Prolonged sitting impairs leg endothelial function, which seems to be mediated by a sustained reduction in blood flow-induced shear stress. However, whether regular endurance training is effective in ...preventing sitting-induced leg endothelial dysfunction remains largely unknown. Herein, we tested the hypothesis that sitting-induced leg endothelial dysfunction is prevented in high endurance-trained individuals.
The endurance-trained group comprised 10 male collegiate cyclists, and the untrained group comprised nine men with no regular endurance training. Peak oxygen uptake (V˙O2peak) was initially determined in all participants using incremental exercise test (37.9 ± 4.7 mL·min·kg in the untrained group versus 60.8 ± 3.6 mL·min·kg in the endurance-trained group). At second visit, the popliteal artery flow-mediated dilation (%FMD) was assessed before and after a 3-h sitting period. During the sitting period, the popliteal artery diameter and blood velocity were measured every hour.
The popliteal artery blood flow and shear rate were significantly and similarly reduced during the sitting period in both groups (P < 0.001). In a 3-h sitting, a significant impairment in popliteal artery %FMD was observed in the untrained group (P = 0.003), but it was prevented in the endurance-trained group (P < 0.196).
In conclusion, the present study revealed that sitting-induced leg endothelial dysfunction is preventable in endurance-trained individuals.
Prolonged sitting impairs endothelial function in the leg vasculature, and this impairment is thought to be largely mediated by a sustained reduction in blood flow-induced shear stress. Indeed, ...preventing the marked reduction of shear stress during sitting with local heating abolishes the impairment in popliteal artery endothelial function. Herein, we tested the hypothesis that sitting-induced reductions in shear stress and ensuing endothelial dysfunction would be prevented by periodic leg movement, or "fidgeting." In 11 young, healthy subjects, bilateral measurements of popliteal artery flow-mediated dilation (FMD) were performed before and after a 3-h sitting period during which one leg was subjected to intermittent fidgeting (1 min on/4 min off) while the contralateral leg remained still throughout and served as an internal control. Fidgeting produced a pronounced increase in popliteal artery blood flow and shear rate (prefidgeting, 33.7 ± 2.6 s(-1) to immediately postfidgeting, 222.7 ± 28.3 s(-1); mean ± SE; P < 0.001) that tapered off during the following 60 s. Fidgeting did not alter popliteal artery blood flow and shear rate of the contralateral leg, which was subjected to a reduction in blood flow and shear rate throughout the sitting period (presit, 71.7 ± 8.0 s(-1) to 3-h sit, 20.2 ± 2.9 s(-1); P < 0.001). Popliteal artery FMD was impaired after 3 h of sitting in the control leg (presit, 4.5 ± 0.3% to postsit: 1.6 ± 1.1%; P = 0.039) but improved in the fidgeting leg (presit, 3.7 ± 0.6% to postsit, 6.6 ± 1.2%; P = 0.014). Collectively, the present study provides evidence that prolonged sitting-induced leg endothelial dysfunction is preventable with small amounts of leg movement while sitting, likely through the intermittent increases in vascular shear stress.
We and others have recently reported that prolonged sitting impairs endothelial function in the leg vasculature; however, the mechanism(s) remain unknown. Herein, we tested the hypothesis that a ...sustained reduction in flow-induced shear stress is the underlying mechanism by which sitting induces leg endothelial dysfunction. Specifically, we examined whether preventing the reduction in shear stress during sitting would abolish the detrimental effects of sitting on popliteal artery endothelial function. In 10 young healthy men, bilateral measurements of popliteal artery flow-mediated dilation were performed before and after a 3-h sitting period during which one foot was submerged in 42°C water (i.e., heated) to increase blood flow and thus shear stress, whereas the contralateral leg remained dry and served as internal control (i.e., nonheated). During sitting, popliteal artery mean shear rate was reduced in the nonheated leg (pre-sit, 42.9 ± 4.5 s(-1); and 3-h sit, 23.6 ± 3.3 s(-1); P < 0.05) but not in the heated leg (pre-sit, 38.9 ± 3.4 s(-1); and 3-h sit, 63.9 ± 16.9 s(-1); P > 0.05). Popliteal artery flow-mediated dilation was impaired after 3 h of sitting in the nonheated leg (pre-sit, 7.1 ± 1.4% vs. post-sit, 2.8 ± 0.9%; P < 0.05) but not in the heated leg (pre-sit: 7.3 ± 1.5% vs. post-sit, 10.9 ± 1.8%; P > 0.05). Collectively, these data suggest that preventing the reduction of flow-induced shear stress during prolonged sitting with local heating abolishes the impairment in popliteal artery endothelial function. Thus these findings are consistent with the hypothesis that sitting-induced leg endothelial dysfunction is mediated by a reduction in shear stress.
Resistance exercise impairs endothelial function. Therefore, it is of paramount importance to devise an effective strategy for restoring endothelial function after resistance exercise. Herein, we ...tested the hypothesis that resistance exercise‐induced endothelial dysfunction would be restored by low‐to‐moderate intensity cycling. Seventeen young healthy subjects completed two randomized experimental trials: (a) resistance exercise only trial; and (b) cycling after the resistance exercise trial. Following baseline brachial artery flow‐mediated dilation (FMD), subjects performed the resistance exercise. Following the resistance exercise, they were asked to rest in the supine position for the assessments of FMD. Subjects in the resistance exercise only trial maintained this supine position for 60 minutes, whereas those in the other trial cycled for 10 minutes after the resistance exercise trial. Subjects were again asked to rest in the supine position after cycling. Then FMD were repeated at 30 and 60 minutes after the resistance exercise in both trials. In the resistance exercise only trial, the increased blood flow and shear rate were disappeared after 1 hour of resting in the supine position, but were maintained in those in the cycling after the resistance trial due to subsequent cycling. Both trials caused a significant impairment in FMD at 10 minutes after the resistance exercise (P < 0.05). This decline was sustained for 60 minutes in the resistance exercise only trial. However, the impaired FMD was restored in the cycling after the resistance exercise trial. In conclusion, impaired endothelial function after the resistance exercise can be restored with 10 minutes of low‐to‐moderate intensity cycling.
Severe hypoxia has been indicated to cause acute changes in appetite-related hormones, which attenuate perceived appetite. However, the effects of moderate hypoxia on appetite-related hormonal ...regulation and perceived appetite have not been elucidated. Therefore, we examined the effects of moderate hypoxia on appetite-related hormonal regulation and perceived appetite. Eight healthy males (21.0 ± 0.6 years; 173 ± 2.3 cm; 70.6 ± 5.0 kg; 23.4 ± 1.1 kg/m
2
) completed two experimental trials on separate days: a rest trial in normoxia (FiO
2
= 20.9%) and a rest trial in hypoxia (FiO
2
= 15.0%). The experimental trials were performed over 7 h in an environmental chamber. Blood samples and scores of subjective appetite were collected over 7 h. Standard meals were provided 1 h (745 kcal) and 4 h (731 kcal) after initiating exposure to hypoxia or normoxia within the chamber. Although each meal significantly reduced plasma active ghrelin concentrations (P < 0.05), the response did not differ significantly between the trials over 7 h. No significant differences in the area under the curves for plasma active ghrelin concentrations over 7 h were observed between the two trials. No significant differences were observed in glucagon-like peptide 1 or leptin concentrations over 7 h between the trials. The subjective feeling of hunger and fullness acutely changed in response to meal ingestions. However, these responses were not affected by exposure to moderate hypoxia. In conclusion, 7 h of exposure to moderate hypoxia did not change appetite-related hormonal responses or perceived appetite in healthy males.
Background
It has been shown that Klotho protects vascular endothelial function. Given that a single bout of resistance‐exercise‐induced hypertensive stimulus causes endothelial dysfunction, we ...postulated that acute resistance exercise would reduce serum Klotho levels. In this respect, the reduction in serum Klotho levels would be associated with the response of flow‐mediated dilation (FMD). Therefore, the purpose of this study was to investigate the impact of acute resistance exercise on the Klotho response in serum. In addition, we examined the relationship between the serum Klotho and FMD responses following acute resistance exercise.
Methods
Twelve untrained men participated in this study (20.4 ± 0.3 years). Following baseline measurements (blood pressure, blood collection, FMD), subjects performed leg extensions, which consisted of 10 repetitions for five sets at 70% of one‐repetition maximum. After the exercise, measurement of blood pressure, blood collection, and FMD assessment were repeated for 60 min. We analyzed Klotho and endothelin‐1 (ET‐1) concentrations in blood serum.
Results
As expected, the exercise significantly elevated blood pressure and led to decreased FMD (p < 0.05). However, Klotho concentrations were significantly increased following exercise (p < 0.05). No correlation was observed in Klotho and FMD responses following acute resistance exercise. However, there was a significant positive correlation between Klotho and ET‐1 in response to resistance exercise (p < 0.05).
Conclusion
In conclusion, the present study reveals that serum Klotho significantly increased following a single bout of resistance exercise. However, the increase in Klotho may not associate with the acute reduction in endothelial function.
Our study reveals that serum Klotho increased following a single bout of resistance exercise. The increase in the Klotho response in serum did not associate with acute reduction in endothelial function following resistance exercise. The increase in the serum Klotho concentration is not responsible for the temporal impairment of endothelial function following a single bout of resistance exercise in healthy young men.
We examined metabolic and endocrine responses during rest and exercise in moderate hypoxia over a 7.5 h time courses during daytime.
Eight sedentary, overweight men (28.6 ± 0.8 kg/m2) completed four ...experimental trials: a rest trial in normoxia (FiO2 = 20.9%, NOR-Rest), an exercise trial in normoxia (NOR-Ex), a rest trial in hypoxia (FiO2 = 15.0%, HYP-Rest), and an exercise trial in hypoxia (HYP-Ex). Experimental trials were performed from 8:00 to 15:30 in an environmental chamber. Blood and respiratory gas samples were collected over 7.5 h. In the exercise trials, subjects performed 30 min of pedaling exercise at 60% of VO2max at 8:00, 10:30, and 13:00, and rested during the remaining period in each environment. Standard meals were provided at 8:30, 11:00, and 13:30.
The areas under the curves for blood glucose and serum insulin concentrations over 7.5 h did not differ among the four trials. At baseline, %carbohydrate contribution was significantly higher in the hypoxic trials than in the normoxic trials (P<0.05). Although exercise promoted carbohydrate oxidation in the NOR-Ex and HYP-Ex trials, %carbohydrate contribution during each exercise and post-exercise period were significantly higher in the HYP-Ex trial than in the NOR-Ex trial (P<0.05).
Three sessions of 30 min exercise (60% of VO2max) in moderate hypoxia over 7.5 h did not attenuate postprandial glucose and insulin responses in young, overweight men. However, carbohydrate oxidation was significantly enhanced when the exercise was conducted in moderate hypoxia.
We have previously shown that local heating or leg fidgeting can prevent prolonged sitting-induced leg endothelial dysfunction. However, whether physical activity prevents subsequent sitting-induced ...leg endothelial dysfunction remains unknown. Herein, we tested the hypothesis that sitting-induced leg endothelial dysfunction would be prevented by prior exercise. We also examined if, in the absence of exercise, standing is an effective alternative strategy to sitting for conserving leg endothelial function. Fifteen young healthy subjects completed three randomized experimental trials: (1) sitting without prior exercise; (2) sitting with prior exercise; and (3) standing without prior exercise. Following baseline popliteal artery flow-mediated dilation (FMD) measurements, subjects maintained a supine position for 45 min in the sitting and standing trials, without prior exercise, or performed 45 min of leg cycling before sitting (i.e. sitting with prior exercise trial). Thereafter, subjects were positioned into a seated or standing position, according to the trial, for 3 h. Popliteal artery FMD measures were then repeated. Three hours of sitting without prior exercise caused a significant impairment in popliteal artery FMD (baseline: 3.8±0.5%, post-sitting: 1.5±0.5%,
<0.05), which was prevented when sitting was preceded by a bout of cycling exercise (baseline: 3.8±0.5%, post-sitting: 3.6±0.7%,
>0.05). Three hours of standing did not significantly alter popliteal artery FMD (baseline: 4.1±0.4%, post-standing: 4.3±0.4%,
>0.05). In conclusion, prolonged sitting-induced leg endothelial dysfunction can be prevented by prior aerobic exercise. In addition, in the absence of exercise, standing represents an effective substitute to sitting for preserving leg conduit artery endothelial function.
The impact of combined aerobic and resistance exercise on Klotho (KL) secretion is unclear. Twelve healthy young men completed two randomized experimental trials: 1) resistance exercise (RE) and 2) ...resistance exercise with prior aerobic exercise (AE + RE). Following baseline blood pressure assessment and blood collection, the subjects in the RE trial maintained a supine position for 45 min, while the subjects in the AE + RE trial performed 45 min of aerobic exercise. After 45 min of resting or aerobic exercise, all subjects performed resistance exercise. Following resistance exercise, the subjects rested in a supine position for 60 min. Blood pressure assessment and blood collection were repeated. Aerobic and resistance exercise significantly increased serum KL concentrations, respectively (P < 0.05), and no additive effect of aerobic exercise on KL secretion was observed immediately after resistance exercise in the AE + RE trial compared with the RE trial. However, serum KL levels at 30 and 60 min after resistance exercise were significantly higher in the AE + RE trial than in the RE trial. Serum ET-1 concentrations were significantly increased only in the RE trial. In conclusion, combined aerobic and resistance exercise could maintain higher levels of serum KL secretion after exercise compared with resistance exercise only.
•Serum KL concentrations were significantly increased following a single bout of combined aerobic and resistance exercise.•The magnitude of the increase in serum KL levels did not differ significantly from the.•Serum KL concentrations immediately after resistance exercise only.•Combined aerobic and resistance exercise maintained higher levels of serum KL secretion with resistance exercise only.
Summary
The present study was conducted to determine change in regional fat accumulation and appetite‐related hormonal response following hypoxic training. Twenty sedentary subjects underwent hypoxic ...(n = 9, HYPO, FiO2 = 15%) or normoxic training (n = 11, NOR, FiO2 = 20·9%) during a 4‐week period (3 days per week). They performed a 4‐week training at 55% of maximal oxygen uptake (V·O2max) for each condition. Before and after the training period, V·O2max, whole body fat mass, abdominal fat area, intramyocellular lipid content (IMCL), fasting and postprandial appetite‐related hormonal responses were determined. Both groups showed a significant increase in V·O2max following training (P<0·05). Whole body and segmental fat mass, abdominal fat area, IMCL did not change in either group. Fasting glucose and insulin concentrations significantly reduced in both groups (P<0·05). Although area under the curve for the postprandial blood glucose concentrations significantly decreased in both groups (P<0·05), the change was significantly greater in the HYPO group than in the NOR group (P<0·05). Changes in postprandial plasma ghrelin were similar in both groups. A significant reduction of postprandial leptin response was observed in both groups (P<0·05), while postprandial glucagon‐like peptide‐1 (GLP‐1) concentrations increased significantly in the NOR group only (P<0·05). In conclusion, hypoxic training for 4 weeks resulted in greater improvement in glucose tolerance without loss of whole body fat mass, abdominal fat area or IMCL. However, hypoxic training did not have synergistic effect on the regulation of appetite‐related hormones.
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