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Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis, 2022, Spaas et al

Discussion in 'Other health news and research' started by Andy, Aug 6, 2022.

  1. Andy

    Andy Committee Member

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    Hampshire, UK
    Abstract

    Background
    Patients with multiple sclerosis (MS) experience reduced exercise tolerance that substantially reduces quality of life. The mechanisms underpinning exercise intolerance in MS are not fully clear. This study aimed to determine the contributions of the cardiopulmonary system and peripheral muscle in MS-induced exercise intolerance before and after exercise training.

    Methods
    Twenty-three patients with MS (13 women) and 20 age-matched and sex-matched healthy controls (13 women) performed a cardiopulmonary exercise test. Muscle fibre type composition, size, succinate dehydrogenase (SDH) activity, capillarity, and gene expression and proteins related to mitochondrial density were determined in vastus lateralis muscle biopsies. Nine MS patients (five women) were re-examined following a 12 week exercise training programme consisting of high-intensity cycling interval and resistance training.

    Results
    Patients with MS had lower maximal oxygen uptake compared with healthy controls (V̇O2peak, 25.0 ± 8.5 vs. 35.7 ± 6.4 mL/kg/min, P < 0.001). The lower gas exchange threshold (MS: 14.5 ± 5.5 vs. controls: 19.7 ± 2.9 mL/kg/min, P = 0.01) and slope of V̇O2 versus work rate (MS: 9.5 ± 1.7 vs. controls: 10.8 ± 1.1 mL/min/W, P = 0.01) suggested an intramuscular contribution to exercise intolerance in patients with MS. Muscle SDH activity was 22% lower in MS (P = 0.004), and strongly correlated with several indices of whole-body exercise capacity in MS patients (e.g. V̇O2peak, Spearman's ρ = 0.81, P = 0.002), but not healthy controls (ρ = 0.24, P = 0.38). In addition, protein levels of mitochondrial OXPHOS complexes I (−40%, P = 0.047) and II (−45%, P = 0.026) were lower in MS patients versus controls. Muscle capillary/fibre ratio correlated with V̇O2peak in healthy controls (ρ = 0.86, P < 0.001) but not in MS (ρ = 0.35, P = 0.22), and did not differ between groups (1.41 ± 0.30 vs. 1.47 ± 0.38, P = 0.65). Expression of genes involved in mitochondrial function, such as PPARA, PPARG, and TFAM, was markedly reduced in muscle tissue samples of MS patients (all P < 0.05). No differences in muscle fibre type composition or size were observed between groups (all P > 0.05). V̇O2peak increased by 23% following exercise training in MS (P < 0.001); however, no changes in muscle capillarity, SDH activity, gene or protein expression were observed (all P > 0.05).

    Conclusions
    Skeletal muscle oxidative phenotype (mitochondrial complex I and II content, SDH activity) is lower in patients with MS, contributing to reduced exercise tolerance. However, skeletal muscle mitochondria appeared resistant to the beneficial effects of exercise training, suggesting that other physiological systems, at least in part, drive the improvements in exercise capacity following exercise training in MS.

    Open access, https://onlinelibrary.wiley.com/doi/10.1002/jcsm.13050
     
    Hutan, RedFox, Sean and 6 others like this.
  2. Andy

    Andy Committee Member

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    Location:
    Hampshire, UK
    "Deconditioning versus MS pathology

    Skeletal muscle weakness in MS patients is often suggested to be caused by physical inactivity-induced deconditioning, as opposed to primary effects of the condition per se.18, 21 We tested the hypothesis that skeletal muscle dysfunction in MS is primarily related to muscle deconditioning (as opposed to MS pathophysiology) in the present study by (i) comparing MS patients with a group of healthy controls with similar levels of physical activity and by (ii) subjecting MS patients to an exercise training regimen similar to that which has previously been shown to result in substantial skeletal muscle mitochondrial adaptations and improvements in muscle size in healthy individuals.30, 31 Hence, if the skeletal muscle alterations that we observed at baseline were due to physical inactivity and/or deconditioning, we would have expected an improvement in these variables following the exercise training intervention. That this was not the case strongly suggests that MS pathophysiology per se, and not deconditioning, is the primary mediator of the skeletal muscle myopathy phenotype observed in MS.18, 21, 22, 32, 33 Moreover, the present data demonstrate that muscle mitochondrial alterations precede the changes in muscle FCSA and fibre type composition in MS pathology observed by other studies.8, 17"
     
    Hutan, RedFox, Sean and 6 others like this.
  3. merylg

    merylg Established Member (Voting Rights)

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    Or that people with a certain muscle myopathy are predisposed to MS?
     
    alktipping and Peter Trewhitt like this.
  4. Snow Leopard

    Snow Leopard Senior Member (Voting Rights)

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    Australia
    That's because these measures don't actually have much to do with VO2Max or muscle strength for people of normal fitness, (except perhaps capillarity for highly trained individuals).
     
    FMMM1, Sean, Medfeb and 4 others like this.
  5. rvallee

    rvallee Senior Member (Voting Rights)

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    12,299
    Location:
    Canada
    It's really hard to process that this is how medical science works. It's so far apart from other fields of science in how there can be open speculation about things that are easily verifiable and professionals simply choose not to verify them because it would end the speculation.

    Because here they do, and let's be honest about it, it won't stop a single future speculative claim from happening. Just like how Wessely pretends that one of the main achievements of his career working on what he calls CFS was thinking, then proving that it's not depression, even though he is very likely aware that this is exactly what most physicians believe, since it's what they're usually taught. More than anything, what they're taught is completely vague, even though the basis for discriminating against us is that our symptoms are vague, even though they are not.

    Exact same thing with deconditioning in ME. It's been debunked thoroughly, and yet no one accepts the debunking. This is the self-correcting process of science being broken entirely for the purpose of maintaining an ideological belief system. It's a lesser process where a higher one is needed. Beyond absurd.
     
    RedFox, merylg, alktipping and 2 others like this.

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