Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure

Donna M. Mancini, Glenn Walter, Nathaniel Reichek, Robert Lenkinski, Kevin K. McCully, James L. Mullen, John R. Wilson

Research output: Contribution to journalArticle

585 Citations (Scopus)

Abstract

Background. The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF). Methods and Results. Peak V̇o2, percent ideal body weight (% IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68% of patients, as evidenced by a decrease in Cr-to-height ratio of <7.4 mg/cm and/or upper arm circumference of <5% of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675±84 cm3/m2; HF, 567±112 cm3/m2; p<0.05). Fat stores were largely perserved with triceps skinfold of <5% of normal and/or IBW of <80% in only 8% of patients. Modest linear correlations were observed between peak V̇o2 and both calf muscle volume per meter squared (r=0.48) and midarm muscle area (r=0.36) (both p<0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r=-0.42, p<0.05). Conclusions. These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.

Original languageEnglish (US)
Pages (from-to)1364-1373
Number of pages10
JournalCirculation
Volume85
Issue number4
StatePublished - Apr 1992

Fingerprint

Muscular Atrophy
Skeletal Muscle
Heart Failure
Exercise
Muscles
Creatinine
Ideal Body Weight
Calcaneus
Patella
Phosphocreatine
Phosphorus
Atrophy
Arm
Magnetic Resonance Spectroscopy
Fats
Magnetic Resonance Imaging
Urine

Keywords

  • Exercise testing
  • Heart failure
  • Skeletal muscle

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Mancini, D. M., Walter, G., Reichek, N., Lenkinski, R., McCully, K. K., Mullen, J. L., & Wilson, J. R. (1992). Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation, 85(4), 1364-1373.

Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. / Mancini, Donna M.; Walter, Glenn; Reichek, Nathaniel; Lenkinski, Robert; McCully, Kevin K.; Mullen, James L.; Wilson, John R.

In: Circulation, Vol. 85, No. 4, 04.1992, p. 1364-1373.

Research output: Contribution to journalArticle

Mancini, DM, Walter, G, Reichek, N, Lenkinski, R, McCully, KK, Mullen, JL & Wilson, JR 1992, 'Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure', Circulation, vol. 85, no. 4, pp. 1364-1373.
Mancini DM, Walter G, Reichek N, Lenkinski R, McCully KK, Mullen JL et al. Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation. 1992 Apr;85(4):1364-1373.
Mancini, Donna M. ; Walter, Glenn ; Reichek, Nathaniel ; Lenkinski, Robert ; McCully, Kevin K. ; Mullen, James L. ; Wilson, John R. / Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. In: Circulation. 1992 ; Vol. 85, No. 4. pp. 1364-1373.
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abstract = "Background. The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF). Methods and Results. Peak V̇o2, percent ideal body weight ({\%} IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68{\%} of patients, as evidenced by a decrease in Cr-to-height ratio of <7.4 mg/cm and/or upper arm circumference of <5{\%} of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675±84 cm3/m2; HF, 567±112 cm3/m2; p<0.05). Fat stores were largely perserved with triceps skinfold of <5{\%} of normal and/or IBW of <80{\%} in only 8{\%} of patients. Modest linear correlations were observed between peak V̇o2 and both calf muscle volume per meter squared (r=0.48) and midarm muscle area (r=0.36) (both p<0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r=-0.42, p<0.05). Conclusions. These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.",
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N2 - Background. The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF). Methods and Results. Peak V̇o2, percent ideal body weight (% IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68% of patients, as evidenced by a decrease in Cr-to-height ratio of <7.4 mg/cm and/or upper arm circumference of <5% of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675±84 cm3/m2; HF, 567±112 cm3/m2; p<0.05). Fat stores were largely perserved with triceps skinfold of <5% of normal and/or IBW of <80% in only 8% of patients. Modest linear correlations were observed between peak V̇o2 and both calf muscle volume per meter squared (r=0.48) and midarm muscle area (r=0.36) (both p<0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r=-0.42, p<0.05). Conclusions. These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.

AB - Background. The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF). Methods and Results. Peak V̇o2, percent ideal body weight (% IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68% of patients, as evidenced by a decrease in Cr-to-height ratio of <7.4 mg/cm and/or upper arm circumference of <5% of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675±84 cm3/m2; HF, 567±112 cm3/m2; p<0.05). Fat stores were largely perserved with triceps skinfold of <5% of normal and/or IBW of <80% in only 8% of patients. Modest linear correlations were observed between peak V̇o2 and both calf muscle volume per meter squared (r=0.48) and midarm muscle area (r=0.36) (both p<0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r=-0.42, p<0.05). Conclusions. These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.

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