The mobilization and activation of natural killer (NK) cells have been proposed as key mechanisms promoting anti oncogenic effects of physical exercise. Although mouse models have proven that physical exercise recruits NK cells to tumor tissue and inhibits tumor growth, this preclinical finding has not been transferred to the clinical setting yet. In this first-in-human study, we found that physical exercise mobilizes and redistributes NK cells, especially those with a cytotoxic phenotype, in line with preclinical models. However, physical exercise did not increase NK cell tumor infiltrates. Future studies should carefully distinguish between acute and chronic exercise modalities and should be encouraged to investigate more immune responsive tumor entities.

The kynurenine (KYN) pathway gains growing research interest concerning the genesis, progression and therapy of solid tumors. Previous studies showed exercise-induced effects on metabolite levels along the KYN pathway. Modulations of the KYN pathway might be involved in the positive impact of exercise on prostate cancer progression and mortality. The objective of this trial was to investigate whether a single-physical exercise alters tryptophan (TRP) metabolism and related inflammatory markers in this population. We conducted a randomized controlled trial with 24 patients suffering from prostate cancer. While the control group remained inactive, the intervention group performed a 30-min aerobic exercise on a bicycle ergometer at 75% of individual VO2peak. Before (t0) and directly after the exercise intervention (t1) KYN, TRP, kynurenic acid, quinolinic acid as well as various inflammation markers (IL6, TNF-α, TGF-β) were measured in blood serum. At baseline, the present sample showed robust correlations between TRP, KYN, quinolinic acid and inflammatory markers. Regarding the exercise intervention, interaction effects for TRP, the KYN/TRP ratio and TGF-β were observed. The results show for the first time that acute physical exercise impacts TRP metabolism in prostate cancer patients. Moreover, baseline associations underline the relationship between inflammation and the KYN pathway in prostate cancer.

Avoiding suture tension in peripheral nerve coaptation seems to be a clinical dogma since 30 years, although experimental data are weak and clinical practice shows good functional outcome after peripheral nerve repair by direct coaptation under "reasonable" tension, defined by local anatomic feasibility and the use of specific suture material. In this article, we focus on the microsurgical technique of nerve stump coaptation and the distribution of tension through epineural sutures with various suture materials; we also analyze the impact on the different nerve tissue layers, the limit of this approach and its combination with other tissue releasing techniques like paraneurolysis, adjacent joint flexion, or bone shortening.

Purpose of reviewThe purpose of this narrative review is to give an overview about the effects of multimodal prehabilitation and current existing and prospectively planned studies. The potential efficacy of exercise in the context of prehabilitation ranges from preoperatively improving patients’ functional capacity to inducing cellular mechanisms that affect organ perfusion via endothelial regeneration, anti-inflammatory processes and tumour defense.Recent findingsCurrent studies show that prehabilitation is capable of reducing certain postoperative complications and length of hospital stay in certain patient populations. These findings are based on small to mid-size trials with large heterogeneity, lacking generalizability and evidence that prehabilitation has positive effects on long term survival.SummaryThe concept of prehabilitation contains the features, namely preoperative exercise, nutritional intervention and psychological support. Preoperative exercise holds potential molecular effects that can be utilized in the perioperative period in order to improve patients’ postoperative outcome. Future multimodal prehabilitation trials must specifically clarify the clinical impact of this concept on patients’ quality of life after major cancer surgery and cancer-specific survival.

The mobilization and activation of natural killer (NK) cells have been proposed as key mechanisms promoting anti oncogenic effects of physical exercise. Although mouse models have proven that physical exercise recruits NK cells to tumor tissue and inhibits tumor growth, this preclinical finding has not been transferred to the clinical setting yet. In this first-in-human study, we found that physical exercise mobilizes and redistributes NK cells, especially those with a cytotoxic phenotype, in line with preclinical models. However, physical exercise did not increase NK cell tumor infiltrates. Future studies should carefully distinguish between acute and chronic exercise modalities and should be encouraged to investigate more immune responsive tumor entities.