Benefit of exercise conditioning for patients with peripheral arterial disease. Exercise rehabilitation improves functional outcomes and peripheral circulation in patients with intermittent claudication: a randomized controlled trial. [Effect of a 2-year ambulatory vascular sports program on walking distance in claudication patients--a controlled study]. Treating peripheral arterial occlusive disease: pentoxifylline vs exercise. Vascular adhesion molecule-1 and markers of platelet function before and after a treatment with iloprost or a supervised physical exercise program in patients with peripheral arterial disease. Exercise training for intermittent claudication: does it adversely affect biochemical markers of the exercise-induced inflammatory response? Upper- vs lower-limb aerobic exercise rehabilitation in patients with symptomatic peripheral arterial disease: a randomized controlled trial. Short-term effects of cycle and treadmill training on exercise tolerance in peripheral arterial disease. The EXercise versus Angioplasty in Claudication Trial (EXACT): reasons for recruitment failure and the implications for research into and treatment of intermittent claudication. The effect of supervised exercise and cilostazol on coagulation and fibrinolysis in intermittent claudication: a randomized controlled trial. PoleStriding exercise and vitamin E for management of peripheral vascular disease. Effect of daily muscular exercise in patients with intermittent claudication. Experimental model of pain-free treadmill training in patients with claudication. Red blood cell deformability in patients with claudication after pain-free treadmill training. Metabolic activity of skeletal muscle in patients with peripheral arterial insufficiency. Effect of exercise training on skeletal muscle histology and metabolism in peripheral arterial disease. Physical training and antiplatelet treatment in stage II peripheral arterial occlusive disease: alone or combined? Intermittent claudication--surgical reconstruction or physical training? A prospective randomized trial of treatment efficiency. Treatment efficacy of intermittent claudication by surgical intervention, supervised physical exercise training compared to no treatment in unselected randomised patients I: one year results of functional and physiological improvements. Improvement of the walking ability in intermittent claudication due to superficial femoral artery occlusion with supervised exercise and pneumatic foot and calf compression: a randomised controlled trial. The effects of exercise training on walking function and perception of health status in elderly patients with peripheral arterial occlusive disease.
Patients with atherosclerotic peripheral arterial disease (PAD) of the lower extremities have impaired walking ability due to exercise-induced muscle ischemia and the resultant pain of intermittent claudication. To evaluate the benefit of exercise training as a treatment for patients with PAD, as well as possible mechanisms associated with improvement, we randomly assigned 19 men with disabling claudication to treated and control groups. Treatment consisted of supervised treadmill walking (1 hr/day, 3 days/wk, for 12 weeks) with progressive increases in speed and grade as tolerated. Graded treadmill testing was performed to maximal toleration of claudication pain on entry and after 12 weeks of training to define changes in peak exercise performance. After 12 weeks, treated subjects had increased their peak walking time 123%, peak oxygen consumption 30%, and pain-free walking time 165% (all p less than 0.05). Control subjects had no change in peak oxygen consumption, but after 12 weeks, peak walking time increased 20% (p less than 0.05). In treated subjects, maximal calf blood flow (measured by a plethysmograph) increased 38 +/- 45% (p less than 0.05), but the change in flow was not correlated to the increase in peak walking time. Elevated plasma concentrations of acylcarnitines have been associated with the functional impairment of PAD and may reflect the metabolic state of ischemic skeletal muscle. In treated subjects, a 26% decrease in resting plasma short-chain acylcarnitine concentration was correlated with improvement in peak walking time (r = -0.78, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS) To determine the effects of a 6-month exercise program on ambulatory function, free-living daily physical activity, peripheral circulation, and health-related quality of life (QOL) in disabled older patients with intermittent claudication.
                Prospective, randomized controlled trial.
                University Medical (Center and Veterans Affairs Medical Center, Baltimore, Maryland.
                Thirty-one of 61 patients with Fontaine stage II peripheral arterial occlusive disease (PAOD) were randomized to exercise rehabilitation and 30 to usual-care control. Three patients from the exercise group and six patients from the control group dropped out, leaving 28 and 24 patients, respectively, completing the study in each group.
                Six months of exercise rehabilitation.
                Treadmill distance walked to onset of claudication and to maximal claudication, ambulatory function, peripheral circulation, perceived QOL, and daily physical activity.
                Compliance with the exercise program was 73% of the possible sessions. Exercise rehabilitation increased treadmill distance walked to onset of claudication by 134% (P < .001) and to maximal claudication by 77% (P < .001), walking economy by 12% (P = .003), 6-minute walk distance by 12% (P < .001), and maximal calf blood flow by 30% (P < .001). Changes in distance walked to maximal pain correlated with changes in walking economy (r = -.50, P = .013) and changes in maximal calf blood flow (r = .38, P = .047). Exercise rehabilitation increased accelerometer-derived daily physical activity by 38% (P < .001); this change correlated with the change in distance walked to maximal pain (r = .45, P = .020). These improvements were significantly better than the changes in the control group (P < .05).
                Improvements in claudication following exercise rehabilitation in older PAOD patients are dependent on improvements in peripheral circulation and walking economy. Improvement in treadmill claudication distances in these patients translated into increased accelerometer-derived physical activity in the community, which enabled the patients to become more functionally independent. nan The effects of three months therapy with Pentoxifylline (800 mg three times daily) and physical training were compared in two age- and sex-matched groups of Stage II PAOD patients. Before therapy and after 12 and 13 weeks each patient underwent a standard treadmill test. The maximum walking time, TcPO2 half recovery time to basal values after the induced ischaemia, granulocyte production of free radicals (by the superoxide dismutase-inhibitable reduction of ferricytochrome) and surface expression of the CD11/CD18 complex of adhesion molecules (by using specific monoclonal antibodies) were determined. Pentoxifylline inhibited free radical production and reduced the percentage of granulocytes expressing adhesion receptors while exercise had no significant effect on these parameters. These changes, which reflect improved microcirculatory functioning, were associated with a greater walking capacity and shorter half recovery time (+14% vs exercise group, p < 0.01; -39% vs exercise group, p < 0.01 respectively). Platelet function and levels of vascular adhesion molecule-1 (VCAM-1) were investigated in 24 patients with peripheral arterial disease at Fontaine stage II undergoing a 2 weeks treatment with iloprost (0.5-2 ng/kg/h i.v. infused, 6 h/day) or a 2 weeks supervised physical training, randomly assigned. Patients were studied before (T0) and after (T14) treatments and 10 days later (T24). The adhesion of washed platelets to fibrinogen coated microwells was reduced after treatment both with iloprost (1.9+/-0.4 vs 6.8+/-0.7%; T24 vs T0; M+/-SEM; p<0.05) and physical exercise (3.0+/-1.0 vs 6.7+/-0.7; p<0.05) while adhesion to human plasma coated microwells was reduced only after treatment with iloprost (1.9+/-0.8 vs 5.8+/-0.9; p<0.05). The expression of fibrinogen receptor (glycoprotein IIb/IIIa) on platelets, measured by flow-cytometry was also reduced after iloprost treatment (17.1+/-1.5 vs 31.8+/-4.8 AU; p<0.05) and physical exercise (14.6+/-1.5 vs 34.0+/-3.3; p<0.05). Theurinaryexcretion of platelet thromboxane A2 metabolite 2,3-dinor-thromboxane B2 decreased only in patients treated with iloprost (154.7+/-97.9 vs 256.2+/-106.4 pg mg creatinine(-1); p<0.05). Similarly plasma VCAM-1 was lower in patients who were treated with iloprost (827.7+/-77.4 vs 999.0+/-83.8 ng ml(-1); p<0.05). In conclusion, both iloprost and physical exercise seem to act on reversible phenomena such as the expression of adhesion molecules or ex vivo adhesion, whereas only iloprost reduces thromboxane A2 biosynthesis in vivo. This anti-platelet activity seems to be extended in time and to be associated with an improvement in vascular function. To identify a stable biochemical marker of disease severity in patients with intermittent claudication and to use these findings to assess the effect of therapeutic exercise training.
                Case-control study: prospective randomised-controlled trial of exercise training.
                Plasma fibrinogen, serum amyloid A protein (SAA), C-reactive protein (CRP) and urinary albumin-creatinine ratio (ACR) were measured in 67 claudicants and 15 controls. Twenty-two patients were randomised to supervised exercise training and 17 randomised to observation. Subjects were reviewed at 3, 6 and 12 months.
                The median (interquartile range) baseline fibrinogen was 3.7 g/l (3.3-4.25) in claudicants and 3.5 g/l (2.9-3.95) in controls (p = 0.045); CRP was 4.7 mg/l (2.2-9.0) and 2.1 mg/l (1.0-2.8), respectively (p < 0.0001); SAA was 72 mg/l (35-132) and 30 mg/l (20-89) (p = 0.0009). Claudicants showed an increased urinary ACR following treadmill exercise (Wilcoxon, p < 0.0001) with no change in controls. Exercise training reduced SAA at 6 months, CRP at 3 months and progressively attenuated the post-exercise increase in ACR. No similar changes were found in controls.
                Repetitive low-grade inflammatory events in claudicants lead to elevation of serum acute-phase proteins. Exercise training is associated with symptomatic improvement and reduction inflammatory markers. The concern that exercise has adverse systemic effects therefore seems to be unjustified. To investigate the effects of a 24-week program of upper- and lower-limb aerobic exercise training on walking performance in patients with symptomatic peripheral arterial disease (PAD) and to study the mechanisms that could influence symptomatic improvement.
                After approval from the North Sheffield Local Research Ethics Committee, 104 patients (median age, 69 years; range, 50 to 85 years) with stable PAD were randomized into an upper- or lower-limb aerobic exercise training group (UL-Ex or LL-Ex), or to a nonexercise training control group. Training was performed twice weekly for 24 weeks at equivalent relative exercise intensities. An incremental arm- and leg-crank test (ACT and LCT) to maximum exercise tolerance was performed before and at 6, 12, 18, and 24 weeks of the intervention to determine peak oxygen consumption (VO(2)). Walking performance, defined as the claudicating distance (CD) and maximum walking distance (MWD) achieved before intolerable claudication pain, was assessed at the same time points by using a shuttle-walk protocol. Peak blood lactate concentration, Borg ratings of perceived exertion (RPE) and pain category ratio (CR-10) were recorded during all assessments.
                CD and MWD increased over time (P < .001) in both training groups. At 24 weeks, CD had improved by 51% and 57%, and MWD had improved by 29% and 31% (all P < .001) in the UL-Ex and LL-Ex groups, respectively. An increase in peak heart rate at MWD in the UL-Ex group (109 +/- 4 vs 115 +/- 4 beats/min; P < .01) and LL-Ex group (107 +/- 3 vs 118 +/- 3 beats/min; P = .01) was accompanied by an increase in the amount of pain experienced in both groups (P < .05), suggesting that exercising patients could tolerate a higher level of cardiovascular stress and an increased intensity of claudication pain before test termination after training. Patients assigned to exercise training also showed an increase in LCT peak VO2 at the 24-week time point in relation to baseline (P < .01) and control patients (P < .01), whereas ACT peak VO2 was only improved in the UL-Ex group (P < .05).
                Our results suggest that a combination of physiologic adaptations and improved exercise pain tolerance account for the improvement in walking performance achieved through upper-limb aerobic exercise training in patients with PAD. Furthermore, that both arm- and leg-crank training could be useful exercise training modalities for improving cardiovascular function, walking performance, and exercise pain tolerance in patients with symptomatic PAD. To explore the efficacy of cycle training in the treatment of intermittent claudication, the present study compared performance and physiologic effects of cycle training with more conventional treadmill walking training in a group of patients with claudication.
                Forty-two individuals with peripheral arterial disease and intermittent claudication (24 men, 18 women) were stratified by gender and the presence or absence of type 2 diabetes mellitus and then randomized to a treadmill (n = 13), cycle (n = 15), or control group (n = 14). Treadmill and cycle groups trained three times a week for 6 weeks, whereas the control group did not train during this period. Maximal and pain-free exercise times were measured on graded treadmill and cycle tests before and after training.
                Treadmill training significantly improved maximal and pain-free treadmill walking times but did not improve cycle performance. Cycle training significantly improved maximal cycle time but did not improve treadmill performance. However, there was evidence of a stronger cross-transfer effect between the training modes for patients who reported a common limiting symptom during cycling and walking at baseline. There was also considerable variation in the training response to cycling, and a subgroup of responsive patients in the cycle group improved their walking performance by more than the average response observed in the treadmill group.
                These findings suggest that cycle exercise is not effective in improving walking performance in all claudication patients but might be an effective alternative to walking in those who exhibit similar limiting symptoms during both types of exercise. nan The prothrombotic, hypofibrinolytic state that develops in patients with intermittent claudication (IC) upon walking due to ischemia-reperfusion injury (IRI) of the leg muscles may contribute to the high incidence of life- and limb-threatening thrombotic events observed in this patient group. Treatments, such as angioplasty, that obtund the IRI also ameliorate the procoagulant diathesis. The effect on this diathesis of supervised exercise and cilostazol, both of which provide symptomatic benefit in IC, but without significantly obtunding IRI, is unknown.
                Thirty-four patients (27 men and 7 women; median age, 67 years; range, 63-72 years) were randomized to receive best medical therapy (BMT) plus supervised exercise (n = 9), BMT plus cilostazol (n = 9), BMT plus supervised exercise plus cilostazol (n = 7), or BMT alone (n = 9) in a 2 x 2 factorial design. Thrombin-antithrombin complex and prothrombin fragments 1 and 2, both markers of thrombin generation; plasminogen activator inhibitor antigen and tissue plasminogen activator antigen, both markers of fibrinolysis; ankle-brachial pressure index (ABPI); and initial and absolute claudication distance (ACD) were measured at baseline and then 3 and 6 months after randomization.
                At 6 months, when compared with receiving BMT only, supervised exercise and cilostazol resulted in improvements in ABPI of 18% and 13% and in ACD of 40% and 64%, respectively. The effects on ABPI and ACD of combining supervised exercise and cilostazol were additive. Supervised exercise, cilostazol, and supervised exercise combined with cilostazol had no significant effect on any of the four hemostatic markers.
                Treatment of IC by supervised exercise or cilostazol results in significant improvements in ABPI and ACD but has no demonstrable effect on the prothrombotic diathesis. This suggests that supervised exercise and cilostazol, unlike angioplasty, are unlikely to have a long-term beneficial effect on the thrombotic risks faced by these patients. The purpose of this investigation was to evaluate the efficacy of PoleStriding exercise (a form of walking that uses muscles of the upper and lower body in a continuous movement similar to cross-country skiing) and vitamin E (alpha-tocopherol) to improve walking ability and perceived quality of life (QOL) of patients with claudication pain secondary to peripheral arterial disease (PAD).
                Fifty-two subjects were randomized into four groups: PoleStriding with vitamin E (N = 13), PoleStriding with placebo (N= 14), vitamin E without exercise (N= 13), and placebo without exercise (N = 12). The dose of vitamin E was 400 IU daily. Only the PoleStriding with vitamin E and PoleStriding with placebo groups received PoleStriding instruction and training. Assignment to vitamin E or placebo was double blind. Subjects trained three times weekly for 30-45 min (rest time excluded). Individuals in vitamin E and placebo groups came to the laboratory biweekly for ankle blood-pressure measurements.
                Results of this randomized clinical trial provide strong evidence that PoleStriding significantly (P< 0.001) improved exercise tolerance on the constant work-rate and incremental treadmill tests. Ratings of perceived claudication pain were significantly less after the PoleStriding training program (P= 0.02). In contrast, vitamin E did not have a statistically significant effect on the subjects' ratings of perceived leg pain (P= 0.35) or treadmill walking duration ( P= 0.36). Perceived distance and walking speed (Walking Impairment Questionnaire) and perceived physical function (Rand Short Form-36) improved in the PoleStriding trained group only (P< 0.001, 0.022 and 0.003, respectively).
                PoleStriding effectively improved the exercise tolerance and perceived QOL of patients with PAD. Little additional benefit to exercise capacity was realized from vitamin E supplementation. nan Treadmill training in claudication is often based on walking exercise to a pain threshold or longer to the maximum muscle pain of the lower limbs. This kind of exercise may cause an inflammatory response. The purpose of this study was to determine whether pain-free treadmill training using walking exercise to 85% of the distance to onset of claudication pain can significantly improve pain-free walking distance in patients with intermittent claudication and to evaluate whether this kind of program may induce an inflammatory response leading to the progression of atherosclerosis.
                A total of 98 patients aged 50-70 yrs with stable intermittent claudication were randomized into a supervised treadmill training program or a comparison group. Patients in the treatment group participated in 12 wks of supervised treadmill training. We examined the effects of 12 wks of pain-free treadmill training on pain-free walking distance, total leukocyte count, neutrophil count, and microalbuminuria in patients with claudication.
                A total of 80 participants completed the program. Exercise rehabilitation increased the time to onset of claudication pain by 119.2%, from 87.4 +/- 38 m to 191.6 +/- 94.8 m (P < 0.001). There was no increase in total leukocyte count, neutrophil count, or microalbuminuria after 12 wks of treadmill exercise (P > 0.05)
                A pain-free training program can be used in the treatment of claudication as a low-risk program, increasing walking ability without potential harmful effects of ischemia-reperfusion injury. To assess the effect of pain-free treadmill training on red blood cell deformability and walking distance in patients with claudication.
                Randomized-controlled trial of exercise training.
                Patients were recruited from the primary care, vascular outpatient clinic.
                A total of 60 patients with peripheral arterial occlusive disease (stage II according to Leriche-Fontaine) were randomized into the treadmill program or a control group. Fifty-five patients completed the study (27 in the exercising group and 28 in the control group).
                Patients in the exercising group were walking on the treadmill 3 times a week for 3 months. Each session consisted of 1 hour repetitive walking [performed to 85% of the pain-free walking time (PFWT)] was supervised by a qualified physiotherapist.
                Changes in erythrocyte deformability and treadmill walking performance (PFWT, maximal walking time) were assessed in both groups before the study and after 3 months.
                After 3 months of treadmill training, red blood cell deformability in the exercising group significantly increased (P<0.01). No significant changes were seen in the erythrocyte deformability in the control group. PFWT was prolonged by 102% from 191+/-34 to 386+/-60 seconds (P<0.01), and maximal walking time increased by 49% from 438+/-62 to 656+/-79 seconds (P<0.01) in the exercising group, whereas these changes were insignificant in the control group.
                A significant improvement of walking ability over 3 months of pain-free treadmill training is associated with a significant increase in red cell deformability in patients with claudication. nan Patients with symptomatic peripheral arterial occlusive disease have a claudication-limited peak exercise performance that is improved with exercise training. The effects of training on skeletal muscle metabolism were evaluated in 26 patients with claudication, randomized into a 12-wk program of treadmill training (enhances muscle metabolic activity in normal subjects), strength training (stimulates muscle hypertrophy in normal subjects), or a nonexercising control group. Gastrocnemius muscle biopsies were performed at rest and before and after training. After 12 wk, only treadmill training improved peak exercise performance and peak oxygen consumption. Treadmill training did not alter type I or type II fiber area and did not increase citrate synthase activity but was associated with an increase in the percentage of denervated fibers (from 7.6 +/- 5.4 to 15.6 +/- 7.5%, P < 0.05). Improvement in exercise performance with treadmill training was associated with a correlative decrease in the plasma (r = -0.67) and muscle (r = -0.59) short-chain acylcarnitine concentrations (intermediates of oxidative metabolism). Patients in the strength and control groups had no changes in muscle histology or carnitine metabolism, but strength-trained subjects had a decrease in citrate synthase activity. Thus treadmill training increased peak exercise performance, but this benefit was associated with skeletal muscle denervation and the absence of a "classic" mitochondrial training response (increase in citrate synthase activity). The present study confirms the relationship between skeletal muscle acylcarnitine content and function in peripheral arterial occlusive disease, demonstrating that the response to treadmill training was associated with parallel improvements in intermediary metabolism. The efficacy of physical training alone or combined with antiplatelet therapy (dipyridamole and aspirin) was studied in 30 patients with stage II peripheral arterial occlusive disease (PAOD). Patients were randomly allocated to one of the following groups: Group A--dipyridamole 75 mg three times daily and aspirin 330 mg once daily: Group B--physical exercise; Group C--physical exercise and dipyridamole 75 mg three time daily and aspirin 330 mg once daily. After six months' treatment the pain-free walking time (PFWT) and the maximum walking time (MWT) improved significantly (p less than 0.05) in all three groups. In group A the PFWT lengthened by 35% (from 101.00 +/- 34.56 to 137.32 +/- 40.50 s) and the MWT by 38% (from 150.34 +/- 55.60 to 207.26 +/- 60.67 s); in group B the PFWT lengthened by 90% (from 90.65 +/- 40.54 to 171.45 +/- 55.60 s) and the MWT by 86% (from 145.39 +/- 60.50 to 270.63 +/- 63.61 s). When physical exercise was associated with drugs as in group C, the PFWT lengthened by 120% (from 89.51 +/- 43.89 to 196.72 +/- 51.73 s) and the MWT by 105% (from 160.43 +/- 59.84 to 329.05 +/- 63.96 s). No significant variations were observed at any stage of the study in the ankle/arm pressure ratio at rest and after standard treadmill exercise, in the plethysmographic rest and peak flows, or in the transcutaneous oxygen pressure in basal conditions and in its half recovery time after an induced ischemia. The results confirm the benefits of regular exercise in stage II PAOD patients but suggest they may be enhanced by antiplatelet therapy. This study reports the initial evaluation of treatment efficiency in 75 patients with intermittent claudication who were randomized to three treatment groups: 1) reconstructive surgery, 2) reconstructive surgery with subsequent physical training, and 3) physical training alone. Before treatment, there were no statistically significant differences between the groups in age, sex, smoking habits, symptom duration of claudication, ankle-arm blood pressure quotient (ankle-index), maximal plethysmographic calf blood flow, symptom-free and maximal walking distance, the history of other atherosclerotic manifestations or in the medical treatment. The walking performance was improved in all three groups at follow-up 13 +/- 0.5 months after randomization. Surgery was most effective, but the addition of training to surgery improved the symptom-free walking distance even further. In pooled observations of the three groups, age, symptom duration, and a history of myocardial ischemic disease correlated negatively with walking performance after treatment. In the operated group, the duration of claudication and a history of myocardial ischemic disease correlated negatively with the walking performance. This was not the case when patients were censored if limited by other symptoms than intermittent claudication after treatment. In the trained group, the duration of claudication correlated negatively to symptom-free and maximal walking distance. Ankle-index and maximal plethysmographic calf blood flow after treatment and the change of these variables with treatment correlated positively with both symptom-free and maximal walking distance when results were pooled for all patients. Although this mainly was a consequence of the improved blood flow after surgery, the change of maximal plethysmographic calf blood flow also correlated with symptom-free but not with maximal walking distance in the trained group. The results demonstrate that, compared with physical training alone, operation alone or in combination with subsequent training are superior treatment modalities in patients with intermittent claudication. to compare the effect of surgery, exercise and simple observation on maximum exercise power in claudicants. Design: prospective, randomised study.
                a total of 264 unselected claudicants were randomised to supervised exercise training, invasive treatment (open surgical or endovascular procedures) or observation. One year treatment outcomes were analysed on an intention to-treat basis.
                invasively treated patients showed a significant improvement in maximum walking power, stopping distance, post-ischaemic blood flow and big toe pressure at one year. Patients randomised to physical exercise training or to the control group did not improve in any outcome measure.
                invasive treatment increased walking capacity, leg blood pressure and flow. Supervised physical exercise training offered no therapeutic advantage compared to untreated controls.
                Copyright 2001 Harcourt Publishers Limited. To compare the effect of unsupervised exercise, supervised exercise and intermittent pneumatic foot and calf compression (IPC) on the claudication distance, lower limb arterial haemodynamics and quality of life of patients with intermittent claudication.
                Thirty-four eligible patients with stable intermittent claudication were randomised to IPC (n = 13, 3h/d for 6 months), supervised exercise (n = 12, three hourly sessions/week for 6 months) or unsupervised exercise (n = 9). In each patient, initial claudication distance (ICD), absolute claudication distance (ACD), resting ankle brachial pressure index (ABPI), and resting hyperaemic calf arterial inflow were measured before, 6 weeks, 6 months and 1 year after randomisation. Quality of life was assessed with the short form (SF)-36, walking impairment (WIQ) and intermittent claudication questionnaires (ICQ).
                Compared with unsupervised exercise, both IPC and supervised exercise, increased ICD and ACD, up to 2.83 times. IPC increased arterial inflow (p < 0.05 at 6 weeks) and ABPI. Supervised exercise decreased arterial inflow and increased ABPI (p < 0.05 at 6 months). Unsupervised exercise had no effect on arterial inflow or ABPI. IPC improved significantly the ICQ score and the speed score of the WIQ, while supervised exercise improved the WIQ claudication severity score. At 1 year clinical effectiveness of supervised exercise and IPC was largely preserved.
                IPC, by augmenting leg perfusion, achieved improvement in walking distance comparable with supervised exercise. Long-term results in a larger number of patients will provide valuable information on the optimal treatment modality of intermittent claudication. To determine the effects of 12-week exercise programme on ambulatory function, free-living daily physical activity and health-related quality of life in disabled older patients with intermittent claudication.
                Prospective, randomized controlled trial.
                University Medical Center and Veterans Affairs Medical Center, Taipei, Taiwan.
                Thirty-two of 64 patients with Fontaine stage II peripheral arterial occlusive disease (PAOD) were randomized to exercise training and 32 to usual care control. Five patients from the exercise group and six patients from the control group dropped out, leaving 27 and 26 patients, respectively, completing the study in each group.
                Twelve weeks of treadmill exercise training.
                Treadmill walking time to onset of claudication pain and to maximal claudication pain, 6-min walk distance, self-reported ambulatory ability and perceived health-related quality of life (QOL).
                Compliance of exercise programme was 83% of the possible sessions. Exercise training increased treadmill walking time to onset of claudication pain by 88% (P < 0.001), time to maximal pain by 70% (P < 0.001), and 6-min walk distance by 21% (P < 0.001).
                Perception of health-related QOL improved from 12% to 178% in the exercise group. These improvements were significantly better than the changes in the control group (P < 0.05).
                Significant improvements in claudication following 12-week exercise training in elderly PAOD patients were observed. Increase in treadmill walking time to maximal claudication pain in these patients translated into the improvement of perceived physical health, which enabled the patients to become more functionally independent.
Exercise programmes were of significant benefit compared with placebo or usual care in improving walking time and distance in selected patients with leg pain from IC.