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

Autor: Craig JC; Department of Internal Medicine, University of Utah, Salt Lake City, Utah.; Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah., Hart CR; Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah.; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah., Layec G; Department of Internal Medicine, University of Utah, Salt Lake City, Utah.; Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah.; Department of Kinesiology, University of Massachusetts, Amherst, Massachusetts.; Institute for Applied Life Sciences, University of Massachusetts, Amherst, Massachusetts., Kwon OS; Department of Internal Medicine, University of Utah, Salt Lake City, Utah.; Department of Kinesiology, University of Connecticut, Storrs, Connecticut., Richardson RS; Department of Internal Medicine, University of Utah, Salt Lake City, Utah.; Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah.; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah., Trinity JD; Department of Internal Medicine, University of Utah, Salt Lake City, Utah.; Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah.; Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
Jazyk: angličtina
Zdroj: American journal of physiology. Regulatory, integrative and comparative physiology [Am J Physiol Regul Integr Comp Physiol] 2022 Nov 01; Vol. 323 (5), pp. R710-R719. Date of Electronic Publication: 2022 Sep 26.
DOI: 10.1152/ajpregu.00159.2022
Abstrakt: 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%WR max , 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 ΔBF, 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 ΔMAP, assessed at 40%WR max , was greater for PAD (PAD: 23 ± 14 vs. Controls: 11 ± 6 mmHg, P = 0.028). The exercise-induced ΔVC 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 ΔMAP response, patients with PAD exhibit an impaired exercise-induced ΔBF and ΔVC, and both inflammation and oxidative stress likely play a role in this attenuated hemodynamic response.
Databáze: MEDLINE