Exercise limitation in cirrhosis is typically attributed to a cirrhoti
c myopathy (without impaired oxygen utilization) and/or a cardiac chro
notropic dysfunction. We performed symptom-limited cardiopulmonary exe
rcise testing in 19 cirrhotics without confounding variables (cardiopu
lmonary disease, beta blockade, anemia, smoking). Twelve concurrently
exercised patients without cirrhosis and with normal resting pulmonary
function were controls. Oxygen consumption ((V) ovet dot (O2),) at pe
ak exercise, at anaerobic threshold ((V) over dot (O2)-AT), work rate
(WR), and heart rate (HR) were measured. Cirrhotics had significantly
lower peak WR (73 +/- 4 vs 107 +/- 7% predicted, p < 0.001), (V) over
dot (O2) (72 +/- vs 98 +/- 5% predicted, P < 0.001), (V) over dot (O2)
-AT (53 +/- 4 vs 71 +/- 5% predicted peak (V) over dot (O2) P < 0.01),
HR (83 +/- 2 vs 91 +/- 2% predicted. P < 0.01) and were more likely t
o have chronotropic dysfunction (peak HR < 85% predicted). Six cirrhot
ics had normal aerobic capacity (peak (V) over dot (O2) > 80% predicte
d), while 13 were abnormal. The abnormals had an earlier AT (46 +/- 2
vs 67 +/- 3% predicted peak (V) over dot (O2), P < 0.05) but no differ
ence in peak HR percent predicted was found. In conclusion, two thirds
of cirrhotics, without confounding factors, have significantly reduce
d aerobic capacity. Cirrhotic myopathy (without impaired O-2 utilizati
on) and cardiac chronotropic dysfunction do not adequately account for
the observed decrease in aerobic capacity.