Impact of moderate-intensity aerobic exercise in combined hypoxic and hot conditions on endothelial function.

There is no study that has investigated the impact of exercise in a combined hypoxic and hot environment on endothelial function. Therefore, we tested whether aerobic exercise in a combined hypoxic and hot conditions induces further enhancement of endothelial function. Twelve healthy males cycled at a constant workload (50% of their maximal oxygen uptake under normoxic/thermoneutral conditions) for 30 min in four different environments: exercise under normoxic condition (NOR: fraction of inspiratory oxygen or FiO2 = 20.9%, 20°C), exercise under hypoxic condition (HYP: FiO2 = 14.5%, 20°C), exercise under hot condition (HOT: FiO2 = 20.9%, 30°C), and exercise under combined hypoxia and hot conditions (HH: FiO2 = 14.5%, 30°C). Before, during, and after exercise, cardiovascular variables (e.g., heart rate, blood flow, and shear rate), blood variables, and endothelial function evaluated by flow-mediated dilation (FMD) were assessed. Heart rates were significantly higher throughout the HH trial's experimental period than the other trials (p < 0.05). However, in the HH trial, brachial artery blood flow and shear rate did not differ from those in other trials after exercise. Plasma catecholamines (epinephrine, norepinephrine, and dopamine) elevations in response to exercise were significantly higher in the HH trial than in the other three trials (p < 0.05). No considerable differences were observed in FMD responses among trials before and after the exercise. In conclusion, aerobic exercise in a combined hot and hypoxic environment further activated sympathetic nervous activity but did not considerably enhance blood flow, shear rate, or endothelial function.

Circulating catecholamines, endothelin-1, and nitric oxide releases do not explain the preserved FMD following acute resistance exercise in strength-trained men.

PURPOSE: Acute resistance exercise decreases endothelial function in sedentary individuals but not in strength-trained (ST) individuals. However, the underlying mechanism(s) of vascular protection in ST individuals remains unclear. Herein, we compared catecholamines, endothelin-1 (ET-1), and nitric oxide (NOx) releases after acute resistance exercise between sedentary and ST individuals. METHODS: The untrained (UT) group comprised 12 male individuals with no regular training, while the ST group comprised 12 male individuals. Participants performed a session of resistance exercise, which consisted of 3 sets of 10 repetitions at 75% of one repetition maximum. Heart rate (HR) and blood pressure were measured during resistance exercise. Brachial artery flow-mediated dilation (FMD), blood pressure, HR, and blood collection were undertaken before and 10, 30, and 60 min after the resistance exercise. RESULTS: No significant difference was found in baseline brachial artery FMD between the groups (P > 0.05). Brachial artery FMD was significantly reduced in the UT group (P < 0.05) but it was prevented in the ST group after the resistance exercise. Significant differences were found at 10, 30, and 60 min after the resistance exercise in brachial artery ΔFMD from baseline between groups (P < 0.05). Blood pressure, HR, plasma epinephrine, norepinephrine, dopamine, serum endothelin-1, and plasma NOx responses did not differ between groups throughout the experimental period. CONCLUSION: In conclusion, preserved endothelial function in response to acute resistance exercise in ST male individuals is independent of catecholamines, ET-1, and NOx responses.

Slow-Speed Low-Intensity but Not Normal-Speed High-Intensity Resistance Exercise Maintains Endothelial Function.

Purpose: High-intensity resistance exercise two or three times a week has been considered optimal for muscle hypertrophy, although it can remarkably elevate blood pressure (BP). In contrast, slow-speed resistance exercise with low intensity and tonic force generation (slow-low) can induce muscle hypertrophy without elevating BP. However, it is unclear how endothelial function changes after slow-low. Therefore, this study examined whether slow-low would maintain brachial artery endothelial function in comparison with normal-speed with high intensity resistance exercise (normal-high) and normal-speed with low-intensity resistance exercise (normal-low). Methods: Eleven healthy young men performed leg-extensions with slow-low (3 sets of 8 repetitions at 50% of 1RM), normal-high (3 sets of 8 repetitions at 80% of 1RM), and normal-low (3 sets of 8 repetitions at 50% of 1RM). Flow-mediated dilation (FMD) in the brachial artery was evaluated at pre-exercise and at 10, 30, and 60 min after exercise. Result: The results showed that normal-high caused significant impairment of FMD at 30 (3.7 ± 2.7%) and 60 (3.7 ± 2.8%) min after exercise (P < .05). In contrast, slow-low and normal-low showed no significant difference from baseline. FMD was significantly lower in normal-high compared with slow-low and normal-low at 30 and 60 min after exercise (P < .05). Additionally, systolic BP was significantly higher during normal-high compared with slow-low and normal-low (P < .05). Conclusion: We concluded that slow-low did not impair brachial artery FMD concomitant with lower systolic BP, and may therefore be a useful mode of exercise training to improve muscle hypertrophy without provoking transient endothelial dysfunction.

Prior beetroot juice ingestion offsets endothelial dysfunction following prolonged sitting.

Nutritional strategies to prevent endothelial dysfunction following prolonged sitting remain largely unknown. Given that beetroot juice (BRJ) ingestion enhances nitric oxide (NO) bioavailability, we aimed to evaluate whether prior BRJ ingestion would prevent sitting-induced endothelial dysfunction in the leg. Eleven healthy young males (n = 7) and females (n = 4) underwent two experimental trials of prolonged sitting with prior: 1) placebo (PL) ingestion (PL trial) and 2) BRJ ingestion (BRJ trial). All subjects ingested 140 mL of PL or BRJ (∼0.0055 or ∼12.8 mmol of nitrate, respectively) immediately before 3 h of sitting. Pre- and post-sitting measurements of popliteal artery flow-mediated dilation (FMD) and blood pressure, and blood collection were undertaken. During the sitting period, an hourly assessment of popliteal artery diameter and blood velocity, blood pressure, and blood collection were performed. Popliteal artery blood flow and shear rate were significantly and similarly reduced during the sitting period in both trials (P < 0.001). Plasma nitrate and NOx (total nitrite and nitrate) concentrations were significantly increased relative to baseline in the only BRJ trial, and the overall concentrations were significantly higher in the BRJ trial (P < 0.001). Popliteal artery FMD was significantly reduced after the sitting period in the PL trial (P < 0.05), whereas no reduction was observed in the BRJ trial. Therefore, prior BRJ ingestion would prevent sitting-induced leg endothelial dysfunction via enhancing NO bioavailability.NEW & NOTEWORTHY The present study elucidates that beetroot juice ingestion before prolonged sitting offsets sitting-induced leg endothelial dysfunction. Data from the present study provides novel physiological information that enhancing NO bioavailability by dietary nitrate supplementation is an effective tool for prevention of the detrimental vascular effects of prolonged sitting.

Effect of combined aerobic and resistance exercise on serum Klotho secretion in healthy young men -a pilot study.

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.

Impact of a single bout of resistance exercise on serum Klotho in healthy young men.

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.

Muscular endurance and muscle metabolic responses to 8 weeks of omega-3 polyunsaturated fatty acids supplementation.

BACKGROUND: It has been well known that exercise training improves muscular endurance; however, whether nutritional strategies can be used to enhance muscular endurance remains unclear. Herein, we tested the hypothesis that 8 weeks of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation, known to promote oxygen availability and lipid metabolism, would attenuate muscular fatigue caused by numerous muscle contractions. METHODS: Nineteen healthy men were randomly assigned to a placebo group (n = 9) and fish oil group (n = 10) in a double-blind fashion. The fish oil group consumed EPA-rich fish oil that contains 600-mg EPA and 260-mg DHA per day for 8 weeks. The placebo group received matching capsules for the same duration of time. After the 8-week intervention, subjects performed muscular endurance test that was repeated knee extensions with weights equal to 40% of the subject's body weight. RESULTS: Maximal repetitions to exhaustion were recorded. In addition, maximum isometric voluntary muscle contraction (MVC), muscle metabolism using near-infrared spectroscopy, and blood lactate were measured during the test. Subjects in both groups reached exhaustion after the muscular endurance test, while the maximal repetitions did not differ between the groups. Similarly, there is no significant difference in oxygen saturation in muscle tissue (StO2), an index of muscle oxygen availability, between the groups. Also, MVC and blood lactate did not change between groups. CONCLUSION: In conclusion, the present study provided evidence that muscle fatigue caused by knee extensions cannot be attenuated by EPA and DHA supplementation in healthy subjects.

Maintenance of endothelial function following acute resistance exercise in females is associated with a tempered blood pressure response.

Acute resistance exercise-induced hypertensive stimulus impairs endothelial function in males. Because prior work indicates that female subjects have a tempered blood pressure response to acute resistance exercise, we hypothesized that, compared with males, females would better maintain endothelial function following resistance exercise and that this preservation would be associated with a lower hypertensive stimulus. Twenty-nine young healthy males (n = 16) and females (n = 13) participated in this study. All subjects performed a session of resistance exercise (leg extension) at the same relative workload [65% of one repetition maximum (1RM)]. The blood pressure response to exercise was characterized, and brachial artery flow-mediated dilation (FMD) was measured before and after. Males performed a second experimental trial in which the blood pressure response to resistance exercise was matched to that of females. This was accomplished by reducing the workload (~25% of 1RM). When resistance exercise was performed at the same relative workload, the systolic blood pressure was greater in males compared with females. Congruently, resistance exercise caused a significant impairment in FMD in males but not in females (P < 0.001). When the exercise workload was reduced in males, they no longer displayed an impairment in FMD following resistance exercise and, as such, the sex difference was abolished (P > 0.05). The present study reveals that acute resistance exercise transiently impairs endothelial function in young, healthy males but not in age-matched females. Notably, the maintenance of endothelial function in females is associated with a lower blood pressure response during resistance exercise.NEW & NOTEWORTHY The present data demonstrate for the first time that acute resistance exercise impairs endothelial function in young, healthy male but not female subjects. In addition, we show that the preservation of endothelial function in females is associated with a mitigated blood pressure response during resistance exercise. Accordingly, this work portrays a sexual dimorphism in the barostress response, and ensuing vascular effects, to resistance exercise.

Sitting-induced Endothelial Dysfunction Is Prevented in Endurance-trained Individuals.

PURPOSE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: In conclusion, the present study revealed that sitting-induced leg endothelial dysfunction is preventable in endurance-trained individuals.

Eight weeks of fish oil supplementation does not prevent sitting-induced leg endothelial dysfunction.

Prolonged sitting impairs leg endothelial function and this impairment is thought to be mediated by a sustained reduction in blood flow-induced shear stress. However, whether nutritional strategies can be used to prevent sitting-induced leg endothelial dysfunction remains unknown. Herein, we tested the hypothesis that 8 weeks of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation would prevent endothelial dysfunction associated with sitting. Nineteen healthy men were randomly assigned to a placebo group or EPA+DHA group in a double-blind fashion. The EPA+DHA group was administered EPA-rich fish oil, containing 600 mg EPA and 260 mg DHA per day for 8 weeks. The placebo group received matching capsules for the same duration of time. Popliteal artery flow-mediated dilation (FMD) was measured at baseline and before and after a 3-h sitting period. During sitting, blood pressure, popliteal artery diameter, and blood velocity were measured every hour. Throughout the sitting period, popliteal artery blood flow and shear rate were markedly and similarly reduced in both groups (P < 0.05). However, counter to the hypothesis, 3 h of sitting impaired popliteal artery FMD to the same extent in both groups (P < 0.05). In conclusion, daily EPA and DHA supplementation is not effective at preventing the detrimental effects of prolonged sitting on leg endothelial function. Novelty We provide evidence that sitting-induced leg endothelial dysfunction in young healthy subjects cannot be remediated by a nutritional strategy known to produce cardiovascular benefits. This could be partially due to the low total dose of EPA and DHA administered.

Prior cycling exercise does not prevent endothelial dysfunction after resistance exercise.

PURPOSE: Resistance exercise impairs endothelial function acutely. Therefore, it becomes important to devise an effective strategy for preventing acute endothelial dysfunction after resistance exercise. Herein, we tested the hypothesis that resistance exercise-induced temporal endothelial dysfunction is prevented by prior cycling. METHODS: Twelve young healthy subjects completed two randomized experimental trials: (1) resistance exercise only trial (RE trial), (2) resistance exercise with prior cycling trial (C + RE trial). Following baseline brachial artery flow-mediated dilation (FMD), the subjects maintained the supine position for 45 min in the RE trial; the subjects performed a 45 min of cycling (67.0 ± 1.7% HRmax) in the C + RE trial. After 45 min of resting or cycling, the subjects performed resistance exercise (69.7 ± 4.0 kg) at the same time points. Following the resistance exercise, they were asked to rest in the supine position for 60 min. Then FMD were repeated at 10, 30 and 60 min after the resistance exercise in both trials. RESULTS: The increased blood flow and shear rate after resistance exercise did not differ between trials, and these changes disappeared following resting in the supine position for 60 min. There was no significant interaction in %FMD responses. Both trials caused impairment in %FMD after the resistance exercise, and statistical significance was observed at 30 and 60 min after resistance exercise in the RE trial. CONCLUSION: The present study revealed that cycling for 45 min prior to resistance exercise was not sufficient to prevent the acute endothelial dysfunction after resistance exercise.

Short-term cycling restores endothelial dysfunction after resistance exercise.

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.

Eicosapentaenoic Acid-Rich Fish Oil Supplementation Inhibits the Decrease in Concentric Work Output and Muscle Swelling of the Elbow Flexors.

OBJECTIVE: The aim of this study was to test the hypothesis that 8-week eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation improves peripheral muscle performance by concentric contractions (CONs) of elbow flexors in humans. METHODS: Sixteen healthy men were randomly administered with EPA and DHA supplement (EPA, n = 8) or placebo (PL, n = 8) by a double-blind method. The EPA group was administered EPA-rich fish oil, containing 600 mg EPA and 260 mg DHA per day for 8 weeks. The subjects performed 5 sets of 6 maximal CONs of elbow flexors. The work output and peak torque were assessed during exercise. Changes in the maximal voluntary isometric contraction torque, range of motion (ROM), upper arm circumference, muscle fatigue by rating of perceived exertion, transverse relaxation time, cross-sectional area (CSA), and lactate in blood were also assessed before, immediately after, and 1 day after exercise. RESULTS: The work output during CONs in the EPA group was greater than that in the placebo group at the fifth set (EPA group; 94.0 ± 11.7%, placebo group; 82.5 ± 11.7%, p < 0.05). In addition, ROM in the EPA group was significantly greater than that in the placebo group immediately after exercise (p < 0.05). The increase of CSA in the EPA group was significantly smaller than that in the placebo group immediately after exercise (p < 0.05). CONCLUSIONS: The present study suggests that the reduction of muscle work output caused by 30 CONs can be attenuated by an 8-week EPA and DHA supplementation. In addition, EPA and DHA supplementation can cause inhibition for reduction of ROM and increase of CSA after CONs.

High-intensity resistance exercise with low repetitions maintains endothelial function.

Resistance exercise impairs endothelial function, and this impairment is thought to be mediated by sustained elevation in blood pressure. Herein, we tested the hypothesis that resistance exercise-induced endothelial dysfunction would be prevented by high-intensity resistance exercise with low repetitions. This type of resistance exercise is known to induce temporal elevation in blood pressure due to low repetitions and a long resting period between sets. Thirteen young healthy subjects completed three randomized experimental trials as follows: 1) moderate-intensity exercise with moderate repetitions (moderate-moderate trial), 2) low-intensity exercise with high repetitions (low-high trial), and 3) high-intensity exercise with low repetitions (high-low trial). After baseline brachial artery flow-mediated dilation (FMD) and blood pressure measurements, subjects performed resistance exercise according to the different types of trials. Thereafter, brachial artery FMD and blood pressure measurements were repeated 10, 30, and 60 min after the exercise. Exercise-induced increases in blood flow and shear rate were significantly lower in the high-low trial than in the other two trials ( P < 0.05). Although systolic blood pressures were significantly elevated after exercise in all trials ( P < 0.05), the magnitudes of rise in blood pressure increase were significantly lower in the high-low trial than in the moderate-moderate and low-high trials ( P < 0.05). Moderate-moderate and low-high trials caused a significant impairment in brachial artery FMD ( P < 0.05), which could be prevented through high-intensity resistance exercise with low repetitions ( > 0.05). In conclusion, endothelial function was maintained by conducting high-intensity resistance exercise with low repetitions. NEW & NOTEWORTHY Data from the present study reveal that high-intensity resistance exercise with low repetitions can maintain endothelial function. Thus, this study provides the first evidence that the detrimental vascular effects of resistance exercise are preventable when resistance exercise is performed in high intensity with low repetitions. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/type-of-resistance-exercise-and-endothelial-function/ (Japanese version: https://ajpheart.podbean.com/e/japanese-language-podcast-type-of-resistance-exercise-and-endothelial-function/ ).

Prior exercise and standing as strategies to circumvent sitting-induced leg endothelial dysfunction.

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%, P<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%, P>0.05). Three hours of standing did not significantly alter popliteal artery FMD (baseline: 4.1±0.4%, post-standing: 4.3±0.4%, P>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.

Prolonged sitting-induced leg endothelial dysfunction is prevented by fidgeting.

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.

Ghrelin, GLP-1, and leptin responses during exposure to moderate hypoxia.

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 (FiO2 = 20.9%) and a rest trial in hypoxia (FiO2 = 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.

Endothelial dysfunction following prolonged sitting is mediated by a reduction in 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.

Influences of increased training volume on exercise performance, physiological and psychological parameters.

BACKGROUND: The aim of this study was to investigate the influence of excessive training on exercise performance and physiological and psychological parameters. METHODS: Eight physically active males (age, mean±standard deviation [SD]: 23±3 years) completed 3 weeks of an intervention program consisting of normal (N), intensified (IT), and recovery (R) training phases (7 days for each phase). Physiological and psychological parameters were measured at rest before the intervention (Pre), and every Monday, Wednesday, and Saturday (day 1, day 3, day 6, respectively), and exercise performance tests were performed before the intervention (Pre) and every Saturday (day 6) during the intervention period. RESULTS: The estimated energy expenditure during a training session revealed a more than two-fold increase from the N phase to the IT phase. During the IT phase, augmented training volume significantly affected the POMS (fatigue) and motivation towards training (P<0.05) scores, and these values returned to baseline levels during the R phase. Moreover, resting serum testosterone concentrations significantly decreased and exercise-induced cortisol responses were diminished during the IT phase (P<0.05). The altered endocrine responses were still observed during the subsequent R phase. Resting serum BAP levels (an index of antioxidant potential) significantly increased during the N phase (P<0.05). Meanwhile, there was no significant change in exercise performance, resting d-ROM (an index of oxidative stress) values, or salivary amylase activity. CONCLUSIONS: Increases in training stress altered psychological parameters, resting testosterone concentrations, and exercise-induced cortisol responses. Exercise performance did not correlate with training stress, suggesting that monitoring endocrine and psychological parameters is essential during intensified training periods.

Augmented Carbohydrate Oxidation under Moderate Hypobaric Hypoxia Equivalent to Simulated Altitude of 2500 m.

Hypoxia itself stimulates glucose uptake mediated by a mechanism independent of insulin. However, whether moderate hypoxia causes similar metabolic effect in humans remains unclear. The present study aimed to determine glycemic regulation following glucose load at a simulated moderate altitude of 2,500 m. Eight healthy young males (mean ± standard error: 24 ± 1 years; 171.3 ± 1.6 cm; 66.9 ± 3.7 kg; 22.8 ± 1.0 kg/m(2)) consumed 75 g of glucose solution under either hypobaric condition (560 mmHg) or normobaric condition (745 mmHg). In the hypobaric chamber, the oxygen partial pressure is proportionally reduced with a reduction of atmospheric pressure, consequently leading to the hypoxic condition. Plasma glucose and serum insulin concentrations increased significantly following glucose load in both conditions (P < 0.05). However, no significant interaction (condition × time) or main effect for condition was observed. There were no significant differences in serum glycerol, plasma epinephrine, or plasma norepinephrine concentrations between the two conditions. No significant differences between the conditions were observed in changes in VO2 or VCO2. However, the hypobaric condition showed significantly higher respiratory exchange ratio (VCO2/VO2) at 90 and 120 min following glucose load (P < 0.05 vs. normobaric condition), suggesting that carbohydrate oxidation following glucose load was enhanced in moderate hypobaric hypoxia. In conclusion, acute exposure to moderate hypobaric hypoxia significantly augmented carbohydrate oxidation following the glucose load, without affecting glucose or insulin responses. Thus, a short-time exposure to moderate hypobaric hypoxia may be beneficial for people with impaired glucose tolerance.