Correction: The effect of an airflow restriction mask (ARM) on metabolic, ventilatory, and electromyographic responses to continuous cycling exercise

AbstractExercise training influences the risk of vascular thrombosis in patients with peripheral arterial disease (PAD). Mitochondrial functionalities in platelets involve the cellular bioenergetics and thrombogenesis. This study aimed to elucidate the effect of cycling exercise training (CET) on platelet mitochondrial bioenergetics in PAD patients. Forty randomly selected patients with PAD engaged in general rehabilitation (GR) with CET (i.e., cycling exercise at ventilation threshold for 30 minute/day, 3 days/week) (GR + CET, n = 20) or to a control group that only received GR course (n = 20) for 12 weeks. Systemic aerobic capacity and platelet mitochondrial bioenergetics that included oxidative phosphorylation (OXPHOS) and electron transport system (ETS) were measured using automatic gas analysis and high-resolution respirometry, respectively. The experimental results demonstrated that GR + CET for 12 weeks significantly (1) elevated VO2peak and lowered VE-VCO2 slope, (2) raised resting ankle-brachial index and enhanced cardiac output response to exercise, (3) increased the distance in 6-minute walk test and raised the Short Form-36 physical/mental component scores, and (4) enhanced capacities of mitochondrial OXPHOS and ETS in platelets by activating FADH2 (complex II)-dependent pathway. Moreover, changes in VO2peak levels were positively associated with changes in platelet OXPHOS and ETS capacities. However, no significant changes in systemic aerobic capacity, platelet mitochondrial bioenergetics, and health-related quality of life (HRQoL) occurred following GR alone. Hence, we conclude that CET effectively increases the capacities of platelet mitochondrial bioenergetics by enhancing complex II activity in patients with PAD. Moreover, the exercise regimen also enhanced functional exercise capacity, consequently improving HRQoL in PAD patients.

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Remote muscle priming anodal transcranial direct current stimulation attenuates short interval intracortical inhibition and increases time to task failure of a constant workload cycling exercise

Experimental Brain Research ◽

10.1007/s00221-021-06103-x ◽

2021 ◽

Author(s):

Simranjit K. Sidhu

Keyword(s):

Direct Current ◽

Transcranial Direct Current Stimulation ◽

Short Interval ◽

Intracortical Inhibition ◽

Cycling Exercise ◽

Task Failure ◽

Direct Current Stimulation

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Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00438.2004 ◽

2005 ◽

Vol 288 (3) ◽

pp. R591-R599 ◽

Cited By ~ 39

Author(s):

Mitsuharu Okutsu ◽

Kenji Ishii ◽

Kai Jun Niu ◽

Ryoichi Nagatomi

Keyword(s):

T Lymphocytes ◽

Mononuclear Cells ◽

Cxcr4 Expression ◽

Peripheral Blood Mononuclear ◽

Cycling Exercise ◽

Ru 486 ◽

Before And After ◽

Stromal Cell Derived Factor ◽

Chemokine Receptor 4

The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol- or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1α/CXCL12. Cortisol dose- and time-dependently augmented CXCR4 expression on T lymphocytes, with <6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise.

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Locomotor exercise induces long-lasting impairments in the capacity of the human motor cortex to voluntarily activate knee extensor muscles

Journal of Applied Physiology ◽

10.1152/japplphysiol.90911.2008 ◽

2009 ◽

Vol 106 (2) ◽

pp. 556-565 ◽

Cited By ~ 84

Author(s):

Simranjit K. Sidhu ◽

David J. Bentley ◽

Timothy J. Carroll

Keyword(s):

Motor Cortex ◽

Motor Nerve ◽

Maximum Voluntary Contraction ◽

Voluntary Activation ◽

Exercise Session ◽

Knee Extensors ◽

Central Component ◽

Control Session ◽

Cycling Exercise ◽

Human Motor Cortex

Muscle fatigue is a reduction in the capacity to exert force and may involve a “central” component originating in the brain and/or spinal cord. Here we examined whether supraspinal factors contribute to impaired central drive after locomotor endurance exercise. On 2 separate days, 10 moderately active individuals completed a locomotor cycling exercise session or a control session. Brief (2 s) and sustained (30 s) isometric knee extension contractions were completed before and after locomotor exercise consisting of eight, 5-min bouts of cycling at 80% of maximum workload. In the control session, subjects completed the isometric contractions in a rested state. Twitch responses to supramaximal motor nerve stimulation and transcranial magnetic stimulation were obtained to assess peripheral force-generating capacity and voluntary activation. Maximum voluntary contraction (MVC) force during brief contractions decreased by 23 ± 6.3% after cycling exercise and remained 12 ± 2.8% below baseline 45 min later ( F1,9 > 15.5; P < 0.01). Resting twitch amplitudes declined by ∼45% ( F1,9 = 28.3; P < 0.001). Cortical voluntary activation declined from 90.6 ± 1.6% at baseline to 80.6 ± 2.1% after exercise ( F1,9 = 28.0; P < 0.001) and remained significantly reduced relative to control 30–45 min later (80.6 ± 3.4%; F1,9 = 10.7; P < 0.01). Thus locomotor exercise caused a long-lasting impairment in the capacity of the motor cortex to drive the knee extensors. Force was reduced more during sustained MVC after locomotor exercise than in the control session. Peripheral mechanisms contributed relatively more to this force reduction in the control session, whereas supraspinal fatigue played a greater role in sustained MVC reduction after locomotor exercise.

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