Chronic Fatigue Commentary

Kelly A Brooks

Abstract


Chronic Fatigue Syndrome  

Currently, there is no accepted theory as to what causes Chronic Fatigue Syndrome (CFS). Certain abnormalities are present in all patients, with a common feature of many patients being the underactivation of the hypothalamic-pituitary-adrenal (HPA) axis, especially in response to stress. A lower than normal variation in the normal circadian pattern of HPA axis activation has been discovered by Pruessner (1999) who studied the underactivation of the HPA axis in CFS patients directly. 

Burnout is the body's protection mechanism against unnecessary and potentially dangerous long-term stress. It appears to be caused by underactivation of the HPA axis

CFS-severe burnout; characterized by the same symptoms and HPA axis disturbances as burnout. All known cases of CFS begin with: long-term stress, negative mental attitude to stress/illness/life or a severe viral illness; a large percentage of CFS patients share every trigger. Mechanisms in the body act to limit HPA axis activation resulting in a reduced ability to cope with stress and a reduced motivation/energy level, causing the person to rest and conserve energy.

 

Exercise Capacity in Chronic Fatigue Syndrome

De Becker, P., et al. (2000) studied a large cohort of female patients with CFS. They performed a maximal test with graded increase on a bicycle ergometer. The RHR of the patient group was higher than controls, while MHR reported at exhaustion was lower. CFS patients had significantly decreased exercise capacity when compared with controls. Reaching the age-predicted target HR seemed to be a limiting factor of the patients with CFS in achieving maximal effort, which could be due to autonomic disturbances.

De Becker et al., (1998) found the maximal workload and oxygen uptake attained by their patients with CFS using a bicycle ergometer. RHR was higher in patients with CFS, suggesting that "alteration in cardiac function is a primary factor associated with the reduction in exercise capacity in CFS." 

Baschetti (2002) noted that CFS and AD share persistent fatigue and debilitation after exercise, but also reduction in cardiac dimensions and increased HR at restZelinskii et al., (1987) noted that adrenal insufficiency, rather than alteration in cardiac function, may primarily account for the reduction in exercise capacity in CFS.  An insufficient production of adrenal hormones results in impaired physical capacities. In patients with CFS (using a bicycle ergometer), working capacity, total volume of work done, and maximum oxygen consumption were lower in patients with AI. 

Baschetti (1999) studied viral reactivation and immunological abnormalities observed in patients with CFS. The abnormalities were accounted for by the cortisol deficiency that characterizes these patients. There are striking similarities between CFS and AD. The conviction that CFS is an AI similar to Addison's disease lies primarily in the fact CFS patients in the previous study recovered from chronic fatigue syndrome symptoms in the course of a few days with consumption of licorice, which is known to aid in the recovery of AI.

Similarity of symptoms in chronic fatigue syndrome and Addison's disease were again reported by Baschetti, R. (1997), through observation that AD is characterized by many CFS-like symptoms. This study revealed evidence of reduced adrenal production of cortisol, both basal and after activity, in patients diagnosed with CFS. Reasons why cortisol levels are lowered is unclear: many factors influence cortisol secretion, including changes in sleep, physical activity and appetite. 

 

Chronic fatigue syndrome, decreased exercise capacity, and adrenal insufficiency

Baschetti, R. (2001) reported that working capacity, total volume of work done, and maximum oxygen consumption were lowered in patients with chronic AI, and noted that CFS shares 39 features with AI, including all the physical and neuropsychological symptoms. De Becker (2002) added to research by finding that CFS and AD share persistent fatigue and debilitation after exercise; and found a reduction in cardiac dimensions and an increased heart rate at rest in both patients. 

CFS and AI patients both share a reduction in exercise capacity. This reduction in exercise capacity in CFS is primarily due to adrenal insufficiency. It is possible that there may be an overlap of CFS with Addison disease, and other related adrenal disorders.

 

Overtraining Syndrome

Overtraining Syndrome (OS) is also described as a form of chronic fatigue, burnout and staleness. It is defined as an imbalance between training/competition, versus recovery. Training alone is seldom the primary cause. OS appears to be caused by the total amount of stress on the athlete exceeding their capacity to cope 

 

Barron, et al.(1985), Gastmann, et al. (1997), and Budgett (1998) were among the first researchers to find that severe overtraining over an extended period can result in AD. They described an Addison-Type overtraining syndrome, where adrenal glands are no longer able to maintain proper hormone levels, and athletic performance is severely compromised. Lehman et al., (1998) described the autonomic imbalance hypothesis and its relationship with OS. He suggested that prolonged training produces an autonomic imbalance. During heavy endurance training or over-reaching periods, there is evidence of reduced adrenal responsiveness to ACTH, which is compensated by an increased pituitary ACTH release. During the early stages of OS, despite increased pituitary ACTH release, the decreased adrenal responsiveness is no longer compensated and the cortisol response decreases. During the advanced stage of OS, the pituitary ACTH release also decreases.  

 

ACTH response

Persson et al. (1980) found reduced ACTH-stimulated adrenal cortisol release in chronically fatigued horses, while Wittert et al. (1996) noted significantly increased ACTH plasma concentrations in ultramarathoners during an early morning period between 3 and 8. Cortisol plasma levels or 24-h renal cortisol excretions did not show any significant differences. This may point to decreased adrenal responsiveness to ACTH

The decreased adrenal responsiveness can be the consequence of an overload during heavy preparatory training sessions before the ultramarathon, the ultramarathon stress itself, and incomplete regeneration.

Lehmann has conducted extensive research on the adrenal axis and OS. He found a 60-80% higher pituitary CRH-stimulated ACTH response in experimentally overtrained athletes in an early stage of OS (Lehmann et al., 1993). The increased response could no longer prevent reduced cortisol response compared to baseline. Measurements were still amplified after 2 weeks of incomplete regeneration (Lehmann et al., 1993, Lehmann et al., 1997). The decreased adrenal responsiveness was no longer completely compensated by increased pituitary ACTH response (Lehmann et al., 1992, 1993). Lehmann also found decreased exercise-related maximum cortisol levels observed in overtrained distance runners (1992) and in recreational athletes (1993) when compared to baseline. 

Barron et al. (1985) found significantly decreased pituitary ACTH response in overtrained distance runners, which reflects a decreased hypothalamic and/or pituitary responsiveness and a reduced adrenal responsiveness to ACTH. Barron described a decreased pituitary release of growth hormone (1988). These findings are paralleled by clearly reduced adrenal cortisol response as also observed in chronically fatigued horses (Persson) and in overtrained human athletes (Lehmann, 1993, 1997). This is characteristic of an advanced stage in the overtraining process. 

Gastmann et al. (1997) observed a reduced pituitary ACTH response to CRH in experienced road cyclists. The study was performed at the end of a heavy road pacing season after an additional 2-wk high-volume training stress without a preceding regeneration period. Researchers found an impaired pituitary hormonal response to exhaustive exercise in overtrained endurance athletes. Urhausen, et al., (1998) studied short-term exhaustive endurance test on a cycle ergometer at an intensity 10% above anaerobic threshold. In OS, the time to exhaustion was significantly decreased by 27% on average. Lower maximal exercise-induced increase of the ACTH and growth hormone was discovered, as well as a trend for a decrease of cortisol and insulin Hypothalamo-pituitary dysregulation during OS was expressed by an impaired response of pituitary hormones to exhaustive short-endurance exercise. 

 

ACTH Response Summary

There is evidence of a reduced adrenal responsiveness to ACTH in the stage of overreaching or early OS. Reduced responsiveness is initially compensated by an increased pituitary ACTH response. This reduction is no longer compensated in an early stage of a Addison -type overtraining syndrome, thus, the cortisol response decreases. A decreased hypothalamic/pituitary responsiveness (CRH) is common in an advanced stage of Addison overtraining syndrome.

 

Conclusion

CFS could be caused by/mistaken for AI. There is commonly a decrease in exercise capacity in CFS, which may be result of AI. Overtraining may contribute to/cause AI. Cortisol levels are lowered and ACTH is increased during overtraining, while a reduced responsiveness to ACTH, and a reduced responsiveness to CRH are found. If the physical stress of overtraining is not removed, adrenal issues may continue or become more severe. Severely overtrained athletes may develop Addison's Disease

Overtraining Syndrome (OS) has been described as chronic fatigue, burnout and staleness, where an imbalance between training/competition, versus recovery occurs. Training alone is seldom the primary cause. In most cases, the total amount of stress on the athlete exceeds their capacity to cope. A triggering stressful event, along with the chronic overtraining, pushes the athlete to start developing symptoms of overtraining syndrome, which is far worse than classic overtraining. Overtraining can be a part of healthy training, if only done for a short period of time. Chronic overtraining is what leads to serious health problems, including adrenal insufficiency. 

Severe overtraining over an extended period can result in adrenal depletion. An Addison- Type overtraining syndrome, where the adrenal glands are no longer able to maintain proper hormone levels and athletic performance is severely compromised has been described by researchers. Other studies have suggested the autonomic imbalance hypothesis is what happens in overtraining syndrome. This suggests that prolonged training produces an autonomic imbalance, and during heavy endurance training or over-reaching periods, there is evidence of reduced adrenal responsiveness to ACTH. This is compensated by an increased pituitary ACTH release. During the early stages of OS, despite increased pituitary ACTH release, the decreased adrenal responsiveness is no longer compensated and the cortisol response decreases. In the advanced stage of OS, the pituitary ACTH release also decreases.

Decreased adrenal responsiveness can be the consequence of an overload during heavy preparatory training sessions before an ultramarathon, for example, or the ultramarathon stress itself, and incomplete regeneration. If a runner continues to chronically overload the adrenals, OS will occur.

There is evidence of a reduced adrenal responsiveness to ACTH in the stage of overreaching or early OS. This reduced responsiveness is initially compensated by an increased pituitary ACTH response. No longer compensated in an early stage of a Addison type overtraining syndrome; the cortisol response decreases. A decreased hypothalamic/pituitary responsiveness (CRH) will be present in an advanced stage of Addison overtraining syndrome. 

Prevention, proper nutrition, balancing training and recovery, and stress-management are all important factors to consider in competitive athletes, as well as recreational athletes. Knowing the signs and symptoms of OS can help aid in intervention, which may prevent adrenal complications. 


Keywords


health, medicine, disease, diagnosis, fatigue, adrenal axis



DOI: https://doi.org/10.12922/jshp.v3i1.43

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