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Emerging evidence suggests that type 2 diabetes (T2D) may impair the ability to properly adjust the circulation during exercise with augmented blood pressure (BP) and an attenuated contracting skeletal muscle blood flow (BF) response being reported. This review provides a brief overview of the current understanding of these altered exercise responses in T2D and the potential underlying mechanisms, with an emphasis on the sympathetic nervous system and its regulation during exercise. The research presented support augmented sympathetic activation, heightened BP, reduced skeletal muscle BF, and impairment in the ability to attenuate sympathetically mediated vasoconstriction (i.e., functional sympatholysis) as potential drivers of neurovascular dysregulation during exercise in T2D. Furthermore, emerging evidence supporting a contribution of the exercise pressor reflex and central command is discussed along with proposed future directions for studies in this important area of research.

Twenty-three young adults (4 Females, 25.13 ± 3.72 years) performed an intermittent maximal handgrip force task using their dominant hand for 20 min (3.5 s squeeze/6.5 s release, 120 blocks) with concurrent cortical activity imaging by functional Near-Infrared Spectroscopy (fNRIS; OMM-3000, Shimadzu Corp., 111 channels). Subjects were grouped as physically active (n = 10) or inactive (n = 12) based on a questionnaire (active-exercise at least four times a week, inactive- exercise less than two times a week). We explored how motor task fatigue affected the vasomotion-induced oscillations in ΔHbO as measured by fNIRS at each hemodynamic frequency band: endothelial component (0.003–0.02 Hz) associated to microvascular activity, neurogenic component (0.02–0.04 Hz) related to intrinsic neuronal activity, and myogenic component (0.04–0.15 Hz) linked to activity of smooth muscles of arterioles. To help understand how these three neurovascular regulatory mechanisms relate to handgrip task performance we quantified several dynamic fNIRS metrics, including directional phase transfer entropy (dPTE), a computationally efficient and data-driven method used as a marker of information flow between cortical regions, and directional connectivity (DC), a means to compute directionality of information flow between two cortical regions. The relationship between static functional connectivity (SFC) and functional connectivity variability (FCV) was also explored to understand their mutual dependence for each frequency band in the context of handgrip performance as fatigued increased. Our findings ultimately showed differences between subject groups across all fNIRS metrics and hemodynamic frequency bands. These findings imply that physical activity modulates neurovascular control mechanisms at the endogenic, neurogenic, and myogenic frequency bands resulting in delayed fatigue onset and enhanced performance. The dynamic cortical network metrics quantified in this work for young, healthy subjects provides baseline measurements to guide future work on older individuals and persons with impaired cardiovascular health.

Abstract Sympathetic vasoconstriction is attenuated in exercising muscles to assist in matching of blood flow with metabolic demand. This “functional sympatholysis” may be impaired in young obese individuals due to greater sympathetic activation and/or reduced local vasodilatory capacity of both small and large arteries, but this remains poorly understood. We tested the hypothesis that functional sympatholysis is impaired in obese individuals compared with normal‐weight counterparts. In 36 obese and normal‐weight young healthy adults (n = 18/group), we measured forearm blood flow and calculated forearm vascular conductance (FVC) responses to reflex increases in sympathetic nerve activity induced by lower body negative pressure (LBNP) at rest and during rhythmic handgrip exercise at 15% and 30% of the maximal voluntary contraction (MVC). FVC was normalized to lean forearm mass. In normal‐weight individuals, LBNP evoked a decrease in FVC (−16.1 ± 5.7%) in the resting forearm, and the reduction in FVC (15%MVC: −8.1 ± 3.3%; 30%MVC: −1.0 ± 4.0%) was blunted during exercise in an intensity‐dependent manner (P 0.05) and was intensity‐dependent (P

BackgroundPostmenopausal women represent the largest cohort of patients with heart failure with preserved ejection fraction, and vascular dementia represents the most common form of dementia in patients with heart failure with preserved ejection fraction. Therefore, we tested the hypotheses that the combination of cardiac pressure overload (aortic banding [AB]) and the loss of female sex hormones (ovariectomy [OVX]) impairs cerebrovascular control and spatial memory. Methods and ResultsFemale Yucatan miniswine were separated into 4 groups (n=7 per group): (1) control, (2) AB, (3) OVX, and (4) AB‐OVX. Pigs underwent OVX and AB at 7 and 8 months of age, respectively. At 14 months, cerebral blood flow velocity and spatial memory (spatial hole‐board task) were lower in the OVX groups (P

The variable pressure neck chamber has provided an invaluable research tool for the non-invasive assessment of carotid baroreflex (CBR) function in human investigations. The ability to construct complete stimulus-response curves and define specific parameters of the reflex function curve permits statistical comparisons of baroreflex function between different experimental conditions, such as rest and exercise. Results have convincingly indicated that the CBR stimulus-response curve is reset during exercise in an intensity-dependent manner to functionally operate around the prevailing pressure elicited by the exercise workload. Furthermore, both at rest and during exercise, alterations in stroke volume do not contribute importantly to the maintenance of arterial blood pressure by the carotid baroreceptors, and therefore, any reflex-induced changes in cardiac output (Q) are the result of CBR-mediated changes in heart rate. However, more importantly, the CBR-induced changes in mean arterial pressure (MAP) are primarily mediated by alterations in vascular conductance with only minimal contributions from Q to the initial reflex MAP response. Thus, the capacity of the CBR to regulate blood pressure depends critically on its ability to alter vascular tone both at rest and during exercise. This review will emphasize the utility of the variable pressure neck chamber to assess CBR function in human experimental investigations and the mechanisms by which the CBR responds to alterations in arterial blood pressure both at rest and during exercise. Experimental Physiology (2003) 88.6, 671-680. [ABSTRACT FROM AUTHOR]

Although square-wave sustained and R wave-triggered pulsatile stimuli have been used to assess carotid baroreflex (CBR) function in humans, it remains unclear whether these different stimulus protocols elicit comparable responses and whether CBR responses adapt during prolonged stimulation. Thus, we measured muscle sympathetic nerve activity (MSNA), heart rate (HR) and mean arterial pressure (MAP) in response to +30 Torr neck pressure (NP) and -30 Torr neck suction (NS) delivered for 20 s either as a sustained or pulsatile stimulus. CBR-mediated changes in MSNA, HR and MAP were similar with sustained and pulsatile stimuli. The time course of MSNA and HR responses identified that significant changes occurred during the initial 5 s and were better maintained over 20 s with NP than with NS. Changes in MAP exhibited a slower onset with the peak increase during NP occurring at 10 s (sustained, 7 ± 1 mmHg; pulsatile, 7 ± 1 mmHg; P > 0.05) and the nadir during NS occurring at 20 s (sustained, -7 ± 1 mmHg; pulsatile, -9 ± 2 mmHg; P > 0.05). These data demonstrate that sustained and pulsatile NP and NS produce comparable CBR-mediated responses. Furthermore, despite MSNA and HR returning towards baseline during NS, CBR-mediated changes in MAP are well maintained over 20 s of NS and NP. Experimental Physiology (2003) 88.5, 595-601. [ABSTRACT FROM AUTHOR]