygen uptake (VO₂max) 64 ml kg⁻¹ min⁻¹ ± SD 4] and eight controls (VO₂max 46 ± 4 ml kg⁻¹ min⁻¹) during one-legged knee extensions (1-KE), two-legged knee extensions (2-KE) and bicycling. Maximal values for power output (P), VO₂max, concentration of blood lactate ([La⁻]), ventilation (VE), heart rate (HR), and arterial oxygen saturation of haemoglobin (SpO₂) were registered. P was 43 (2), 89 (3) and 298 (7) W (mean ± SE); and VO₂max: 1,387 (80), 2,234 (113) and 4,115 (150) ml min⁻¹) for controls in 1-KE, 2-KE and bicycling, respectively. The ET subjects achieved 126, 121 and 126% of the P of controls (p < 0.05) and 127, 124, and 117% of their VO₂max (p < 0.05). HR and [La⁻] were similar for both groups during all modes of exercise, while VE in ET was 147 and 114% of controls during 1-KE and bicycling, respectively. For mass-specific VO₂max (VO₂max divided by the calculated active muscle mass) during the different exercises, ET achieved 148, 141, and 150% of the controls’ values, respectively (p < 0.05). During bicycling, both groups achieved 37% of their mass-specific VO₂ during 1-KE. Finally we conclude that ET subjects have the same utilization of the muscular metabolic capacity during whole body exercise as active control subjects.     

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.     

Effect of secretin and inhibitors of HCO3 −/H+ transport on the membrane voltage of rat pancreatic duct cells

The aim of the present study was to study the effect of secretin on the electrophysiological response of pancreatic ducts. Furthermore, we investigated the effects of lipid-soluble buffers and inhibitors of HCO₃ ^–/H⁺ transport. Ducts obtained from fresh rat pancreas were perfused in vitro. Secretin depolarized the basolateral membrane voltage, V _bl, by up to 35 mV (n=37); a halfmaximal response was obtained at 3×10^–11 mol/l. In unstimulated ducts a decrease in the luminal Cl^– concentration (120 to 37 mmol/l) had a marginal effect on V _bl, but after maximal secretin stimulation it evoked a 14±2 mV depolarization (n=6), showing that a luminal Cl^– conductance G _Cl- was activated. The depolarizing effect of secretin on V _bl was often preceded by about a 6 mV hyperpolarization, most likely due to an increase in the basolateral G _K+. Perfusion of ducts with DIDS (4,4 — diisothiocyanatostilbene — 2,2 — disulphonic acid, 0.01 mmol/l) or addition of ethoxzolamide (0.1 mmol/l) to the bath medium diminished the effect of secretin. Acetate or pre-treatment of ducts with NH₄ ⁺/NH₃ (10 mmol/l in the bath) depolarized the resting V _bl of –65±2 mV by 16±4 mV (n=7) and 19±3 mV (n=10), respectively. The fractional resistance of the basolateral membrane (FR _bl) doubled, and the depolarizing responses to changes in bath K⁺ concentrations (5 to 20 mmol/l) decreased from 22±1 to 11±2 mV. The Na⁺/H⁺ antiporter blocker EIPA (5-[N-ethyl-N-isopropyl]-amiloride, 0.1 mmol/l) also depolarized V _bl by 10±1 mV, FR_bl increased and the response to K⁺ concentration changes decreased (n=7). Effects of EIPA and ethoxzolamide on V _bl were greater in ducts deprived of exogenous HCO₃ ^–/CO₂. Taken together, the present study shows that secretin increased the basolateral G _K+ and the luminal G _Cl-. The depolarizing effect of secretin was diminished following inhibition of HCO₃ ^– transport (DIDS), or HCO₃ ^–/H⁺ generation (ethoxzolamide). Manoeuvres that presumably led to lowered intracellular pH (NH₄ ⁺/NH₃ removal, acetate, EIPA) decreased the basolateral G _K+. The present data support our previously published model for pancreatic HCO₃ ^– secretion, and indicate that the basolateral membrane possesses a pH-sensitive G _K+.     

Active NaCl transport in the cortical thick ascending limb of Henle's loop of the mouse does not require the presence of bicarbonate

The aim of the present study was to investigate whether bicarbonate buffer (CO₂ + HCO ₃ ^– ) is required to sustain maximal NaCl transport in the cortical thick ascending limb of Henle's loop (cTAL) of the mouse. Transepithelial Na⁺ and Cl^– net fluxes (J _Na, J _Cl, pmol min^–1 mm^–1), measured by electron microprobe analysis, were similar irrespective of the presence or absence of CO₂ + HCO ₃ ^– in luminal and bathing solutions J _NaCl with CO₂ + HCO ₃ ^– =203±25 pmol min^–1 mm^–1; J NaCl without CO₂ + HCO ₃ ^– =213±13 pmol min^–1 mm^–1, n=14). Furthermore the transepithelial potential difference, V _te, the transepithelial resistance, R _te, and the basolateral membrane potential, V _bl, were unaffected by CO₂ + HCO ₃ ^– . In the absence of CO₂ + HCO ₃ ^– , V _te was +17.0±1.7 mV(n=9) (lumen positive), R _te was 28±2 cm² (n=9) and V _bl was –76±4 mV (n=6). In the presence of CO₂ + HCO ₃ ^– , V _te, R _te and V _bl were +15.9±1.5 mV, 29±1 cm² and –73±5 mV, respectively. 4-Acetamido-4-isothiocyanatostilbene-2,2-disulphonic acid (SITS; 0.1 mmol l^–1) and amiloride (1 mmol l^–1) added to the (CO₂ + HCO ₃ ^– )-containing lumen perfusate were without effect on V _te and R _te. Finally, the effect of furosemide (0.1 mmol l^–1) on V _te and V _bl in the presence of CO₂ + HCO ₃ ^– was investigated. Furosemide reversibly decreased V _te from +13.7±1.1 mV to +1.7±0.7 mV (n=6) and hyperpolarized V_bl from –70±1 to –89±3 mV (n=5), suggesting passive distribution of Cl^– across the basolateral membrane. In conclusion, these data suggest that active NaCl transport in the cTAL of the mouse does not require the presence of CO₂ + HCO ₃ ^– .     

Oxygen uptake kinetics during severe intensity running and cycling

The purpose of this study was to investigate the effect of exercise mode on the characteristics of the oxygen uptake ( V̇O₂) response to exercise within the severe intensity domain. Twelve participants each performed a treadmill running test and a cycle ergometer test to fatigue at intensities selected to elicit a mode-specific V̇O₂max and to cause fatigue in ~5 min. The tests were at 234 (30) m·min⁻¹ and 251 (59) W, and times to fatigue were 297 (15) s and 298 (14) s, respectively. The overall rapidity of the V̇O₂response was influenced by exercise mode [ V̇O₂max was achieved after 115 (20) s in running versus 207 (36) s in cycling; p<0.01]. V̇O₂ responses were fit to a three-phase exponential model. The time constant of the primary phase was faster in treadmill tests than in cycle ergometer tests [14 (6) s versus 25 (4) s; p<0.01], and the amplitude of the primary phase was greater in running than in cycling when it was expressed in absolute terms [2327 (393) ml·min⁻¹ versus 2036 (301) ml·min⁻¹; p=0.02] but not when it was expressed as a percentage of the total increase in V̇O₂ [86 (6)% versus 82 (6)%; p=0.09]. When quantified as the difference between the end-exercise V̇O₂ and the V̇O₂ at 2 min, the amplitude of the slow component was ~40% smaller in running [177 (92) ml·min⁻¹ versus 299 (153) ml min⁻¹; p=0.03]. It is concluded that exercise modality affects the characteristics of the V̇O₂ response at equivalent intensities in the severe domain.     

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.     

The effect of prolonged submaximal exercise on gas exchange kinetics and ventilation during heavy exercise in humans

This study compared ventilation, gas exchange (oxygen uptake, V̇O₂) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% V̇O_2peak. The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [V̇O_2peak=60.2 (1.7) ml·kg⁻¹·min⁻¹] completed two identical 6-min bouts of cycling performed at high intensity [~90% V̇O_2peak; 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). V̇O₂ at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml·min⁻¹, respectively, P<0.05) than in Pre-Ex but there was a ~25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml·min⁻¹, respectively, P<0.05]. The greater whole-body V̇O₂ after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (~12–16 l·min⁻¹ and ~10 beats·min⁻¹, respectively, P<0.05) as were the ratios V̇ _E/O₂ and V̇ _E/V̇CO₂ in the Post-Ex tests. It was concluded that the V̇O₂ and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.     

The relationship between anaerobic threshold and electromyographic fatigue threshold in college women

Summary The purpose of this study was to investigate the relationship between anaerobic threshold (Th_an) and muscle fatigue threshold (EMG_FT) as estimated from electromyographic (EMG) data taken from the quadriceps muscles (vastus lateralis) during exercise on a cycle ergometer. The subjects in this study were 20 female college students, including highly trained endurance athletes and untrained sedentary individuals, whose fitness levels derived from their maximal oxygen consumption ranged from 24.9 to 62.2 ml · kg^–1·min^–1. The rate of increase in integrated EMG (iEMG) activity as a function of time (iEMG slope) was calculated at each of four constant power outputs (350, 300, 250, 200 W), sufficiently high to bring about muscle fatigue. The iEMG slopes so obtained were plotted against the exercise intensities imposed, resulting in linear plots which were extrapolated to zero slope to give an intercept on the power axis which was in turn interpreted as the highest exercise intensity sustainable without electromyographic evidence of neuromuscular fatigue (EMGF_FT). The Th_an was estimated from gas exchange parameters during an incremental exercise test on the same cycle ergometer. The mean results indicated that oxygen uptake (VO₂) at Th_an was 1.391·min^–1, SD 0.44 andVO₂ at EMG_FT was 1.33 1·min^–1, SD 0.57. There was no significant difference between these mean values (P>0.05) and there was a highly significant correlation betweenVO₂ at Th_an andVO₂ at EMG_FT (r=0.823,P<0.01). These data supported the concept of Th_an on the basis that Than was associated with the highest exercise intensity that could be sustained without evidence of neuromuscular fatigue and thus suggested that EMG_FT may provide an attractive alternative to the measurement of Th_an.     

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.     

Ba2+ and amiloride uncover or induce a pH-sensitive and a Na+ or non-selective cation conductance in transitional cells of the inner ear

The membrane potential V _m the cytosolic pH (pH_i), the transference numbers (t) for K⁺, Cl^– and Na⁺/ non-selective cation (NSC) and the pH-sensitivity of V _m were investigated in transitional cells from the vestibular labyrinth of the gerbil. V _m, pH_i, , and the pH_i sensitivity of V _m were under control conditions were –92±1 mV (n=89 cells), pH_i 7.13±0.07 (n=11 epithelia), 0.87±0.02 (n=22), 0.02±0.01 (n=19), 0.01±0.01 (n=24) and –5 mV/pH unit (n=13 cells/n=11 epithelia), respectively. In the presence of 100 mol/l Ba²⁺ the corresponding values were: –70±1 mV (n=32), pH_i 7.16±0.08 (n=6), 0.31±0.05 (n=4), 0.06±0.01 (n=6), 0.20±0.03 (n=10) and -16 mV/pH-unit (n=15/n=6). In the presence of 500 mol/l amiloride the corresponding values were: –72±2mV (n=34), pH_i 7.00±0.07 (n=5), 0.50±0.04 (n=6), 0.04±0.01 (n=11), 0.28±0.04 (n=9) and –26 mV/pH-unit (n=20/n=5). In the presence of 20 mmol/l propionate plus amiloride the corresponding values were: –61±2 mV (n=27), pH_i 6.72±0.06 (n=5), 0.30±0.02 (n=6), 0.06±0.01 (n=5) and 0.40±0.02 (n=8), respectively. V _m was depolarized and and pH_i decreased due to (a) addition of 1 mmol/l amiloride in 150 mmol/l Na⁺ by 38±1 mV (n=8), from 0.82±0.02 to 0.17±0.02 (n=8) and by 0.13±0.01 pH unit (n=6), respectively; (b) reduction of [Na⁺] from 150 to 1.5 mmol/l by 3.3±0.5 mV (n=30), from 0.83±0.02 to 0.75±0.04 (n=9) and by 0.33±0.07 pH unit (n=4), respectively and (c) addition of 1 mmol/l amiloride in 1.5 mmol/l Na⁺ by 20±1 mV (n=11) and from 0.83±0.03 to 0.53±0.02 (n=5), respectively. These data suggest that the K⁺ conductance is directly inhibited by amiloride and Ba²⁺ and that Ba²⁺ and amiloride uncover or induce a pH-sensitive and a Na⁺/NSC conductance which may or may not be the same entity.Some of the data have been presented at various meetings and appear in abstract form in [31, 35, 37]     

Isolated perfused rabbit colon crypts: stimulation of Cl− secretion by forskolin

The aim of this study was to characterize ion conductances and carrier mechanisms of isolated in vitro perfused rabbit colonic crypts. Crypts were isolated from rabbit colon mucosa and mounted on a pipette system which allowed controlled perfusion of the lumen. In non-stimulated conditions basolateral membrane voltage (V _b1) was –65±1 mV (n=240). Bath Ba²⁺ (1 mmol/ l) and verapamil (0.1 mmol/l) depolarized V _b1 by 21±2 mV (n=7) and 31±1 (n=4), respectively. Lowering of bath Cl^– concentration hyperpolarized V _b1 from –69±3 to –75±3 mV (n=9). Lowering of luminal Cl^– concentration did not change V _b1. Basolateral application of loop diuretics (furosemide, piretanide, bumetanide) had no influence on V _b1 in non-stimulated crypts. Forskolin (10^–6 mol/l) in the bath depolarized V _b1 by 29±2 mV (n=54) and decreased luminal membrane resistance. In one-third of the experiments a spontaneous partial repolarization of V _b1 was seen in the presence of forskolin. During forskolin-induced depolarization basolateral application of loop diuretics hyperpolarized V _b1 significantly and concentration dependently with a potency sequence of bumetanide > piretanide furosemide. Lowering bath Cl^– concentration hyperpolarized V _b1. Lowering of luminal Cl^– concentration from 120 to 32 mmol/l during forskolin-induced depolarization led to a further depolarization of V_b1 by 7±2 mV (n=10). We conclude that V_b1 of rabbit colonic crypt cells is dominated by a K⁺ conductance. Stimulation of the cells by forskolin opens a luminal Cl^– conductance. Basolateral uptake of Cl^– occurs via a basolateral Na⁺ : 2Cl^– : K⁺ cotransport system.     

Excess post-exercise oxygen consumption in spinal cord-injured men

This study examined excess post-exercise oxygen consumption (EPOC) following arm cranking in men who had a traumatic spinal cord injury (SCI). Six physically active SCI men with a lesion level between T10 and T12 and six able-bodied (AB) men who were matched according to upper body peak VO₂ performed 30 min of arm-cranking at 65–70% peak VO₂. Baseline measurements were recorded during the last 10 min of a 40-min seated rest. Subjects remained seated during recovery for 40 min or until VO₂ returned to baseline, whichever was longer. Plasma lactate concentration was measured at rest, at the end of exercise, and at 10, 20 and 40 min of recovery. EPOC duration was not significantly different (P>0.05) between SCI [23.2 (7.9) min; mean (SE)] and AB [35.0 (15.4) min] men, nor was there a significant group difference in EPOC magnitude [36.8 (7.8) kJ for SCI and 53.0 (22.8) kJ for AB]. There was no significant difference in recovery heart rate (HR) or respiratory exchange ratio (RER) between SCI and AB. However, HR measured at the end of the EPOC period was significantly elevated (P<0.001) and RER significantly lower (P<0.03) for both groups when compared to baseline. Lactate concentration was not significantly different between the groups at any sampling period. The findings suggest that physically active SCI men have a similar energy expenditure and time frame for recovery from arm crank exercise as their AB counterparts. Similar to what has been reported following lower body exercise, arm crank exercise elicits a higher HR and lower RER at end-EPOC when compared to pre-exercise values.     

Early adaptations in gas exchange,cardiac function and haematology to prolonged exercise training in man

Summary In order to determine the effect of shortterm training on central adaptations, gas exchange and cardiac function were measured during a prolonged submaximal exercise challenge prior to and following 10–12 consecutive days of exercise. In addition, vascular volumes and selected haematological properties were also examined. The subjects, healthy males between the ages of 19 and 30 years of age, cycled for 2 h per day at approximately 59% of pre-training peak oxygen consumption (VO₂) i.e., maximal oxygen consumption (VO_{2 max}). Following the training,VO_{2 max} (1·min^–1) increased (P<0.05) by 4.3% (3.94, 0.11 vs 4.11, 0.11; mean, SE) whereas maximal exercise ventilation (V _E,max) and maximal heart rate (_c,max) were unchanged. During submaximal exercise,VO₂ was unaltered by the training whereas carbon dioxide production (V _E) and respiratory exchange ratio were all reduced (P<0.05). The altered activity pattern failed to elicit adaptations in either submaximal exercise cardiac output or arteriovenous O₂ difference. _c was reduced (P<0.05). Plasma volume (PV) as measured by¹²⁵I human serum albumin increased by 365 ml or 11.8%, while red cell volume (RCV) as measured by⁵¹chromium-labelled red blood cells (RBC) was unaltered. The increase in PV was accompanied by reductions (P<0.05) in haematocrit, haemoglobin concentration (g. 100 ml^–1), and RBCs (10⁶ mm^–3). Collectively these changes suggest only minimal adaptations in maximal oxygen transport during the early period of prolonged exercise training. However, as evidenced by the changes during submaximal exercise, both the ventilatory and the cardiodynamic response were altered. Since RCV did not change, it is suggested that the elevated PV accompanying training is instrumental in eliciting the change in cardiac function.     

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.