Short-term unilateral leg immobilization alters peripheral but not central arterial structure and function in healthy young humans

Rakobowchuk, Mark; Crozier, Jennifer; Glover, Elisa I.; Yasuda, Naomi; Phillips, Stuart M.; Tarnopolsky, Mark A.; MacDonald, Maureen J.

doi:10.1007/s00421-010-1636-y

Cited by 15 publications

(17 citation statements)

References 22 publications

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“…The brace was removed to check for pressure points daily and resealed with a custom-modified plastic strap that was melted to seal the strap and to prevent removal of the brace. Previous use of this model has, in our hands, proved effective and has resulted in degrees of muscle atrophy on par with that seen with casting and short-term bed rest (15, 17, 30–32).…”

Section: Methodsmentioning

confidence: 69%

A Novel Amino Acid Composition Ameliorates Short-Term Muscle Disuse Atrophy in Healthy Young Men

et al. 2019

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Skeletal muscle disuse leads to atrophy, declines in muscle function, and metabolic dysfunction that are often slow to recover. Strategies to mitigate these effects would be clinically relevant. In a double-blind randomized-controlled pilot trial, we examined the safety and tolerability as well as the atrophy mitigating effect of a novel amino acid composition (AXA2678), during single limb immobilization. Twenty healthy young men were randomly assigned (10 per group) to receive AXA2678 or an excipient- and energy-matched non-amino acid containing placebo (PL) for 28d: days 1–7, pre-immobilization; days 8–15, immobilization; and days 16–28 post-immobilization recovery. Muscle biopsies were taken on d1, d8 (immobilization start), d15 (immobilization end), and d28 (post-immobilization recovery). Magnetic resonance imaging (MRI) was utilized to assess quadriceps muscle volume (Mvol), muscle cross-sectional area (CSA), and muscle fat-fraction (FF: the fraction of muscle occupied by fat). Maximal voluntary leg isometric torque was assessed by dynamometry. Administration of AXA2678 attenuated muscle disuse atrophy compared to PL ( p < 0.05) with changes from d8 to d15 in PL: ΔMvol = −2.4 ± 2.3% and ΔCSA = −3.1% ± 2.1%, both p < 0.001 vs. zero; against AXA2678: ΔMvol: −0.7 ± 1.8% and ΔCSA: −0.7 ± 2.1%, both p > 0.3 vs. zero; and p < 0.05 between treatment conditions for CSA. During immobilization, muscle FF increased in PL but not in AXA2678 (PL: 12.8 ± 6.1%, AXA2678: 0.4 ± 3.1%; p < 0.05). Immobilization resulted in similar reductions in peak leg isometric torque and change in time-to-peak (TTP) torque in both groups. Recovery (d15–d28) of peak torque and TTP torque was also not different between groups, but showed a trend for better recovery in the AXA2678 group. Thrice daily consumption of AXA2678 for 28d was found to be safe and well-tolerated. Additionally, AXA2678 attenuated atrophy, and attenuated accumulation of fat during short-term disuse. Further investigations on the administration of AXA2678 in conditions of muscle disuse are warranted. Clinical Trial Registration: https://clinicaltrials.gov , identifier: NCT03267745.

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Section: Methodsmentioning

confidence: 69%

A Novel Amino Acid Composition Ameliorates Short-Term Muscle Disuse Atrophy in Healthy Young Men

et al. 2019

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“…Within 4-5 days of inactivity induced by bed rest there are reductions in limb blood flow [76] and signs of endothelial dysfunction [77]. As little as 2 weeks of limb immobilization has been shown to increase arterial stiffness [78]. Thus immobility in the elderly may perpetuate inactivity and reduce muscle power further promulgating a state of “extreme” vascular deconditioning.…”

Section: Discussionmentioning

confidence: 99%

Systemic Vascular Function Is Associated with Muscular Power in Older Adults

Heffernan

Chalé

Hau

et al. 2012

Journal of Aging Research

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Age-associated loss of muscular strength and muscular power is a critical determinant of loss of physical function and progression to disability in older adults. In this study, we examined the association of systemic vascular function and measures of muscle strength and power in older adults. Measures of vascular endothelial function included brachial artery flow-mediated dilation (FMD) and the pulse wave amplitude reactive hyperemia index (PWA-RHI). Augmentation index (AIx) was taken as a measure of systemic vascular function related to arterial stiffness and wave reflection. Measures of muscular strength included one repetition maximum (1RM) for a bilateral leg press. Peak muscular power was measured during 5 repetitions performed as fast as possible for bilateral leg press at 40% 1RM. Muscular power was associated with brachial FMD (r = 0.43, P < 0.05), PWA-RHI (r = 0.42, P < 0.05), and AIx (r = −0.54, P < 0.05). Muscular strength was not associated with any measure of vascular function. In conclusion, systemic vascular function is associated with lower-limb muscular power but not muscular strength in older adults. Whether loss of muscular power with aging contributes to systemic vascular deconditioning or vascular dysfunction contributes to decrements in muscular power remains to be determined.

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“…Animal studies have reported arteriolar rarefaction (reduced number of arterioles) in rodent muscle with ageing (Behnke et al 2006). This may be facilitated by a combination of factors including reduced physical activity (Sugawara et al 2004; Rakobowchuk et al 2011), endothelial dysfunction (Taddei et al 2001) and lower nitric oxide bioavailability (Nyberg et al 2012 a ), leading to remodelling of the vascular tree (rarefaction). Other mechanisms, like altered sympatholysis, may also play a role (see below).…”

Section: Muscle Fibre Type Training and Reduced Physical Activitymentioning

confidence: 99%

Skeletal muscle vasodilatation during maximal exercise in health and disease

Calbet

Lundby

2012

The Journal of Physiology

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Maximal exercise vasodilatation results from the balance between vasoconstricting and vasodilating signals combined with the vascular reactivity to these signals. During maximal exercise with a small muscle mass the skeletal muscle vascular bed is fully vasodilated. During maximal whole body exercise, however, vasodilatation is restrained by the sympathetic system. This is necessary to avoid hypotension since the maximal vascular conductance of the musculature exceeds the maximal pumping capacity of the heart. Endurance training and high-intensity intermittent knee extension training increase the capacity for maximal exercise vasodilatation by 20-30%, mainly due to an enhanced vasodilatory capacity, as maximal exercise perfusion pressure changes little with training. The increase in maximal exercise vascular conductance is to a large extent explained by skeletal muscle hypertrophy and vascular remodelling. The vasodilatory capacity during maximal exercise is reduced or blunted with ageing, as well as in chronic heart failure patients and chronically hypoxic humans; reduced vasodilatory responsiveness and increased sympathetic activity (and probably, altered sympatholysis) are potential mechanisms accounting for this effect. Pharmacological counteraction of the sympathetic restraint may result in lower perfusion pressure and reduced oxygen extraction by the exercising muscles. However, at the same time fast inhibition of the chemoreflex in maximally exercising humans may result in increased vasodilatation, further confirming a restraining role of the sympathetic nervous system on exercise-induced vasodilatation. This is likely to be critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity.

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Short-term unilateral leg immobilization alters peripheral but not central arterial structure and function in healthy young humans

Cited by 15 publications

References 22 publications

A Novel Amino Acid Composition Ameliorates Short-Term Muscle Disuse Atrophy in Healthy Young Men

A Novel Amino Acid Composition Ameliorates Short-Term Muscle Disuse Atrophy in Healthy Young Men

Systemic Vascular Function Is Associated with Muscular Power in Older Adults

Skeletal muscle vasodilatation during maximal exercise in health and disease

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