Hormonal and metabolic changes during exercise in cirrhotic patients

The metabolic response to exercise was compared in 10 cirrhotic patients (P) in a stable clinical condition and in 6 sedentary, age-matched, normal subjects (C) performing 32 minutes of treadmill exercise with the same constant workload corresponding to three to four times their resting oxygen uptake. Taking indirect calorimetry as reference, respiratory exchanges indicated that cirrhotic patients consumed carbohydrates almost exclusively, unlike the normal controls, who consumed lipids and glucids in about the same proportions (RQ : 0.98 ± 0.04 v 0.87 ± 0.04, P < .0001). In the patients, this carbohydrate path of exercise metabolism lowered glycemia from the resting value of 5.23 ± 0.16 mmol/L to 4.03 ± 0.37 mmol/L ( P < .0001) and raised the plasma lactate concentration from 2.08 ± 0.24 mmol/L at rest to 3.48 ± 0.32 mmol/L at the eighth minute of exercise ( P < .001), thus suggesting defective liver glyconeogenesis. Fatty free acids and glycerol remained almost constant during exercise, whereas catecholamines increased. Insulin levels were high in patients at rest (67.1 ± 14.5 U/mL v 15.1 ± 3.5 U/mL); they declined sharply at the onset of exercise but nevertheless remained high compared to those observed in the controls ( P < .0001). Glucagon increased in exercising patients from 88.3 ± 21.3 pg/mL to 127.4 ± 30.6 pg/mL (NS). Esterified plasma carnitine declined in the patients from 13.0 ± 2.2 μmol/L to 8.6 ± 1.5 μmol/L ( P < .05). Several possibilities might account for these results: (1) insulin and exercise might act synergistically to increase glucose use; (2) insulin might not allow other hormones to express their effects, hence the lipolysis inhibition and reduced liver glycogen release; (3) the decrease in esterified carnitine might be due either to hyperinsulinemia and small lipid use or to some defect of synthesis connected with liver cell damage, a defect that becomes evident when carnitine requirements increase.