Using sucrose-sweetened diet as a control, increased weight gain with the ingestion of NNS was observed. However, using a nonsweetened control, neither increased caloric intake nor weight gain occurred with NNS intake. Alternating diets between NNS, NS, and control did not affect the appetite.

Studies using nuclear magnetic resonance have shown that undernutrition affects muscle performance and energetics. It is unclear to what extent underfeeding and refeeding influence the availability of muscle glycogen, net glycogenolysis, skeletal muscle wasting, and recovery. We hypothesized that muscle performance is independent of muscle size and weight, is specific to muscle type, and is unrelated to muscle glycogen concentrations. Slow- and fast-twitch muscles were studied in three groups of adult male Wistar rats: well-fed controls, hypoenergetically fed (Hypo) rats, and rats refed for 4 d after the hypoenergetic diet. Glycogen concentrations and net glycogenolysis; serum glucose, insulin, and protein concentrations; and muscle weight, protein, and cross-sectional area were studied relative to the performance of both types of muscles. Our study controlled for muscle size, weight, and type and electrolyte-micronutrient deficiency. Undernutrition affected muscle performance in five ways. First, compared with controls, fatigue increased only in the soleus muscles of Hypo rats yet the maximal relaxation rate (MRR) decreased in both the soleus and extensor digitorum longus (EDL) muscles. Second, muscle glycogen concentrations did not significantly correlate with fatigue in either the soleus or the EDL although net glycogenolysis was significantly correlated with fatigue in the soleus (r = -0.64; P > 0.01 < 0.05). Third, lower glycogen concentrations did not hinder net glycogenolysis in the EDL of Hypo rats or the soleus of refed rats. Fourth, muscle weight, size, and protein were dissociated from function. Fifth, refeeding did not restore muscle endurance; however, the MRR of the soleus normalized. In conclusion, glycogen values and muscle performance did not correlate but net glycogenolysis correlated with fatigue in the soleus. Also, there was a dissociation between muscle weight, size, and protein and muscle function during hypoenergetic feeding and refeeding.

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Muscle glycogen concentrations in underfed (HYPO) and refed rats (RE) in an earlier study did not correlate with fatigue. We hypothesized that underfeeding slowed glycolysis in the slow-twitch soleus, but not in the fast-twitch extensor digitorum longus (EDL). Thirty adult male Wistar rats were randomly assigned to receive one of two isovolemic and micronutrient-complete liquid diets, a control (CN) energy-complete diet for 10 d or a diet 80% lower in energy (HYPO) for 7 d producing a 20% loss of initial weight. Rats were refed an energy-complete diet for 1 or 4 d (RE1, RE4). Rats were then anesthetized, and the soleus and EDL muscles of the hindlimbs were isolated and electrically stimulated in situ. The pre- and postfatigued muscles were freeze-clamped, lyophilized and stored at -70 degreesC until assayed for specific glycolytic and Krebs cycle metabolites. The HYPO diet caused significantly slower glycolysis in the stimulated soleus but not the EDL compared with the CN diet as supported by the following: 1) a lower fructose-1,6-bisphosphate (F-1,6-P2)/fructose-6-phosphate (F-6-P) ratio; 2) a greater glucose-6-phosphate (G-6-P)/lactate ratio; 3) a lower lactate/glycogen ratio; and 4) lower lactate concentration. Four days of refeeding normalized the F-1,6-P2/F-6-P ratio, but did not improve the lactate/glycogen or the G-6-P/lactate ratios. We conclude that undernutrition compromises glycolysis only in slow-twitch muscles and that 4 d of refeeding restores phosphofructokinase activity.