Mettauer 2001 J Am Coll Cardiol

Mettauer B, Zoll J, Sanchez H, Lampert E, Ribera F, Veksler V, Bigard X, Mateo P, Epailly E, Lonsdorfer J, Ventura-Clapier R (2001) Oxidative capacity of skeletal muscle in heart failure patients versus sedentary or active control subjects. J Am Coll Cardiol 38:947-54.

» PMID: 11583863 Open Access

Mettauer B, Zoll J, Sanchez H, Lampert E, Ribera F, Veksler V, Bigard X, Mateo P, Epailly E, Lonsdorfer J, Ventura-Clapier R (2001) J Am Coll Cardiol

Abstract: OBJECTIVES: We investigated the in situ properties of muscle mitochondria using the skinned fiber technique in patients with chronic heart failure (CHF) and sedentary (SED) and more active (ACT) controls to determine: 1) whether respiration of muscle tissue in the SED and ACT groups correlates with peak oxygen consumption (pVO(2)), 2) whether it is altered in CHF, and 3) whether this results from deconditioning or CHF-specific myopathy.

BACKGROUND: Skeletal muscle oxidative capacity is thought to partly determine the exercise capacity in humans and its decrease to participate in exercise limitation in CHF.

METHODS: M. Vastus lateralis biopsies were obtained from 11 SED group members, 10 ACT group members and 15 patients with CHF at the time of transplantation, saponine-skinned and placed in an oxygraphic chamber to measure basal and maximal adenosine diphosphate (ADP)-stimulated (V(max)) respiration rates and to assess mitochondrial regulation by ADP. All patients received angiotensin-converting enzyme (ACE) inhibitors.

RESULTS: The pVO(2) differed in the order CHF < SED < ACT. Compared with SED, muscle alterations in CHF appeared as decreased citrate synthase, creatine kinase and lactate dehydrogenase, whereas the myosin heavy chain profile remained unchanged. However, muscle oxidative capacity (V(max), CHF: 3.53 +/- 0.38; SED: 3.17 +/- 0.48; ACT: 7.47 +/- 0.73, micromol O(2).min(-1).g(-1)dw, p < 0.001 vs. CHF and SED) and regulation were identical in patients in the CHF and SED groups, differing in the ACT group only. In patients with CHF, the correlation between pVO(2) and muscle oxidative capacity observed in controls was displaced toward lower pVO(2) values.

CONCLUSIONS: In these patients, the disease-specific muscle metabolic impairments derive mostly from extramitochondrial mechanisms that disrupt the normal symmorphosis relations. The possible roles of ACE inhibitors and level of activity are discussed.

• Bioblast editor: Gnaiger E

MitoEAGLE V_O2max/BME database

• Human vastus lateralis
• 2 females & 8 males
• 46.9 years
• Active
• H = 1.72 m
• M = 71.5 kg
• BME = 0.20
• BMI = 24.2 kg·m^-2
• V_O2max/M = 46.2 mL·min^-1·kg^-1 (= V_O2peak/BM/0.93)
• Permeabilized muscle fibres; 22 °C; GM_P; m_d; conversions: Gnaiger 2009 Int J Biochem Cell Biol
• J_O2,P(NS) = 137.8 µmol·s^-1·kg^-1 wet muscle mass (37 °C)

• J_O2,P(GM) = 100.6 µmol·s^-1·kg^-1 wet muscle mass (37 °C)
• J_O2,P(NS) = J_O2,P(GM)/0.73
• Fiber wet mass to dry mass ratio = 3.5 (N'Guessan 2004 Mol Cell Biochem)

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• Human vastus lateralis
• 1 female & 10 males
• 51.2 years
• Sedentary
• H = 1.76 m
• M = 87.2 kg
• BME = 0.37
• BMI = 28.2 kg·m^-2
• V_O2max/M = 29.4 mL·min^-1·kg^-1 (= V_O2peak/M/0.93)
• Permeabilized muscle fibres; 22 °C; GM_P; m_d; conversions: Gnaiger 2009 Int J Biochem Cell Biol
• J_O2,P(NS) = 58.5 µmol·s^-1·kg^-1 wet muscle mass (37 °C)

• J_O2,P(GM) = 42.7 µmol·s^-1·kg^-1 wet muscle mass (37 °C)
• J_O2,P(NS) = J_O2,P(GM)/0.73
• Fiber wet mass to dry mass ratio = 3.5 (N'Guessan 2004 Mol Cell Biochem)

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References: BME and VO2max

» VO2max

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Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Cardiovascular 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Intact organism, Permeabilized tissue 

Coupling state: LEAK, OXPHOS  Pathway: N 

MitoEAGLE BME, BMI, VO2max, BME