Are There Limitations to Exercise Benefits in Peripheral Arterial Disease?

Abstract

Substantial evidence exists indicating that inactivity contributes to the progression of chronic disease, and conversely, that regular physical activity can both prevent the onset of disease as well as delay the progression of existing disease. To that end “exercise as medicine” has been advocated in the broad context as general medical care, but also in the specific context as a therapeutic, to be considered in much the same way as other drugs. As there are non-responders to many medications, there also are non-responders to exercise; individual who participate but do not demonstrate appreciable improvement/benefit. In some settings, the stress induced by exercise may aggravate an underlying condition, rather than attenuate chronic disease. As personalized medicine evolves with ready access to genetic information, so too will the incorporation of exercise in the context of those individual genetics. The focus of this brief review is to distinguish between the inherent capacity to perform, as compared to adaptive response to active exercise training in relation to cardiovascular health and peripheral arterial disease.

Patients with Diabetes Complicated by Peripheral Artery Disease: the Current State of Knowledge on Physiotherapy Interventions

“…Other important exercising contraindications include advanced heart failure and rest dyspnea of any origin, recent myocardial infarction or active signs of ischemia in electrocardiogram (unstable angina), complete heart block, myocarditis, endocarditis, pericarditis, left ventricular outflow tract obstruction, pleuritis, pericarditis, and if systolic blood pressure falls by 30% of baseline during exercise. When blood pressure exceeds >160/100 mmHg, the exercise should be periodically discontinued [69][70][71]. Contraindications are also common in rheumatoid arthritis and osteoarthritis when there is acute inflammation or pain during exercising.…”

Low Intrinsic Aerobic Capacity Limits Recovery Response to Hindlimb Ischemia

“…From the images, measurements were obtained in five fields per section, 50 myocytes/field, and in at least five separate sections, with care taken to avoid repeated sampling of the same field in sequential sections. The following indices were measured: (1) number of capillaries around a fiber (NCAF), (2) the capillary to fiber ratio on an individual fiber basis (Cap/Fi), (3) the number of fibers sharing each capillary [share factor (SF)], and (4) capillary density (CD). This stain also provides the ability to distinguish between different muscle fiber types.…”

“…Exercise training has been shown to increase capillary number within healthy skeletal muscle through the process of angiogenesis, mediated, at least in part, by vascular endothelial growth factor (VEGF) driven pathways (5)(6)(7)(8). The mechanisms by which exercise training improves intermittent claudication in PAOD patients remains unclear (2,9,10). Clinical studies of PAOD indicate that patients limited by intermittent claudication who engage in any amount of weekly physical activity beyond light intensity, have a lower mortality rate than their sedentary counterparts who perform either no physical activity or only light-intensity activities (11), even after adjusting for other predictors of mortality, which include age, and body mass index (BMI).…”

“…These outcomes are determined by at least two genetic components (12)(13)(14)(15)(16)(17). One component establishes the innate aerobic exercise capacity that each individual possesses irrespective of any subsequent training or activity (12)(13)(14)(15)(16)(17), and the second genetic component establishes the pattern of responses to active exercise training (1,2,11,(18)(19)(20). It is estimated that up to 70% of the variation in exercise capacity are due to the genetic predisposition of an individual (12,13).…”

“…It is estimated that up to 70% of the variation in exercise capacity are due to the genetic predisposition of an individual (12,13). Many studies have focused on the active exercise training component (1,2,6,7,11,(18)(19)(20)(21), but even within these studies, there is a heterogeneous response in subjects to training protocols (2,6,7,11,(18)(19)(20)(21)(22). It is this finding that suggests the importance of investigating intrinsic exercise capacity and its impact on the response to ischemic stress.…”