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Physiological cost of walking (Rafferty, Marshall, 2009)

WillowJ

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Rafferty, Marshall "Physiological cost of walking in those those with chronic fatigue syndrome (CFS): a case-control study." Disabil Rehabil. 2009;31(19):1598-604. PMID: 19848558

Faculty of Medicine, Nursing and Health Care, University of Glasgow, Glasgow, UK.

Abstract

PURPOSE: To examine the physiological cost of walking in subjects with chronic fatigue syndrome (CFS) and a matched control group, walking at their preferred and at matched walking speeds.

METHODS: Seventeen people with CFS and 17 matched-controls participated in this observational study of physiological cost during over-ground gait. Each subject walked for 5 min at their preferred walking speed (PWS). Controls then walked for 5 min at the same pace of their matched CFS subject. Gait speed and oxygen uptake, gross and net were measured and oxygen uptake was expressed per unit distance ambulated. CFS subjects completed the CFS-Activities and Participation Questionnaire (CFS-APQ).

RESULTS: At PWS the CFS group walked at a slower velocity of 0.84 +/- 0.21 m s(-1) compared to controls with a velocity of 1.19 +/- 0.13 m s(-1) (p < 0.001). At PWS both gross and net oxygen uptake of CFS subjects was significantly less than controls (p = 0.023 and p = 0.025 respectively). At matched-velocity both gross and net physiological cost of gait was greater for CFS subjects than controls (p = 0.048 and p = 0.001, respectively).

CONCLUSION: The physiological cost of walking was significantly greater for people with CFS compared with healthy subjects. The reasons for these higher energy demands for walking in those with CFS have yet to be fully elucidated.

Has this been discussed already? It looks really interesting. I can't find the full text anywhere.
 

Dolphin

Senior Member
Messages
17,567
No, I don't have that one to read either.

I read this one by the same team:
Gait characteristics of subjects with chronic fatigue syndrome and controls at self-selected and matched velocities.

J Neuroeng Rehabil. 2008 May 27;5:16.

Paul L, Rafferty D, Wood L, Maclaren W.
which is open access: http://www.jneuroengrehab.com/content/5/1/16 which I didn't find that exciting but the one you highlighted does sound more interesting. I may have been slightly prejudiced as I was able to compete and run at a high level before the illness so I feel my gait was not particularly bad before the illness (so not sure about the idea I think they suggested that it might be modifiable). Anyway, going from memory on that but will look up if it gets discussed.
 

Cort

Phoenix Rising Founder
That's pretty impressive; a recent study by Vermoulen suggested that oxygen transport to the tissues was the cause of the impaired aerobic functioning during repeat exercise tests. Here we have reduced oxygen transport - I think that's what they are saying - simply during walking!
 

Sean

Senior Member
Messages
7,378
Papers like the two mentioned above may not seem exciting but I wouldn't underestimate them, I suspect they are giving us some important clues.

Apart from anything else, they are hard objective evidence, and we need all of that we can get.
 

eric_s

Senior Member
Messages
1,925
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Switzerland/Spain (Valencia)
Yes, i think this is very interesting. Anything that's measurable is very valuable for us, to prove what we are telling people. And especially for me, as i don't walk a lot. This tells me that there seems to be some scientific evidence why walking (and probably every other form of excercise) is different for me than for a healthy person.

Could those results be the effect of deconditoning? I know this is not our problem but this is the question i'm expecting from "doubters".

And i like the fact that this comes out of the UK.
 

shannah

Senior Member
Messages
1,429
Glad to see some studies in this area.

A number of years ago, both my son and I ended up with pneumonia after walking about a mile. Then trying it again about 5 years ago, we ended up with immediate and severe ear/throat/head infections. His ear drum actually burst. Any sort of increased activity really kicks up some infection going on in us.
 

WillowJ

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Yes, i think this is very interesting. Anything that's measurable is very valuable for us, to prove what we are telling people. And especially for me, as i don't walk a lot. This tells me that there seems to be some scientific evidence why walking (and probably every other form of excercise) is different for me than for a healthy person.

Could those results be the effect of deconditoning? I know this is not our problem but this is the question i'm expecting from "doubters".

And i like the fact that this comes out of the UK.

This is my response to that (from a handout I prepared):

Is CFS causally related to deconditioning, and does exercise improve ME/CFS? Does CBT?
Is there any evidence to support the use of pacing?​

Carruthers et al. "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols" J CFS, Vol. 11(1) 2003, pp. 7-115 (pp 46-49). http://cfids-cab.org/MESA/ccpc-1.html
Explains that most CBT/GET studies are done on fatigued patients using the name but not any specific criteria for CFS. Refusal and drop-out rates may be very high. Assessment is chiefly subjective. When used respectfully, cognitive therapy may be useful as an adjunct therapy. Some CF patients may see modest improvement from increased activity; but ME/CFS patients report adverse effects, consistent with the definitions and clinical and research findings.

Price JR, Mitchell E, Tidy E, Hunot V. Cognitive behaviour therapy for chronic fatigue syndrome in adults. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD001027. Review. PMID: 18646067
Claims effectiveness based on symptoms of fatigue, a purely subjective measure, and states, The evidence base at follow-up is limited to a small group of studies with inconsistent findings. There is a lack of evidence on the comparative effectiveness of CBT alone or in combination with other treatments, and further studies are required to inform the development of effective treatment programmes for people with CFS.​

Nijs J et al. "Comparison of two exercise testing protocols in patients with chronic fatigue syndrome." J Rehabil Res Dev. 2007;44(4):553-9. PMID: 18247252
Symptoms are typically worsened after modest amounts of exercise [2], after increased daily physical activity [3], and after a maximal exercise stress test [4-5]. A delayed recovery from exercise typically occurs in patients with CFS [6].... [further discussion of findings and problems of exercise in ME/CFS and of CFS assessment]​

Clapp LL, et al. "Acute effects of thirty minutes of light-intensity, intermittent exercise on patients with chronic fatigue syndrome." Phys Ther. 1999;79(8):749-56 PMID: 10440661
Although clinical findings and self-reported symptoms vary among patients with CFS, a worsening of symptoms, especially of fatigue, after previously well-tolerated levels of exercise continues to be the hallmark of this incapacitating disorder.[25]... Patients with CFS typically feel much worse after modest amounts of physical exercise. Some investigators have suggested the onset of severe symptoms to be 6 to 48 hours following exercise[25] and to last from 2 days to 2 weeks.[2,26]... some individuals with CFS may be able to use low-level, intermittent exercise [3 min sessions] without exacerbating their [condition].​

Nijs J, et al. "Can exercise limits prevent post-exertional malaise in chronic fatigue syndrome? An uncontrolled clinical trial." Clin Rehabil. 2008 May;22(5):426-35. PMID: 18441039
It was shown that the use of exercise limits (limiting both the intensity and duration of exercise) prevents important health status changes following a walking exercise in people with chronic fatigue syndrome, but was unable to prevent short-term symptom increases.​

Note that both of the above are time-limited trials and do not measure the effect of an ongoing program over time. Nor do they asses how adding an exercise program might affect ability to carry out important ADLs such as meal preparation.

Black CD, McCully KK. (U Georgia). Time course of exercise induced alterations in daily activity in chronic fatigue syndrome. Dyn Med. 2005 Oct 28;4:10. PMID: 16255779
Over the first 4-10 days of walking the subjects with CFS were able to reach the prescribed activity goals each day. After this time, walking and total activity counts decreased. Sedentary controls subjects were able to maintain their daily walking and total activity goals throughout the 4 weeks. Unlike our previous interpretation of the data, we feel this new analysis suggests that CFS patients may develop exercise intolerance as demonstrated by reduced total activity after 4-10 days. The inability to sustain target activity levels, associated with pronounced worsening of symptomology, suggests the subjects with CFS had reached their activity limit.​

Bazelmans E, Bleijenberg G, Van Der Meer JW, Folgering H. "Is physical deconditioning a perpetuating factor in chronic fatigue syndrome? A controlled study on maximal exercise performance and relations with fatigue, impairment and physical activity." Psychol Med. 2001 Jan;31(1):107-14. PMID: 11200949
There were no statistically significant differences in physical fitness between CFS patients and their controls. Nine CFS patients had a better fitness than their control.... Physical deconditioning does not seem a perpetuating factor in CFS.​

VanNess JM, Stevens SR, Bateman L, Stiles TL, Snell CR. "Postexertional malaise in women with chronic fatigue syndrome." J Womens Health (Larchmt). 2010 Feb;19(2):239-44. PMID: 20095909
The results of this study suggest that PEM is both a real and an incapacitating condition for women with CFS and that their responses to exercise are distinctively different from those of sedentary controls.​

Sorensen, et al. "Complement activation in a model of chronic fatigue syndrome." J Allergy and Clin Immunol. 2003 Aug;112(2):397-403. PMID: 12897748
Activity produces immune response, which is associated with symptom flare (PEM).

Lane RJ, Barrett MC, Woodrow D, Moss J, Fletcher R, Archard LC. "Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome." J Neurol Neurosurg Psychiatry. 1998 Mar;64(3):362-7. PMID: 9527150
Muscle histometry in patients with chronic fatigue syndrome generally did not show the changes expected as a result of inactivity. However, patients with abnormal lactate responses to exercise had a significantly lower proportion of mitochondria rich type 1 muscle fibres.​

De Becker P, Roeykens J, Reynders M, McGregor N, De Meirleir K. "Exercise capacity in chronic fatigue syndrome." Arch Intern Med. 2000 Nov 27;160(21):3270-7.
When compared with healthy sedentary women, female patients with CFS show a significantly decreased exercise capacity. This could affect their physical abilities to a moderate or severe extent. Reaching the age-predicted target heart rate seemed to be a limiting factor of the patients with CFS in achieving maximal effort, which could be due to autonomic disturbances.​

Nijs J, van Eupen I, Vandecauter J, et al. "Can pacing self-management alter physical behavior and symptom severity in chronic fatigue syndrome? A case series." J Rehabil Res Dev. 2009;46(7):985-96.
When comparing pre- versus post-treatment data, we found that the patients' ability to perform daily activities and the severity of their symptom complexes were improved (p = 0.043). Concentration difficulties, mood swings, muscle weakness, and intolerance to bright light improved as well.... We found that 3 weeks of pacing self-management was accompanied by a modest improvement in symptom severity and daily functioning.​

Lehman AM, Lehman DR, Hemphill KJ, Mandel DR, Cooper LM. "Illness experience, depression, and anxiety in chronic fatigue syndrome." J Psychosom Res. 2002 Jun;52(6):461-5. PMID: 12069870
Those who believed that limiting their physical exertion was the path to recovery (55%) had lower depression and anxiety scores (P's<.01) than their counterparts.​

Jason L, Benton M, Torres-Harding S, Muldowney K. "The impact of energy modulation on physical functioning and fatigue severity among patients with ME/CFS." Patient Educ Couns. 2009 Nov;77(2):237-41. PMID: 19356884
Those who were able to stay within their energy envelope had significant improvements in physical functioning and fatigue severity. Health care professionals that treat patients with ME/CFS might incorporate strategies that help patients self-monitor and self-regulate energy expenditures.​

No, the effects of this disease cannot be caused by deconditioning. In fact, longitudinal studies show that in CF and CFS patients, the fatigue came first and the reduction in activity came second. Again, no, this disease cannot possibly be caused by deconditioning. If these effects were caused by deconditioning, they would likely have already been noticed in some of the other better-studied disabling diseases that result in secondary deconditioning.

Back to the study, it would be valuable if they used sedentary controls. That should ideally be always a part of the matching process and then this "caused be deconditioning" bologna would be shut up forever. Some of the researchers make a point of doing using sedentary controls (Yammes, for instance, does). I can't tell if these authors did or not.

Often I can find full text of a study I want to read on one of the sites (MESA or someplace like that), but I couldn't find this one.
 

WillowJ

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No, I don't have that one to read either.

I read this one by the same team:
which is open access: http://www.jneuroengrehab.com/content/5/1/16 which I didn't find that exciting but the one you highlighted does sound more interesting. I may have been slightly prejudiced as I was able to compete and run at a high level before the illness so I feel my gait was not particularly bad before the illness (so not sure about the idea I think they suggested that it might be modifiable). Anyway, going from memory on that but will look up if it gets discussed.

I didn't find the gait one very interesting, either, particularly since they thought the gait difference could be due to self-selected slow speed of walking. Evidently they must have gotten curious why such a (usually) inefficient walking speed would be preferred. :)
 
Messages
24
Willow, thanks for the great summation and compilation of research on exercise and pacing. I'd read most of these before but putting them in one place amplifies the findings.

Singularly, I wouldn't bother bringing these abstracts to my doctor. Together, I will because they provide a clear picture of the physiology of exercise in ME/CFS and they show the real but limited value of pacing.
 

WillowJ

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WA, USA
Willow, thanks for the great summation and compilation of research on exercise and pacing. I'd read most of these before but putting them in one place amplifies the findings.

Singularly, I wouldn't bother bringing these abstracts to my doctor. Together, I will because they provide a clear picture of the physiology of exercise in ME/CFS and they show the real but limited value of pacing.

no problem--my pleasure. You're quite right about the amplified effect of multiple studies, especially when produced by different groups. :)
 

IamME

Too sick for an identity
Messages
110
Here we have reduced oxygen transport - I think that's what they are saying - simply during walking!

Why does it surprise you to have an abnormality on walking, given that it's a demanding thing for most sufferers?
 

Dolphin

Senior Member
Messages
17,567
Discussion section

Here's the discussion section - as one can see, deconditioning is mentioned a few times as a possible explanation so this study doesn't seem to prove much:

Discussion

Results of the study demonstrated that the average
PWS of subjects with CFS was significantly lower
than that of the control subjects. The PWS of the
CFS subjects was around 25% less than the reported
normal range of walking speed of approximately 1.2
1.4 m s71 [19] whereas control subjects were within
the reported range. The walking speed of the CFS
subjects reported here is lower than that previously
reported by our group (1.05 m s71and 0.99 m s71)
[6,7]. However, in our previous study subjects
walked for relatively short time and distance. In
contrast the present study required subjects to walk
continuously for 5 min. The PWS of our CFS
subjects was higher than that recorded by Clapp
et al. [20] (0.71 m s71) however these subjects were
walking on a motorised treadmill rendering direct
comparisons questionable.

In summary, those with CFS had a slower walking
speed and lower oxygen uptake when walking at
PWS. Although the relative oxygen uptake requirement
for walking was lower in those with CFS, when
the speed of walking was taken into consideration,
the metabolic cost of walking in those with CFS was
higher than that of controls. The fact that there
remained a difference between the two groups when
the speeds were matched suggests that the relatively
high energy demands which occur when walking for
those with CFS are in some way related to the
condition itself, or deconditioning associated with
the condition, and not just to the relatively slow PWS
observed.

These results demonstrate that CFS subjects, for
whatever reason, adopt a PWS that reduces their
oxygen uptake but increases the energy cost of
walking as measured by oxygen uptake per unit
distance. This maybe explained by a desire to
conserve energy (reduce oxygen uptake) and prevent
fatigue but has the opposite effect (increase oxygen
uptake per unit distance). One possible explanation
for this may be kinesiophobia, an excessive and
debilitating fear of movement which may be a
common feature of CFS [21]. Although no significant
correlation between kinesophobia and maximal
exercise capacity has been found [18] the presence of
kinesiophobia would explain the slow walking speed
observed in this study. In addition it may be that fear
of movement in those with CFS leads, like fear of
falling in other patient groups, to an increase in
muscle activation which in turn increases the oxygen
demand per unit distance ambulated.

Higher energy cost of walking may be due to
biomechanical or metabolic factors [9]. A number of
biomechanical factors have been proposed to explain
the reason for relatively low PWS seen in other
patient groups; these factors include poor balance,
fear of falling, spasticity, joint stiffness [9,22]. There
is some evidence that those with CFS may suffer
from dizziness which is related to orthostatic intolerance
[23]. This may lead to impaired balance
although the consequential effect on gait has not
been reported. Indeed our group have previously
reported no difference between CFS subjects and
healthy controls in terms of standing balance [6].

There is debate within the literature as to the
presence and extent of metabolic impairments in
those with CFS. Some studies have proposed that
metabolic differences between CFS and control
subjects may be due to mitochondrial abnormality.
McCully et al. [24] reported reduced muscle
oxidative capacity in those with CFS and suggested
this might be due to mitochondrial abnormality or
deconditioning. Barnes et al. [25] argued against
mitochondrial abnormality but again suggested that
observed metabolic differences between CFS and
control subjects could be explained by deconditioning.
It is possible that the present results may be partly
explained by the presence of deconditioning in those
with CFS. Even though the IPAQ was used to
exclude control subjects with high levels of physical
activity and thus to match CFS and control subjects
more closely in terms of physical activity profiles it
may be that overall CFS subjects had lower activity
levels than control subjects and, as such an increased
likelihood of deconditoning.

A high energy cost of walking can limit the type
and duration of everyday activity [26] as reflected in
the results obtained from the CFS-APQ. These
scores suggest that this group of CFS subjects
experienced limitations in at least some aspects of
their daily life and this may be due to the increased
energy requirements discussed.

Graded exercise and cognitive behavioural therapy
are management strategies which may be useful for
some people with CFS to try to reduce the adverse
physiological effects of inactivity and possible deconditioning.
However, exercise in itself can exacerbate
the symptoms of CFS as exercise performed at too
high an intensity can trigger immune dysfunction
[27]. To increase physical activity, reduce deconditioning
and reduce the physiological cost of walking,
whilst avoiding exacerbations, any exercise programme
for people with CFS should be undertaken
under direction of an appropriately qualified practitioner.

Previous research has investigated oxygen uptake
per unit distance, or the related energy expenditure,
in other pathophysiological conditions. Even allowing
for the methodological differences between the
studies the situation appears to be that the physiological
cost of walking for those with CFS is not very
dissimilar to that of other patient groups such as
those with Multiple Sclerosis [10], Post-poliomyelitis
Syndrome [28], patients with orthopaedic conditions
such as post-hip fracture [22] or patients 4 years
following a stroke [9].
 

richvank

Senior Member
Messages
2,732
Hi, all.

It amazes me that researchers continue to take seriously the notion that the physical problems in ME/CFS are the result of deconditioning. To me, in view of the evidence we have, the explanation is very clear. It is well-known that by far the biggest user of oxygen in the body is normally the mitochondria. It is also clear, especially from the work of Booth, Myhill and McLaren-Howard, as well as supporting data in the literature, that the mitochondria are dysfunctional in ME/CFS, and that the degree of mito dysfunction correlates well with the degree of physical disability. (In my view, this dysfunction is due mainly to glutathione depletion in the skeletal muscle cells and certain other types of cells, including the neutrophils in which McLaren-Howard has done his measurements).

Dysfunctioning mitochondria present a lower demand for oxygen (unless they are decoupled, in which case they produce a lot of heat, but this is not observed in ME/CFS, in which the peripheral body temperature is usually lower than normal, rather than higher). The dyfunctional mitochondria also produce ATP at a lower rate. ATP is needed to power muscle contraction. If it is being produced at a lower rate, the person is not going to be able to walk as fast for a sustained period of time. This accounts for the lower preferrred walking speed.

The inefficiency in oxygen utilization is explained by the fact that because the mitochondria are dysfunctional in the skeletal muscles in ME/CFS, the person has to rely more on anaerobic metabolism to produce their muscle ATP. This produces lactic acid, which must be sent to the liver for reconversion to glucose, via the Cori cycle. The liver, which does not have dysfunctional mitochondria, because it has a complete transsulfuration pathway and can thus convert methionine to cysteine to maintain its glutathione level, has to use oxygen to do this. This cycle is a much less efficient way to produce ATP than the normal oxidation of glucose by the mitochondria.

I think that this is very consistent with Dr. Paul Cheney's observation that the arterial oxygen percent saturation as monitored by a pulse oximeter does not drop in people with ME/CFS as fast as it does in normal, healthy people when they exhale and then hold their breath for 30 seconds. The mitochondria in people with ME/CFS are simply not demanding as much oxygen as in normal, healthy people, because they are dysfunctional, so the level in the blood stays higher when no additional oxygen is being put into the blood by breathing.

Best regards,

Rich
 

mellster

Marco
Messages
805
Location
San Francisco
Hi Rich,

Having been making good strides of aerobic exercise with methylation (I fit the slightly lower body temp profile) and other protocols I have been wondering why my muscle strength does not seem to decrease even during times of (very) limited exercise. In fact, sometimes I feel stronger (e.g. doing push-ups or presses) than before even though I am only very gradualy increasing the length/intensity of aerobic exercise (if at all). Could the forced takeover of anaerobic fibers account for the presence of relative good muscle strength while aerobic tolerance is lacking and occasional post-exertion muscle-twitch (or even PEM) be due to increased effort of said anaerobic fibers? This is a very interesting topic..