We studied the effect of breathing at various levels of transdiaphragmatic pressure (Pdi) on the EMG power spectrum of the diaphragm. The diaphragmatic EMG was measured simultaneously with a bipolar esophageal electrode (EE) and surface electrode (SE) placed on the ventral portion of the sixth and seventh intercostal spaces in five normal subjects breathing at functional residual capacity (FRC) against an inspiratory resistance. During each fatigue run the subjects generated a Pdi, with each inspiration, that was 25, 50, or 75% of maximum Pdi (Pdimax) for a period up to 15 min. During runs at 50 and 75% of the Pdimax, which are known to produce fatigue, we found for both EE and SE a progressive increase in the amplitude of the low-frequency (L = 20-46.7 Hz) and a decrease in the high-frequency (H = 150-350 Hz) component of the EMG. These changes were not seen at 25% of Pdimax. The diaphragmatic H/L ratio was independent of Pdi when the diaphragm was not fatigued. H/L fell while the diaphragm performed fatiguing work and this was more rapid at higher Pdi's. It was thus concluded that frequency spectrum analysis of the EMG can detect diaphragmatic fatigue reliably, prior to the time when the diaphragm fails as a pressure generator.

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Background/Aims: Cardiovascular disease (CVD) is increased in chronic kidney disease (CKD), and contributed to by the CKD-mineral bone disorder (CKD-MBD). CKD-MBD begins in early CKD and its vascular manifestations begin with vascular stiffness proceeding to increased carotid artery intima-media thickness (cIMT) and vascular calcification (VC). Phosphorus is associated with this progression and is considered a CVD risk factor in CKD. We hypothesized that modifying phosphorus balance with lanthanum carbonate (LaCO₃) in early CKD would not produce hypophosphatemia and may affect vascular manifestations of CKD-MBD. Methods: We randomized 38 subjects with normophosphatemic stage 3 CKD to a fixed dose of LaCO₃ or matching placebo without adjusting dietary phosphorus in a 12-month randomized, double-blind, pilot and feasibility study. The primary outcome was the change in serum phosphorus. Secondary outcomes were changes in measures of phosphate homeostasis and vascular stiffness assessed by carotid-femoral pulse wave velocity (PWV), cIMT and VC over 12 months. Results: There were no statistically significant differences between LaCO₃ and placebo with respect to the change in serum phosphorus, urinary phosphorus, tubular reabsorption of phosphorus, PWV, cIMT, or VC. Biomarkers of the early CKD-MBD such as plasma fibroblast growth factor-23, Dickkopf-related protein 1 (DKK1), and sclerostin were increased 2- to 3-fold at baseline, but were not affected by LaCO₃. Conclusion: Twelve months of LaCO₃ had no effect on serum phosphorus and did not alter phosphate homeostasis, PWV, cIMT, VC, or biomarkers of CKD-MBD.