Brachial and Femoral Artery Responses to Prolonged Sitting
Brachial and Femoral Artery Responses to Prolonged Sitting
The purpose of this study was to investigate whether the effects of prolonged sitting on BA and SFA endothelial function are similar. We hypothesized that prolonged sitting will lead to decline in SFA endothelial function, but not in the BA endothelial function. Indeed, we found a decline in FMD in SFA during 3 hours of sitting (also published in). We also saw a decline in antegrade and mean shear rate in the SFA. In the BA, we found no significant decline in FMD during prolonged sitting; however to our surprise we found a decline in BA antegrade shear rate along with a significant increase in OSI 3 hours of sitting. This is the first study to our knowledge which compares the physiological effects of prolonged sitting on the upper and lower extremity vasculature.
We have previously discovered and discussed that prolonged sitting led to decreases in antegrade and mean shear rates in addition to impairment in endothelial function in the SFA. Padilla and colleagues in a similar study showed that when subjected to a similar inactivity model, there is a decline in shear rate patterns in the popliteal artery but no significant change in the FMD. Our shear rate results are similar to these authors but the FMD results differ primarily because of the study design, as discussed elsewhere.
The focus of this discussion will be our novel finding which is the decline in the antegrade shear rate in the BA along with an increase in OSI during 3 hrs prolonged sitting. We did not expect any change in the vascular parameters in the BA during sitting, primarily because upper extremity movement was not controlled and subjects moved their upper extremities, although the movement was minimal. We have previously shown that minimal activity during breaking sitting time prevents the impairment in shear rates and FMD in the SFA during prolonged sitting. Indeed, in this design, moving the upper extremities is similar to breaking sitting time for the lower extremities and therefore we did not expect any change in vascular parameters in the BA. There is only one study which has looked at the effects of acute inactivity on BA FMD. Padilla and colleagues had their subjects' arm hanging to mimic the increased hydrostatic load and inactivity. They showed that the shear rates decreased from baseline through 150 min which is similar to our results and a significant decline in BA FMD which is contrary to our findings. The type of inactivity in our protocol does not change the hydrostatic load in the upper extremities and mimics what most people do in sedentary jobs, for example using a computer or reading. Despite the movement in the arms, the antegrade shear rate declined and OSI increased. It is known that a decline in antegrade shear rate represents an aging profile in the vasculature. It is also known that oscillatory shear affects nitric oxide production thus inducing oxidative stress and monocyte adhesion. Oscillatory shear patterns are also associated with increased atherosclerosis. Newcomer and colleagues have shown that in the upright posture, mean blood velocity and shear rate are lower in SFA than BA. In view of this result and our data, it is clear that prolonged sitting causes an impairment in the BA shear rate patterns, although the BA FMD appears to be preserved as compared to SFA FMD. There are indeed other studies which have looked at the effect of physical inactivity on upper extremity vascular function during bed rest, dry water immersion, spinal cord injury among other inactivity models. However our results are directly important for public health and are shown in a study design simulating normal human behavior.
There are various possibilities why BA FMD might not have changed even in the presence of a reduced antegrade shear rate and increased OSI. It is possible that longer duration of sitting may have shown an effect on BA FMD. Antegrade shear rate declined in the SFA at 1 hr but it declined in the BA at 3 hours. This possibly shows some latency in the impairment of BA function on prolonged sitting, perhaps due to the regular movement of the upper extremities. It is possible that multiple bouts of prolonged sitting may impair BA FMD which is a marker of systemic vascular function. The possibility that the decline in FMD in the SFA during sitting signifies a true local phenomenon and not a systemic phenomenon cannot be discounted. A chronic environment of impaired endothelial function may lead to the increased atherosclerosis in the legs. Indeed 2 hours of siting has been shown to increase whole blood viscosity in the legs but not the arm. Furthermore, there are known differences in vascular reactivity between BA and FA and hence one can speculate that the FMD in the BA may be preserved even when the FMD in SFA is blunted, chronically exposing the lower extremity to a pro-atherogenic milieu. Finally it is possible that BA FMD may not be a sensitive measure of systemic endothelial function during prolonged sitting.
There are various possible mechanisms leading to an impaired shear pattern in the BA. For example, increase in muscle sympathetic nerve activity may lead to impaired shear patterns. We could not measure MSNA in our study due to logistical reasons. It is also possible that prolonged sitting may have led to an increased blood pressure which further led impaired shear patterns in the BA. It is known that lower extremity exercise increases BA FMD via an increase in shear rates. Based on our results, we can postulate that although 3 hours of sitting does not change BA FMD, it does promote pro-atherogenic shear patterns.
This study is not without limitations. For example, we did not measure blood pressure during the seated period. We contemplated measuring blood pressure but this was logistically difficult to do in the ipsilateral leg for concerns of changing blood flow patterns and in the contralateral leg for concerns of moving the lower extremity. It could have been done in the arm but because the primary purpose was comparing the two arteries it was not measured in the BA as well. It is known that uninterrupted sitting is associated with increased resting BP albeit in overweight adults which could lead to impaired shear rates and endothelial function. We acknowledge that not having blood pressure measures is a mechanistic limitation. We did not measure viscosity. It is known that whole blood viscosity increases in the leg but not in the arm during 2 hours of sitting. Our design consisted of 3 hours of prolonged sitting and it is possible that viscosity increases in the arm after 3 hours especially since increased viscosity is associated with low shear rates. Furthermore, measuring viscosity would also have allowed us to measure shear stresses. We did not measure MSNA. As discussed earlier increased MSNA has been shown to impair shear rate patterns in conduit arteries. Finally, we had young inactive men as our participants and more research needs to be done in women and different age groups to generalize these results to other populations.
Despite these limitations, our study adds significant new information to the existing literature on physical inactivity and the vascular differences between upper and lower extremities. This is the first study which shows that 3 hrs of sitting decreases antegrade shear rate and increases OSI in the BA, both shear patterns harmful to vascular health.
Discussion
The purpose of this study was to investigate whether the effects of prolonged sitting on BA and SFA endothelial function are similar. We hypothesized that prolonged sitting will lead to decline in SFA endothelial function, but not in the BA endothelial function. Indeed, we found a decline in FMD in SFA during 3 hours of sitting (also published in). We also saw a decline in antegrade and mean shear rate in the SFA. In the BA, we found no significant decline in FMD during prolonged sitting; however to our surprise we found a decline in BA antegrade shear rate along with a significant increase in OSI 3 hours of sitting. This is the first study to our knowledge which compares the physiological effects of prolonged sitting on the upper and lower extremity vasculature.
We have previously discovered and discussed that prolonged sitting led to decreases in antegrade and mean shear rates in addition to impairment in endothelial function in the SFA. Padilla and colleagues in a similar study showed that when subjected to a similar inactivity model, there is a decline in shear rate patterns in the popliteal artery but no significant change in the FMD. Our shear rate results are similar to these authors but the FMD results differ primarily because of the study design, as discussed elsewhere.
The focus of this discussion will be our novel finding which is the decline in the antegrade shear rate in the BA along with an increase in OSI during 3 hrs prolonged sitting. We did not expect any change in the vascular parameters in the BA during sitting, primarily because upper extremity movement was not controlled and subjects moved their upper extremities, although the movement was minimal. We have previously shown that minimal activity during breaking sitting time prevents the impairment in shear rates and FMD in the SFA during prolonged sitting. Indeed, in this design, moving the upper extremities is similar to breaking sitting time for the lower extremities and therefore we did not expect any change in vascular parameters in the BA. There is only one study which has looked at the effects of acute inactivity on BA FMD. Padilla and colleagues had their subjects' arm hanging to mimic the increased hydrostatic load and inactivity. They showed that the shear rates decreased from baseline through 150 min which is similar to our results and a significant decline in BA FMD which is contrary to our findings. The type of inactivity in our protocol does not change the hydrostatic load in the upper extremities and mimics what most people do in sedentary jobs, for example using a computer or reading. Despite the movement in the arms, the antegrade shear rate declined and OSI increased. It is known that a decline in antegrade shear rate represents an aging profile in the vasculature. It is also known that oscillatory shear affects nitric oxide production thus inducing oxidative stress and monocyte adhesion. Oscillatory shear patterns are also associated with increased atherosclerosis. Newcomer and colleagues have shown that in the upright posture, mean blood velocity and shear rate are lower in SFA than BA. In view of this result and our data, it is clear that prolonged sitting causes an impairment in the BA shear rate patterns, although the BA FMD appears to be preserved as compared to SFA FMD. There are indeed other studies which have looked at the effect of physical inactivity on upper extremity vascular function during bed rest, dry water immersion, spinal cord injury among other inactivity models. However our results are directly important for public health and are shown in a study design simulating normal human behavior.
There are various possibilities why BA FMD might not have changed even in the presence of a reduced antegrade shear rate and increased OSI. It is possible that longer duration of sitting may have shown an effect on BA FMD. Antegrade shear rate declined in the SFA at 1 hr but it declined in the BA at 3 hours. This possibly shows some latency in the impairment of BA function on prolonged sitting, perhaps due to the regular movement of the upper extremities. It is possible that multiple bouts of prolonged sitting may impair BA FMD which is a marker of systemic vascular function. The possibility that the decline in FMD in the SFA during sitting signifies a true local phenomenon and not a systemic phenomenon cannot be discounted. A chronic environment of impaired endothelial function may lead to the increased atherosclerosis in the legs. Indeed 2 hours of siting has been shown to increase whole blood viscosity in the legs but not the arm. Furthermore, there are known differences in vascular reactivity between BA and FA and hence one can speculate that the FMD in the BA may be preserved even when the FMD in SFA is blunted, chronically exposing the lower extremity to a pro-atherogenic milieu. Finally it is possible that BA FMD may not be a sensitive measure of systemic endothelial function during prolonged sitting.
Mechanisms
There are various possible mechanisms leading to an impaired shear pattern in the BA. For example, increase in muscle sympathetic nerve activity may lead to impaired shear patterns. We could not measure MSNA in our study due to logistical reasons. It is also possible that prolonged sitting may have led to an increased blood pressure which further led impaired shear patterns in the BA. It is known that lower extremity exercise increases BA FMD via an increase in shear rates. Based on our results, we can postulate that although 3 hours of sitting does not change BA FMD, it does promote pro-atherogenic shear patterns.
Limitations
This study is not without limitations. For example, we did not measure blood pressure during the seated period. We contemplated measuring blood pressure but this was logistically difficult to do in the ipsilateral leg for concerns of changing blood flow patterns and in the contralateral leg for concerns of moving the lower extremity. It could have been done in the arm but because the primary purpose was comparing the two arteries it was not measured in the BA as well. It is known that uninterrupted sitting is associated with increased resting BP albeit in overweight adults which could lead to impaired shear rates and endothelial function. We acknowledge that not having blood pressure measures is a mechanistic limitation. We did not measure viscosity. It is known that whole blood viscosity increases in the leg but not in the arm during 2 hours of sitting. Our design consisted of 3 hours of prolonged sitting and it is possible that viscosity increases in the arm after 3 hours especially since increased viscosity is associated with low shear rates. Furthermore, measuring viscosity would also have allowed us to measure shear stresses. We did not measure MSNA. As discussed earlier increased MSNA has been shown to impair shear rate patterns in conduit arteries. Finally, we had young inactive men as our participants and more research needs to be done in women and different age groups to generalize these results to other populations.
Despite these limitations, our study adds significant new information to the existing literature on physical inactivity and the vascular differences between upper and lower extremities. This is the first study which shows that 3 hrs of sitting decreases antegrade shear rate and increases OSI in the BA, both shear patterns harmful to vascular health.
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