Relationship between breath-hold time and physical performance in patients with cystic fibrosis

Rehabilitation including physiotherapy is an important part of the treatment used to help improve the quality of life of patients with cystic fibrosis (CF). The aim of this study was to determine the value of the breath-hold time as an index of exercise tolerance in patients with CF. Eighteen patients in different states of CF were included. The breath-hold time was measured in all patients. The fitness level was assessed by means of a progressive exercise test on a cycle-ergometer. During the test, oxygen uptake (VO₂) and carbon dioxide elimination (VCO₂) were measured breath by breath. The VO₂ and working capacity (WC) were computed at the anaerobic threshold (AT) and at peak. Duration of breath-hold was 24.7±2.87 (mean ± SEM) seconds, varying between 10 and 58. The breath-hold time (BHT) displayed a significant correlation with VO₂ (r=0.898), WC (r=0.899) at the AT, and the peak VO₂ (r=0.895). Regression equations were: VO₂ at the AT (ml/kg)=5.53+0.42×BHT and WC at the AT (watt/kg)=0.56+0.38×BHT Our results suggest that the voluntary breath-hold time might be a useful index for prediction of the exercise tolerance of CF patients.The institutional review board was the Human Ethics Committee of The Hospital of Chest Diseases of the Protestant Church of Hungary, Mosdós. The rights of human subjects were fully protected.     

A comparison of various methods for the determination of VO2max

Summary Previous studies have shown that true maximal oxygen uptake (VO₂max) obtained by means of cycle ergometer and step test are lower than the VO₂max measured during uphill treadmill running. The predicted VO₂max measured by ergometer was even lower. Four different methods for the determination of VO₂max within the same group of examinees were compared: True VO₂max by treadmill, ergometer, step test, and predicted VO₂max (Astrand-Rhyming). This study was performed on 15 healthy non-professional sportsmen. They underwent progressive test protocols on alternating days and the results were as follows — VO₂max expressed in ml O₂ kg BW/min (mean±SD): treadmill running 63.8±4.7; ergometer cycling 60.2±5.6; step test 59.6±5.2 and predicted VO₂max 59.9±6.9.The VO₂max as determined by uphill treadmill running was significantly higher than with the other methods. No significant difference was found between true VO₂max determined by the ergometer and step test. However, step test and properly executed Astrand-Rhyming test again proved to be reliable and deviate from the treadmill test by only 6%. Maximal heart rate was sgnificantly higher in the treadmill and step tests than in the direct ergometer test.     

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.     

New acquisitions in the assessment of breath-by-breath alveolar gas transfer in humans

We summarise recent results obtained in testing some of the algorithms utilised for estimating breath-by-breath (BB) alveolar O₂ transfer (VO_2A) in humans. VO_2A is the difference of the O₂ volume transferred at the mouth minus the alveolar O₂ stores changes. These are given by the alveolar volume change at constant O₂ fraction (F _AiO₂ V _Ai) plus the O₂ alveolar fraction change at constant volume [V _Ai–1(F _Ai–F _Ai–1)O₂], where V _Ai–1 is the alveolar volume at the beginning of the breath i. All these quantities can be measured BB, with the exception of V _Ai–1, which is usually set equal to the subjects functional residual capacity (FRC) (Auchincloss algorithm, AU). Alternatively, the respiratory cycle can be defined as the time elapsing between two equal O₂ fractions in two subsequent breaths (Grønlund algorithm, GR). In this case, F _AiO₂=F _Ai–1O₂ and the term V _Ai–1(F _Ai–F _Ai–1)O₂ disappears. BB alveolar gas transfer was first determined at rest and during exercise at steady-state. AU and GR showed the same accuracy in estimating alveolar gas transfer; however GR turned out to be significantly more precise than AU. Secondly, the effects of using different V _Ai–1 values in estimating the time constant of alveolar O₂ uptake (O_2A) kinetics at the onset of 120 W step exercise were evaluated. O_2A was calculated by using GR and by using (in AU) V _Ai–1 values ranging from 0 to FRC +0.5 l. The time constant of the phase II kinetics (₂) of O_2A increased linearly, with V _Ai–1 ranging from 36.6 s for V _Ai–1=0 to 46.8 s for V _Ai–1=FRC+0.5 l, whereas ₂ amounted to 34.3 s with GR. We concluded that, when using AU in estimating O_2A during step exercise transitions, the ₂ value obtained depends on the assumed value of V _Ai–1.     

Effect of training intensity in adult females on aerobic power,related to lean body mass

Summary The aim of this study was to investigate the effect of training intensity on maximal aerobic power on the basis of the subjects lean body mass. Seven sedentary adult females aged 23–40 years participated in a 44-week training experiment. They trained on a bicycle ergometer at progressive intensities of 60, 75, and 90% VO₂ max for 13, 18, and 13 consecutive weeks, respectively. The total amount of work was between 9,000 and 12,000 kpm a day and frequency between 2 and 4 days a week, keeping both factors approximately constant for each subject throughout the 44-week training period. Mean VO₂ max increased significantly during 60 and 90% VO₂ max training. The increase during 75% VO₂ max training was not significant. The final values during the three training periods were not necessarily the highest ones. Keeping the effect of age statistically constant, a significant partial correlation developed between the initial values and the total gains (%) of VO₂ max, V _E, and O₂ pulse, expressed per lean body mass (LBM). The final attained values of VO₂ max per LBM were significantly correlated with age. Therefore, if training intensity is sufficiently effective, it might be assumed that everyone has the same capacity for the improvement of cardiorespiratory function corresponding to their lean body mass, which is related to the magnitude of muscle mass. Furthermore, it might be said that the attainable level of aerobic power is greatly limited by the effects of age.     

Limiting factors in peak oxygen uptake and the relationship with functional ambulation in ambulating children with Spina Bifida

The objective of this study is to interpret the outcomes of peak oxygen uptake (VO_2peak) in children with SB and explore the relationship between VO_2peak and functional ambulation using retrospective cross-sectional study. Twenty-three ambulating children with SB participated at Wilhelmina’s Children’s Hospital Utrecht, the Netherlands. VO_2peak was measured during a graded treadmill-test. Eschenbacher’s and Maninna’s algorithm was used to determine limiting factors in reaching low VO_2peak values. Energy expenditure during locomotion (both O₂ rate and O₂ cost) and percentage of VO_2peak and HR_peak were determined during a 6-min walking test (6MWT). Differences between community and normal ambulators were analyzed. VO_2peak, VO_2peak/kg, HR_peak, RER_peak and VE _peak were significantly lower compared to reference values, with significant differences between normal and community ambulators. Limiting factors according to the algorithm were mostly “muscular and/or deconditioning” (47%) and ventilatory “gasexchange” (35%). Distance walked during 6MWT was 48.5% of predicted distance. Both O₂ rate and O₂ cost were high with significant differences between normal and community ambulators [17.6 vs. 21.9 ml/(kg min) and 0.27 vs 0.43 ml/(kg m)]. Also %HR_peak and %VO_2peak were significantly higher in community ambulators when compared to normal ambulators (resp. 97.6 vs. 75% and 90.2 vs. 55.9%). VO_2peak seems to be mostly limited by deconditioning and/or muscular components and possible ventilatory factors. For both peak values and functional ambulation, community ambulators were significantly more impaired than normal ambulators. High energy expenditure, %VO_2peak and %HR_peak reflect high level of strain during ambulation in the community ambulators. Future exercise testing in children with SB should include assessment of ventilatory reserve. Exercise training in ambulatory children should focus on increasing both VO_2peak and muscular endurance, as well as decreasing energy cost of locomotion.     

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 relation of ventilation to metabolic rate during moderate exercise in man

Summary To characterize more precisely the relationship between ventilation (V _E) and CO₂ output (VCO₂) during incremental exercise, 35 healthy males were studied at rest and during upright cycle ergometry, with the work rate incremented every 4 min up to each subject's anaerobic threshold ( _an). Twenty-one subjects had arterial blood sampled at rest and in the steady state at each work rate to determine the relationship between physiological dead space ventilation (V _D) and VCO₂. At these work rates arterial PCO₂ was regulated at the resting, control value. V _E (BTPS) was linearly related to VCO₂ from rest to _an with a slope of 24.6. However, the regression had a significant positive intercept of 3.2 L·min^–1. This causes the ventilatory equivalent for CO₂ (i.e., V _E/VCO₂) to decrease with increasing work rates. V _D also increased linearly with increasing VCO₂. However, this was consequent to increased breathing frequency as V _D remained constant. Thus, the observed fall in V _E/VCO₂ with increasing work rates is due to the positive intercept but the inherent relationship between V _E and VCO₂, reflected by the linear regression slope, remains unchanged from rest through moderate exercise.This investigation was supported by National Institutes of Health Grant HL-11907     

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.     

Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO₂) and carbon dioxide (PCO₂) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions,PO₂ was significantly lower in the subendocardium (13.5±4.5 mm Hg) than in the subepicardium (20.7±2.3 mm Hg), whereasPCO₂ did not differ significantly (43±8.8 and 51±9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardialPO₂ decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardialPO₂ was 4.1±6.3 mm Hg while subepicardialPO₂ was 6.7±15.0 mm Hg (P<0.05).PCO₂ reached peak values of 56±25 mm Hg subendocardial and 82±22 mm Hg subepicardial at 2.67±0.71 min and 3.43±0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows whilePO₂ recovered with different kinetics. SubendocardialPO₂ increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.     

Acute EPOC response in women to circuit training and treadmill exercise of matched oxygen consumption

The purpose of the study was to evaluate the effects of circuit training (CT) and treadmill exercise performed at matched rates of oxygen consumption and exercise duration on elevated post-exercise oxygen consumption (EPOC) in untrained women, while controlling for the menstrual cycle. Eight, untrained females (31.3±9.1 years; 2.04±0.26 l min^–1 estimated VO_2max; BMI=24.6±3.9 kg/m²) volunteered to participate in the study. Testing was performed during the early follicular phase for each subject to minimize hormonal variability between tests. Subjects performed two exercise sessions approximately 28 days apart. Resting, supine energy expenditure was measured for 30 min preceding exercise and for 1 h after completion of exercise. Respiratory gas exchange data were collected continuously during rest and exercise periods via indirect calorimetry. CT consisted of three sets of eight common resistance exercises. Pre-exercise and exercise oxygen consumption was not different between testing days (P>0.05). Thus, exercise conditions were appropriately matched. Analysis of EPOC data revealed that CT resulted in a significantly higher (p<0.05) oxygen uptake during the first 30 min of recovery (0.27±0.01 l min^–1 vs 0.23±0.01 l min^–1); though, at 60 min, treatment differences were not present. Mean VO₂ remained significantly higher (0.231±0.01 l min^–1) than pre-exercise measures (0.193±0.01 l min^–1) throughout the 60-min EPOC period (p<0.05). Heart rate, RPE, V_E and RER were all significantly greater during CT (p<0.05). When exercise VO₂ and exercise duration were matched, CT was associated with a greater metabolic disturbance and cost during the early phases of EPOC.     

CO2 responsivity in the mouse measured by rebreathing

We have modified the rebreathing method to study CO₂ responsivity in very small mammals. Tidal volume (V _T) and frequency (f) of pentobarbital-anesthetized mice were measured during rebreathing from a closed circuit, primed with 95% O₂, 5% CO₂, through which the gas was constantly circulated at 0.5 l·min^–1. The circuit consisted of T-tube from a plethysmograph, Tygon tubing with compliant element, CO₂ analyzer and pump, in series. CircuitPCO₂ (PctCO₂), which was recorded continuously during spontaneous breathing, rapidly equilibrated with end-tidalPCO₂. CO₂ response curves were constructed from extrapolated minute ventilation ( ),V _T,f and parameters of breath-to-breath timing, respectively, onPctCO₂. Analyses of slopes of the response curves, change from onset of rebreathing to peak response, andPctCO₂ at which the response peaked revealed that CO₂ stimulates by increasingf andV _T and that this is effected by facilitation of central inspiratory-expiratory phase switching and inspiratory drive mechanisms. However, the stimulatory effect of CO₂ on phase switching was not sustained, with maximal effect occurring before peak . The advantages and facility of the modified rebreathing method make it suitable for studies of other small mammals, including neonates.     

Breath-by-breath alveolar oxygen transfer at the onset of step exercise in humans: methodological implications

The effects of using different algorithms to estimate the time constant of changes in oxygen uptake at the onset of square-wave 120 W cycloergometric exercise were evaluated in seven subjects. The volume of oxygen taken up at the alveoli (VO_2Ai) was determined breath-by-breath (BB) from the volume of O₂ transferred at the mouth (VO_2mi) minus the corresponding volume changes in O₂ stores in the alveoli: VO_2Ai=VO_2mi–[V _Ai–1(FO_2Ai–FO_2Ai–1)+FO_2Ai·ΔV _Ai], where V _Ai–1 is the alveolar volume at the end of the previous breath, FO_2Ai and FO_2Ai–1 are estimated from the fractions of end-tidal O₂ in the current and previous breaths, respectively, and ΔV _Ai is the change in volume during breath i. These quantities can be measured BB, with the exception of V _Ai–1 which must be assumed. The respiratory cycle has been defined as the time elapsing between identical fractions of expiratory gas in two successive breaths. Using this approach, since FO_2Ai=FO_2Ai–1, any assumption regarding V _Ai–1 becomes unnecessary. In the present study, VO_2Ai was calculated firstly, by using this approach, and secondly by setting different V _Ai–1 values (from 0 to FRC+0.5 l, where FRC is the functional residual capacity). Values for alveolar O₂ flow (V˙O_2Ai), as calculated from the quotient of VO_2Ai divided by breath duration, were then fitted bi-exponentially. The time constant of the phase II kinetics of V˙O_2Ai (τ₂) was linearly related to V _Ai–1, increasing from 36.6 s (V _Ai–1=0) to 46.8 s (V _Ai–1=FRC+0.5 l) while τ₂ estimated using the first approach amounted to 34.3 s. We concluded that, firstly, the first approach allowed us to calculate V˙O_2A during transitions in step exercise; and secondly, when using methods wherein V _Ai–1 must be assumed, τ₂ depended on V _Ai–1. Electronic Publication     

Transcutaneous,noninvasiveP O 2 monitoring in adults during exercise and hypoxemia

A new, commercially available, transcutaneous (tc)P _{O 2} monitor was tested in adult females and in laboratory animals to assess its applicability in measuring arterial oxygen tension during physiological stress. Observed values on dogs correlated well with direct measurements of arterialP _{O 2} and with previous data obtained from measurements of arterial blood during exercise and hypoxemia. In our female subjects the unit responded rapidly to changes in inspired ambient oxygen and electrical stability was excellent during maximal exercise tests. TranscutaneousP _{O 2} decreased to an average of 87.8 Torr during maximum exercise breathing 20.9% O₂, and to 32 Torr while breathing 12.6% O₂ at maximum work. Two distinct patterns of response in tcP _{O 2} were observed during hypoxic and normoxic exercise. The technique appears to have substantial future application both in clinical and physiological investigation involving adult subjects.     

Effect of alteration of peripheral blood flow on the central circulation in man during supine cycling in different ambient temperatures

Summary Whether the alteration of peripheral circulation caused by changing ambient temperature (T_a) affects central circulatory changes in man during supine cycling was investigated in four well-trained men, who exercised at two levels (117.7 or 176.6 W). Exercise metabolic rate (VO₂) in cold (0 C or 10 C) was the same as it was at 20 C, whereas the cardiac output (CO; CO₂ rebreathing technique) and heart rate were significantly lower (e.g., 176.6 W at 0 C, both p<0.01). In heat (30 C or 40 C), the VO₂ reduced with falling CO and mean arterial blood pressure from those at 20 C (e.g., 176.6 W at 40 C, all cases p<0.01), whereas the peak post-exercise calf blood flow (CBF_p) increased (p<0.01). The VO₂ and stroke volume (SV) were inversely proportional to the ratio of CBF_p to CO/kg body weight (CBF_p/CO) (r>–0.78, p<0.001). Total peripheral resistance (TPR) was related to arteriovenous oxygen difference (A-VO₂ difference) (r>0.78, p<0.001). The TPR and A-VO₂ difference decreased as T_a rose, while CBF_p/CO was almost the same. As CBF_p/CO had exceeded 50 and further progressed, however, the two parameters elevated until the same level as that at 0 C. The present results suggest that during moderately prolonged (16–60 min) supine cycling in different T_a's the central circulatory changes are mainly affected by the altered peripheral blood flow in competing between skin and muscle for blood flow.     

Effects of training on plasma FFA during exercise in women

Summary The purpose of this study was to investigate the effects of training on plasma FFA concentrations in women during 60 min of work. All subjects (n=10) exercised at 55% of their initial VO_{2 max} for 60 min on a bicycle ergometer. Five subjects then participated in a training program, consisting of bicycling five days per week for four weeks while five control subjects remained inactive. Following the training or control period, all 10 subjects repeated the initial 1-h test at the same absolute work load. The training program resulted in a 14% increase in VO_{2 max} and a decreased resting HR (p<0.05). The submaximal exercise HR and R were also lower following training (p<0.05). Plasma FFA were significantly lower (p<0.05) during exercise in the experimental group following training. The average increase in plasma FFA during the 60 min bicycle test was 0.22 mol/l, from 0.48 mol/l at rest to 0.70 mol/l after 60 min of exercise prior to training. After training the same absolute work load resulted in an increased plasma FFA of only 0.10 mol/l from 0.29 to 0.39 mol/l. No significant changes due to training were observed for glycerol or lactate. The results suggest that the metabolic response of women is similar to men during exercise before and after training. Possible mechanisms for the decreased plasma FFA response after training are discussed.     

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.     

Comparison of arterial,end-tidal and transcutaneous PCO2 during moderate exercise and external C02 loading in humans

Summary Static relationships between arterial, transcutaneous[/p] and end-tidal PCO₂ (P _aCO₂, P _tc CO ₂, P _etCO₂) as well as the dynamic relationship between P _etCO₂ and P _tcCO₂ were studied during moderate bicycle ergometer exercise with and without external C0₂ loading. The exercise pattern consisted of 5-min intervals of constant power at 40 W and 100 W and 900 s of randomised changes between these two power levels. The external CO₂ loading was achieved by means of controlled variations of inspiratory gas compositions aimed at a constant P _etCO₂ of 6.5 kPa (49 mm Hg). The P_etO2 was regulated at 17.3 kPa (130 mm Hg). Under steady-state conditions all PCO₂ parameters showed close linear relationships. P _aCO₂/P _tcCO₂ was near to identity while the P _etCO₂ systematically overestimated changes in P _aCO₂. No relationship showed a significant influence of the exercise intensity. Transients of P _tcCO₂ are considerably slower than P _etCO₂ transients. The dynamic relationship between both parameters was found to be independent of whether internal or external C0₂ loadings were applied. It is concluded that the combination of P _etCO₂ and P _tcCO₂ measurements allows an improved non-invasive assessment of P _aCO₂. While P _etC0₂ better reflects the transients, P _tcCO₂ can be employed to determine slow changes of the absolute P _aCO₂.     

Ventilatory response to oscillating and non-oscillatingPa CO 2 in the anesthetized cat

Summary In 11 adult cats, lightly anesthetized with chloralose-urethane, blood from both common carotid arteries was led into a plastic chamber of 15–20 ml and returned to the carotids at a point 1.5 cm more cranial. By doing so arterial blood was assumed to pool within the chamber and lose itsP _{CO 2} oscillations which are normally known to exist as a result of the respiratory cycle. In control periods blood bypassed the chamber, thus maintaining respiratoryP _{CO 2} oscillations. Spontaneous ventilation was measured spirometrically. The animals were breathing pure O₂.Results. 1. When the sinus (carotid) nerves were intact or sectioned there was no significant difference in ventilation before or after switching from non-oscillating to oscillatingPa _{CO 2}. 2. When the vertebral arteries were ligated a drop in ventilation occurred after turning to oscillatingPa _{CO 2} which was followed by a slight rise above control values after 30–50 sec. This phenomenon was independent of sinus nerve integrity. Thus in hyperoxie condition the smallPa _{CO 2} oscillations known to occur in phase with respiration do not seem to provide a respiratory stimulus to resting ventilation above that generated by the mean level ofPa _{CO 2}. The ventilatory depression after vertebral artery ligation must at this time remain unexplained.     

Step vs. progressive exercise: the kinetics of phosphocreatine hydrolysis in human muscle

It is well known that the VPO ₂ readjustment rate of the whole body is faster when carrying out a given constant work load starting from a baseline of moderate exercise than from rest. However, it has not been established whether the above change is the result of faster kinetics of the oxidative machinery or, alternatively, the consequence of a reduced involvement of confounding factors such as anaerobic glycolysis or tissue O₂ stores. The problem, earlier approached by chemical methods, was studied in man by ³¹P-NMRS assessment of the kinetics of phosphocreatine (PC) hydrolysis at the muscle level which is known to reflect the readjustment rate of the oxidative reactions. Twelve normal subjects carried out in a 90 cm bore modified Picker (1.5 T) magnet, a series of contractions by the plantar flexors reaching pre-set submaximal loads either in single steps (constant load, CL) or progressively (incremental exercise, I). If preceding exercise (I), compared to rest, influenced the rate of oxidations, the PC concentration at the target loads would be different for the two exercise modes, reflecting different energy deficits. This was not the case. Thus the present results show that the rate of readjustment of oxidations at the muscle level is not affected by priming exercise confirming previous findings and showing that theoretical models of VPO ₂ control are experimentally applicable to man.