Principles of postoperative anterior cruciate ligament rehabilitation

It is known that anterior cruciate ligament(ACL) reconstruction needs to be combined with detailed postoperative rehabilitation in order for patients to return to their pre-injury activity levels, and that the rehabilitation process is as important as the reconstruction surgery. Literature studies focus on how early in the postoperative ACL rehabilitation period rehabilitation modalities can be initiated. Despite the sheer number of studies on this topic, postoperative ACL rehabilitation protocols have not been standardized yet. Could common, "ossified" knowledge or modalities really prove themselves in the literature? Could questions such as "is postoperative brace use really necessary?", "what are the benefits of early restoration of the range of motion(ROM)?", "to what extent is neuromuscular electrical stimulation(NMES) effective in the protection from muscular atrophy?", "how early can proprioception training and open chain exercises begin?", "should strengthening training start in the immediate postoperative period?" be answered for sure? My aim is to review postoperative brace use, early ROM restoration, NMES, proprioception, open/closed chain exercises and early strengthening, which are common modalities in the very comprehensive theme of postoperative ACLrehabilitation, on the basis of several studies(Level of Evidence 1 and 2) and to present the commonly accepted ways they are presently used. Moreover, I have presented the objectives of postoperative ACL rehabilitation in tables and recent miscellaneous studies in the last chapter of the paper.

Neuromuscular,biomechanical,and energetic adjustments following repeated bouts of downhill running

Purpose This study used downhill running as a model to investigate the repeated bout effect(RBE)on neuromuscular performance,running biomechanics,and metabolic cost of running.Methods Ten healthy recreational male runners performed two 30-min bouts of downhill running(DR1 and DR2)at a-20%slope and 2.8 m/s 3 weeks apart.Neuromuscular fatigue,level running biomechanics during slow and fast running,and running economy parameters were recorded immediately before and after the downhill bouts,and at 24 h,48 h,72 h,96 h,and 168 h thereafter(i.e.,follow-up days).Results An RBE was confirmed by attenuated muscle soreness and serum creatine kinase rise after DR2 compared to DR1.An RBE was also observed in maximum voluntary contraction(MVC)force loss and voluntary activation where DR2 resulted in attenuated MVC force loss and voluntary activation immediately after the run and during follow-up days.The downhill running protocol significantly influenced level running biomechanics;an RBE was observed in which center of mass excursion and,therefore,lower-extremity compliance were greater during follow-up days after DR1 compared to DR2.The observed changes in level running biomechanics did not influence the energy cost of running.Conclusion This study demonstrated evidence of adaptation in neural drive as well as biomechanical changes with the RBE after DR.The higher neural drive resulted in attenuated MVC force loss after the second bout.It can be concluded that the RBE after downhill running manifests as changes to global and central fatigue parameters and running biomechanics without substantially altering the energy cost of running.

The Role of Autophagy Regulator HMGB1 in Skeletal Muscle Autophagy After Eccentric Exercise

High mobility group box-1 protein(HMGB1)is an evolutionarily ancient protein,which,as an important non-histone chromosome-binding protein in organism cells,is involved in a variety of important biological processes,including DNA repair,gene transcription,cellular inflammatory response,and autophagy.In this study,we established an eccentric exercise model to observe the effect of HMGB1 on skeletal muscle autophagy and to investigate the underlying molecular mechanisms.Forty-eight male 8-week-old SD rats were randomly divided into control group(C)and exercise group(E).Group E was subjected to a bout of eccentric exercise on a treadmill and sampled soleus at 0 h,12 h,24 h,48 h,and 72 h post-exercise.The speed of the exercise protocol in this study was 16 m/min,the slope was−16°,and the time was 90 min.The ultrastructural changes of skeletal muscle were observed by transmission electron microscopy.The protein expressions of HMGB1,Beclin1,and LC3 were detected by Western Blot.The co-localizations of Beclin1/Bcl-2,Beclin1/HMGB1,and Beclin1/Vps34 were measured by immunofluorescence.The results show that eccentric exercise leads to abnormal changes in the ultrastructure of skeletal muscle,and the protein levels of Beclin1,LC3-II/LC3-I,and the content of HMGB1 in nuclear and cytoplasm were significantly increased at 24 h post-exercise(P<0.05).The co-localization of Beclin1/Bcl-2 and Beclin1/HMGB1 were increased significantly at 0 h post-exercise and then decreased,while the co-localization of Beclin1/Vps34 showed the highest level at 24 h post-exercise.In conclusion,HMGB1 facilitates the separation of Beclin1 from Bcl-2 and promotes Beclin1 binding to Vps34,which may play an important role in eccentric exercise-induced skeletal muscle autophagy.

Response of macrophages in rat skeletal muscle after eccentric exercise

Purpose： Macrophages are known to be important for healing numerous injured tissues depending on their functional phenotypes in response to different stimuli. The objective of this study was to reveal macrophage phenotypic changes involved in exercise-induced skeletal muscle injury and regeneration. Methods： Adult male Sprague-Dawley rats experienced one session of downhill running （16~ decline, 16 m/min） for 90 min. After exercise the blood and soleus muscles were collected at 0 h, 6 h, 12 h, 1 d, 2 d, 3 d, 1 w and 2 w after exercise, separately. Results： It was showed that CD6B＋ M1 macrophages mainly infiltrated into musc｜e necrotic sites at 1-3 d, while CD163＋ M2 macrophages were present in muscles from 0 h to 2 weeks after exercise. Using transmission electron microscopy, we observed activated satellite cells 1 d after exercise. Thl-associated transcripts of iNOS and Cc12 were inhibited post exercise, while COX-2 mRNA was dramatically increased 12 h after running （p 〈 0.01 ）. M2 phenotype marker Arg-1 increased 12 h and 3 d （p 〈 0.05, p 〈 0.01 ） after exercise, and Clecl0a and Mrc2 were up-regulated in muscles 12 h following exercise （p 〈 0.05, p 〈 0.05）. Conclusion： The data demonstrate the dynamic patterns of macrophage phenotype in skeletal muscle upon eccentric exercise stimuli, and M1 and M2 phenotypes perform different functions during exercise- induced skeletal muscle injury and recovery.