A B S T R A C T Muscle glycogen stores are depleted during exercise and are rapidly repleted during the recovery period. To investigate the mechanism for this phenomenon, untrained male rats were run for 45 min on a motor-driven treadmill and the ability of their muscles to utilize glucose was then assessed during perfusion of their isolated hindquarters. Glucose utilization by the hindquarter was the same in exercised and control rats perfused in the absence of added insulin; however, when insulin (30-40,000 MU/ml) was added to the perfusate, glucose utilization was greater after exercise. Prior exercise lowered both, the concentration of insulin that half-maximally stimulated glucose utilization (exercise, 150 ,U/ml; control, 480 ,gU/ml) and modestly increased its maximum effect.The increase in insulin sensitivity persisted for 4 h following exercise, but was not present after 24 h. The rate-limiting step in glucose utilization enhanced by prior exercise appeared to be glucose transport across the cell membrane, as in neither control nor exercised rats did free glucose accumulate in the muscle cell.Following exercise, the ability of insulin to stimulate the release of lactate into the perfusate was unaltered; however its ability to stimulate the incorporation of ['4C]glucose into glycogen in certain muscles was enhanced. Thus at a concentration of 75 AU/ml insulin stimulated glycogen synthesis eightfold more in the fast-twitch red fibers of the red gastrocnemius than it did in the same muscle of nonexercised rats. In contrast, insulin only minimally increased glycogen synthesis in the fast-twitch white fibers of the gastrocnemius, which were not glycogen-depleted. The uptake of 2-deoxyglucose by these muscles followed a similar pattern suggesting that glucose transport was also differentially enhanced. Prior exercise did not enhance

The use of conventional dental implants for orthodontic anchorage is limited by their large size. The purpose of this study was to quantify the histomorphometric properties of the bone-implant interface to analyze the use of small titanium screws as an orthodontic anchorage and to establish an adequate healing period. Overall, successful rigid osseous fixation was achieved by 97% of the 96 implants placed in 8 dogs and 100% of the elastomeric chain-loaded implants. All of the loaded implants remained integrated. Mandibular implants had significantly higher bone-implant contact than maxillary implants. Within each arch, the significant histomorphometric indices noted for the "three-week unloaded" healing group were: increased labeling incidence, higher woven-to-lamellar-bone ratio, and increased osseous contact. Analysis of these data indicates that small titanium screws were able to function as rigid osseous anchorage against orthodontic load for 3 months with a minimal (under 3 weeks) healing period.

Studies in the rat suggest that after voluntary exercise there are two phases of glycogen repletion in skeletal muscle (preceding study). In phase I glucose utilization and glycogen synthesis are enhanced both in the presence and absence of insulin, whereas in phase II only the increase in the presence of insulin is found. To determine whether these alterations and in particular those mediated by insulin are due to local or systemic factors, one hindlimb of an anesthetized rat was electrically stimulated, and both hindlimbs were perfused immediately thereafter. Glucose and glycogen metabolism in the stimulated leg closely mimicked that observed previously after voluntary exercise on a treadmill. With no insulin added to the perfusate, glucose incorporation into glycogen was markedly enhanced in muscles that were glycogen depleted as were the uptake of 2-deoxyglucose and 3-O-methylglucose. Likewise, the stimulation of these processes by insulin was enhanced and continued to be so 2 h later when the muscles of the stimulated leg had substantially repleted their glycogen stores. The results suggest that the increases in insulin-mediated glucose utilization and glycogen synthesis in muscle after exercise are modulated by local contraction-induced factors.