School of Sport, Exercise and Nutrition, Massey University, Auckland, New Zealand.
Sports Performance Research Institute New Zealand (SPRINZ), Auckland University of Technology, Auckland, New Zealand.
Exp Physiol. 2023 May;108(5):706-714. doi: 10.1113/EP090729. Epub 2023 Feb 26.
What is the central question of this study? Does a ketogenic diet (KD) modulate circulating counts of natural killer (NK) cells, including CD56 and CD56 subsets, and their ability to activate (CD69 expression) following in vitro antigen stimulation in response to exhaustive moderate-intensity exercise? What is the main finding and its importance? The KD amplified the biphasic exercise-induced NK cell response due to a greater mobilisation of the cytotoxic CD56 subset but did not alter NK cell CD69 expression. The KD appears to modulate exercise-induced circulating NK cell mobilisation and egress, but not antigen-stimulated circulating NK cell activation.
We investigated the effect of a 31-day ketogenic diet (KD) compared with a habitual, carbohydrate (CHO)-based diet on total circulating natural killer (NK) CD3 CD56 , dim and bright subset count, and antigen-stimulated CD3 CD56 cell activation (CD69 ) in response to exhaustive running. In a randomised, repeated-measures, cross-over study, eight trained, male endurance athletes ingested a 31-day low-CHO KD or their habitual diet (HD). On day 31, participants ran to exhaustion at 70% (∼3.5-4 h, ∼45-50 km). A low-CHO (<10 g) meal was ingested prior to the KD trial, with fat ingested during exercise. A high-CHO (2 g kg ) meal was ingested prior to the HD trial, with CHO (∼55 g h ) ingested during exercise. Venous blood samples were collected at pre-exercise, post-exercise and 1 h post-exercise. The KD amplified the classical exercise-induced biphasic CD3 CD56 cell response by increasing the post-exercise counts (P = 0.0004), which appeared to be underpinned by the cytotoxic CD3 CD56 subset (main effect of time point, P < 0.0001). The KD had no effect on NK cells' expression of CD69 or their geometric mean fluorescence intensity of CD69 expression, either for unstimulated or for antigen-stimulated NK cells (all P > 0.05). In conclusion, adaptation to a KD may alter the number of circulating NK cells but not their ability to activate to an antigenic challenge.
本研究的核心问题是什么?生酮饮食(KD)是否会调节自然杀伤(NK)细胞的循环计数,包括 CD56 和 CD56 亚群,以及它们在体外抗原刺激后对剧烈中等强度运动的反应中激活(CD69 表达)的能力?主要发现及其重要性是什么?KD 通过更大程度地动员细胞毒性 CD56 亚群,放大了双相运动诱导的 NK 细胞反应,但不会改变 NK 细胞 CD69 的表达。KD 似乎调节运动诱导的循环 NK 细胞动员和迁出,但不调节抗原刺激的循环 NK 细胞激活。
我们研究了与习惯性碳水化合物(CHO)饮食相比,31 天的生酮饮食(KD)对耗尽性跑步后总循环自然杀伤(NK)CD3 CD56 、dim 和 bright 亚群计数以及抗原刺激的 NK CD3 CD56 细胞激活(CD69)的影响。在一项随机、重复测量、交叉研究中,8 名训练有素的男性耐力运动员摄入 31 天的低 CHO KD 或他们的习惯性饮食(HD)。第 31 天,参与者以 70%的速度(约 3.5-4 小时,约 45-50 公里)耗尽性跑步。在 KD 试验前摄入低 CHO(<10g)餐,在运动期间摄入脂肪。在 HD 试验前摄入高 CHO(2g kg)餐,在运动期间摄入 CHO(约 55g h)。在运动前、运动后和运动后 1 小时采集静脉血样。KD 通过增加运动后的计数(P=0.0004)放大了经典的运动诱导的双相 CD3 CD56 细胞反应,这似乎是由细胞毒性 CD3 CD56 亚群支撑的(时间点的主要影响,P<0.0001)。KD 对未刺激或抗原刺激的 NK 细胞的 CD69 表达或其 CD69 表达的几何平均荧光强度均无影响(所有 P>0.05)。总之,适应 KD 可能会改变循环 NK 细胞的数量,但不会改变它们对抗原挑战的激活能力。