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Hormonal responses to exercise in chronic fatigue syndrome (Ottenweller et al., 2001)

Dolphin

Senior Member
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17,567
Hormonal responses to exercise in chronic fatigue syndrome.

Neuropsychobiology. 2001 Jan;43(1):34-41.

Ottenweller JE, Sisto SA, McCarty RC, Natelson BH.

Source
Department of Neurosciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, USA. jeo@nbunj.jvnc.net

Abstract*

Chronic fatigue syndrome (CFS) is a debilitating disease characterized by severe, unexplained fatigue and postexertional exacerbation of symptoms.

We examined basal endocrine function in a group of CFS patients and a carefully matched group of sedentary controls.

The subjects then completed a graded, maximal exercise test on a treadmill, and additional blood samples were drawn 4 min and a day after the end of exercise.

There were no differences in basal hormone levels before exercise.

Plasma adrenocorticotropin, epinephrine, prolactin and thyrotropin responses 4 min after exercise were lower in the CFS group, but the growth hormone response may have been exaggerated, and the plasma norepinephrine response was similar to that in controls.

The next day, there were no differences in hormone levels between the groups, which suggests that long-term changes in endocrine function are unlikely to be a cause of the prolonged fatigue that occurs in CFS patients after a bout of exertion.

Copyright 2001 S. Karger AG, Basel

PMID: 11150897 [PubMed - indexed for MEDLINE]

*I gave each sentence its own paragraph
 

Dolphin

Senior Member
Messages
17,567
I always find exercise studies that find differences of interest. Here are some extracts:
---
A subset of the the CFS subjects did not achieve maximum effort

Figures 1 and 2 present the differences in hormone levels between basal samples and those drawn 4 min after exercise, i.e. the acute responses to exercise. CFS subjects had lower plasma ACTH (F = 5.73 with 1, 25 d.f., p < 0.05), TSH (F = 4.99 with 1, 25 d.f., p < 0.05) and PRL (F = 4.94 with 1, 25 d.f., p < 0.05) responses than controls, and a trend toward greater GH responses (F = 4.17 with 1, 25 d.f., p = 0.08; fig. 1). Similar results were obtained in the analyses of GH responses when body mass index was included as a covariate. The plasma EPI response was also lower in CFS subjects than in controls (F = 7.80 with 1, 25 d.f., p < 0.01), but the NE response was not (F < 1 with 1, 25 d.f., p > 0.1; fig. 2). With maximum heart rate in the ANCOVA model, the groups did not differ significantly in their EPI responses because of a correlation between these variables (see below and fig. 3). There were smaller changes in the catecholamine metabolites of CFS subjects than controls after exercise (fig. 2). Four minutes after exercise, none of the following plasma hormones showed any significant change from the baseline levels described in table 1: CORT, T4, T3, E2, DHEA-S or IGF-1. In addition, plasma levels of all hormones 24 h after the exercise were similar to the baseline levels presented in table 1 and were not different between CFS and control subjects.

Reanalyses of the hormonal response data including only these 12 subjects in the CFS group produced the same results as the initial analyses. In the case of GH, a marginal effect (fig. 1) became a significant difference between CFS and control subjects.

The second way we examined the effect of effort on the hormone responses was to use linear regressions to look at the relationships between the physiological variables and hormonal responses. A significant relationship was found in CFS subjects between maximum heart rate during exercise and the EPI response, but not in control subjects (fig. 3a). In addition, for CFS subjects alone, baseline CORT levels before the start of exercise predicted how long subjects continued on the treadmill, i.e. CFS subjects with higher CORT levels continued on the treadmill longer than those with lower levels (fig. 3b).

Discussion:
The CFS subjects in this study showed no differences from sedentary controls in baseline hormone levels, but there were lower plasma levels of two primary catecholamine metabolites. Because catecholamines are quickly metabolized, these lower baseline levels suggest an ongoing state of lower catecholamine synthesis and/or metabolism in CFS subjects. In addition, lower plasma DOPA levels have been interpreted by others as a sign of decreased tyrosine hydroxylase activity [25]. However, we failed to find differences in basal plasma levels of any other hormones.

Plasma ACTH, PRL and TSH responses to exercise were also lower in CFS subjects than controls, as was the EPI response. The lower pituitary hormone responses were not due to altered levels of peripheral hormones that affect their secretion, namely CORT, E2 or thyroid hormones. The lower responses in CFS patients were not due to differences in exertion, because these reduced responses compared to controls were found in the subset of CFS subjects who attained a physiologically maximal effort, as well as in the entire CFS sample. The lower responses were probably not due to the CFS subjects being less stressed by the procedure for two reasons: first, they were frequently concerned about the adverse effects of exercise due to the fact that exertion worsens their symptoms, and second, they reported levels of perceived exertion that were consistently as high as or higher than those reported by controls throughout the exercise test [21]. Thus, these data indicate that exercise can uncover subtle endocrinological abnormalities that differentiate CFS patients from healthy controls.

One of our most intriguing findings was a relatively good, positive correlation between basal CORT levels before exercise and the amount of time the subjects could run on the treadmill. This finding suggests that the mild hypocortisolemia in CFS patients might be helped by exogenous glucocorticoids, and two treatment trials have found that low-dose hydrocortisone may produce some improvements in CFS patients [27, 28].

The fact that the GH response to exercise was exaggerated in CFS means that not all pituitary hormonal systems respond less to an exercise probe. Since GH is an acute stress respondent [30], the increased responses in the CFS group might reflect an increased stressfulness of the test for these subjects.


Various changes related to catecholamines have been reported in CFS patients. NE levels are an index of sympathetic nerve activity, whereas plasma EPI levels reflect adrenomedullary secretion [32]. Although we found normal baseline plasma catecholamines in CFS patients, we also found they had lower plasma levels of catecholamine metabolites, which is consistent with findings of lower cerebrospinal fluid MHPG, an NE metabolite, in CFS patients [33]. Our findings of lower basal plasma DHPG and DOPAC suggest that catecholamine metabolism, synthesis or release might be lower in CFS subjects.

33 Demitrack MA, Gold PW, Dale JK, Krahn DD, Kling MA, Strauss SE: Plasma and cerebrospinal fluid monoamine metabolism in patients with chronic fatigue syndrome: Preliminary findings. Biol Pyschiatry 1992;32:1065– 1077.
 

Dolphin

Senior Member
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17,567
Final extract - thought I'd give it its own message:
The diminished responses of CFS subjects to exercise, particularly the EPI response, was unexpected, given that people with greater levels of fitness have lower NE and EPI responses to exercise [17, 38]. Not only is this true in healthy subjects, but catecholamine responses to exercise also decrease after training and increased fitness in cardiac patients with ischemic heart disease [15]. In addition to changes in catecholamine responses, exercise training in healthy subjects will increase the GH response to exercise testing [17]. Given these findings, it might be expected that deconditioned CFS patients would have exaggerated NE and EPI responses to exercise and perhaps lower GH responses. However, our results indicate the contrary. They suggest that it is the illness process and not the deconditioning which is responsible for the abnormal endocrine responses to exercise in CFS patients.
 

heapsreal

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Interesting. Several attempts with exercise at different levels of function for me seem to possibly correlate with this. Pre cfs i would get that exercise high. With cfs and feeling crap there would be no exercise high just feeling sick and yuk as i attempted it and then paying for it for along time afterwards. When i have been feeling well and exercise with cfs i notice that same exercise high i use to get, now in the past if i continued to exercise and was well then the exercise high continued but then when it starts to disappear is when my general cfs starts to decline and after alot of unsuccessful attempts i notice this now and know its time to just stop altogether until i feel myself improving. These exercise attempts could be once session or have been semi regular over a few weeks.

Maybe this exercise high and feeling good is from noradrenaline and cortisol levels. I think our ability to recovery relates to good dhea, testosterone and growth hormone levels which poor sleep can blow these out of the water which i think can also be a reason for PEM??
 

Seven7

Seven
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I think our ability to recovery relates to good dhea, testosterone and growth hormone levels which poor sleep can blow these out of the water which i think can also be a reason for PEM??

I think the PEM comes from OI (see the dinet forum and the struggles of the OI plp) IS something to do with the cytokines and the role they have on vassocontricion/dialiation, I am surprised they do not look at the known hormones for OI like neuroprenine (something like that) I think is time for the OI people and CFS to do a think tank also.
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
I think the PEM comes from OI (see the dinet forum and the struggles of the OI plp) IS something to do with the cytokines and the role they have on vassocontricion/dialiation, I am surprised they do not look at the known hormones for OI like neuroprenine (something like that) I think is time for the OI people and CFS to do a think tank also.
Probably a big connection between hormones, cytokines, oi and pem. a study testing post exercise hormones and cytokines and maybe do positional blood pressure testing too and then again 24 hours later, with a control group?
 

*GG*

senior member
Messages
6,389
Location
Concord, NH
Interesting. Several attempts with exercise at different levels of function for me seem to possibly correlate with this. Pre cfs i would get that exercise high. With cfs and feeling crap there would be no exercise high just feeling sick and yuk as i attempted it and then paying for it for along time afterwards. When i have been feeling well and exercise with cfs i notice that same exercise high i use to get, now in the past if i continued to exercise and was well then the exercise high continued but then when it starts to disappear is when my general cfs starts to decline and after alot of unsuccessful attempts i notice this now and know its time to just stop altogether until i feel myself improving. These exercise attempts could be once session or have been semi regular over a few weeks.

Maybe this exercise high and feeling good is from noradrenaline and cortisol levels. I think our ability to recovery relates to good dhea, testosterone and growth hormone levels which poor sleep can blow these out of the water which i think can also be a reason for PEM??

@hearps You still get an exercise high? Mine has not come back yet!

GG
 

heapsreal

iherb 10% discount code OPA989,
Messages
10,089
Location
australia (brisbane)
@hearps You still get an exercise high? Mine has not come back yet!

GG

occassionally, depends how im functioning but havent done anything regular for months. played tennis last wednesday and felt really good afterwards, but sore the next few days but thats expected. Time again to test my boundaries??
 
Messages
15,786
I think the PEM comes from OI (see the dinet forum and the struggles of the OI plp) IS something to do with the cytokines and the role they have on vassocontricion/dialiation, I am surprised they do not look at the known hormones for OI like neuroprenine (something like that) I think is time for the OI people and CFS to do a think tank also.
I get PEM even when OI is completely under control, or if I'm using muscles while laying down. BP and heart rate are normal then, but I still get very sick the next day.

OI does seem to contribute to a more immediate and short term exercise intolerance though.