Functional and metabolic early changes in calf muscle occurring during nutritional repletion in malnourished elderly patients.
BACKGROUND
Metabolic alterations in skeletal muscle associated with malnutrition and the potential reversibility of such alterations during refeeding are not fully understood.


OBJECTIVE
We characterized early changes in muscle during refeeding in malnourished, hospitalized elderly subjects.


METHODS
Muscle function, metabolism, and mass were evaluated in 24 clinically stable patients (11 were malnourished) by using isokinetic plantar flexor torque measurements and nuclear magnetic resonance (NMR) imaging for medial gastrocnemius mass assessment and 31P and 13C NMR spectroscopy for inorganic phosphate (Pi), phosphocreatine, and glycogen quantitation.


RESULTS
Malnourished subjects had lower muscle mass (P < 0.02) and tended to have lower strength than did control subjects. In malnourished subjects, muscle strength increased after refeeding (P < 0.01) whereas muscle mass was unchanged. The ratio of Pi to ATP was lower in malnourished than in control subjects (P < 0.001) and increased during refeeding (P < 0.01). The mean ratio of phosphocreatine to ATP was lower in malnourished than in control subjects (P < 0.01) and increased to control values after refeeding. Muscle glycogen showed a scattered distribution for malnourished subjects; the mean value did not differ significantly from that of control subjects, either at baseline or after refeeding.


CONCLUSIONS
The lower ratio of phosphocreatine to ATP in malnourished subjects could have resulted from either lower total muscle creatine or reduced oxidative capacities. High or normal glycogen associated with a low Pi-to-ATP ratio in malnourished subjects suggested preferential use of lipid over carbohydrate for energy supply, which is known to reduce muscle performance. The data suggest that normalization of muscle metabolite content after refeeding improves muscle strength in malnourished subjects.
Département de Gériatrie du Centre Hospitalo-Universitaire de Bordeaux, Hôpital Xavier Arnozan, Centre Hospitalier-Universitaire de Bordeaux, Pessac, France. isabelle.bourdel-marchasson@chu-bordeaux.fr
I
I
Bourdel-Marchasson
P A
PA
Joseph
P
P
Dehail
M
M
Biran
P
P
Faux
M
M
Rainfray
J P
JP
Emeriau
P
P
Canioni
E
E
Thiaudière
D000255:Adenosine Triphosphate / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism / Q000502:physiology*; D002247:Carbon Isotopes; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006760:Hospitalization; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D009748:Nutrition Disorders / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009752:Nutritional Status; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010759:Phosphorus Isotopes
D002247:Carbon Isotopes; D010710:Phosphates; D010759:Phosphorus Isotopes; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006003:Glycogen