4.3 Article

Impaired hemodynamic response to exercise in patients with peripheral artery disease: evidence of a link to inflammation and oxidative stress

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00159.2022

关键词

blood flow; exercise pressor response; peripheral vascular disease

资金

  1. National Heart, Lung, and Blood Institute [T32HL007576, T32HL139451, K99HL125756, P01HL091830, R01HL142603]
  2. Flight Attendant Medical Research Institute
  3. Veterans Administration Rehabilitation Research and Development Service Awards [E6910-R, E1697-R, E1433-P, I01CX001999]
  4. Small Projects in Rehabilitation Research Award [E1572P]

向作者/读者索取更多资源

This study found that patients with peripheral artery disease (PAD) have an exaggerated mean arterial blood pressure (MAP) response to exercise, likely driven by inflammation and oxidative stress. However, the blood flow response to exercise in patients with PAD remains equivocal.
An exaggerated mean arterial blood pressure (MAP) response to exercise in patients with peripheral artery disease (PAD), likely driven by inflammation and oxidative stress and, perhaps, required to achieve an adequate blood flow response, is well described. However, the blood flow response to exercise in patients with PAD actually remains equivocal. Therefore, eight patients with PAD and eight healthy controls completed 3 min of plantar flexion exercise at both an absolute work rate (WR) (2.7 W, to evaluate blood flow) and a relative intensity (40%WRmax, to evaluate MAP). The exercise-induced change in popliteal artery blood flow (BF, Ultrasound Doppler), MAP (Finapress), and vascular conductance (VC) were quantified. In addition, resting markers of inflammation and oxidative stress were measured in plasma and muscle biopsies. Exercise-induced DBF, assessed at 2.7 W, was lower in PAD compared with controls (PAD: 251 +/- 150 vs. Controls: 545 +/- 187 mL/min, P < 0.001), whereas Delta MAP, assessed at 40%WRmax, was greater for PAD (PAD: 23 +/- 14 vs. Controls: 11 +/- 6 mmHg, P = 0.028). The exercise-induced Delta VC was lower for PAD during both the absolute WR (PAD: 1.9 +/- 1.6 vs. Controls: 4.7 +/- 1.9 mL/min/mmHg) and relative intensity exercise (PAD: 1.9 +/- 1.8 vs. Controls: 5.0 +/- 2.2 mL/min/mmHg) trials (both, P < 0.01). Inflammatory and oxidative stress markers, including plasma interleukin-6 and muscle protein carbonyls, were elevated in PAD (both, P < 0.05), and significantly correlated with the hemodynamic changes during exercise (r = -0.57 to -0.78, P < 0.05). Thus, despite an exaggerated DMAP response, patients with PAD exhibit an impaired exercise-induced Delta BF and Delta VC, and both inflammation and oxidative stress likely play a role in this attenuated hemodynamic response.

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