Inspiratory muscle training reduces blood lactate concentration during volitional hyperpnoea.

Although reduced blood lactate concentrations ([lac(-)](B)) have been observed during whole-body exercise following inspiratory muscle training (IMT), it remains unknown whether the inspiratory muscles are the source of at least part of this reduction. To investigate this, we tested the hypothesis that IMT would attenuate the increase in [lac(-)](B) caused by mimicking, at rest, the breathing pattern observed during high-intensity exercise. Twenty-two physically active males were matched for 85% maximal exercise minute ventilation (.V(E) max) and divided equally into an IMT or a control group. Prior to and following a 6 week intervention, participants performed 10 min of volitional hyperpnoea at the breathing pattern commensurate with 85% .V(E) max. The IMT group performed 6 weeks of pressure-threshold IMT; the control group performed no IMT. Maximal inspiratory mouth pressure increased (mean +/- SD) 31 +/- 22% following IMT and was unchanged in the control group. Prior to the intervention in the control group, [lac(-)](B) increased from 0.76 +/- 0.24 mmol L(-1) at rest to 1.50 +/- 0.60 mmol L(-1) (P < 0.05) following 10 min volitional hyperpnoea. In the IMT group, [lac(-)](B) increased from 0.85 +/- 0.40 mmol L(-1) at rest to 2.02 +/- 0.85 mmol L(-1) following 10 min volitional hyperpnoea (P < 0.05). After 6 weeks, increases in [lac(-)](B) during volitional hyperpnoea were unchanged in the control group. Conversely, following IMT the increase in [lac(-)](B) during volitional hyperpnoea was reduced by 17 +/- 37% and 25 +/- 34% following 8 and 10 min, respectively (P < 0.05). In conclusion, increases in [lac(-)](B) during volitional hyperpnoea at 85% .V(E) max were attenuated following IMT. These findings suggest that the inspiratory muscles were the source of at least part of this reduction, and provide a possible explanation for some of the IMT-mediated reductions in [lac(-)](B), often observed during whole-body exercise.

Hypophosphatemia and phosphorus depletion in respiratory and peripheral muscles of patients with respiratory failure due to COPD.

In 22 patients (19 men, 3 women; mean [+/- SD] age, 63 +/- 6 years) with chronic obstructive pulmonary disease (COPD), phosphorus content was measured by spectrophotometric methods on muscle fragments of both peripheral (quadriceps femoris needle biopsy in 22 patients) and respiratory muscles (external intercostal muscle surgical biopsy in 14 patients). Thirty age- and sex-matched subjects were used as controls (19 for quadriceps femoris muscle biopsy and 11 for intercostal muscle biopsy). Serum phosphorus levels, as well as the main determinants of overall phosphorus metabolism (dietary intake of phosphorus and renal phosphate handling), were also obtained in all patients and control subjects. Muscle phosphorus content of both respiratory and peripheral muscles was significantly reduced in the COPD patient group, no matter what reference index was used (fat-free dry muscle weight or muscle fragment DNA content); muscle phosphorus depletion was present in about 50 percent of patients with COPD. In the same patient group, a significant relationship between muscle and serum phosphorus levels was demonstrable in the case of peripheral muscles only. No relationship was found between phosphorus content of both types of skeletal muscles and dietary phosphorus intake levels or with nutritional status, even though patients with COPD had significantly reduced anthropometric, biochemical, and immunologic indices as compared with controls. Renal phosphorus handling indices of the COPD patient group were compatible with a condition of inadequacy of the renal compensatory mechanism to hypophosphatemia and phosphorus depletion (low percent tubular reabsorption of phosphorus, low renal threshold concentration values). Our study suggests that phosphorus depletion occurs frequently in COPD, but in this clinical condition serum phosphorus levels are not representative of cellular phosphorus levels. Phosphorus depletion, which is equally severe in respiratory and peripheral muscles, could depend, at least in part, on malnutrition and a condition of renal phosphorus wasting possibly linked to some drugs commonly used in patients with COPD (xanthine derivatives, diuretics, etc).

Influence of volume on the spread of local anesthetic-methylene blue solution after injection for intercostal block.

The purpose of this study was to evaluate the influence of the volume of methylene blue-local anesthetic on the spread of the injectate along the costal pleura. Twenty patients undergoing elective thoracotomy were studied. Twelve patients received intercostal nerve injection with 10 mL of 0.5% bupivacaine with methylene blue (10-mL group), and eight patients received 5 mL of 0.5% bupivacaine with methylene blue (5-mL group). The area of spread of the methylene blue was measured after the pleural cavity was incised. The 10-mL group had a mean area of spread of 51.1 cm2 as opposed to 17.6 cm2 for the 5-mL group (P less than 0.05). In the 10-mL group, eight patients had bupivacaine-methylene blue spread to two intercostal spaces, three patients to three intercostal spaces, and one patient to four intercostal spaces. In the 5-mL group, seven patients had bupivacaine methylene blue spread confined to one intercostal space and one patient to two intercostal spaces. We conclude that a potential anatomic space exists between the costal pleura and the internal intercostal muscle and that the spread of local anesthetic after intercostal nerve block injection is volume dependent.