You’ve probably heard about pacing, or maybe you haven’t. If you have, you may know that it is a management technique used in illnesses that give low energy levels and pain. Pacing consists of listening to your body, and seeing symptoms as signs, usually of overactivity. You use information from your body to reorganise your activities to get as low a symptom level as possible. This usually means splitting activities into smaller bits and taking frequent rest breaks. It also means finding less strenuous ways of performing activities. When less energy is spent on some activities, you’ll have more energy left over to have fun. Although that is an obvious boon, you’re probably not jumping up and down right now thinking “Hooray, pacing is what I’ve always dreamed of”. So why bother? Is there any point in even trying?
Why Bother About Pacing?
Let’s have a brief look at some of the relevant research. Several studies have shown that people with ME produce less energy in their cells than healthy people. Dr Sarah Myhill and colleagues looked at five different aspects of cell metabolism, and found that it varied from person to person how compromised each part of the metabolism was. However, the total amount of energy production problems for each person correlated almost perfectly with the person’s level on a disability scale. In other words, the worse the energy production problems were, the more ill the people were and the less they could do. This shows that the feeling of lack of energy in ME isn’t just a feeling; it’s a sign that the energy production is actually lower than in healthy people.
Several groups of researchers have looked at the effect of exercise testing in ME, particularly maximal exercise testing done twice 24 hours apart. The oxygen uptake dropped significantly on the second test in people with ME, whereas healthy people either did just as well as the day before or even a bit better. The changes in the bodies of ME patients are so characteristic that these tests have been considered a possible diagnostic test. However, people with ME don’t just perform worse on the second day of the test; their gene expression also changes on the second day. Gene expression is about which genes are turned on and which genes are turned off. When people with ME are overexerted, genes that lower the metabolism and change the immune system are activated. This does not happen in healthy people. Basically, these tests show that overexertion activates the disease process in ME, and it also actively worsens the disease process and the functional ability of the patients. In other words, doing too much makes you more ill. That’s why it’s so important to learn pacing, as the whole point of pacing is to stay within one’s energy limits, thereby avoiding overexertion. You can read more about this in the next article in this series.
References:
Betsy A Keller, John Luke Pyor and Ludovic Giloteaux. (2014) “Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO2peak indicates functional impairment” Journal of Translational Medicine 12:104
Bouquet J, Li T, Gardy JL, Kang X, Stevens S, Stevens J, et al. (2019) “Whole blood human transcriptome and virome analysis of ME/CFS patients experiencing post-exertional malaise following cardiopulmonary exercise testing.” PLoS ONE 14(3):e0212193
Christopher R. Snell, J. Mark Vanness, David R. Strayer. (2005) “Exercise Capacity and Immune Function in Male and Female Patients with Chronic Fatigue Syndrome (CFS)” In Vivo 19:237-390
Katarina Lien, Bjørn Johansen, Marit B. Veierød, Annicke S. Haslestad, Siv K. Bøhn, Morten N. Melsom, et al. “Abnormal blood lactate accumulation during repeated exercise testing in myalgig encephalomyelitis/chronic fatigue syndrome” (2019) Physol Rep, 7(11):e14138
J. Mark Vanness, Christopher R. Snell, Dean M. Fredrickson, David R. Strayer & Staci R. Stevens (2001) “Assessment of Functional Impairment by Cardiopulmonary Exercise Testing in Patients with Chronic Fatigue Syndrome”, Journal of Chronic Fatigue Syndrome, 8:3-4, 103-109
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2009) “Chronic fatigue syndrome and mitochondrial dysfunction” International Journal of Clinical and Experimental Medicine 2, 1-16
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2012) “Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)” International Journal of Clinical and Experimental Medicine 5(3):208-220
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2013) “Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) – a clinical audit” International Journal of Clinical and Experimental Medicine 6(1):1-15
Snell CR, Stevens SR, Davenport TE, Van Ness JM. (2013) “Discriminative validity of metabolic and workload measurements for identifying people with chronic fatigue syndrome” Physical Therapy 93:1484-1492
©Copyright Ingebjørg Midsem Dahl 2019
ME groups are welcome to reprint this article in their newsletter or link to it, provided that nothing is changed. If you wish to translate it, please email me: [email protected]
Why Bother About Pacing?
Let’s have a brief look at some of the relevant research. Several studies have shown that people with ME produce less energy in their cells than healthy people. Dr Sarah Myhill and colleagues looked at five different aspects of cell metabolism, and found that it varied from person to person how compromised each part of the metabolism was. However, the total amount of energy production problems for each person correlated almost perfectly with the person’s level on a disability scale. In other words, the worse the energy production problems were, the more ill the people were and the less they could do. This shows that the feeling of lack of energy in ME isn’t just a feeling; it’s a sign that the energy production is actually lower than in healthy people.
Several groups of researchers have looked at the effect of exercise testing in ME, particularly maximal exercise testing done twice 24 hours apart. The oxygen uptake dropped significantly on the second test in people with ME, whereas healthy people either did just as well as the day before or even a bit better. The changes in the bodies of ME patients are so characteristic that these tests have been considered a possible diagnostic test. However, people with ME don’t just perform worse on the second day of the test; their gene expression also changes on the second day. Gene expression is about which genes are turned on and which genes are turned off. When people with ME are overexerted, genes that lower the metabolism and change the immune system are activated. This does not happen in healthy people. Basically, these tests show that overexertion activates the disease process in ME, and it also actively worsens the disease process and the functional ability of the patients. In other words, doing too much makes you more ill. That’s why it’s so important to learn pacing, as the whole point of pacing is to stay within one’s energy limits, thereby avoiding overexertion. You can read more about this in the next article in this series.
References:
Betsy A Keller, John Luke Pyor and Ludovic Giloteaux. (2014) “Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO2peak indicates functional impairment” Journal of Translational Medicine 12:104
Bouquet J, Li T, Gardy JL, Kang X, Stevens S, Stevens J, et al. (2019) “Whole blood human transcriptome and virome analysis of ME/CFS patients experiencing post-exertional malaise following cardiopulmonary exercise testing.” PLoS ONE 14(3):e0212193
Christopher R. Snell, J. Mark Vanness, David R. Strayer. (2005) “Exercise Capacity and Immune Function in Male and Female Patients with Chronic Fatigue Syndrome (CFS)” In Vivo 19:237-390
Katarina Lien, Bjørn Johansen, Marit B. Veierød, Annicke S. Haslestad, Siv K. Bøhn, Morten N. Melsom, et al. “Abnormal blood lactate accumulation during repeated exercise testing in myalgig encephalomyelitis/chronic fatigue syndrome” (2019) Physol Rep, 7(11):e14138
J. Mark Vanness, Christopher R. Snell, Dean M. Fredrickson, David R. Strayer & Staci R. Stevens (2001) “Assessment of Functional Impairment by Cardiopulmonary Exercise Testing in Patients with Chronic Fatigue Syndrome”, Journal of Chronic Fatigue Syndrome, 8:3-4, 103-109
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2009) “Chronic fatigue syndrome and mitochondrial dysfunction” International Journal of Clinical and Experimental Medicine 2, 1-16
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2012) “Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)” International Journal of Clinical and Experimental Medicine 5(3):208-220
Sarah Myhill, Norman E Booth and John McLaren-Howard. (2013) “Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) – a clinical audit” International Journal of Clinical and Experimental Medicine 6(1):1-15
Snell CR, Stevens SR, Davenport TE, Van Ness JM. (2013) “Discriminative validity of metabolic and workload measurements for identifying people with chronic fatigue syndrome” Physical Therapy 93:1484-1492
©Copyright Ingebjørg Midsem Dahl 2019
ME groups are welcome to reprint this article in their newsletter or link to it, provided that nothing is changed. If you wish to translate it, please email me: [email protected]