Physical inactivity, sarcopenia, and frailty are highly prevalent, independent predictors of morbidity and mortality in patients with cirrhosis. Across a range of chronic diseases, exercise training is a key recommendation supported by guidelines and, for some conditions, even by governmental funding of exercise programmes. Consistent with the broader chronic disease literature, the evidence for a benefit of exercise in cirrhosis is promising. Several small trials have reported significant improvements in muscle health (mass, strength, functional capacity), quality of life, fatigue, and reductions in the hepatic venous pressure gradient, without adverse events. With strong emerging evidence surrounding the substantial risks of sarcopenia/frailty and our first-hand experiences with liver pre-transplant exercise programmes, we contend that routine patient care in cirrhosis should include an exercise prescription. Some clinicians may lack the resources and necessary background to translate the existing evidence into a practicable intervention. Our team, comprised of physiotherapists, exercise physiologists, hepatologists, transplant specialists, and knowledge translation experts from six North American centres, has distilled the essential background information, tools, and practices into a set of information ready for immediate implementation into clinics ranging from a family practice setting to specialty cirrhosis clinics. Augmenting the rationale and evidence are supplementary materials including video and downloadable materials for both patients and the physician. Supporting the exercising patient is a section regarding information about nutrition, providing practical tips suitable for all patients with cirrhosis.

Renal transplant recipients (RTR) have reduced peak aerobic capacity, muscle strength, arterial function and an unfavorable cardiovascular disease risk (CVD) profile. This study compared the effects of 12 weeks of supervised endurance and strength training (EST, n = 16) versus usual care (UC, n = 15) on peak aerobic capicity, cardiovascular and skeletal muscle function, CVD risk profile, and quality of life (QOL) in RTR (55 ± 13 years). Peak aerobic capacity and exercise hemodynamics, arterial compliance, 24-h blood pressure, muscle strength, lean body mass, CVD risk score, and QOL were assessed before and after 12 weeks. The change in peak aerobic capacity (EST: 2.6 ± 3.1 vs. UC: -0.5 ± 2.5 mL/(kg·min)), cardiac output (EST: 1.7 ± 2.6 vs. UC: -0.01 ± 0.8 L/min), leg press (EST: 48.7 ± 34.1 vs. UC: -10.5 ± 37.7 kg) and leg extension strength (EST: 9.5 ± 10.3 vs. UC: 0.65 ± 5.5 kg) improved significantly after EST compared with UC. The overall change in QOL improved significantly after 12 weeks of EST compared with UC. No significant difference was found between groups for lean body mass, arterial compliance, 24-h blood pressure or CVD risk score. Supervised EST is an effective intervention to improve peak exercise aerobic capacity and cardiac output, muscle strength and QOL in clinically stable RTR.

We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean ± SE; age: 53 ± 3 years; years posttransplant: 6 ± 4) and five age- and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (V̇o2p), heart rate (HR), stroke volume (SV), cardiac output (Q̇), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve V̇o2p, Q̇, and systemic arterial-venous oxygen difference (a-vO2diff) were 23–52% lower ( P < 0.05) in HTR. The reduced Q̇ and a-vO2diff reserves were associated with lower HR and HHb reserves, respectively. The phase II V̇o2p time delay was greater (HTR: 38 ± 2 vs. CON: 25 ± 1 s, P < 0.05), while time constants for phase II V̇o2p (HTR: 54 ± 8 vs. CON: 31 ± 3 s), Q̇ (HTR: 66 ± 8 vs. CON: 28 ± 4 s), and HHb (HTR: 27 ± 5 vs. CON: 13 ± 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 ± 21 s) vs. CON (21 ± 2 s, P < 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 ± 8 s vs. CON 31 ± 6 s). The lower peak V̇o2p and prolonged V̇o2p kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.

Compromised arterial compliance and poor aerobic endurance may partially explain the high incidence of cardiovascular disease in KTR. Interventions demonstrated to improve these parameters may afford substantial clinical benefit in this population.

TOTR and AOTR have abnormal VO2p kinetics, which is secondary to prolonged heart rate kinetics and impaired vascular function in TOTR, but not AOTR.

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