a Laboratory of Biological Structure Biomechanics , IRCCS Istituto Ortopedico Galeazzi , Milano , Italia.
b Laboratory of Experimental Biochemistry & Molecular Biology , IRCCS Istituto Ortopedico Galeazzi , Milano , Italia.
Chronobiol Int. 2018 Sep;35(9):1185-1197. doi: 10.1080/07420528.2018.1475395. Epub 2018 Jun 28.
Rhythms can be observed at all levels of the biologic integration in humans. The observation that a biological or physiological variable shows a circadian rhythm can be explained by several multifactorial systems including external (exogenous), internal (endogenous) and psychobiological (lifestyle) mechanisms. Our body clock can be synchronized with the environment by external factors, called "synchronizers", i.e. the light-dark cycle, but it is also negatively influenced by some pathological conditions or factors, called "chronodisruptors," i.e. aging or low physical activity (PA). The desynchronization of a 24-h rhythm in a chronic manner has been recently defined "chronodisruption" or "circadian disruption." A very large number of hormonal variables, such as adrenal and gonadal stress steroids, are governed by circadian rhythmicity. Such hormones, in normal conditions, show a peak in the first part of the day, while their typical diurnal fluctuations are totally out of sync in subjects affected by cancer or metabolic diseases, such as obesity, diabetes and metabolic syndrome. In general, a flatter slope with altered peaks in cortisol and testosterone circadian rhythms has been observed in pathological individuals. PA, specifically chronic exercise, seems to play a key role as synchronizer for the whole circadian system in such pathologies even if specific data on steroids circadian pattern are still sparse and contradictory. Recently, it has been proposed that low-intensity chronic PA could be an effective intervention to decrease morning cortisol levels in pathological subjects. The standardization of all confounding factors is needed to reach more clear evidence-based results.
在人类的生物整合的各个层次都可以观察到节律。可以用几种多因素系统来解释一个生物或生理变量显示出昼夜节律的现象,这些系统包括外部(外源性)、内部(内源性)和心理生物学(生活方式)机制。我们的生物钟可以通过外部因素(称为“同步器”)与环境同步,例如光-暗周期,但它也会受到一些病理状况或因素(称为“时间破坏者”)的负面影响,例如衰老或低体力活动(PA)。24 小时节律的慢性失同步最近被定义为“时间破坏”或“昼夜节律破坏”。大量的激素变量,如肾上腺和性腺应激类固醇,受昼夜节律的控制。在正常情况下,这些激素在一天的前半部分达到峰值,而在癌症或代谢疾病(如肥胖、糖尿病和代谢综合征)患者中,其典型的昼夜波动完全不同步。一般来说,在病理个体中,皮质醇和睾酮昼夜节律的峰变化更平坦。PA,特别是慢性运动,似乎在这些疾病的整个昼夜节律系统中起着同步器的关键作用,即使关于类固醇昼夜节律模式的具体数据仍然很少且相互矛盾。最近,有人提出低强度慢性 PA 可能是降低病理个体晨峰皮质醇水平的有效干预措施。需要标准化所有混杂因素,以获得更明确的基于证据的结果。