Effects of Age on $$ (\dot V{O_2}) $$ Kinetics During Calf and Cycling Exercise

1995 ◽  
pp. 195-200 ◽  
Author(s):  
P. D. Chilibeck ◽  
D. H. Paterson ◽  
D. A. Cunningham
Keyword(s):  
Cycling Exercise

Cycling Exercise Training Enhances Platelet Mitochondrial Bioenergetics in Patients with Peripheral Arterial Disease: A Randomized Controlled Trial

2021 ◽  
Author(s):  
Tieh-Cheng Fu ◽  
Ming-Lu Lin ◽  
Chih-Chin Hsu ◽  
Shu-Chun Huang ◽  
Yu-Ting Lin ◽  
...  
Keyword(s):  
Exercise Training ◽  
Peripheral Arterial Disease ◽  
Aerobic Capacity ◽  
Short Form ◽  
Arterial Disease ◽  
Control Group ◽  
Mitochondrial Bioenergetics ◽  
Cycling Exercise ◽  
Complex Ii ◽  
Peripheral Arterial

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.

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

2005 ◽  
Vol 288 (3) ◽  
pp. R591-R599 ◽  
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.

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

2009 ◽  
Vol 106 (2) ◽  
pp. 556-565 ◽  
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.

COMPARISON OF WALKING AND LOW-SIT CYCLING EXERCISE IN THE ELDERLY

1991 ◽  
Vol 11 (5) ◽  
pp. 318
Author(s):  
Tom R. Thomas ◽  
Lucy P. Zahler ◽  
Karen K. Mcmillan ◽  
Vaskar Mukerji
Keyword(s):  
The Elderly ◽  
Cycling Exercise

Cycling exercise with functional electrical stimulation improves postural control in stroke patients

2012 ◽  
Vol 35 (3) ◽  
pp. 506-510 ◽  
Author(s):  
Hsin-Chang Lo ◽  
Yung-Chun Hsu ◽  
Ya-Hsin Hsueh ◽  
Chun-Yu Yeh
Keyword(s):  
Electrical Stimulation ◽  
Postural Control ◽  
Functional Electrical Stimulation ◽  
Stroke Patients ◽  
Cycling Exercise

Oxidation of combined ingestion of glucose and fructose during exercise

2004 ◽  
Vol 96 (4) ◽  
pp. 1277-1284 ◽  
Author(s):  
Roy L. P. G. Jentjens ◽  
Luke Moseley ◽  
Rosemary H. Waring ◽  
Leslie K. Harding ◽  
Asker E. Jeukendrup
Keyword(s):  
Power Output ◽  
Statistical Significance ◽  
Random Order ◽  
Carbohydrate Oxidation ◽  
Maximum Power ◽  
The Other ◽  
Cycling Exercise ◽  
Oxidation Rates ◽  
Maximum Power Output ◽  
Exercise Period

The purpose of the present study was to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenous carbohydrate oxidation rates >1 g/min. Eight trained cyclists (maximal O2consumption: 62 ± 3 ml·kg-1·min-1) performed four exercise trials in random order. Each trial consisted of 120 min of cycling at 50% maximum power output (63 ± 2% maximal O2consumption), while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose + 1.2 g/min of glucose (Fruc+Glu), or water. The ingested fructose was labeled with [U-13C]fructose, and the ingested glucose was labeled with [U-14C]glucose. Peak exogenous carbohydrate oxidation rates were ∼55% higher ( P < 0.001) in Fruc+Glu (1.26 ± 0.07 g/min) compared with Med-Glu and High-Glu (0.80 ± 0.04 and 0.83 ± 0.05 g/min, respectively). Furthermore, the average exogenous carbohydrate oxidation rates over the 60- to 120-min exercise period were higher ( P < 0.001) in Fruc+Glu compared with Med-Glu and High-Glu (1.16 ± 0.06, 0.75 ± 0.04, and 0.75 ± 0.04 g/min, respectively). There was a trend toward a lower endogenous carbohydrate oxidation in Fruc+Glu compared with the other two carbohydrate trials, but this failed to reach statistical significance ( P = 0.075). The present results demonstrate that, when fructose and glucose are ingested simultaneously at high rates during cycling exercise, exogenous carbohydrate oxidation rates can reach peak values of ∼1.3 g/min.

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