Middle cerebral artery blood velocity during exercise in patients with atrial fibrillation

Atrial fibrillation limits the ability to increase cardiac output during exercise and may, in turn, affect the exercise-associated elevation in cerebral perfusion. In nine patients with atrial fibrillation (AF) and in five age-matched healthy subjects, middle cerebral artery blood velocity (MCA V_mean) was measured during incremental exercise using the transcranial Doppler. The AF patient group exhibited a lower aerobic capacity than the control group [peak work rate: 106 W (71–153 W; median and range) vs. 129 W (118–159 W) and maximal oxygen uptake: 1·4 l min^–1 (1·0–1·9 l min^–1) vs. 1·7 l min^–1 (1·4–2·2 l min^–1); P = 0·05]. At rest, MCA V_mean was not significantly different between the two groups [43 cm s^–1 (39–56 cm s^–1) vs. 52 cm s^–1 (40–68 cm s^–1)]. During intense cycling, the increase in MCA V_mean was to 51 cm s^–1 (40–78 cm s^–1) (9%) in the AF group and lower than in the healthy subjects [to 62 cm s^–1 (50–81 cm s^–1) 23%; P<0·05], which corresponded with the smaller than expected increase in cardiac output [156% (130–169%) vs. 180%]. Thus, there was a correlation between the increase in MCA V_mean and the ability to increase cardiac output (r² = 0·55, P<0·01). We suggest that, during exercise with a large muscle mass, atrial fibrillation affects the ability to elevate cerebral perfusion, and this results from an impaired ability to increase cardiac output.     

Ventilatory response and arterial potassium concentration during incremental exercise in patients with chronic airways obstruction

Summary. The relationship of ventilation response (V?_E) to arterial potassium concentration (K⁺) during ramp incremental exercise was assessed in nine patients with chronic obstructive pulmonary disease (COPD), and in 10 healthy subjects. For COPD patients the maximum oxygen uptake (VO_max) was 19.6±3.8 ml kg^-1 min^-1 (± SD), and percentage of forced expired volume at 1 s (% FEV₁) was 47.8 ± 10.4%. In healthy subjects, Vo₂max was 44.4±7.0 ml kg^-1 min^-1 and FEV₁, was 89.7 ± 7.4%. Breath-by-breath determinations for V?_E, oxygen uptake (V?o₂) and carbon dioxide output (V?co₂), as well as determinations for K⁺, partial pressure of oxygen (Po₂), partial pressure of carbon dioxide (Pco₂), pH and lactate in arterial blood were performed during a workout on an exercise bicycle at a ramp function work rate of 20 W min^-1, preceded by a 40 min warm-up period. The major findings in the present study are: (1) that there is a linear relation between ventilation and arterial K⁺ concentration during ramp exercise in both healthy subjects and COPD patients; (2) that the slope of the V?_E-K⁺ relationship is significantly lower in COPD patients (16.2 ± 7.31 min^-1 mM^-1) than in normal subjects (37.4 ± 6.91 min^-1 mM^-1, P<0.01); and, (3) that the slope of the V?_E-K⁺ relationship is significantly related to the ability to ventilate during maximal exercise in both healthy subjects and COPD patients (P<0.05). It is thought that the significantly reduced slope of the V?_E-K⁺ relationship in the COPD patients could be interpreted as a reduced sensitivity to the stimulus and/or as a mechanical impairment of the ventilation.     

Kinetics of 13CO2 elimination after ingestion of 13C bicarbonate: the effects of exercise and acid base balance

Abstract. In order to investigate the effects of muscular work and preceding exercise on the retention of exogenous labelled bicarbonate, we studied the effects of oral administration of [¹³C]bicarbonate (0·1 mg kg^-1) in five subjects at rest before exercise and during and after 1 h of treadmill walking at 73% VO_2max on three separate occasions. Elimination of CO₂ from labelled bicarbonate was 62·6±8·1% at rest, 103·6±11·3% during exercise (P<0·01) and 43·0±4·7% during recovery from exercise (P= 0·01). During exercise mean residence time (MRT) was shorter than at rest (35±7 min vs. 54±9min, P < 0·02) and CO₂ pool size was larger (998±160 ml CO₂kg^-1, vs. 194±28ml CO₂kg^-1, P < 0·001). Compared to values obtained at rest, during recovery from exercise, MRT and CO₂ pool size were reduced (34±5min, P < 0·05; 116±19 ml CO₂kg^-1, P < 0·02, respectively). In an additional five subjects acidosis and alkalosis were induced prior to administration of oral [¹³C]bicarbonate at rest. Elimination of bicarbonate was lower during acidosis (46·1±5·6%, P < 0·01) but was unaltered (50·9±5·6%, NS) during alkalosis, compared to the values obtained at resting pH. During acidosis MRT and CO₂ pool size decreased (37±3min, P<0·01 and 123±10ml CO₂kg^-1, P < 0·01, respectively) whereas in alkalosis MRT was unchanged (65±8 min NS) but CO₂ pool size was increased (230±23ml CO₂kg^-1, P < 0·05). The kinetics of elimination of ¹³CO₂ from administered bicarbonate after exercise are different to those at rest and resemble acidosis. The appropriate correction factor for sequestered ¹³C should be used in metabolic studies of the post-exercise state when using ¹³C tracers.     

Anticipating maximal or submaximal exercise: no differences in cardiopulmonary responses

Background: Anticipation before the start of exercise may influence the cardiopulmonary responses during exercise. If anticipation influences the responses differently with maximal and submaximal exercises, normative values for submaximal responses will not be comparable unless exercise has been continued to the same end point. Methods: Twelve healthy subjects (five men) aged 18–27 years had a maximal exercise test and a submaximal exercise test on a cycle ergometer on different days and in random order. They were not aware of the specific purpose of the study and were informed 15 min before the tests whether it should be maximal or submaximal. Workload increased with 15 W min^?1 until exhaustion or to 80% of predicted maximal heart rate (HR). HR, oxygen uptake (VO₂), carbon dioxide production (VCO₂), minute ventilation (V_E) and tidal volume (V_T) were averaged over 20 s intervals. Linear regression of the HR–VO₂ relationship and quadratic regression of the V_T–V_E relationship were performed for each individual, and the regression coefficients for maximal and submaximal tests were compared. Results: The regression models described the V_T–V_E responses with a R² > 0·85 in 23 of 24 tests, and the HR‐VO₂ responses with a R² > 0·90 in all tests. The regression coefficients of the relationships were not significantly different with maximal and submaximal exercises. Conclusion: Anticipation appears not to influence the responses to progressive maximal and submaximal exercise tests with the same rate of increase in load. Normative values at submaximal exercise levels are not influenced by the targeted end point of exercise.     

Ventilation–perfusion inequality and carbon dioxide sensitivity in hypoxaemic chronic obstructive pulmonary disease (COPD) and effects of 6 months of long‐term oxygen treatment (LTOT)

The aim of our study was to find out how blood gas disturbances in stable, eucapnic, severe chronic obstructive pulmonary disease (COPD) patients with an arterial oxygen tension (PaO₂) value of 7·7 (6·1–8·4) kPa are affected by ventilation–perfusion (V_A/Q) relationships and carbon dioxide (CO₂) sensitivity and how these parameters are influenced by 6 months of long‐term oxygen treatment (LTOT). V_A/Q ratios were measured using the multiple inert gas elimination technique (MIGET). Mouth occlusion pressure 0·1 s after onset of inspiration (Pi0·1) and minute ventilation (V_E) were measured to assess respiratory drive response (ΔPi0·1/ΔPCO₂) and hypercapnic ventilatory response (HCVR) to CO₂ rebreathing. At the start of LTOT, a normal median respiratory drive response level of 1·2 (0·2–2·3) cm H₂O/kPa and a low median HCVR as compared with healthy individuals (P<0·001) were found. However, 7·9 (0–29·8)% of the V_E, was directed towards hypoperfused lung areas. The dispersion of ventilation (log SDV; 0·47–1·76), and the dispersion of perfusion (log SDQ; 0·66–1·07) were wider than normal. The PaO₂ level correlated inversely with mean V_A/Q ratio for ventilation (V mean) and shunt. The PaCO₂ level correlated inversely with HCVR and vital capacity. After 6 months of LTOT, no significant changes in daytime blood gas levels, CO₂‐sensitivity or V_A/Q ratios were found. V_E tended to be reduced by 1·0 l min^–1. Conclusions: An elevated V mean and probably shunting are important contributing factors for the reduced PaO₂ and hypercapnic ventilatory response is a major determinant of PaCO₂ in eucapnic stable hypoxaemic COPD. Six months of LTOT does not affect blood gases, CO₂ sensitivity or ventilation–perfusion relationships.     

Metabolic cost of locomotion during treadmill walking with blood flow restriction

We explored whether interval walking with blood flow restriction (BFR) increases net metabolic cost of locomotion in healthy young men at their optimal walking speed. We also determined whether decreased walking economy resulting from BFR might be accompanied by an increase in ventilation relative to VO₂ and VCO₂. Finally, we examined possible relationships between the changes in ratings of perceived exertion (RPE) and those obtained in minute ventilation (V_E) during walking with BFR. Eighteen healthy men (age: 22·5 ± 3·4 years) performed graded treadmill exercise to assess VO_2max. In a randomized fashion, participants also performed five bouts of 3‐min treadmill exercise with and without BFR at their optimal walking speed. Walking with BFR elicited an overall increase in net VO₂ (10·4%) compared with that seen in the non‐BFR condition (P<0·05). The participants also demonstrated greater V_E and V_E/VO₂ values while walking with BFR (P<0·05). Conversely, V_E/VCO₂ was similar between conditions at each walking bout. We found no significant correlation between the changes in V_E and RPE induced by walking with BFR (r = 0·38, P>0·05). Our results indicate that (i) BFR decreases net walking economy in healthy young men, even at their optimal walking speed; (ii) heightened ventilatory drive may explain a small proportion of BFR effects on walking economy; and (iii) the ventilatory responses to BFR walking may be largely independent of changes in perceived exertion and are likely matched to the flux of CO₂ between muscles and respiratory centres.     

Measurement of cardiac output with non-invasive Aesculon impedance versus thermodilution

Background: This study compared the non‐invasive thoracic electrical bioimpedance Aesculon^® technique (TEB_Aesculon) with thermodilution (TD) to evaluate whether TEB_Aesculon may offer a reliable means for estimating cardiac output (CO) in humans. Material and method: Cardiac output was measured with TD and TEB_Aesculon in 33 patients, with a mean age ± SEM of 59 ± 2·7 years, that underwent right heart catheterization for clinical investigation of pulmonary hypertension or severe heart failure. Four to five CO measurements were performed with each technique simultaneously in 33 patients at rest, 11 during exercise and seven during NO inhalation. Result: Cardiac output correlated poorly between TEB_Aesculon and TD at rest (r = 0·46, P<0·001), during exercise (r = 0·35, P<0·013) and NO inhalation (r = 0·41, P<0·017). CO was higher for TEB_Aesculon than TD with 0·86 ± 0·14 l min^?1 at rest (P<0·001) and 2·95 ± 0·69 l min^?1 during exercise (P<0·003), but similar during NO inhalation, with a tendency (P<0·079) to be 0·44 ± 0·19 l min^?1 higher for TEB_Aesculon than TD. CO increased from rest to exercise for TEB_Aesculon and TD with 6·11 ± 0·6 l min^?1 (P<0·001) and 3·91 ± 0·36 l min^?1 (P<0·001), respectively; an increase that was higher (P<0·002) for TEB_Aesculon than TD. During NO inhalation, compared to rest, CO decreased for TEB_Aesculon with 0·62 ± 0·11 l min^?1 (P<0·002), but not significantly for TD with 0·21 ± 0·12 l min^?1 (P<0·11). Bland–Altman analysis showed a poor agreement between TEB_Aesculon and TD. Conclusion: TEB_Aesculon overestimated CO compared to TD with ～17% at rest and ～34% during exercise, but the techniques showed similar results during NO inhalation. CO, furthermore, correlated poorly between TEB_Aesculon and TD. TEB_Aesculon may at present not replace TD for reliable CO measurements in humans.     

Physical working capacity determined by different types of bicycle exercise tests

Summary. Forty-three pairs and 10 triplets of bicycle exercise tests were performed. Seven different workload incremental procedures were used. Triplets and nine pairs of tests were performed by healthy subjects (n= 19) and 34 pairs of tests by patients (n= 19) 3 and 15 months after coronary by-pass operation. From each test result a hypothetical maximal workload sustainable for 6 min (W_max6) was calculated. The two and three W_max6. values obtained for each pair and each triplet of tests, respectively, were compared. The ratios between the corresponding W_max6 values were 1·00 ± 0·01 (mean±SE) for healthy subjects and 0·96 ± 0·03 for patients. It is concluded that working capacities determined by bicycle exercise tests with different workload incremental procedures can be compared via the W_max6.     

Intensity of Nordic Walking in young females with different peak O2 consumption

The purpose of this cross‐sectional study was to determine the physiological reaction to the different intensity Nordic Walking exercise in young females with different aerobic capacity values. Twenty‐eight 19–24‐year‐old female university students participated in the study. Their peak O₂ consumption (VO₂ peak kg^?1) and individual ventilatory threshold (IVT) were measured using a continuous incremental protocol until volitional exhaustion on treadmill. The subjects were analysed as a whole group (n = 28) and were also divided into three groups based on the measured VO₂ peak kg^?1 (Difference between groups is 1 SD) as follows: 1. >46 ml min^?1 kg^?1 (n = 8), 2. 41–46 ml min^?1 kg^?1 (n = 12) and 3. <41 ml min^?1 kg^?1 (n = 8). The second test consisted of four times 1 km Nordic Walking with increasing speed on the 200 m indoor track, performed as a continuous study (Step 1 – slow walking, Step 2 – usual speed walking, Step 3 – faster speed walking and Step 4 – maximal speed walking). During the walking test expired gas was sampled breath‐by‐breath and heart rate (HR) was recorded continuously. Ratings of perceived exertion (RPE) were asked using the Borg RPE scale separately for every 1 km of the walking test. No significant differences emerged between groups in HR of IVT (172·4 ± 10·3–176·4 ± 4·9 beats min^?1) or maximal HR (190·1 ± 7·3–191·6 ± 7·8 beats min^?1) during the treadmill test. During maximal speed walking the speed (7·4 ± 0·4–7·5 ± 0·6 km h^?1) and O₂ consumption (30·4 ± 3·9–34·0 ± 4·5 ml min^?1 kg^?1) were relatively similar between groups (P > 0·05). However, during maximal speed walking, the O₂ consumption in the second and third groups was similar with the IVT (94·9 ± 17·5% and 99·4 ± 15·5%, respectively) but in the first group it was only 75·5 ± 8·0% from IVT. Mean HR during the maximal speed walking was in the first group 151·6 ± 12·5 beats min^?1, in the second (169·7 ± 10·3 beats min^?1) and the third (173·1 ± 15·8 beats min^?1) groups it was comparable with the calculated IVT level. The Borg RPE was very low in every group (11·9 ± 2·0–14·4 ± 2·3) and the relationship with VO₂and HR was not significant during maximal speed Nordic Walking. In summary, the present study indicated that walking is an acceptable exercise for young females independent of their initial VO₂ peak level. However, females with low initial VO₂ peak can be recommended to exercise with the subjective ‘faster speed walking’. In contrast, females with high initial VO₂ peak should exercise with maximal speed.     

Pulmonary clearance of inhaled [99Tcm]DTPA: effects of ventilation pattern

Summary. While a rise in lung volume is known to increase the pulmonary clearance of technetium-99m-labelled dietylene triamine pentaacetate ([⁹⁹Tc^m]DTPA), little interest has been focused on the effects of changes in ventilation frequency, tidal volume and airway pressure. We studied adult, anaesthetized and intubated rabbits during three ventilation patterns (VP) using pressure controlled ventilation (Servo Ventilator 900C). VP was either deep slow (f=20 min^-1, tidal volume (V_T) = 30 ± 4 ml kg^-1 and positive end-expiratory pressure (PEEP) = 0·2 kPa [VP 20/ 0·2, n= 8]) or rapid shallow (f=80 min^-1, V_T= 11 ±2 ml kg^-1 and PEEP = 0·2 or 0·4 kPa [VP 80/0·2, n= 6 and VP 80/0·4, n= 6]). The mean airway pressure was similar at VP 20/0·2 and VP 80/0·4. During administration of [⁹⁹Tc^m]DTPA aerosol all animals were ventilated under the same conditions (f=40 min^-1 and PEEP = 0·2 kPa). The pulmonary clearance rate expressed as the half-life time (T^1/2) of [⁹⁹Tc^m]DTPA was at VP 80/0·2 = 113 ± 31 min, at VP 80/0·4 = 70 ± 24 min (P < 0·01 compared to VP 80/0·2) and at VP 20/0·2 = 36± 18 min (P <0·001 compared to VP 80/0·2 and P <0·01 compared to VP 80/0·4). We conclude that the pulmonary clearance of [⁹⁹Tc^m]DTPA increases

• 1 during rapid shallow ventilation when PEEP is increased from 0·2 to 0·4 kPa;
• 2 during deep slow ventilation relative to rapid shallow ventilation even when the mean airway pressure is similar.

     

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25–40) in the LHD group and 44 W (33–49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31·0 ± 5·5 to 8·8 ± 5·0 mmHg in the LHD group, compared with from 13·7 ± 1·0 to 2·1 ± 2·4 mmHg in the controls, while ventilation/O₂ intake ratio (V˙/V˙O₂) and physiological dead space/tidal volume ratio (V_D/V_T) showed a tendency to rise, from 36·3 ± 8·8 to 39·2 ± 7·4, and from 0·35 ± 0·11 to 0·39 ± 0·09, respectively, in the LHD group, and from 27·5 ± 3·1 to 28·7 ± 5·3, and from 0·19 ± 0·09 to 0·21 ± 0·12 in the controls. Mixed venous O₂ tension (PvO ₂) showed a marked decline from 3·60 ± 0·33 to 3·26 ± 0·36 kPa in the LHD group, as compared with from 3·94 ± 0·28 to 3·71 ± 0·29 kPa in the controls, while the calculated physiologic shunt (Q˙_s/Q˙_t) suggested improved alveolo‐arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia‐induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.     

The effects of beta‐alanine supplementation on physical working capacity at heart rate threshold

Beta‐alanine (BA) supplementation has been shown to delay neuromuscular fatigue as a result of increased muscle carnosine concentrations. Carnosine has also been found in brain and cardiac tissue. The physical working capacity test at heart rate threshold (PWC_HRT) is a global estimate of the onset of fatigue during exercise, influenced by central and peripheral factors. The purpose of this study was to determine the effects of 28 days of BA supplementation on the PWC_HRT. Thirty subjects (mean ± SD; age: 21·0 ± 2·1 years; body mass: 72·7 ± 14·5 kg; height: 170·1 ± 7·9 cm) were randomly assigned to BA (n = 15) or placebo (PL, n = 15) groups. Testing included eight to nine total visits: an enrolment day, physical screening, peak oxygen consumption (V^·O_2peak) and two PWC_HRT assessments over 4 days. Significant differences existed between BA and PL for PWC_HRT (P = 0·001; mean?: BA? = +24·2 watts, PL? = +11·2 watts), but not for V^·O_2peak (P = 0·222), time to exhaustion (TTE; P = 0·562) or ventilatory threshold (VT; P = 0·134). Results suggest that BA may increase heart rate training threshold. These results, in combination with one previous study reporting a potential effect of BA on HR, suggest that future studies should evaluate both central and peripheral aspects of fatigue with BA intake.     

Acute physiological and perceptual responses to high‐load resistance exercise in hypoxia

This study assessed whether hypoxia during high‐load resistance exercise could enhance the acute physiological responses related to muscular development. Twelve trained men performed exercise in three conditions: normoxia (fraction of inspired oxygen [F_IO₂] = 21%), moderate‐level hypoxia (F_IO₂ = 16%) and high‐level hypoxia (F_IO₂ = 13%). Exercise comprised high‐load squats and deadlifts (5 × 5 using 80% of 1‐repetition maximum with 180‐s rest). Muscle oxygenation and activation were monitored during exercise. Metabolic stress was estimated via capillary blood sampling. Perceived fatigue and soreness were also quantified following exercise. While the hypoxic conditions appeared to affect muscle oxygenation, significant differences between conditions were only noted for maximal deoxyhaemoglobin in the deadlift (P = 0·009). Blood lactate concentration increased from 1·1 to 1·2 mmol l^?1 at baseline to 9·5–9·8 mmol l^?1 after squats and 10·4–10·5 mmol l^?1 after deadlifts (P≤0·001), although there were no between‐condition differences. Perceived fatigue and muscle soreness were significantly elevated immediately and at 24 h following exercise, respectively, by similar magnitudes in all conditions (P≤0·001). Muscle activation did not differ between conditions. While metabolic stress is thought to moderate muscle activation and subsequent muscular development during hypoxic resistance training, it is not augmented during traditional high‐load exercise. This may be explained by the low number of repetitions performed and the long interset rest periods employed during this training. These findings suggest that high‐load resistance training might not benefit from additional hypoxia as has been shown for low‐ and moderate‐load training.     

The exercise heart rate profile in master athletes compared to healthy controls

Endurance exercise protects the heart via effects on autonomic control of heart rate (HR); however, its effects on HR indices in healthy middle‐aged men are unclear. This study compared HR profiles, including resting HR, increase in HR during exercise and HR recovery after exercise, in middle‐aged athletes and controls. Fifty endurance‐trained athletes and 50 controls (all male; mean age, 48·7 ± 5·8 years) performed an incremental symptom‐limited exercise treadmill test. The electrocardiographic findings and HR profiles were evaluated. Maximal O₂ uptake (52·6 ± 7·0 versus 34·8 ± 4·5 ml kg^?1 min^?1; P<0·001) and the metabolic equivalent of task (15·4 ± 1·6 versus 12·2 ± 1·5; P<0·001) were significantly higher in athletes than in controls. Resting HR was significantly lower in athletes than in controls (62·8 ± 6·7 versus 74·0 ± 10·4 beats per minute (bpm), respectively; P<0·001). Athletes showed a greater increase in HR during exercise than controls (110·1 ± 11·0 versus 88·1 ± 15·4 bpm; P<0·001); however, there was no significant between‐group difference in HR recovery at 1 min after cessation of exercise (22·9 ± 5·6 versus 21·3 ± 6·7 bpm; P = 0·20). Additionally, athletes showed a lower incidence of premature ventricular contractions (PVCs) during exercise (0·0% versus 24·0%; P<0·001). Healthy middle‐aged men participating in regular endurance exercise showed more favourable exercise HR profiles and a lower incidence of PVCs during exercise than sedentary men. These results reflect the beneficial effect of endurance training on autonomic control of the heart.     

High anaerobic energy release during submaximal arm exercise

Summary. The anaerobic energy release during submaximal arm (AE) and leg exercise (LE) has been estimated from O₂ deficit measured at the onset of exercise. Eight male subjects were studied during 8–10 min of arm or leg cycling at the same relative workload (53% of the peak exercise-induced increase in pulmonary oxygen uptake, VO₂). The workloads were 78 ± 4 W during AE and 173 ± 11 W during LE and Vo₂ was 1.51 ± 006 1 min^-1 for AE and 2.33 ±0.15 1 min^-1 for LE. The half-time of the Vo₂ on-response was considerably longer (P<0.01) during AE (62 ± 9 s) than during LE (33 ± 4 s) and the peak blood lactate concentration was higher (P<0.05) during AE (4.8 ± 0.5 mmol-l^-1) than during LE (3.5 ±0.4 mmol-l^-1). Oxygen deficil was 1.64 ±016 and 1.78 ±0.16 1 for AE and LE respectively. Oxygen deficit was higher during AE than during LE when related to absolute workload (P<0.01), or tc Vo₂ at steady state (P<0.001) or to limb volume (P<0.001). The proportion of the total energy demand covered by anaerobic energy release at the onset of exercise (0–8 min) was about 54% higher (P<0.01) during AE than during LE. It is concluded thai the energy release to a greater extend is covered by anaerobic processes during AE than during LE.     

Leg uptake of calcitonin gene‐related peptide during exercise in spinal cord injured humans

Exercise‐induced increases in cardiac output (CO) and oxygen uptake (VO₂) are tightly coupled, as also in absence of central motor activity and neural feedback from skeletal muscle. Neuromodulators of vascular tone and cardiac function – such as calcitonin gene related peptide (CGRP) – may be of importance. Spinal cord injured individuals (six tetraplegic and four paraplegic) performed electrically induced cycling (FES) with their paralyzed lower limbs for 29 ± 2 min to fatigue. Voluntary cycling performed both at VO₂ similar to FES and at maximal exercise in six healthy subjects served as control. In healthy subjects, CGRP in plasma increased only during maximal exercise (33·8 ± 3·1 pmol l^?1 (rest) to 39·5 ± 4·3 (14%, P<0·05)) with a mean extraction over the working leg of 10% (P<0·05). Spinal cord injured individuals had more pronounced increase in plasma CGRP (33·2 ± 3·8 to 46·9 ± 3·6 pmol l^?1, P<0·05), and paraplegic and tetraplegic individuals increased in average by 23% and 52%, respectively, with a 10% leg extraction in both groups (P<0·05). The exercise induced increase in leg blood flow was 10–12 fold in both spinal cord injured and controls at similar VO₂ (P<0·05), whereas CO increased more in the controls than in spinal man. Heart rate (HR) increased more in paraplegic subjects (67 ± 7 to 132 ± 15 bpm) compared with controls and tetraplegics (P<0·05). Mean arterial pressure (MAP) was unchanged during submaximal exercise and increased during maximal exercise in healthy subjects, but decreased during the last 15 min of exercise in the tetraplegics. It is concluded that plasma CGRP increases during exercise, and that it is taken up by contracting skeletal muscle. The study did not allow for a demonstration of the origin of the CGRP, but its release does not require activation of motor centres. Finally, the more marked increase in plasma CGRP and the decrease in blood pressure during exercise in tetraplegic humans may indicate a role of CGRP in regulation of vascular tone during exercise.     

Breathing patterns during progressive incremental cycle and treadmill exercise are different

Perceived breathlessness at comparable minute ventilation (V_E) is higher with cycling than with running. Different use of the upper extremities and chest wall may influence the breathing pattern. It was hypothetized that the relationship between tidal volume (V_T) and V_E throughout progressive incremental exercise is different with the two modes of exercise. Twelve well trained subjects (seven men) 20–25 years had incremental maximal exercise tests on a treadmill and a cycle ergometer on different days in random order. Heart rate, respiratory gases, V_E and V_T were measured on a computerized exercise testing system, and data were averaged over 20 s periods. The V_E?V_T relationship was characterized by maximum V_T, V_T at a V_E of 30 l min^?1 (V_T30), the Hey plot and by a least squares quadratic regression model. The increase in V_T by V_E was steeper and V_T30 was higher with cycling compared to running. V_Tmax was not different, but was achieved at a lower V_E with cycling. Breathing strategies are different with running and cycling in young well trained subjects, and exercise mode must be accounted for in normative studies of breathing pattern.     

The influence of a fast ramp rate on peak cardiopulmonary parameters during arm crank ergometry

The influence of a very fast ramp rate on cardiopulmonary variables at ventilatory threshold and peak exercise during a maximal arm crank exercise test has not been extensively studied. Considering that short arm crank tests could be sufficient to achieve maximal oxygen consumption (VO₂), it would be of practical interest to explore this possibility. Thus, this study aimed to analyse the influence of a fast ramp rate (20 W min^?1) on the cardiopulmonary responses of healthy individuals during a maximal arm crank ergometry test. Seventeen healthy individuals performed maximal cardiopulmonary exercise tests (Ultima CardiO2; Medical Graphics Corporation, St Louis, USA) in arm ergometer (Angio, LODE, Groningen, The Netherlands) following two protocols in random order: fast protocol (increment: 2 w/6 s) and slow protocol (increment: 1 w/6 s). The fast protocol was repeated 60–90 days after the 1st test to evaluate protocol reproducibility. Both protocols elicited the same peak VO₂ (fast: 23·51 ± 6·00 versus slow: 23·28 ± 7·77 ml kg^?1 min^?1; P = 0·12) but peak power load in the fast ramp protocol was higher than the one in the slow ramp protocol (119 ± 43 versus. 102 ± 39 W, P < 0·001). There was no other difference in ventilatory threshold and peak exercise variables when 1st and 2nd fast protocols were compared. Fast protocol seems to be useful when healthy young individuals perform arm cardiopulmonary exercise test. The usefulness of this protocol in other populations remains to be evaluated.     

Endurance training,overtraining and baroreflex sensitivity in female athletes

We examined heavy training-induced changes in baroreflex sensitivity, plasma volume and resting heart rate and blood pressure variability in female endurance athletes. Nine athletes (experimental training group, ETG) increased intense training (70–90% VO _2max) volume by 130% and low-intensity training (<70% VO _2max) volume by 100% during 6–9 weeks, whereas the corresponding increases in six control athletes (CG) were 5% and 10% respectively. Maximal oxygen uptake (VO _2max) in the ETG and CG did not change, but in five ETG athletes VO _2max decreased from 53·0 ± 2·2 (mean ± SEM) (CI 46·8–59·2) ml kg^–1 min^–1 to 50·2 ± 2·3 (43·8–56·6) ml kg^–1 min^–1 (P<0·01), indicating overtraining. Baroreflex sensitivity (BRS) measured using the phenylephrine technique and blood pressure variability (BPV) did not change, but the low-frequency power of the R–R interval variability increased in the ETG (P<0·05). The relative change in plasma volume was 7% in the ETG and 3% in the CG. The changes in BRS did not correlate with the changes in plasma volume, heart rate variability and BPV. We conclude that heavy endurance training and overtraining did not change baroreflex sensitivity or BPV but significantly increased the low-frequency power of the R–R interval variability during supine rest in female athletes as a marker of increased cardiac sympathetic modulation.     

The lymphocyte Na+/H+ antiport: activation in primary hypertension and during chronic NaCl-loading

Abstract. Increased activity of the Na⁺/H⁺ antiport may be a major abnormality in essential hypertension. The activity of this transport system was investigated in lymphocytes from 13 patients with untreated essential hypertension (Ht) and 13 normotensive control subjects (Nt) on an ad libitum (130–170 mmol d^-1) NaCl intake. Furthermore, the effects of different states of NaCl balance on lymphocyte Na⁺/H⁺ antiport were evaluated in two groups of Nt volunteers receiving 20 vs. 300 mmol d^-1 (n= 8) and 85 vs. 200 mmol d^-1 (n= 14) of NaCl for 1 week each and in seven Ht patients (20 vs. 300 mmol NaCl d^-1 for 1 week each). Additionally, during the 20 and 300 mmol/d NaCl intake red blood cell membrane transport was studied in eight subjects. For the determination of lymphocyte antiport activity, cells were loaded with the cytosolic pH (pH_i) indicator bis-carboxyethyl carboxyfluorescein (BCECF-AM) and acidified by addition of different amounts of Na⁺-propionate (5–40 mM). Initial pH_i-recovery was taken as the activity of the antiport system and plotted against pH_i-values after acidification. Non-linear regression analysis yielded higher ’apparent’ maximal transport rates in Ht than Nt (Nt: 2·00 pL 0·22; Ht: (3·81 pL 0·59)·10^-3 s^-1; P < 0·025). In contrast, baseline pH_i-values and pH_i-values at half-maximal activity (pK) were identical in Nt and Ht. In normotensive control subjects on an NaCl intake of 20, 85, 200 and 300 mmol d^-1 for 7 d, ’apparent’ maximal transport rates averaged 2.75 0·20, 2·89 0·17, 2·81 ± 0·18 and (3·62 ± 0·25) · 10^-3 s^-1, respectively. Thus, antiport activity was significantly (P < 0·05) stimulated on the 300 mmol d^-1 intake as compared to the three other NaCl intakes. The extreme intakes of NaCl (20 vs. 300 mmol d^-1) in normotensive volunteers did not affect the erythrocyte Na⁺/K⁺ pump, Na⁺/K⁺ cotransport and Na⁺/Li⁺ countertransport. Our study supports the concept that a group of patients with primary hypertension exhibit an activated Na⁺/H⁺ antiport. Furthermore, our data demonstrate that a chronic high intake of NaCl is associated with an increase in lymphocyte antiport activity towards the high values observed in primary hypertension.