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We investigated 8 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) for diaphragmatic strength and the neuromechanical efficiency of the diaphragm while the abdomen was filled with dialysate and while it was empty. Maximum transdiaphragmatic pressure (Pdimax) served as parameter for diaphragmatic strength; diaphragmatic efficiency was assessed by simultaneously monitoring transdiaphragmatic pressure (Pdi) and diaphragmatic electromyogram (EMGdi) during room-air breathing and hyperoxic CO2-rebreathing. After instilling dialysate, Pdimax increased from 76.7 ± 12.1 cmH2O to 92.2 ± 16.3 cmH2O (P < 0.05). While the slopes of the regression lines relating minute ventilation (VE) to arterial CO2 tension, and the change in VE for a given change in Pdi during hypercapnic rebreathing were similar in both states, the slope of EMGdi vs Pdi was significantly steeper when the abdomen was filled (P < 0.05). The increase in Pdimax observed in the filled state may suggest an adaptive rightward shift in the diaphragm's force-length relationship in CAPD patients, although this mechanism is insufficient to prevent a reduction of neuromechanical efficiency of the diaphragm.

Phrenic nerve latency was studied in 14 male type 1 diabetic patients with impaired diaphragm function and in 14 healthy control subjects. The diabetics showed significantly decreased values regarding inspiratory vital capacity and forced volume in 1 s compared with the control subjects. All other lung function parameters were similar in both groups. Although motor and sensory nerve conduction studies provided evidence for peripheral neuropathy in all patients, phrenic nerve latencies turned out to be normal. These results rule out a neuropathic disorder of the phrenic nerve. Thus, impaired diaphragm function in type 1 diabetic patients is not caused by phrenic neuropathy.

The energy demand during physical exercise causes an increased oxygen uptake and supply to active tissues, which may increase the rate of free oxygen radical production and thereby affect the capacity of endogenous cellular defense systems. This could result in DNA base modifications, among which 8-hydroxydeoxyguanosine (8OHdG) is one of the most important and has widely been used as a biomarker of in vivo oxidative lesions. Therefore, we examined the effect of regular running exercise on the urinary levels of 8OHdG in 32 long-distance runners and in a group of untrained healthy subjects. The range of 8OHdG in urine was 0.12-6.45 mumol/mol creatinine in both groups, and no significant difference in the mean excretion levels between runners and control probands was observed. This gives no reason to believe that physical exercise in trained individuals may induce a disturbance of the oxidant-to-antioxidant balance.

Plasma beta-endorphin (beta-E) concentration was determined before, during, and after a standardized incremental exercise test to maximal capacity in eight type I diabetic patients and eight normal control subjects. Diabetic patients were studied under normoglycemic and hyperglycemic conditions in a single-blind random fashion to differentiate between the effects of acute hyperglycemia and of diabetes per se on the beta-E response to exercise. The perceived magnitude of leg effort elicited by exercise was evaluated using a category scale. Whereas plasma beta-E concentrations increased in control subjects with increasing workload, causing significantly higher beta-E levels at the end of exercise than at the beginning (P.001), no such increase could be observed in the diabetic patients under normoglycemic and hyperglycemic conditions. In addition, baseline plasma beta-E concentrations were significantly lower in normoglycemic (P.01) and hyperglycemic (P.001) diabetic patients than in control subjects. Even during the recovery period, patients' beta-E levels remained significantly lower than those of control subjects. At submaximal levels of power output, the perceived intensity of leg effort was significantly higher in normoglycemic and hyperglycemic diabetic patients than in control subjects. We conclude that in type I diabetic patients, the ability of the endogenous opioid system to respond to exercise-induced stress is impaired under hyperglycemic and even under normoglycemic conditions. Considering the effect of endogenous opioids on stress tolerance, such changes may compromise exercise performance in diabetic patients.

Cycle ergometer training plays an important role in the rehabilitation of patients with chronic obstructive pulmonary disease (COPD), but the usefulness of specific inspiratory muscle training as part of pulmonary rehabilitation remains uncertain. To determine whether inspiratory muscle training could intensify the known beneficial effects of cycle ergometer training on exercise performance in these patients, we compared the effect of an 8 week inspiratory muscle training combined with cycle ergometer training with that of an 8 week cycle ergometer training alone on inspiratory muscle performance and general exercise capacity. Patients were randomly assigned to the two training groups; 21 patients received additional inspiratory muscle training (Group 1) and 21 did not (Group 2). Maximal sniff assessed oesophageal and transdiaphragmatic pressures served as parameters for global inspiratory muscle strength and diaphragmatic strength, respectively. The duration for which the patient could breathe against a constant inspiratory pressure load was used as an index of inspiratory muscle endurance. Exercise capacity was determined by an incremental symptom-limited cycle ergometer test. After the training period, inspiratory muscle performance improved significantly in the patients with inspiratory muscle training, but not in those without. Both training regimens increased maximal power output and oxygen uptake, but this improvement was significantly greater in the patients with inspiratory muscle training than in those without.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of opioids on inspiratory muscle function under high mechanical load is still unknown. Even less clear is the extent to which opioids influence the shift of the electromyographic power spectrum of the inspiratory muscles to lower frequencies during ventilatory stress. We studied seven healthy subjects breathing against high inspiratory threshold loads until exhaustion while keeping the minute ventilation constantly high. We compared runs with and without administration of 0.2 mg kg-1 of morphine sulphate intramuscularly; two subjects were given 30 mg morphine sulphate so that we could study the effect of higher opioid concentration. The endurance time (Tlim), the diaphragmatic electromyogram (EMG), the transdiaphragmatic pressures (Pdi) and the ventilatory effort sensation were analysed. Morphine did not have any effect on Tlim or on the effort sensation elicited by the inspiratory resistance in both concentrations. Analysing the spectral shifts of the diaphragmatic EMG, we did not find any significant difference in the decrease of the centroid frequency between drug and control runs. Furthermore, the activation pattern of the diaphragm and the intercostal muscles, evaluated from the percentage contribution of oesophageal and gastric pressures on the transdiaphragmatic pressure swings, did not change following the administration of morphine. Our study shows that morphine does not change the function of the inspiratory muscles during high-resistive breathing. Morphine does not affect the electromyographic power spectrum of the diaphragm during those resistive breathing runs, either. This points out that during stressful ventilatory situations, the shift of the electromyographic power spectrum is attributed to a peripheral (muscular) event consequent to muscle fatigue and not to the elaboration of endogenous opioids.

BACKGROUND--The high prevalence of obstructive sleep apnoea (OSA) in patients with systemic hypertension and of hypertension in patients with OSA suggests a causal link between the two disorders. This study was carried out to determine whether nasal continuous positive airway pressure (CPAP) and weight loss affect daytime hypertension in OSA. METHODS--Sixty hypertensive patients with OSA took part in the study; 33 accepted nasal CPAP and used their machine for 5.7 (0.2) hours per night, and the remaining 27 patients refused nasal CPAP and upper airway surgery so the only therapeutic intervention was a recommendation of weight loss. A significant change in hypertension during follow up was defined as either a change in mean blood pressure of at least 10 mm Hg (or more than 8%) without a change in drug treatment, or a reduction in drug dosage with mean blood pressure within these limits. Weight loss was defined as a body mass index of at least 5% below the baseline value. RESULTS--After 512 (41) days, hypertension had become less severe in seven of 12 patients (58%) treated with weight loss only, in eight of 28 patients (29%) with nasal CPAP only, in two of five patients with nasal CPAP and weight loss, and in one of 15 patients without nasal CPAP or weight loss. Multivariate analysis of variance with the outcome of hypertension at follow up as the dependent variable revealed that only the percentage change in body mass index significantly contributed to the course of hypertension. CONCLUSION--The course of hypertension in OSA is more closely linked to weight loss than to elimination of sleep apnoea by nasal CPAP.

In order to investigate pulmonary gas exchange and cardiopulmonary performance in Type 1 diabetes, 36 patients underwent a progressive incremental exercise test on a cycle ergometer. Cardiopulmonary variables were measured, and arterial blood gases determined on samples obtained from an indwelling catheter in the radial artery. The results were compared with those from 40 control subjects. In the patients, the maximum power (Wmax) and maximum oxygen uptake (VO2max) were lower than in the control subjects (Wmax 186 +/- 52 (+/- SD) vs 233 +/- 48 W, p less than 0.05; VO2max 2.56 +/- 0.71 vs 3.17 + 0.77 l min-1, p less than 0.05). At comparable levels of power output, however, no significant abnormality was observed in the difference between alveolar and arterial oxygen pressure (P(A-a)O2), and the ratio of physiological dead space to tidal volume (VD/VT ratio). These data indicate that in Type 1 diabetic patients, despite their reduced maximum oxygen uptake, gas transfer during exercise is not limited and thus does not contribute to the impairment of exercise capacity.

The aim of our study was to examine the effect of posture on inspiratory muscle activity response to hypercapnia. Recent research has revealed that in normal subjects the activation of the rib cage muscles and of the diaphragm is actually greater in the upright than in the supine position during resting tidal breathing. In this study we examined whether the upright position necessarily entails a greater activation of the inspiratory muscles also under conditions of ventilatory stress. For this purpose we compared the responses to CO2-rebreathing in the supine and sitting positions in five volunteers, by simultaneously recording the electromyogram of the diaphragm (EMGdi) and the intercostal muscles (EMGint). The electromyogram was recorded by means of surface electrodes to measure the EMG amplitude. While the slopes of ventilatory (VE) response to increasing arterial CO2 tension (PaCO2) were similar in the two positions, both the EMGdi-VE and EMGint-VE relationship showed steeper slopes in the supine than in the sitting position. In each CO2 run the increases in EMGdi were linearly related to those in EMGint. This relationship was not affected by the body position. These results suggested that, in spite of similar ventilatory responses to CO2-rebreathing in the lying and sitting positions, the supine position, in humans, required a higher activation of the inspiratory muscles.

An incremental cycle ergometer test performed with a total of 40 healthy subjects (25 male, 15 female) was used to study the mechanical load on the ventilatory muscles. The parameters for the mechanical load on the ventilatory muscles are the time integral of the oesophageal pressure and the mean oesophageal pressure change per time unit (dPoe/dTI) of each breathing manoeuvre. The pressure-time integral is the area delimited by the oesophageal pressure trace and the inspiratory time axis. It is expressed as a fraction of the product of the subject's maximum oesophageal pressure (Poe(max)) and total breath cycle duration (TTOT). This parameter is called oesophageal tension time index (TTIoe). The relationship between minute ventilation and these two parameters during ergometer test showed gender-specific variations because of the differences between men and women as to anthropometric data, lung function parameters and maximum ventilatory muscle strength. Moreover, the dPoe/dTI values significantly depend on the breathing frequency. The present study has provided evidence that, in general, the TTIoe and dPoe/dTI values in terms of a specific minute ventilation (VE) are higher in women than in men. Parameters for the mechanical load on the ventilatory muscles regarding the level of pressure to be generated as well as the duration and velocity of muscle contraction should therefore also allow for the gender of the patients.