Song-Young Park

Impact of age on the vasodilatory function of human skeletal muscle feed arteries

Although advancing age is often associated with attenuated skeletal muscle blood flow and skeletal muscle feed arteries (SMFAs) have been recognized to play a regulatory role in the vasculature, little is known about the impact of age on the vasodilatory capacity of human SMFAs. Therefore, endothelium-dependent and -independent vasodilation were assessed in SMFAs (diameter: 544 ± 63 μm) obtained from 24 (equally represented) young (33 ± 2 yr) and old (71 ± 2 yr) subjects in response to three stimuli: 1) flow-induced shear stress, 2) ACh, and 3) sodium nitropusside (SNP). Both assessments of endothelium-dependent vasodilation, flow (young subjects: 68 ± 1% and old subjects: 32 ± 7%) and ACh (young subjects: 92 ± 3% and old subjects: 73 ± 4%), were significantly blunted (P < 0.05) in SMFAs of old compared with young subjects, with no such age-related differences in endothelium-independent vasodilation (SNP). In response to an increase in flow-induced shear stress, vasodilation kinetics (time constant to reach 63% of the amplitude of the response: 55 ± 1 s in young subjects and 92 ± 7 s in old subjects) and endothelial nitric oxide synthase (eNOS) activation (phospho-eNOS(s1177)/total eNOS: 1.0 ± 0.1 in young subjects and 0.2 ± 0.1 in old subjects) were also significantly attenuated in old compared with young subjects (P < 0.05). Furthermore, the vessel superoxide concentration was greater in old subjects (old subjects: 3.9 ± 1.0 area under curve/mg and young subjects: 1.7 ± 0.1 area under the curve/mg, P < 0.05). These findings reveal that the endothelium-dependent vasodilatory capacity, including vasodilation kinetics but not smooth muscle function, of human SMFAs is blunted with age and may be due to free radicals. Given the potential regulatory role of SMFAs in skeletal muscle blood flow, these findings may explain, at least in part, the often observed attenuated perfusion of skeletal muscle with advancing age that may contribute to exercise intolerance in the elderly.

Quadriceps exercise intolerance in patients with chronic obstructive pulmonary disease: the potential role of altered skeletal muscle mitochondrial respiration

This study sought to determine if qualitative alterations in skeletal muscle mitochondrial respiration, associated with decreased mitochondrial efficiency, contribute to exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). Using permeabilized muscle fibers from the vastus lateralis of 13 patients with COPD and 12 healthy controls, complex I (CI) and complex II (CII)-driven State 3 mitochondrial respiration were measured separately (State 3:CI and State 3:CII) and in combination (State 3:CI+CII). State 2 respiration was also measured. Exercise tolerance was assessed by knee extensor exercise (KE) time to fatigue. Per milligram of muscle, State 3:CI+CII and State 3:CI were reduced in COPD (P < 0.05), while State 3:CII and State 2 were not different between groups. To determine if this altered pattern of respiration represented qualitative changes in mitochondrial function, respiration states were examined as percentages of peak respiration (State 3:CI+CII), which revealed altered contributions from State 3:CI (Con 83.7 ± 3.4, COPD 72.1 ± 2.4%Peak, P < 0.05) and State 3:CII (Con 64.9 ± 3.2, COPD 79.5 ± 3.0%Peak, P < 0.05) respiration, but not State 2 respiration in COPD. Importantly, a diminished contribution of CI-driven respiration relative to the metabolically less-efficient CII-driven respiration (CI/CII) was also observed in COPD (Con 1.28 ± 0.09, COPD 0.81 ± 0.05, P < 0.05), which was related to exercise tolerance of the patients (r = 0.64, P < 0.05). Overall, this study indicates that COPD is associated with qualitative alterations in skeletal muscle mitochondria that affect the contribution of CI and CII-driven respiration, which potentially contributes to the exercise intolerance associated with this disease.

Combined exercise reduces arterial stiffness, blood pressure, and blood markers for cardiovascular risk in postmenopausal women with hypertension.

Objective: Postmenopausal women exhibit elevated brachial-ankle pulse wave velocity (baPWV), an indicator of arterial stiffness, which is associated with an increased risk of cardiovascular events and mortality. The purpose of this study is to examine the impact of combined resistance and aerobic exercise training on baPWV, blood pressure (BP), and cardiovascular fitness in postmenopausal women with stage 1 hypertension. Methods: Twenty postmenopausal women (age, 75 ± 2 y; systolic BP, 152 ± 2 mm Hg, diastolic BP, 95 ± 3 mm Hg) were randomly assigned to a “no-exercise” (CON, n = 10) or combined exercise (EX, n = 10) group. The EX group performed resistance and aerobic exercise for 12 weeks, 3 times per week. Exercise intensity was increased gradually, from 40% to 70% of heart rate reserve, every 4 weeks. BaPWV, BP, blood nitrite/nitrate, endothelin-1 (ET-1), cardiovascular fitness, and body composition were measured before and after the 12-week intervention. Results: BP, baPWV (−1.2 ± 0.4 m/s), ET-1 (−2.7 ± 0.3 &mgr;mol/mL), nitrite/nitrate (+4.5 ± 0.5 &mgr;M), functional capacity, and body composition were significantly improved (P < 0.05) in the EX group after 12 weeks of training, but no changes were observed in the CON group. Conclusions: These findings indicate that 12 weeks of combined exercise training improves arterial stiffness, BP, ET-1, blood nitrite/nitrate, functional capacity, and body composition in postmenopausal women with stage 1 hypertension. Thus, this study provides evidence that combined exercise training is a useful therapeutic method to improve cardiovascular health which can reduce cardiovascular disease risk in postmenopausal women with hypertension.

Exercise training improves vascular mitochondrial function.

Exercise training is recognized to improve cardiac and skeletal muscle mitochondrial respiratory capacity; however, the impact of chronic exercise on vascular mitochondrial respiratory function is unknown. We hypothesized that exercise training concomitantly increases both vascular mitochondrial respiratory capacity and vascular function. Arteries from both sedentary (SED) and swim-trained (EX, 5 wk) mice were compared in terms of mitochondrial respiratory function, mitochondrial content, markers of mitochondrial biogenesis, redox balance, nitric oxide (NO) signaling, and vessel function. Mitochondrial complex I and complex I + II state 3 respiration and the respiratory control ratio (complex I + II state 3 respiration/complex I state 2 respiration) were greater in vessels from EX relative to SED mice, despite similar levels of arterial citrate synthase activity and mitochondrial DNA content. Furthermore, compared with the SED mice, arteries from EX mice displayed elevated transcript levels of peroxisome proliferative activated receptor-γ coactivator-1α and the downstream targets cytochrome c oxidase subunit IV isoform 1,isocitrate dehydrogenase(Idh)2, and Idh3a, increased manganese superoxide dismutase protein expression, increased endothelial NO synthase phosphorylation (Ser(1177)), and suppressed reactive oxygen species generation (all P< 0.05). Although there were no differences in EX and SED mice concerning endothelium-dependent and endothelium-independent vasorelaxation, phenylephrine-induced vasocontraction was blunted in vessels from EX compared with SED mice, and this effect was normalized by NOS inhibition. These training-induced increases in vascular mitochondrial respiratory capacity and evidence of improved redox balance, which may, at least in part, be attributable to elevated NO bioavailability, have the potential to protect against age- and disease-related challenges to arterial function.

Human skeletal muscle feed arteries: evidence of regulatory potential

Recently, it has been recognized that human skeletal muscle feed arteries can be harvested during exploratory surgery for melanoma. This approach provides vessels for in vitro study from a wide spectrum of relatively healthy humans. Although, the regulatory role of skeletal muscle feed arteries in rodent models has been documented, whether such vessels in humans possess this functionality is unknown.

Low Intensity Resistance Exercise Training with Blood Flow Restriction: Insight into Cardiovascular Function, and Skeletal Muscle Hypertrophy in Humans

Attenuated functional exercise capacity in elderly and diseased populations is a common problem, and stems primarily from physical inactivity. Decreased function and exercise capacity can be restored by maintaining muscular strength and mass, which are key factors in an independent and healthy life. Resistance exercise has been used to prevent muscle loss and improve muscular strength and mass. However, the intensities necessary for traditional resistance training to increase muscular strength and mass may be contraindicated for some at risk populations, such as diseased populations and the elderly. Therefore, an alternative exercise modality is required. Recently, blood flow restriction (BFR) with low intensity resistance exercise (LIRE) has been used for such special populations to improve their function and exercise capacity. Although BFR+LIRE has been intensively studied for a decade, a comprehensive review detailing the effects of BFR+LIRE on both skeletal muscle and vascular function is not available. Therefore, the purpose of this review is to discuss previous studies documenting the effects of BFR+LIRE on hormonal and transcriptional factors in muscle hypertrophy and vascular function, including changes in hemodynamics, and endothelial function.

Effectiveness of Tai Chi on Cardiac Autonomic Function and Symptomatology in Women With Fibromyalgia: A Randomized Controlled Trial

The present study examined the effects of a 12-week Tai Chi (TC) training regimen on heart rate variability (HRV), symptomatology, muscle fitness and body composition in women with fibromyalgia. Participants were randomly assigned to either a TC training group (n = 18) or a control group (n = 19). HRV, symptomatology, muscle fitness and body composition were measured before and after 12 weeks. There were significant decreases (p < 0.05) in sympathovagal balance (LnLF/LnHF), sympathetic tone (LnLF, nLF), pain, and fatigue, and significant increases (p < 0.05) in parasympathetic tone (LnHF, nHF), strength and flexibility following TC compared with no changes after control. The changes in LnLF and LnLF/LnHF were correlated with changes in pain. There were no significant changes in HR, sleep quality and body composition after TC or control. TC may be an effective therapeutic intervention for improving sympathovagal balance, pain, fatigue, strength and flexibility in women with fibromyalgia.

The Clinical Evaluation between Overtraining Syndrome and Exercise-related Immunity

The present study was performed to analyze and review the physical and immune responses to over- training syndrome in humans. Overreaching refers to the initial phage of overtraining syndrome and has been known as a physical fatigue which is mainly from metab olic imbalance. It has been known that overtraining also results in a loss of adaptability which may lead to an attenuation of exercise performance, sleeping disorder, central fatigue, neurohormonal changes, difficulty recovery to physical stress, and immunological changes. Additionally, overtraining syndrome is characterized by persistent fatigue, poor performance in sport due to the prolonged and strenuous physical training. Also, pre- vious studies reported that endurance athletes experienced a hi gh incidence of URTI during intense training and the post training. And also, high-performance athletes reported that suppression of cell mediated and anti-body mediated immune function. NK cell number s were also reduced in the period of overtraining syndrome. Major components of prevention and treatment for the overtraining syn- drome are screening, education, and detraining. Furthermore, the combination of these prevention and treatment strategies will be much helpful. Therefore, the curre nt review will be helpful for athletes and individuals who are at the risk of overtraining syndrome.

The Effects of Aerobic Exercise Training on Blood Lipid Profiles, Fibrinolytic Activities, and Nitric Oxide Levels in High-fat-diet induced Rats

Although exercise training has been utilized to improve vascular function in animals and humans, the impact of moderate intensity exercise training on fibrinolytic activities and nitric oxide (NO) bioavailability has not been well documented. Therefore, the purpose of the current study was to examine the impact of moderate intensity aerobic exercise training on fat mass, blood lipid profiles, fibrinolytic activity, and NO levels in high-fat-diet induced rats. The body weight, fat mass, blood lipid profiles, fibrinolytic activity, and nitrite/nitrate were measured pre- and postexercise (10 weeks) training. The body weight and fat mass reduced significantly in the exercise (EX) group compared to the control (CON) group. Blood lipid profiles and low-density lipoprotein were unchanged in the EX group compared to the CON group. However, triglyceride and free fatty acid were significantly lower in the EX group compared to the CON group, and high-density lipoprotein was significantly greater in the EX group compared to the CON group. In addition, fibrinolytic activity and nitrite/nitrate were significantly greater in the EX compared to the CON group. These results suggest that 10 weeks of the moderated intensity aerobic exercise training improves blood lipid profiles, fibrinolytic activity, and the nitrite/nitrate ratio, which may improve vascular health and reduce obesity-related cardiovascular disease risks in high-fat- diet induced rats.