Postexercise Hemodynamics in Patients With Type 2 Diabetes: Effect of Exercise Intensity and Duration

2017 ◽  
Vol 6 (1) ◽  
pp. 1-8
Author(s):  
Thomas K. Pellinger ◽  
Catherine B. Pearce ◽  
Grant H. Simmons ◽  
Jack L. Snitzer

Background: For individuals with type 2 diabetes (T2D), the hemodynamic response to regular exercise is critical for regulating blood glucose, protecting vascular function, and reducing cardiovascular disease risk, but the hemodynamic responses to differing doses of acute exercise in T2D are unclear. We aimed to compare postexercise (PE) hemodynamics in patients with T2D in response to 4 doses of dynamic exercise. Methods: Eight subjects with well-controlled T2D (42–64 years old.; hemoglobin A1c: 6.6% ± 0.9%) participated in 4 study days, during which they exercised on a cycle ergometer at 4 different combinations of exercise duration and intensity: 30 min at 40% V˙O2peak (30@40), 30 min at 60% V˙O2peak (30@60), 60 min at 40% V˙O2peak (60@40), and 60 min at 60% V˙O2peak (60@60). Heart rate, arterial pressure, and femoral blood flow (Doppler ultrasound) were measured pre-exercise and every 15 min through 120 min PE. Femoral vascular conductance was calculated as flow/pressure. Results: Compared with pre-exercise baseline, femoral blood flow and femoral vascular conductance were higher through at least 105 min of recovery in all conditions (all P < .05), except for the 30@40 trial. Compared with the pre-exercise measures, systolic blood pressure was lower through at least 75 min of recovery in all conditions (all P < .05), except for the 30@40 trial. Conclusion: These results suggest that exercise must be at least moderate in intensity or prolonged in duration (>30 min) to promote sustained PE elevations in skeletal muscle blood flow and reductions in systolic blood pressure in patients with T2D.

2006 ◽  
Vol 101 (5) ◽  
pp. 1351-1355 ◽  
Author(s):  
Maria M. Anton ◽  
Miriam Y. Cortez-Cooper ◽  
Allison E. DeVan ◽  
Daria B. Neidre ◽  
Jill N. Cook ◽  
...  

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 ± 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 ± 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested ( P < 0.05). Whole body lean body mass increased ( P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55–60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.


BMJ Open ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. e027906
Author(s):  
Yijia Chen ◽  
Jie Yang ◽  
Jian Su ◽  
Yu Qin ◽  
Chong Shen ◽  
...  

ObjectiveInvestigating the association between total physical activity, physical activity in different domains and sedentary time with clustered metabolic risk in patients with type 2 diabetes from Jiangsu province, China.DesignInterview-based cross-sectional study conducted between December 2013 and January 2014.Setting44 selected townships across two cities, Changshu and Huai’an, in Jiangsu province.Participants20 340 participants selected using stratified cluster-randomised sampling and an interviewer-managed questionnaire.MethodsWe constructed clustered metabolic risk by summing sex-specific standardised values of waist circumference, fasting triacylglycerol, fasting plasma glucose, systolic blood pressure and the inverse of blood high-density lipoprotein cholesterol (HDL-cholesterol). Self-reported total physical activity included occupation, commuting and leisure-time physical activity. The un-standardised regression coefficient [B] and its 95% CI were calculated using multivariate linear regression analyses.ResultsThis study included 17 750 type 2 diabetes patients (aged 21–94 years, 60.3% female). The total (B=−0.080; 95% CI: −0.114 to −0.046), occupational (B=−0.066; 95% CI: −0.101 to− 0.031) and leisure-time physical activity (B=−0.041; 95% CI: −0.075 to −0.007), and sedentary time (B=0.117; 95% CI: 0.083 to 0.151) were associated with clustered metabolic risk. Total physical activity, occupational physical activity and sedentary time were associated with waist circumference, triacylglycerol and HDL-cholesterol, but not with systolic blood pressure. Commuting physical activity and sedentary time were significantly associated with triacylglycerol (B=−0.012; 95% CI: −0.019 to −0.005) and fasting plasma glucose (B=0.008; 95% CI: 0.003 to 0.01), respectively. Leisure-time physical activity was only significantly associated with systolic blood pressure (B=−0.239; 95% CI: −0.542 to− 0.045).ConclusionsTotal, occupational and leisure-time physical activity were inversely associated with clustered metabolic risk, whereas sedentary time increased metabolic risk. Commuting physical activity was inversely associated with triacylglycerol. These findings suggest that increased physical activity in different domains and decreased sedentary time may have protective effects against metabolic risk in type 2 diabetes patients.


2012 ◽  
Vol 112 (4) ◽  
pp. 560-565 ◽  
Author(s):  
John McDaniel ◽  
Stephen J. Ives ◽  
Russell S. Richardson

Although a multitude of factors that influence skeletal muscle blood flow have been extensively investigated, the influence of muscle length on limb blood flow has received little attention. Thus the purpose of this investigation was to determine if cyclic changes in muscle length influence resting blood flow. Nine healthy men (28 ± 4 yr of age) underwent a passive knee extension protocol during which the subjects' knee joint was passively extended and flexed through 100–180° knee joint angle at a rate of 1 cycle per 30 s. Femoral blood flow, cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded during the entire protocol. These measurements revealed that slow passive changes in knee joint angle did not have a significant influence on HR, SV, MAP, or CO; however, net femoral blood flow demonstrated a curvilinear increase with knee joint angle ( r2 = 0.98) such that blood flow increased by ∼90% (125 ml/min) across the 80° range of motion. This net change in blood flow was due to a constant antegrade blood flow across knee joint angle and negative relationship between retrograde blood flow and knee joint angle ( r2 = 0.98). Thus, despite the absence of central hemodynamic changes and local metabolic factors, blood flow to the leg was altered by changes in muscle length. Therefore, when designing research protocols, researchers need to be cognizant of the fact that joint angle, and ultimately muscle length, influence limb blood flow.


Author(s):  
Jay S Mishra ◽  
Sathish Kumar

Abstract Preeclampsia is a pregnancy-related hypertensive disorder with unclear mechanisms. While hypersensitivity to angiotensin II via vasoconstrictive angiotensin type-1 receptor (AT1R) is observed in preeclampsia, the importance of vasodilatory angiotensin type-2 receptor (AT2R) in the control of vascular dysfunction is less clear. We assessed whether AT1R, AT2R and eNOS expression is altered in placental vessels of preeclamptic women and tested if ex vivo incubation with AT2R agonist Compound 21 (C21; 1 μM) could restore AT1R, AT2R and eNOS balance. Further, using a rat model of gestational hypertension induced by elevated testosterone, we examined whether C21 (1 μg·kg−1·day−1, oral) could preserve AT1R and AT2R balance and improve blood pressure, uterine artery blood flow, and vascular function. Western blots revealed that AT1R protein level was higher while AT2R and eNOS protein were reduced in preeclamptic placental vessels, and AT2R agonist C21 decreased AT1R and increased AT2R and eNOS protein levels in preeclamptic vessels. In testosterone-dams, blood pressure was higher, and uterine artery blood flow was reduced, and C21 treatment reversed these levels similar to those in controls dams. C21 attenuated the exaggerated Ang II contraction and improved endothelium-dependent vasorelaxation in uterine arteries of testosterone-dams. These C21-mediated vascular effects were associated with decreased AT1R and increased AT2R and eNOS protein levels. C21 also increased serum nitrate/nitrite and bradykinin production in testosterone-dams and attenuated the feto-placental growth restriction. Thus, AT1R upregulation and AT2R downregulation is observed in preeclampsia and testosterone-model, and increasing AT2R activity could help restore AT1R and AT2R balance and improve gestational vascular function.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Pablo Lapuerta ◽  
Paul Strumph ◽  
Philip Banks ◽  
Ikenna Ogbaa ◽  
Brian Zambrowicz ◽  
...  

Introduction: Selective sodium-glucose cotransporter 2 (SGLT2) inhibitors target only the kidney, and they have reduced efficacy when patients with type 2 diabetes mellitus (T2DM) have renal impairment (RI). LX4211 blocks sodium and glucose absorption in the gastrointestinal tract by inhibition of SGLT1, and it enhances urinary sodium and glucose excretion in the urine through inhibition of SGLT2. The dual SGLT1/2 action of LX4211 was anticipated to reduce systolic blood pressure (SBP) in addition to improving glucose control in the setting of RI. Methods: This analysis explored the effect of LX4211 on SBP in a clinical trial of patients with T2DM and moderate to severe RI. Patients (N=31) were randomly assigned to be treated with LX4211 (400 mg, N=16) or placebo (N=15) qd for 7 consecutive days. Postprandial glucose levels after a standard high glucose meal served as the primary measure of pharmacodynamic activity. Baseline and Day 8 trough SBP measures were each an average of 3 seated assessments. Results: Mean baseline characteristics included age 66.4 years, estimated glomerular filtration rate (eGFR) 43.4 mL/min/1.73 m 2 , and SBP 130.9 mmHg. Postprandial glucose area under the curve (sampled from pre-dose to 4 hours post meal) was reduced from Baseline to Day 7 by 169.3 mg*hr/dL on LX4211 compared to placebo (p=0.003). Day 8 SBP reductions were 11.4 mmHg on LX4211 and 0.0 mmHg on placebo (p=0.045 for difference between groups). Patients with greater RI (eGFR <45 mL/min/1.73 m2) treated with LX4211 (N=6) had a 10.5 mmHg SBP reduction compared to 0.3 mmHg on placebo (N=9). The difference between seated and standing SBP did not change with LX4211 (0.0 mmHg change, Day 8 vs. Baseline). There were no reports of hypotension, hypovolemia, no serious adverse events, and no patient discontinued due to an adverse event. Mild hypoglycemia was reported in 1 LX4211 patient compared to 2 placebo patients. Conclusions: LX4211 may reduce SBP and enhance glycemic control in T2DM patients with moderate to severe RI.


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