Positive energy balance is associated with accelerated muscle atrophy and increased erythrocyte glutathione turnover during 5 wk of bed rest.
BACKGROUND
Physical inactivity is often associated with positive energy balance and fat gain.


OBJECTIVE
We aimed to assess whether energy intake in excess of requirement activates systemic inflammation and antioxidant defenses and accelerates muscle atrophy induced by inactivity.


METHODS
Nineteen healthy male volunteers were studied before and at the end of 5 wk of bed rest. Subjects were allowed to spontaneously adapt to decreased energy requirement (study A, n = 10) or were provided with an activity-matched diet (study B, n = 9). Groups with higher (HEB) or lower (LEB) energy balance were identified according to median values of inactivity-induced changes in fat mass (DeltaFM, assessed by bioelectrical impedance analysis).


RESULTS
In pooled subjects (n = 19; median DeltaFM: 1.4 kg), bed rest-mediated decreases in fat-free mass (bioelectrical impedance analysis) and vastus lateralis thickness (ultrasound imaging) were significantly greater (P < 0.03) in HEB(AB) (-3.8 +/- 0.4 kg and -0.32 +/- 0.04 cm, respectively) than in LEB(AB) (-2.3 +/- 0.5 kg and -0.09 +/- 0.04 cm, respectively) subjects. In study A (median DeltaFM: 1.8 kg), bed rest-mediated increases in plasma leptin, C-reactive protein, and myeloperoxidase were greater (P < 0.04) in HEB(A) than in LEB(A) subjects. Bed rest-mediated changes of glutathione synthesis rate in eythrocytes (l-[3,3-(2)H(2)]cysteine incorporation) were greater (P = 0.03) in HEB(A) (from 70 +/- 19 to 164 +/- 29%/d) than in LEB(A) (from 103 +/- 23 to 84 +/- 27%/d) subjects.


CONCLUSIONS
Positive energy balance during inactivity is associated with greater muscle atrophy and with activation of systemic inflammation and of antioxidant defenses. Optimizing caloric intake may be a useful strategy for mitigating muscle loss during period of chronic inactivity.
Department of Clinical, Morphological and Technological Sciences, Division of Internal Medicine, and the Department of Mathematics and Informatics, University of Udine, Udine, Italy. biolo@units.it
Gianni
G
Biolo
Francesco
F
Agostini
Bostjan
B
Simunic
Mariella
M
Sturma
Lucio
L
Torelli
Jean Charles
JC
Preiser
Ginette
G
Deby-Dupont
Paolo
P
Magni
Felice
F
Strollo
Pietro
P
di Prampero
Gianfranco
G
Guarnieri
Igor B
IB
Mekjavic
Rado
R
Pisot
Marco V
MV
Narici
D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D001510:Bed Rest / Q000009:adverse effects; D015415:Biomarkers; D001823:Body Composition / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D017097:Electric Impedance; D002149:Energy Intake / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D004912:Erythrocytes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000453:epidemiology; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000502:physiology; D008297:Male; D009133:Muscular Atrophy / Q000453:epidemiology / Q000378:metabolism*; D009751:Nutritional Requirements; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D012307:Risk Factors; D015430:Weight Gain / Q000502:physiology
D015415:Biomarkers; D020738:Leptin; D002097:C-Reactive Protein; D005978:Glutathione