耿青青 郝選明

摘要:綜述了評(píng)定運(yùn)動(dòng)員的機(jī)能狀態(tài)的免疫指標(biāo),并從造血細(xì)胞的源頭骨髓探討了應(yīng)激對(duì)骨髓髓系細(xì)胞與淋巴系細(xì)胞前體的影響。今后運(yùn)動(dòng)免疫學(xué)研究應(yīng)注重與延遲性肌肉酸痛癥等研究的免疫學(xué)指標(biāo)的綜合性分析。

關(guān)鍵詞:運(yùn)動(dòng)生物化學(xué);原B細(xì)胞;運(yùn)動(dòng)免疫;大負(fù)荷訓(xùn)練;綜述

中圖分類號(hào):G804.7 文獻(xiàn)標(biāo)識(shí)碼:A文章編號(hào):1006-7116(2009)12-0107-06

Review of the relationship between immunocyte/cytokine and

delayed muscle soreness symptom

GENG Qing-qing,HAO Xuan-ming

(School of Physical Education,South China Normal University,Guangzhou 510006,China)

Abstract: The authors gave an overview of immunological indexes for evaluating athletes functional conditions, and probed into the effects of stress on myeloid lineages and lymphocyte progenitors from the perspective of the source bone marrow of hematopoietic cells. In the study of sports immunology henceforward, we should focus on the comprehensive analysis of immunological indexes for the study of delayed muscle soreness symptom and such.

Key words: sports biochemistry;pro-B cell;sports immunity;heavy load training;overview

大強(qiáng)度運(yùn)動(dòng)訓(xùn)練或比賽可以引起運(yùn)動(dòng)員免疫功能的抑制[1-2]。因此,在訓(xùn)練期間對(duì)運(yùn)動(dòng)員的免疫機(jī)能監(jiān)控顯得極為重要。本文就運(yùn)動(dòng)員的免疫機(jī)能監(jiān)控指標(biāo)、運(yùn)動(dòng)對(duì)骨髓髓系細(xì)胞與淋巴系細(xì)胞前體的影響、延遲性肌肉酸痛癥的免疫介導(dǎo)等作一綜述。

1免疫細(xì)胞

目前,免疫機(jī)能監(jiān)控的常用指標(biāo)是T 淋巴細(xì)胞亞群,但研究發(fā)現(xiàn),這些指標(biāo)對(duì)訓(xùn)練不夠敏感,有的指標(biāo)(如CD4+/CD8+)是否能準(zhǔn)確反映機(jī)體免疫機(jī)能還存在爭(zhēng)議[3-5]。

Rall LC等[6]觀察了12周的遞增負(fù)荷力量訓(xùn)練:以8名類風(fēng)濕性關(guān)節(jié)炎患者、8名健康青年、8名健康年長(zhǎng)者為受試組,6名無訓(xùn)練的老人做安靜對(duì)照組。受試者以80%的個(gè)體最大運(yùn)動(dòng)量運(yùn)動(dòng),每周2次,每次3組,每組重復(fù)8次。結(jié)果,與安靜對(duì)照組相比,運(yùn)動(dòng)的3組受試者外周血單核細(xì)胞、淋巴細(xì)胞增殖反應(yīng)、DTH(遲發(fā)型超敏反應(yīng))均無明顯變化。

Buyukyazi G等[7]比較了大強(qiáng)度、長(zhǎng)時(shí)間訓(xùn)練的11名競(jìng)技運(yùn)動(dòng)員以及進(jìn)行中等強(qiáng)度長(zhǎng)時(shí)間訓(xùn)練的11名業(yè)余運(yùn)動(dòng)員(訓(xùn)練年限均大于10年),11名靜坐男性為對(duì)照組。結(jié)果顯示:3組人的總T淋巴細(xì)胞(CD3+)、輔助性T淋巴細(xì)胞(CD4+)、抑制殺傷性T細(xì)胞(CD8+)、NK、CD4+/CD8+、CD19+細(xì)胞、HLA-DR+活化TXB均無顯著性差異,作者對(duì)大強(qiáng)度訓(xùn)練導(dǎo)致的免疫抑制提出質(zhì)疑。

一般情況下,運(yùn)動(dòng)員如果出現(xiàn)免疫功能低下,可表現(xiàn)為WBC、NK細(xì)胞、T細(xì)胞總數(shù)、CD4+/CD8+等下降[8]?；蛘哒f,隨著運(yùn)動(dòng)員訓(xùn)練負(fù)荷加大及訓(xùn)練時(shí)間延長(zhǎng),總T淋巴細(xì)胞(CD3+)、輔助性T淋巴細(xì)胞(CD4+)及CD4+/CD8+應(yīng)當(dāng)出現(xiàn)下降,細(xì)胞毒性T細(xì)胞(CD8+)應(yīng)增加。

免疫指標(biāo)的變化往往沒有或沒有完全遵循上述規(guī)律,說明訓(xùn)練中上述免疫細(xì)胞的變化具有階段性的特點(diǎn),不同的測(cè)量點(diǎn)可能出現(xiàn)不同的變化趨勢(shì),這可能是造成以往的研究結(jié)果不一致或相互矛盾的原因之一。因此,在研究中應(yīng)當(dāng)重視縱向的觀察和測(cè)量點(diǎn)的密度。

對(duì)B系淋巴細(xì)胞前體的研究發(fā)現(xiàn)[9-11],為了模仿應(yīng)激下產(chǎn)生的同濃度的GC[12-14],片劑的CS皮下植入雄性小鼠(實(shí)驗(yàn)組) 36 h內(nèi)血液中產(chǎn)生CS為60~95 μg/ dL,而在對(duì)照組CS值為5~15 μg /dL。24 h,實(shí)驗(yàn)組CS對(duì)早期原B細(xì)胞、前B細(xì)胞和不成熟B細(xì)胞造成30%~70%的缺失。36 h,前B細(xì)胞,幾乎消失;幸存的循環(huán)原B細(xì)胞和前B細(xì)胞減少了70%~80%。最早的B細(xì)胞、前祖B細(xì)胞,對(duì)于CS 顯示了相當(dāng)大的耐受力,36 h僅減少20%。36 h,實(shí)驗(yàn)組骨髓中祖細(xì)胞、紅細(xì)胞系、單核細(xì)胞所占的百分比沒有變化,有核細(xì)胞的數(shù)量也沒有變化,粒系細(xì)胞卻以13%的絕對(duì)細(xì)胞數(shù)量增加。推斷應(yīng)激下GC對(duì)淋巴細(xì)胞前體的影響可能是通過糖皮質(zhì)激素受體活性的改變以及基質(zhì)細(xì)胞所產(chǎn)生的細(xì)胞因子等因素造成的。

切除腎上腺的或抗孕酮片處理的小鼠,發(fā)現(xiàn)骨髓B系淋巴細(xì)胞前體有異常的升高。這表明在正常情況下,糖皮質(zhì)激素可能促進(jìn)了淋巴細(xì)胞增殖的穩(wěn)態(tài)調(diào)節(jié)[15]。研究揭示,在用糖皮質(zhì)激素治療中,人類的淋巴細(xì)胞增殖分化的最早期階段是極其敏感的[16]。

筆者認(rèn)為:GC可能對(duì)B系細(xì)胞的增殖存在一個(gè)閾值。紅系、單核系、造血前體祖細(xì)胞雖然只有微小的變化,但各系的分裂效率以及對(duì)合成底物的聚集與利用是否相同等一系列問題值得探究。

對(duì)骨髓造血祖細(xì)胞的細(xì)胞周期的研究發(fā)現(xiàn):在小鼠14 d的胎肝有80%原始B祖細(xì)胞是活躍的,而在成年階段30%是活躍的[17-19]。因此,研究人員認(rèn)為在成年階段淋巴細(xì)胞產(chǎn)生的維持是由處于靜止期的原始祖細(xì)胞間歇性的分裂而促成的。

筆者設(shè)想,應(yīng)激下產(chǎn)生的GS,對(duì)B系細(xì)胞的增殖作用,是否是在GS對(duì)骨髓B細(xì)胞發(fā)生作用的一定閾值內(nèi),由于處于靜止期的原始B祖細(xì)胞(成年骨髓中原始B祖細(xì)胞30%是活躍的)分裂活躍而產(chǎn)生的呢?

最近研究發(fā)現(xiàn)1 h的中等強(qiáng)度運(yùn)動(dòng)中T淋巴細(xì)胞分裂無明顯的變化,但運(yùn)動(dòng)后淋巴細(xì)胞的凋亡率增加,T淋巴細(xì)胞凋亡的增加與其數(shù)量的減少對(duì)應(yīng),說明中等強(qiáng)度運(yùn)動(dòng)對(duì)T淋巴細(xì)胞的增殖分裂影響并不大[20]。以往的研究?jī)A向于認(rèn)為運(yùn)動(dòng)后淋巴細(xì)胞數(shù)量減少主要是因?yàn)門淋巴細(xì)胞增殖能力下降[21-22]。這一結(jié)論是通過絲裂原刺激全淋巴細(xì)胞增殖得出的,但近年來通過磁珠分離技術(shù)去除NK細(xì)胞發(fā)現(xiàn),運(yùn)動(dòng)后絲裂原刺激下的全淋巴細(xì)胞增殖能力下降,但絲裂原刺激下的單純T淋巴細(xì)胞的增殖能力沒有下降[23]。有研究發(fā)現(xiàn),1 h的無氧閾強(qiáng)度運(yùn)動(dòng)對(duì)外周血CD69+ T細(xì)胞并無影響[24]。

總之,單純的CD3+、CD4+、CD8+、CD4+/CD8+還不足以反映免疫機(jī)能的變化。T細(xì)胞是一個(gè)高度不均一的細(xì)胞群,存在功能不同的亞群,輔助性T細(xì)胞(CD4+,主要發(fā)揮輔助和誘導(dǎo)作用)和細(xì)胞毒性T細(xì)胞(CD8+,主要發(fā)揮殺傷和抑制作用)又可按照它們分泌的細(xì)胞因子分為Th1和Th2細(xì)胞亞群,前者可產(chǎn)生IL-2、IFN-γ等,后者可產(chǎn)生IL-4、IL-6等。

2細(xì)胞因子

免疫系統(tǒng)是具有高度復(fù)雜性的系統(tǒng),其內(nèi)部的精細(xì)調(diào)節(jié)大多通過免疫分子來實(shí)現(xiàn)。近年來免疫系統(tǒng)中重要的免疫分子-細(xì)胞因子與運(yùn)動(dòng)的關(guān)系備受重視,但急性實(shí)驗(yàn)研究較多,慢性實(shí)驗(yàn)研究相對(duì)較少,研究結(jié)果也很不一致[25-26]。

久坐不運(yùn)動(dòng)女性,一組進(jìn)行45 min的55% VO2max的中等強(qiáng)度自行車運(yùn)動(dòng),一組進(jìn)行1 h的70% VO2max的大強(qiáng)度自行車運(yùn)動(dòng)。IL-4在中等強(qiáng)度運(yùn)動(dòng)后增加,而大強(qiáng)度運(yùn)動(dòng)后下降;IFN-γ只在大強(qiáng)度運(yùn)動(dòng)后顯著上升;IL-12只在大強(qiáng)度運(yùn)動(dòng)后24 h增加;IL-2在中等強(qiáng)度運(yùn)動(dòng)后下降顯著。提示,抗炎(致炎)因子在中等強(qiáng)度運(yùn)動(dòng)后都有增加趨勢(shì)[27]。

25只Wistar雄性大鼠隨機(jī)分為4組:左冠狀動(dòng)脈結(jié)扎靜坐組(MI-S組)、訓(xùn)練組(MI-T組,跑臺(tái)坡度為0°,13~20 m/min,60 min/d,5 d/周,持續(xù)8~10周);模擬手術(shù)靜坐組(sham-S組)、訓(xùn)練組(sham-T組,訓(xùn)練方案同上)。PHA刺激淋巴細(xì)胞,MI-S組比sham-S組IL-4表達(dá)升高;MI-T組比 MI-S組的頸部淋巴結(jié)IL-2產(chǎn)量增加,提示充血性心力衰竭大鼠模型中,中等強(qiáng)度運(yùn)動(dòng),雖然IL-4增加而導(dǎo)致的Th1/Th2細(xì)胞向Th2漂移,但I(xiàn)L-2分泌增加,有扭轉(zhuǎn)此效應(yīng),使得Th1/Th2細(xì)胞向Th1漂移,進(jìn)而增強(qiáng)免疫功能[28]。

觀察中等強(qiáng)度運(yùn)動(dòng)(跑步,21 m/min,每次35 min,5 d/周,共14周)與一次性運(yùn)動(dòng)(跑步,21 m/min,35 min)對(duì)代謝綜合癥的致炎因子IL-1β和IFN-γ的影響。巨噬細(xì)胞(未受抗原刺激)分泌的IL-1β,在肥胖Zucker大鼠有較高的濃度。在LPS刺激下,巨噬細(xì)胞分泌的IL-1β和IFN-γ明顯低于正常體重組。運(yùn)動(dòng)方案并未改變肥胖大鼠巨噬細(xì)胞IL-1β和IFN-γ的分泌,但增加了LPS刺激下的巨噬細(xì)胞分泌的細(xì)胞因子量。一次性運(yùn)動(dòng)僅增加了靜坐和訓(xùn)練組肥胖鼠的LPS刺激下巨噬細(xì)胞分泌的IL-1β量。結(jié)果提示:代謝綜合癥大鼠,在LPS刺激下,肥胖組巨噬細(xì)胞分泌的IL-1β和IFN-γ受到抑制,中等強(qiáng)度運(yùn)動(dòng)可以改善此效應(yīng)[29]。

不一致的結(jié)果可能與多種因素有關(guān),如運(yùn)動(dòng)方式、運(yùn)動(dòng)強(qiáng)度、運(yùn)動(dòng)持續(xù)時(shí)間、兩次運(yùn)動(dòng)之間的間隔、以前的訓(xùn)練情況、運(yùn)動(dòng)后取樣時(shí)間、細(xì)胞因子的檢測(cè)部位(如全血培養(yǎng)基、血清、尿液)以及檢測(cè)方法(如方法的敏感性、特異性)等。

IL-6主要是由免疫細(xì)胞產(chǎn)生的細(xì)胞因子, 可促進(jìn)淋巴細(xì)胞增殖,增強(qiáng)細(xì)胞免疫功能,但近年來研究證實(shí),運(yùn)動(dòng)期間的血漿細(xì)胞因子,尤其是IL-6主要來源于收縮的骨骼肌細(xì)胞,而不是免疫細(xì)胞,并認(rèn)為運(yùn)動(dòng)過程中肌肉產(chǎn)生的IL-6有免疫抑制作用[30]?？赡艿慕忉屖莿×疫\(yùn)動(dòng)引起血漿IL-6活性增強(qiáng),可刺激垂體前葉分泌ACTH,使糖皮質(zhì)激素增加[31-32]。體外給受試者注射重組IL-6 (rhIL-6)可引起血漿可的松含量明顯增加[33]。血清IL-6濃度增加與Cor共同參與應(yīng)激反應(yīng),IL-6促進(jìn)免疫機(jī)能效應(yīng)表現(xiàn)不明顯,或被Cor對(duì)免疫機(jī)能的抑制效應(yīng)掩蓋了。

此外,糖皮質(zhì)激素增加對(duì)免疫細(xì)胞產(chǎn)生IL-6有負(fù)反饋調(diào)節(jié)作用,可直接抑制巨噬細(xì)胞表達(dá)IL-1,并能抑制T-細(xì)胞表達(dá)IL-2和IL-2受體[34]。IL-2受體與IL-6受體同屬 Jaks蛋白酪氨酸激酶家族,因此,糖皮質(zhì)激素也可能對(duì)IL-6受體的表達(dá)有影響。這就有可能削弱IL-6促進(jìn)淋巴細(xì)胞增殖的效應(yīng)。

運(yùn)動(dòng)期間,骨骼肌本身要產(chǎn)生IL-6以調(diào)節(jié)肌糖原的動(dòng)用,同時(shí),也向血液中釋放并增加血漿IL-6的水平。這些研究結(jié)果提示,運(yùn)動(dòng)應(yīng)激時(shí)血漿IL-6濃度升高與糖代謝的調(diào)節(jié)有關(guān)[35]。

有報(bào)道認(rèn)為,IL-6可加速葡萄糖的氧化分解作用,促進(jìn)骨骼肌的葡萄糖吸收。讓受試者做分級(jí)負(fù)荷的伸膝運(yùn)動(dòng),隨運(yùn)動(dòng)強(qiáng)度增大,運(yùn)動(dòng)腿釋放IL-6和吸收血糖均增加[36]。這有可能加速工作肌的糖酵解,以保證在較大強(qiáng)度運(yùn)動(dòng)時(shí)的能量供應(yīng)。

有研究發(fā)現(xiàn),外源性給受試者注射重組IL-6的確可提高安靜時(shí)的肝臟葡萄糖的合成和血糖濃度,并表現(xiàn)出劑量依賴關(guān)系,這可能是IL-6增加血糖的機(jī)制之一[37]。

以上研究表明,IL-6在運(yùn)動(dòng)應(yīng)激期間主要參與糖代謝的調(diào)節(jié),對(duì)細(xì)胞免疫功能有一定抑制作用。因此,從運(yùn)動(dòng)應(yīng)激的角度可以把IL-6理解為與糖皮質(zhì)激素一樣,是參與應(yīng)激反應(yīng)的應(yīng)激因子[38]。

3延遲性肌肉酸痛癥(DOMS)

近年來,延遲性肌肉酸痛癥(DOMS)的免疫介導(dǎo)學(xué)說備受關(guān)注。

延遲性肌肉酸痛癥,也有學(xué)者稱為運(yùn)動(dòng)性肌肉損傷(EIMD),其病理本質(zhì),目前尚無統(tǒng)一認(rèn)識(shí)。國(guó)內(nèi)學(xué)者則多傾向認(rèn)為DOMS尚不是真正意義上的損傷,也許只是運(yùn)動(dòng)訓(xùn)練學(xué)中超量恢復(fù)學(xué)說的物質(zhì)基礎(chǔ),將其定義為疲勞而不是損傷更能反映其與運(yùn)動(dòng)訓(xùn)練的關(guān)系。

國(guó)外學(xué)者多傾向于認(rèn)為其病理本質(zhì)屬于“損傷”,如肌纖維的破壞、Z線的斷裂、細(xì)胞膜的破壞等等。引起破壞的原因則可能是高應(yīng)力牽拉導(dǎo)致的直接破壞、局部代謝產(chǎn)物堆積、Ca2+濃度增加引起的膜通透性改變、局部炎癥反應(yīng)、自由基造成的破壞、局部的氧化還原反應(yīng)以及免疫介導(dǎo)物介導(dǎo)的免疫反應(yīng)等等。提出的假說主要有:乳酸堆積學(xué)說、肌肉痙攣學(xué)說、結(jié)締組織損傷學(xué)說、骨骼肌超微結(jié)構(gòu)損傷學(xué)說、炎癥反應(yīng)學(xué)說、酶外溢學(xué)說等,其中炎癥反應(yīng)學(xué)說認(rèn)為DOMS是由機(jī)械性損傷引起的一系列炎癥反應(yīng),有研究顯示,DOMS與普通炎癥有著相似的循環(huán)和組織免疫反應(yīng):肌纖維損傷后,蛋白水解酶便啟動(dòng)了細(xì)胞類脂和蛋白結(jié)構(gòu)的降解。受損肌纖維和結(jié)締組織的快速降解,加之緩激肽、組織胺和前列腺素的堆積,吸引了單核細(xì)胞和中性粒細(xì)胞快速聚集損傷部位[39]。白細(xì)胞增多、白細(xì)胞介素IL-1、IL-6濃度上升,DOMS局部白細(xì)胞數(shù)量及IL-6的mRNA含量增加。有報(bào)道中等強(qiáng)度運(yùn)動(dòng)可使中性粒細(xì)胞提高2倍。但是DOMS 反應(yīng)高峰在運(yùn)動(dòng)后24~48 h,炎癥反應(yīng)高峰在運(yùn)動(dòng)后72~96 h,且使用抗生素和維生素不能或不能明顯減輕 DOMS,而且用順勢(shì)療法、用能加深炎癥反應(yīng)的藥物處理,也不能加重DOMS。說明DOMS有獨(dú)立的代謝過程。對(duì)此學(xué)說是由于水腫還是炎癥細(xì)胞浸入仍存在爭(zhēng)論[40-46]。

無論是損傷還是疲勞,肌細(xì)胞本身出現(xiàn)形態(tài)學(xué)改變已為鏡下觀察所證實(shí),那么免疫介導(dǎo)物介導(dǎo)的免疫反應(yīng)與運(yùn)動(dòng)免疫學(xué)的指標(biāo)體系的異同,關(guān)聯(lián)性如何?

筆者等推測(cè)現(xiàn)已有的運(yùn)動(dòng)免疫學(xué)研究的各免疫指標(biāo)的結(jié)果的不一致可能忽略了:1)研究的運(yùn)動(dòng)模型下肌肉的損傷程度與延遲性肌肉酸痛癥的異同;2)在各不同的運(yùn)動(dòng)模型下,測(cè)得的各免疫指標(biāo)結(jié)果與DOMS的免疫指標(biāo)結(jié)果的綜合性分析。

免疫系統(tǒng)對(duì)運(yùn)動(dòng)訓(xùn)練下骨骼肌適應(yīng)性變化的影響已有報(bào)導(dǎo),但人體實(shí)驗(yàn)還較少。有研究采用了免疫組織化學(xué)和流式細(xì)胞術(shù)觀察離心運(yùn)動(dòng)后人血液和骨骼肌的免疫反應(yīng)以及多極活組織檢查[47]。13名健康男受試者(19~32歲)隨機(jī)分為運(yùn)動(dòng)訓(xùn)練組和對(duì)照組,進(jìn)行遞增自行車運(yùn)動(dòng),起始功率為100 W(60 r/min),每2 min增加50 W直至力竭,持續(xù)7 d。受試者可以維持30 min 的功率為60 r/min相當(dāng)于離心運(yùn)動(dòng)VO2max測(cè)試的最高離心運(yùn)動(dòng)功率2 min。所有的受試者離心運(yùn)動(dòng)功率達(dá)250 W或300 W?；顧z前于前臂抽取靜脈血,在運(yùn)動(dòng)前、運(yùn)動(dòng)后即刻和6、24、48 h,運(yùn)動(dòng)后第4天、第7天取樣。結(jié)果發(fā)現(xiàn):(1)離心運(yùn)動(dòng)同時(shí)影響血液和人骨骼肌的免疫指標(biāo)。免疫組織化學(xué)結(jié)果發(fā)現(xiàn)離心運(yùn)動(dòng)后人骨骼肌配合多極活檢,中性粒細(xì)胞(CD11b、CD15)、巨噬細(xì)胞(CD163)、衛(wèi)星細(xì)胞(CD56)和IL-1β特異抗體含量增加,并且與只有多極活檢情況類似,即多極活檢類似于離心運(yùn)動(dòng)對(duì)人骨骼肌的影響。(2)血液與肌肉的免疫指標(biāo)的變化相互關(guān)聯(lián),單核細(xì)胞(MNC)和自然殺傷細(xì)胞(NK)對(duì)人骨骼肌免疫功能起重要的統(tǒng)領(lǐng)作用。(3)DOMS情況下,發(fā)現(xiàn)血清CK活性和C-反應(yīng)性蛋白含量與人類骨骼肌白細(xì)胞浸潤(rùn)不相關(guān),即血清CK活性與肌肉炎癥并不相關(guān);DOMS與肌肉炎癥不相關(guān),與肌肉損傷相比較,DOMS與肌肉適應(yīng)有更多關(guān)聯(lián)。(4)血液激素的變化與血液而非骨骼肌中的白細(xì)胞變化相關(guān)。(5)運(yùn)動(dòng)訓(xùn)練的骨骼肌適應(yīng)性改變的發(fā)生可能伴隨非經(jīng)典的炎癥反應(yīng),如中性粒細(xì)胞和吞噬細(xì)胞在肌肉損傷處聚集等。(6)離心自行車運(yùn)動(dòng)和(或)肌肉活檢并未導(dǎo)致人骨骼肌T細(xì)胞浸潤(rùn)。由于缺少T細(xì)胞浸潤(rùn),離心自行車運(yùn)動(dòng)并不是研究肌炎的適宜模型。因此,應(yīng)該建立排除離心性運(yùn)動(dòng)的應(yīng)激模型,以更好的研究人肌炎情況。(7)以往對(duì)運(yùn)動(dòng)訓(xùn)練下肌肉適應(yīng)性變化的研究并未考慮肌肉炎癥,實(shí)際上,粒細(xì)胞卻對(duì)于人骨骼肌的修復(fù)、再生和適應(yīng)性變化起到了重要的作用。此篇文章的發(fā)現(xiàn)很有新意,也得到其它文獻(xiàn)的數(shù)據(jù)支持[48-50],值得運(yùn)動(dòng)免疫學(xué)研究者們的進(jìn)一步探討論證。

縱觀人類進(jìn)化史,人類的免疫系統(tǒng)由保護(hù)機(jī)體免受感染防御侵害進(jìn)化到產(chǎn)生新的適應(yīng)性功能。在機(jī)體對(duì)運(yùn)動(dòng)訓(xùn)練的適應(yīng)性變化中,單核細(xì)胞和NK細(xì)胞比T、B細(xì)胞更活躍也不足為奇。人類進(jìn)化離不開勞動(dòng),而正是這名為“運(yùn)動(dòng)訓(xùn)練”導(dǎo)致了人類骨骼肌的損傷。如果證實(shí)了運(yùn)動(dòng)后人骨骼肌會(huì)出現(xiàn)粒細(xì)胞,這將反映粒細(xì)胞在骨骼肌適應(yīng)中的機(jī)能作用而非功能退化。

4運(yùn)動(dòng)過程中的Th1/Th2細(xì)胞漂移

最新研究觀點(diǎn)認(rèn)為,運(yùn)動(dòng)后感染性疾病的高發(fā),本質(zhì)上并非運(yùn)動(dòng)后的免疫抑制,而是和免疫功能重心遷移(altered focus)有關(guān)[51]。這是由于運(yùn)動(dòng)中的組織損傷激發(fā)了Th2分化,同時(shí)抑制了CMI以及運(yùn)動(dòng)應(yīng)激所致激素(皮質(zhì)醇、兒茶酚胺、前列腺E2等)水平的上升進(jìn)一步支持了Th2的上調(diào),使Th1和Th2細(xì)胞失衡所致。其結(jié)果是體液免疫增強(qiáng),細(xì)胞免疫受抑,運(yùn)動(dòng)員對(duì)感染的易感性提高。綜合國(guó)內(nèi)學(xué)者們的觀點(diǎn)[52-54],筆者認(rèn)為研究Th1和Th2細(xì)胞平衡、細(xì)胞因子及其受體網(wǎng)絡(luò)與運(yùn)動(dòng)訓(xùn)練的關(guān)系及可能的機(jī)制,對(duì)尋求免疫調(diào)控措施具有重要意義。

5小結(jié)

1)運(yùn)動(dòng)訓(xùn)練中免疫細(xì)胞的變化還不足以準(zhǔn)確反映免疫機(jī)能的變化,今后的研究應(yīng)重視縱向的觀察和測(cè)量點(diǎn)的密度。

2)應(yīng)激水平的糖皮質(zhì)激素對(duì)骨髓早期B細(xì)胞發(fā)育有負(fù)性調(diào)節(jié)作用,但運(yùn)動(dòng)對(duì)早期B細(xì)胞發(fā)育各階段的變化及相關(guān)調(diào)節(jié)因素的研究還很少。

3)以往研究多認(rèn)為運(yùn)動(dòng)后淋巴細(xì)胞數(shù)量減少主要是因?yàn)門細(xì)胞增殖能力下降,而忽略了其凋亡率的增加。

4)今后運(yùn)動(dòng)免疫學(xué)研究應(yīng)注重與延遲性肌肉酸痛癥等研究的免疫學(xué)指標(biāo)的綜合性分析。

5)離心自行車運(yùn)動(dòng)和(或)肌肉活檢并未導(dǎo)致人骨骼肌T細(xì)胞浸潤(rùn)。因此,應(yīng)該建立排除離心性運(yùn)動(dòng)的應(yīng)激模型,以便更好地研究人肌炎情況。

6)以往對(duì)運(yùn)動(dòng)訓(xùn)練下肌肉適應(yīng)性變化的研究并未考慮肌肉炎癥,實(shí)際上,粒細(xì)胞對(duì)于人骨骼肌的修復(fù)、再生和適應(yīng)性變化起到了重要的作用,可能具有進(jìn)化論意義。

感謝華南師范大學(xué)體育科學(xué)學(xué)院劉承宜教授對(duì)本文提出的修改意見!

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[編輯:鄭植友]