Verde T, Thomas S, Shephard R J
School of Physical and Health Education, University of Toronto, Canada.
Br J Sports Med. 1992 Sep;26(3):167-75. doi: 10.1136/bjsm.26.3.167.
Markers of a heavy increase in training were examined in ten highly trained distance runners (mean(s.d.) age 29.8(1.7) years, maximal oxygen intake 65.3 ml kg-1 min-1, personal best 10-km time 31 min 4 s) who undertook a deliberate 38% increment of training over a 3-week period. Their running performance did not improve, and six of the ten subjects developed sustained fatigue, suggesting that training was excessive, although the full clinical picture of overtraining did not develop. The Profile of Mood States was the best single marker of disturbed function, indicating increased fatigue and decreased vigour. There were no useful changes of resting heart rate or perceived exertion during submaximal running, sleep was undisturbed, and there were no orthopaedic injuries. Two subjects developed rhinoviral infections following the heavy training, and a third complained of symptoms that were diagnosed 2 weeks later as exercise-induced asthma. The increase of serum cortisol normally induced by 30 min of submaximal exercise was no longer seen when the same acute exercise was performed after heavy training. Resting lymphocyte proliferation tended to increase in response to phytohaematoglutinin (PHA) and concanavalin A (Con A), the ratio of helper to suppressor cells (H/S) decreased, and pokeweed mitogen induced smaller increases in IgG and IgM synthesis. Whereas before heavy training, PHA-stimulated lymphocyte proliferation was unchanged by 30 min of acute submaximal exercise, after 3 weeks of heavy training the same bout of exercise caused an 18% suppression of proliferation. Likewise, heavy training brought about a decrease of T-lymphocytes in response to acute submaximal exercise, but an abolition of the acute exercise-induced decrease in the H/S ratio. The previously observed exercise-induced decrease of IgG synthesis did not occur when the same acute bout of exercise was performed after heavy training. We conclude that such minor and transient changes of immune function may possibly be a warning that training is becoming excessive, but they have only a limited significance for overall immune function.
对10名训练有素的长跑运动员(平均(标准差)年龄29.8(1.7)岁,最大摄氧量65.3 ml·kg⁻¹·min⁻¹,个人最佳10公里跑成绩31分04秒)进行了研究,这些运动员在3周内有意将训练量增加了38%。他们的跑步成绩没有提高,10名受试者中有6人出现了持续疲劳,这表明训练过量,尽管尚未出现过度训练的完整临床症状。情绪状态剖面图是功能紊乱的最佳单一指标,表明疲劳加剧和活力下降。静息心率或次最大强度跑步时的主观用力感觉没有明显变化,睡眠不受干扰,也没有骨科损伤。两名受试者在高强度训练后患上了鼻病毒感染,第三名受试者抱怨有症状,两周后被诊断为运动诱发哮喘。在高强度训练后进行相同的急性运动时,通常由30分钟次最大强度运动诱导的血清皮质醇升高不再出现。静息淋巴细胞对植物血凝素(PHA)和刀豆球蛋白A(Con A)的增殖反应趋于增加,辅助性T细胞与抑制性T细胞的比例(H/S)降低,商陆有丝分裂原诱导的IgG和IgM合成增加较小。在高强度训练前,30分钟的急性次最大强度运动对PHA刺激的淋巴细胞增殖没有影响,而在高强度训练3周后,相同的运动导致增殖抑制了18%。同样,高强度训练使急性次最大强度运动后的T淋巴细胞减少,但消除了急性运动诱导的H/S比例下降。在高强度训练后进行相同的急性运动时,先前观察到的运动诱导的IgG合成减少并未发生。我们得出结论,免疫功能的这种轻微和短暂变化可能是训练过量的一个警告,但它们对整体免疫功能的意义有限。