Slowed Exercise-Onset Vo<sub>2</sub> Kinetics During Submaximal Endurance Exercise in Subjects With Multiple Sclerosis

Hansen, Dominique; Wens, Inez; Kosten, Lauren; Verboven, Kenneth; Eijnde, Bert O.

doi:10.1177/1545968312451916

Cited by 26 publications

(42 citation statements)

References 34 publications

(50 reference statements)

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“…Next, subjects were instructed to cycle at a rate of 70 rpm, against a resistance corresponding to 25% of predicted cycling power output ( W max⁡ ), for six minutes [19]. After six minutes of cycling subjects remained seated on bike for additional six minutes, after which a second 6-minute exercise bout was initiated.…”

Section: Methodsmentioning

confidence: 99%

“…Exercise-onset VO 2 kinetics were calculated algebraically and expressed as mean response time (MRT), as explained previously [19]. The two MRT's that were obtained from the two exercise bouts were averaged.…”

Section: Methodsmentioning

confidence: 99%

“…It is thus generally accepted that assessing exercise-onset VO 2 kinetics is a sensitive tool for the specific evaluation of muscle oxidative capacity [18]. Intriguingly, exercise-onset VO 2 kinetics are significantly slowed in subjects with MS [19]. Such impaired muscle oxidative capacity might thus interfere with walking capacity in subjects with MS.…”

Section: Introductionmentioning

confidence: 99%

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Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Hansen

Feys

Wens

et al. 2014

Multiple Sclerosis International

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Background and Purpose. Walking capacity is reduced in subjects with multiple sclerosis (MS). To develop effective exercise interventions to enhance walking capacity, it is important to determine the impact of factors, modifiable by exercise intervention (maximal muscle strength versus muscle oxidative capacity), on walking capacity. The purpose of this pilot study is to discriminate between the impact of maximal muscle strength versus muscle oxidative capacity on walking capacity in subjects with MS. Methods. From 24 patients with MS, muscle oxidative capacity was determined by calculation of exercise-onset oxygen uptake kinetics (mean response time) during submaximal exercise bouts. Maximal muscle strength (isometric knee extension and flexion peak torque) was assessed on dynamometer. All subjects completed a 6-minute walking test. Relationships between walking capacity (as a percentage of normal value) and muscle strength (of knee flexors and extensors) versus muscle oxidative capacity were assessed in multivariate regression analyses. Results. The expanded disability status score (EDSS) showed a significant univariate correlation (r = −0.70, P < 0.004) with walking capacity. In multivariate regression analyses, EDSS and mean response time, but not muscle strength, were independently related to walking capacity (P < 0.05). Conclusions. Walking distance is, next to disability level and not taking neurologic symptoms/deficits into account, primarily related to muscle oxidative capacity in subjects with MS. Additional study is needed to further examine/verify these findings.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Hansen

Feys

Wens

et al. 2014

Multiple Sclerosis International

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“…In brief, after a 3-min period to obtain resting data, subjects were instructed to cycle (70 rpm) against a resistance corresponding to 25% of their predicted maximal cycling power output (W max ) for 6 min [23,24]. By multiplying the resultant MRT by 60, a value expressed in seconds was produced, which was used to quantify exercise-onset VO 2 kinetics [25] and which is reported for both exercise bouts separately. Next, subjects remained seated on the bike for 6 min of rest, followed by a 6 min exercise bout, applying the same intensity as during the first cycling period.…”

Section: Compliance Measures (For Persons With Ms Only)mentioning

confidence: 99%

“…MRT then equals the division of this oxygen deficit by the difference between resting VO 2 and steady state VO 2 . By multiplying the resultant MRT by 60, a value expressed in seconds was produced, which was used to quantify exercise-onset VO 2 kinetics [25] and which is reported for both exercise bouts separately.…”

Section: Compliance Measures (For Persons With Ms Only)mentioning

confidence: 99%

Brain derived neurotrophic factor in multiple sclerosis: effect of 24 weeks endurance and resistance training

Wens

Keytsman

Deckx

et al. 2016

Euro J of Neurology

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Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis

Spaas

Goulding

Keytsman

et al. 2022

J cachexia sarcopenia muscle

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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 (V ˙O2peak , 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 V ˙O2 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. V ˙O2peak , 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 (À40%, P = 0.047) and II (À45%, P = 0.026) were lower in MS patients versus controls. Muscle capillary/fibre ratio correlated with V ˙O2peak 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). V ˙O2peak 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.

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Slowed Exercise-Onset Vo₂ Kinetics During Submaximal Endurance Exercise in Subjects With Multiple Sclerosis

Cited by 26 publications

References 34 publications

Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Brain derived neurotrophic factor in multiple sclerosis: effect of 24 weeks endurance and resistance training

Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis

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Slowed Exercise-Onset Vo2 Kinetics During Submaximal Endurance Exercise in Subjects With Multiple Sclerosis

Cited by 26 publications

References 34 publications

Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Is Walking Capacity in Subjects with Multiple Sclerosis Primarily Related to Muscle Oxidative Capacity or Maximal Muscle Strength? A Pilot Study

Brain derived neurotrophic factor in multiple sclerosis: effect of 24 weeks endurance and resistance training

Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis

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Slowed Exercise-Onset Vo₂ Kinetics During Submaximal Endurance Exercise in Subjects With Multiple Sclerosis