Exercise capacity in heart failure patients: relative importance of heart and skeletal muscle

Abstract

The knee extensor and the whole-body exercise capacities were measured in 11 chronic heart failure (CHF) patients and 11 healthy age- and sex-matched controls, and were related to ejection fraction and to biochemical and histochemical markers of the musculature. The CHF patients had a 39% lower maximal oxygen uptake measured on an ergometer cycle than the healthy controls (1.54 +/- 0.57 vs. 2.51 +/- 0.70 1 min-1, P < 0.001). The low exercise capacity was markedly related to the ejection fraction (r = 0.77, P < 0.001). The maximal strength of m. quadriceps femoris was 15% lower in the CHF patients than in the controls (P < 0.05). The cross-sectional area (CSA) of m. quadriceps femoris explained 55% (r = 0.74, P < 0.001) of the difference in strength between both groups. The endurance capacity of m. quadriceps femoris was 30% lower in CHF patients than in controls, partly as a result of the 25% lower capillary density (P < 0.05) and the 27% lower aerobic enzyme capacity (P < 0.05), as estimated by the citrate synthase activity, in the CHF patients. The citrate synthase activity correlated with the maximal oxygen uptake (r = 0.61, P < 0.05). Moreover, the ejection fraction, together with the CSA of m. quadriceps femoris, explained 75% (r = 0.86%, P < 0.01) of the difference in maximal oxygen uptake between CHF patients and controls. These results demonstrate that CHF patients have both a lower local and a lower whole-body work capacity than healthy controls. This is a function of a smaller leg muscle mass and a lower capillary density and mitochondrial enzyme capacity in the CHF patients; however, a lowered pump capacity of the heart is the factor which limits the exercise capacity the most.

Heart Failure Affects Mitochondrial but Not Myofibrillar Intrinsic Properties of Skeletal Muscle

“…Many studies, including the close relation between peak V O 2 and mitochondrial enzyme activity or volume, 3,4,28 have pointed out that impaired aerobic metabolism may play a role in the limitation of systemic exercise capacity. The decreased oxidative capacity and altered mitochondrial regulation and energy transfer demonstrated here could be the mechanistic basis for decreased oxygen utilization and exercise capacity in CHF.…”

Skeletal muscle abnormalities and exercise intolerance in older patients with heart failure and preserved ejection fraction

“…HFPEF, heart failure with preserved ejection fraction; HC, healthy age-matched control. have reported that the capillary-to-fiber ratio is also reduced in HFREF patients compared with HC subjects (42,43,58,64,72).…”

“…However, our results are believable given what is known from many reports regarding skeletal muscle fiber composition and capillarity in patients with HFREF and other populations. Specifically, several investigators have reported that HFREF patients have decreased type I fibers compared with HC subjects (12,39,42,45,64,66,67) and that this is related to peak V O 2 (49). Moreover, several investigators Values are means Ϯ SD or numbers of patients/subjects per group (n) with percentages.…”

“…It is known that aging results in alterations in skeletal muscle, including a reduction in the relative number of type II fibers (40) and in capillary density (9), and that these are associated with a decline in physical performance (51). Furthermore, it is well established that patients with HF with reduced ejection fraction (HFREF) have multiple skeletal muscle abnormalities (12,39,42,43,45,58,64,66,72), including a reduced percentage of type I (oxidative) fibers and a decreased number of capillaries per fiber, and that these contribute significantly to their severe exercise intolerance (49,64,65). However, despite the high prevalence of HFPEF and the impact of exercise intolerance as its key chronic symptom, there is no information available regarding skeletal muscle phenotype and its relationship to peak V O 2 in HFPEF.…”

Exercise training in chronic heart failure: improving skeletal muscle O2transport and utilization

“…As mentioned above, the literature is equivocal regarding the effects of CHF on skeletal muscle oxidative metabolism. For instance, some studies report that HFrEF induces significant structural/functional mitochondrial impairments and/or reductions in oxidative enzyme capacity (68,156,197,281,297) that vary as function of disease severity (14,61,65), whereas others do not (90,154,210,274,305,319,340). Recently, impaired skeletal muscle oxidative metabolism has also been reported in HFpEF patients (37) and animal models (43,333).…”