Oxygen uptake kinetics and exercise capacity in children with cystic fibrosis.

Exercise capacity, an objective measure of exercise intolerance, is known to predict quality of life and mortality in cystic fibrosis (CF). The mechanisms for exercise intolerance in patients with cystic fibrosis (CF), however, have yet to be fully elucidated. Accordingly, this study sought to investigate oxygen uptake kinetics and the impact of fat-free mass (FFM) on exercise capacity in young patients with CF. 16 young patients with CF (age 13 ± 4 years; 10 female) and 15 matched controls (age 14 ± 3 years; nine female) participated. Pulmonary function and a maximal exercise test on a cycle ergometer using the Godfrey protocol were performed. Exercise capacity (VO2 peak), VO2 response time (VO2 RT), and functional VO2 gain (ΔVO2 /ΔWR) were all determined. Lung function was the only demographic parameter significantly lower (P < 0.05) in CF compared to controls. Exercise capacity was lower in CF (P < 0.014) only when VO2 peak was normalized for FFM (43.5 ± 7.7 vs. 50.6 ± 7.4 ml/kg-FFM/min) or expressed as % predicted (70.1 ± 14.3 vs. 85.4 ± 16.0%). The VO2 RT was slower (36.1 ± 15.1 vs. 25.0 ± 12.4 sec; P = 0.03) and the ΔVO2 /ΔWR slope was lower (8.4 ± 3 ml/min/watt vs. 10.1 ± 1.4 ml/min/watt; P = 0.02) in patients compared to controls, respectively. In conclusion, a delayed VO2 response time coupled with the lower functional VO2 gain (ΔVO2 /ΔWR) suggest that young patients with CF have impairment in oxygen transport and oxygen utilization by the muscles. These data in addition to differences in VO2 peak normalized for FFM provide some insight that muscle mass and muscle metabolism contribute to exercise intolerance in CF.

Association beween resting heart rate, shear and flow-mediated dilation in healthy adults.

Preclinical data have demonstrated that heart rate (HR) can directly impact vascular endothelial function, in part, through a shear-stress mechanism. This study sought to explore, in humans, the associations between resting heart rate and both shear and endothelial function assessed by flow-mediated dilation (FMD). The brachial artery FMD test was performed in 31 apparently healthy volunteers. Basal (B) and hyperaemic (H) shear were quantified in the following two ways using data from the FMD test: the traditional cumulative shear area under the curve up to peak dilation (Shearcum) method; and our novel method of shear summation (Shearsum), which accounts for HR by summing each individual cardiac cycle shear up to peak dilation. Data were grouped by tertiles based on resting HR as follows: low (LHR = 43-56 beats min(-1); n = 10); middle (MHR = 58-68 beats min(-1); n = 11); and high (HHR = 69-77 beats min(-1); n = 10). Within the LHR group, both B-Shearcum and H-Shearcum were significantly higher (P < 0.001) than B-Shearsum and H-Shearsum, respectively, whereas in the HHR group B-Shearcum and H-Shearcum were significantly lower (P < 0.001) than B-Shearsum and H-Shearsum, respectively. The FMD in the LHR group (8.8 ± 0.8%) was significantly greater than that in both the MHR group (5.5 ± 0.8%; P = 0.009) and the HHR group (5.9 ± 0.8%; P = 0.024). These findings demonstrate the existence of a relationship between heart rate and both shear and endothelial function in humans. Moreover, these findings have implications for considering heart rate as an important physiological variable when quantifying shear and performing the FMD test.