Purpose: The exercise capacity of cardiac asymptomatic subjects with hereditary hemochromatosis (HH) has not been well described. In this study, we tested whether the iron overload associated with HH affected exercise capacity with a case control study design.
Methods: Forty-three HH and 21 normal control subjects who were New York Heart Association functional class I underwent metabolic stress testing using the Bruce protocol at the clinical center of the National Institutes of Health. Exercise capacity was assessed with minute ventilation (V˙E), oxygen uptake (V˙O2), and carbon dioxide production (V˙CO2) using a breath-by-breath respiratory gas analyzer.
Results: The exercise capacity of HH subjects was not statistically different from that of control subjects (exercise time 564 ± 135 vs 673 ± 175 s, P = 0.191; peak V˙O2 29.6 ± 6.4 vs 32.5 ± 6.7 mL·kg−1·min−1, P = 0.109; ventilatory threshold 19.0 ± 3.4 vs 21.0 ± 5.0 mL·min−1·kg−1, P = 0.099; data are for HH vs control subjects). Ventilatory efficiency was comparable between groups (V˙E/V˙CO2 slope 23.7 ± 3.2 vs 23.4 ± 4.2, P = 0.791). No significant correlation between the markers of iron levels and the markers of exercise capacity was noted. Iron depletion by 6-month phlebotomy therapy in 18 subjects who were newly diagnosed did not affect exercise testing variables (exercise time 562 ± 119 vs 579 ± 118 s, P = 0.691; peak V˙O2 29.5 ± 3.7 vs 29.1 ± 4.7 mL·kg−1·min−1, P = 0.600; ventilatory threshold 18.5 ± 2.8 vs 17.9 ± 3.8 mL·kg−1·min−1, P = 0.651; data are from before and after phlebotomy therapy). Abnormal ischemic electrocardiographic responses and complex arrhythmias were more frequently seen in HH subjects.
Conclusions: The aerobic exercise capacity of asymptomatic HH subjects seems not to be statistically different from that of normal subjects. The iron levels do not seem to affect exercise capacity in asymptomatic HH subjects.