During peak exercise HR, stroke volume and cardiac output were not different between the groups with and without diabetes; however, forced expiratory flow at 50% of the forced vital capacity was lower in subjects with diabetes (P < 0.05). Within the group with diabetes, HbA1c was lower in the low-HbA1c versus high-HbA1c group (6.5 +/- 0.3 vs 7.8 +/- 0.4, respectively; P < 0.05), but training volume was not different. At rest, the low-HbA1c group had greater cardiac output and lower systemic vascular resistance than the high-HbA1c group, and all pulmonary function measurements were greater in the low-HbA1c group (P < 0.05). During peak exercise, the VO2, workload, HR, stroke volume, and cardiac output were greater in the low-HbA1c versus the high-HbA1c group (P < 0.05). In addition, all indices of pulmonary function were higher in the low-HbA1c group (P < 0.05). Finally, within the subjects with diabetes, there was a weak inverse correlation between HbA1c and exercise training volume (r2 = -0.352) and stroke volume (r2 = -0.339). These data suggest that highly trained individuals with type I diabetes can achieve the same cardiopulmonary exercise responses as trained subjects without diabetes, but these responses are reduced by poor glycemic control.

These results suggest a limitation in exercise-mediated increases in membrane conductance in CF which may contribute to a drop in SaO(2) and that resting DLNO can account for a large portion of the variability in SaO(2).

Lung diffusing capacity (DLCO) is influenced by alveolar-capillary membrane conductance (D (M)) and pulmonary capillary blood volume (V (C)), both of which can be impaired in sedentary type 1 diabetes mellitus (T1DM) subjects due to hyperglycemia. We sought to determine if T1DM, and glycemic control, affected DLNO, DLCO, D (M), V (C) and SaO(2) during maximal exercise in aerobically fit T1DM subjects. We recruited 12 T1DM subjects and 18 non-diabetic subjects measuring DLNO, DLCO, D (M), and V (C) along with SaO(2) and cardiac output (Q) at peak exercise. The T1DM subjects had significantly lower DLCO/Q and D (M)/Q with no difference in Q, DLNO, DLCO, D (M), or V (C) (DLCO/Q = 2.1 ± 0.4 vs. 1.7 ± 0.3, D (M)/Q = 2.8 ± 0.6 vs. 2.4 ± 0.5, non-diabetic and T1DM, p < 0.05). In addition, when considering all subjects there was a relationship between DLCO/Q and SaO(2) at peak exercise (r = 0.46, p = 0.01). Within the T1DM group, the optimal glycemic control group (HbA1c <7%, n = 6) had higher DLNO, DLCO, and D (M)/Q than the poor glycemic control subjects (HbA1c ≥ 7%, n = 6) at peak exercise (DLCO = 38.3 ± 8.0 vs. 28.5 ± 6.9 ml/min/mmHg, DLNO = 120.3 ± 24.3 vs. 89.1 ± 21.0 ml/min/mmHg, D (M)/Q = 3.8 ± 0.8 vs. 2.7 ± 0.2, optimal vs. poor control, p < 0.05). There was a negative correlation between HbA1c with DLCO, D (M) and D (M)/Q at peak exercise (DLCO: r = -0.70, p = 0.01; D (M): r = -0.70, p = 0.01; D (M)/Q: r = -0.68, p = 0.02). These results demonstrate that there is a reduction in lung diffusing capacity in aerobically fit athletes with T1DM at peak exercise, but suggests that maintaining near-normoglycemia potentially averts lung diffusion impairments.

In these healthy subjects, administration of a nebulized β(2)-agonist resulted in enhanced ventricular function and a decrease in SVR, suggesting peripheral vasodilation. In addition, the increase in norepinephrine level with albuterol, but not placebo, may have important implications in patients with known cardiovascular disease.

The assessment of inflammatory markers and ions in exhaled breath condensate (EBC) is being utilized more frequently in diseases such as asthma and cystic fibrosis with marked variability in EBC measures, including those of exhaled Na+. We sought to determine if variability in exhaled Na+ was due to differences in pulmonary blood flow (PBF) or Na+ in the mouth (salivary Na+). We measured exhaled Na+ three times with coinciding sampling of salivary Na+ and assessment of PBF (using acetylene rebreathing) in 13 healthy subjects (54% female, age = 27 ± 7 yrs., ht. = 172 ± 10 cm, wt. = 70 ± 21 kg, BMI = 22 ± 7 kg/m2 mean ± SD). Exhaled Na+ averaged 2.7 ± 1.2 mmol/l, and salivary Na+ averaged 5.51 ± 4.58 mmol/l. The coefficients of variation across all three measures in all 13 subjects averaged 30% for exhaled Na+ and 83% for salivary Na+, within subjects the variability across the three measures averaged 30% for exhaled Na+ and 38% for salivary Na+. Across all three measures in all 13 subjects the relationship between PBF and exhaled Na+ averaged 0.027 (P = 0.87), and the relationship between salivary Na+ and exhaled Na+ concentrations averaged 0.59 (P = 0.001). Also, we sought to determine the relationship between exhaled Na+ and serum Na+ in an addition 20 subjects. There was a moderate and significant relationship between serum Na+ and exhaled Na+ (r = 0.37, P = 0.04). These findings suggest there that the variability in exhaled Na+ is caused, at least in part, by droplet formation from within the mouth as turbulent air passes through and that there is a flux of ions from the pulmonary blood into the airways.