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.
Increased daily sitting time is associated with greater cardiovascular risk, and, on average, women are more sedentary than men. Recent reports have demonstrated that prolonged sitting reduces lower ...leg microvascular (reactive hyperemia) and macrovascular flow-mediated dilation (FMD) vasodilator function. However, these studies have predominately included men, and the effects of sitting in young women are largely unexplored. This becomes important given known sex differences in vascular function. Thus, herein, we assessed popliteal artery reactive hyperemia and FMD before and after a 3-h sitting period in healthy young women (
= 12) and men (
= 8). In addition, resting popliteal artery hemodynamics (duplex Doppler ultrasound) and calf circumference were measured before, during, and after sitting. Resting popliteal artery shear rate was reduced to a similar extent in both groups during the sitting period (women: -48.5 ± 8.4 s
and men: -52.9 ± 12.3 s
,
= 0.45). This was accompanied by comparable increases in calf circumference in men and women (
= 0.37). After the sitting period, popliteal artery FMD was significantly reduced in men (PreSit: 5.5 ± 0.9% and PostSit: 1.6 ± 0.4%,
< 0.001) but not women (PreSit: 4.4 ± 0.6% and PostSit: 3.6 ± 0.6%,
= 0.29). In contrast, both groups demonstrated similar reductions in hyperemic blood flow area under the curve (women: -28,860 ± 5,742 arbitrary units and men: -28,691 ± 9,685 arbitrary units,
= 0.99), indicating impaired microvascular reactivity after sitting. These findings indicate that despite comparable reductions in shear rate during 3 h of uninterrupted sitting, macrovascular function appears protected in some young women but the response was variable, whereas men exhibited more consistent reductions in FMD. In contrast, the leg microvasculature is susceptible to similar sitting-induced impairments in men and women.
We demonstrate that leg macrovascular function was consistently reduced in young men but not young women after prolonged sitting. In contrast, both men and women exhibited similar reductions in leg microvascular reactivity after sitting. These data demonstrate, for the first time, sex differences in vascular responses to prolonged sitting.
Blacks have the highest prevalence of hypertension, putting them at greater risk of cardiovascular disease and death. Previous studies have reported that, relative to whites, healthy black men have ...augmented pressor responses to sympathoexcitatory stressors. Although important, these studies do not inform about the resting state and the influence of spontaneous changes in resting muscle sympathetic nerve activity (MSNA). Likewise, little is known about the transduction of MSNA into a vascular response at rest on a beat-to-beat basis. Accordingly, we tested the hypothesis that relative to whites, blacks would exhibit greater vasoconstriction and pressor responses following spontaneous bursts of MSNA. Mean arterial pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 minutes of supine rest in 35 young healthy men (17 blacks and 18 whites). Signal averaging was used to characterize changes in leg vascular conductance, total vascular conductance, and mean arterial pressure following spontaneous MSNA bursts. Blacks demonstrated significantly greater decreases in leg vascular conductance (blacks: -15.0±1.0%; whites: -11.5±1.2%;
=0.042) and total vascular conductance (blacks: -8.6±0.9%; whites: -5.1±0.4%;
=0.001) following MSNA bursts, which resulted in greater mean arterial pressure increases (blacks: +5.2±0.6 mm Hg; whites: +3.9±0.3 mm Hg;
=0.04). These exaggerated responses in blacks compared with whites were present whether MSNA bursts occurred in isolation (singles) or in combination (multiples) and were graded with increases in burst height. Collectively, these findings suggest that healthy young black men exhibit augmented sympathetic vascular transduction at rest and provide novel insight into potential mechanism(s) by which this population may develop hypertension later in life.
New and effective strategies are needed to manage the autonomic and cardiovascular sequelae of obstructive sleep apnea (OSA). We assessed the effect of daily inspiratory muscle strength training ...(IMT) on sleep and cardiovascular function in adults unable to use continuous positive airway pressure (CPAP) therapy.
This is a placebo-controlled, single-blind study conducted in twenty four adults with mild, moderate, and severe OSA. Subjects were randomly assigned to placebo or inspiratory muscle strength training. Subjects in each group performed 5 min of training each day for 6 w. All subjects underwent overnight polysomnography at intake and again at study close.
We evaluated the effects of placebo training or IMT on sleep, blood pressure, and plasma catecholamines. Relative to placebo-trained subjects with OSA, subjects with OSA who performed IMT manifested reductions in systolic and diastolic blood pressures (-12.3 ± 1.6 SBP and -5.0 ± 1.3 DBP mmHg; P < 0.01); plasma norepinephrine levels (536.3 ± 56.6 versus 380.6 ± 41.2 pg/mL; P = 0.01); and registered fewer nighttime arousals and reported improved sleep (Pittsburgh Sleep Quality Index scores: 9.1 ± 0.9 versus 5.1 ± 0.7; P = 0.001). These favorable outcomes were achieved without affecting apneahypopnea index.
The results are consistent with our previously published findings in normotensive adults but further indicate that IMT can modulate blood pressure and plasma catecholamines in subjects with ongoing nighttime apnea and hypoxemia. Accordingly, we suggest IMT offers a low cost, nonpharmacologic means of improving sleep and blood pressure in patients who are intolerant of CPAP.
Background
Inspiratory muscle strength training (IMST) has been shown to bring about improvements in respiratory muscle strength and reductions in blood pressure after 6 weeks of daily high intensity ...training. However, there has been little investigation into the effects of IMST on limb blood flow, and it is unclear how hemodynamics are altered within a single bout of training.
Purpose
To investigate the acute effects of one session of either low or high intensity IMST on blood flow in the upper and lower limbs.
Methods
Participants (n=7, 57% female) aged 20 to 47 years completed two randomized laboratory visits wherein resting blood flow was measured via duplex Doppler ultrasound at the left brachial and popliteal arteries. Following baseline measures, participants' maximal inspiratory pressure (PImax) was measured using a PowerBreathe K3 device. Participants performed one session (30 breaths) of IMST at either 15% or 75% of their PImax, and blood flow was measured again at each artery for five breaths during the final ten breaths of the training. At their second visit, subjects performed whichever training level had yet to be completed and blood flow was assessed as described above.
Results
Mean blood flow at the brachial artery appeared reduced during both 15% (p=0.070) and 75% training (p=0.078), which may be attributed to a significant increase in retrograde blood flow in both cases (p=0.014 and p=0.037, respectively). This increase in retrograde blood flow tended to be greater during the 75% training (p=0.066). Popliteal artery blood flow showed similar trends to brachial artery blood flow.
Conclusions
While IMST appears to reduce brachial artery mean blood flow during a single training session, this may be due to alterations in retrograde blood flow, which tended to increase in an intensity‐dependent manner. Further investigation into the chronic hemodynamic effects of IMST is warranted.
This study was conducted to determine if there was a difference in bone strength between men and post‐menopausal women. Prior research suggests that women are four times more likely to be affected by ...osteoporosis and experience fractures twice as often as men. Bone mass loss found in osteoporosis increases in women after menopause due to marked estrogen deficiency. However, it is unclear whether this bone mass difference between men and women contributes to a reduction in bone strength. Therefore, the hypothesis of this study was that men will have a higher bone density than women and will therefore have stronger bones when tested to failure. To test this hypothesis, eight cadavers (four men, four women) from the Wayne State University Willed Body Program were used (age: 81±16, range: 51‐104). The bone density of the ulna was calculated via a volume displacement test and its mass. The ulna was then secured and weight was added incrementally until failure. There was no significant difference found in ulna bone density between men and women (p=0.776); however, the weight required to break the ulnas in men was greater (p=0.0001). Once normalized by the mass of the ulna this effect was reduced (p>0.05). These data suggest potential sex differences in bone strength, independent of bone density, indicating future investigation is needed at different locations in the body.
Patients with type 2 diabetes (T2D) exhibit greater daytime blood pressure (BP) variability, increasing their cardiovascular risk. Given the number of daily activities that incorporate short-duration ...isometric muscle contractions (e.g., carrying groceries), herein we investigated BP and muscle sympathetic nerve activity (MSNA) responses at the onset of isometric handgrip (HG). We tested the hypothesis that, relative to control subjects, patients with T2D would exhibit exaggerated pressor and MSNA responses to the immediate onset of HG. Mean arterial pressure (MAP) and MSNA were quantified during the first 30 s of isometric HG at 30% and 40% of maximal voluntary contraction (MVC) and during a cold pressor test (CPT), a nonexercise sympathoexcitatory stimulus. The onset of 30% MVC HG evoked similar increases in MAP between groups (
= 0.17); however, the increase in MSNA was significantly greater in patients with T2D versus control subjects with the largest group difference at 20 s (
< 0.001). At the onset of 40% MVC HG, patients with T2D demonstrated greater increases in MAP (e.g., 10 s, T2D: 9 ± 1 mmHg, controls: 5 ± 2 mmHg;
= 0.04). MSNA was also greater in patients with T2D at 40% MVC onset but differences were only significant at the 20-30 s timepoint (T2D: 15 ± 3 bursts/min, controls: -2 ± 4 bursts/min;
< 0.001). Similarly, MAP and MSNA responses were augmented during the onset of CPT in T2D patients. These findings demonstrate exaggerated pressor and MSNA reactivity in patients with T2D, with rapid and robust responses to both isometric contractions and cold stress. This hyper-responsiveness may contribute to daily surges in BP in patients with T2D, increasing their short-term and long-term cardiovascular risk.
New Findings
What is the central question of this study?
We aimed to examine leg vascular responses to brief periods of inactivity.
What is the main finding and its importance?
We demonstrate that a ...mere 10 min of sitting is sufficient to impair leg microvascular function (reactive hyperaemia). However, conduit artery vasodilatation (flow‐mediated dilatation) was unaffected, indicating maintained macrovascular function. Interestingly, immobile supine rest also resulted in a reduction in microvascular function alone that was prevented when calf muscle contractions were performed. Collectively, these data highlight the susceptibility of the microcirculation to short periods of inactivity and the beneficial role of skeletal muscle contraction for vascular health.
Prolonged sitting for 1–6 h has been shown to impair leg macrovascular i.e. reduced flow‐mediated dilatation (FMD) and microvascular (i.e. reduced reactive hyperaemia) function. These impairments appear to be mediated through reductions in shear stress. Interestingly, a reduction in shear rate has been observed as early as 10 min into sitting. However, it is unknown whether this acute reduction in shear stress is sufficient to affect vascular function. Accordingly, we studied 18 young men and assessed popliteal artery FMD and reactive hyperaemia before (Baseline) and after (PostSit) a 10 min sitting period. Popliteal artery shear rate was significantly reduced during sitting (Baseline, 62 ± 35 s−1; 10 min sitting, 27 ± 13 s−1; P < 0.001). Macrovascular function was unaffected by 10 min of sitting (Baseline, 4.4 ± 2.1%; PostSit, 4.3 ± 2.3%; P = 0.97), but microvascular function was reduced (Baseline, 4852 ± 2261 a.u.; PostSit, 3522 ± 1872 a.u.; P = 0.02). In a subset of individuals, we extended the recovery period after sitting and demonstrated that resting shear rate and reactive hyperaemia responses remained low up to 1 h post‐sitting (P < 0.001), whereas FMD was unchanged throughout (P = 0.99). Additionally, time control experiments were performed with participants in an immobile supine position, which demonstrated no change in macrovascular function (P = 0.94) but, unexpectedly, a reduction in microvascular function (P = 0.008). Importantly, when calf muscle contractions were performed during supine rest, reactive hyperaemia responses were maintained (P = 0.76), along with FMD (P = 0.88). These findings suggest that the leg microcirculation might be more vulnerable to short periods of inactivity, whereas conduit artery vasodilatation appears well maintained. Moreover, intermittent skeletal muscle contractions are beneficial for microvascular function.
PDF
