The mechanism of calf claudication: Studies of simultaneous clearance of 99Tcm from the calf and thigh

Angelides, N.S.; Nicolaides, Andrew; Needham, Terry; Dudley, H. A. F.

doi:10.1002/bjs.1800650319

Cited by 29 publications

(14 citation statements)

References 14 publications

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“…57 This increase in leg VO 2 occurred through increases in leg blood flow from 79 to 342 ml min À1 and the a-VO 2 from 0.09 to 0.171 ml min À1 blood. The increase in leg blood flow would, on the basis of calf perfusion measurements made during or after walking, 59,60 be no more than 40% of that seen in healthy controls; whereas the increase in a-VO 2 is the same as that observed in young, healthy subjects performing maximal calf exercise 61 or even greater than controls during cycling or walking. 62,63 These data show that calf muscle peak VO 2 in claudicants is limited by leg blood flow and not a-VO 2 .…”

Section: Walking Performance and Metabolismmentioning

confidence: 85%

“…Although this response was similar to that seen in mitochondrial myopathies, 34 it is important to note two things: that blood flow was not measured; and that, compared with normal conditions, a reduction in muscle blood flow during exercise lowers muscle [ATP] and [PCr], and thus increases [ADP], 34 at a given rate of muscle O 2 consumption. 76 Since muscle blood flow during and after exercise is blunted in claudicants, 58,59 the altered NMR responses in claudicants are consistent with hemodynamic, rather than mitochondrial, limitations. When limb perfusion was assessed using NIRS simultaneous with NMR measurements of metabolism recently, 77 the impaired muscle metabolism in PAD was attributed to an impaired hemodynamic response.…”

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confidence: 94%

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Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

2004

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Patients with claudication have a marked impairment in exercise performance. Several factors contribute to this limitation, including reductions in large vessel blood flow and oxygen delivery as well as metabolic abnormalities in skeletal muscle. The relative contribution of these factors and their role in the pathophysiology of the exercise limitation is discussed using a point-counterpoint approach. Future directions for research conclude the discussion.

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Section: Walking Performance and Metabolismmentioning

confidence: 85%

mentioning

confidence: 94%

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

2004

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“…resting ABI) was not different between the groups and so it alone cannot explain the poorer exercise tolerance in the diabetic group. However, the ABI is a poor predictor of the lower-limb haemodynamic response to exercise [25,26], and there is evidence of more severe atherosclerosis in distal segments of the lower extremity in diabetic compared with non-diabetic patients with claudication [27]. Therefore, we cannot exclude the possibility that muscle blood flow during exercise was more impaired in diabetic patients with claudication.…”

Section: Discussionmentioning

confidence: 97%

Effect of type 2 diabetes mellitus on exercise intolerance and the physiological responses to exercise in peripheral arterial disease

2007

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Aims/hypothesis There are conflicting data about the effect of type 2 diabetes mellitus on exercise tolerance in peripheral arterial disease. To elucidate this problem, we compared the tolerance and physiological responses to treadmill and cycle exercise in 31 patients with peripheral arterial disease and intermittent claudication. Materials and methods One group of these patients had type 2 diabetes (n=12) and its members were matched for sex and age with a group of patients who did not have diabetes (n=12). Since BMI and body weight were greater in the diabetic group (28.4±3.7 vs 25.2±2.4 kg/m 2 ; 84.0± 14.6 vs 73.8±8.0 kg), we also studied a third, 'heavy' group of non-diabetic patients with claudication of similar age (n=7; BMI = 30.9±5.3 kg/m 2 ; body weight = 85.2± 8.2 kg). Results Compared with the 'light' non-diabetic group, maximum treadmill times were shorter for the diabetic and heavy non-diabetic groups (1,448 vs 845 and 915 s; ANOVA p=0.01); maximum cycle time also tended to be shorter (ANOVA, p=0.08) in the diabetic and heavy nondiabetic groups (median = 1,231 vs 730 and 797 s). The majority of physiological responses assessed were not different between the groups, although the time constant of oxygen uptake during submaximal treadmill and cycle exercise was significantly larger (ANOVA p<0.05) for the diabetic group. Conclusions/interpretation These data demonstrate that exercise tolerance is lower in diabetic than non-diabetic patients with claudication, but that this difference is due to obesity rather than diabetes itself.

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“…Moreover, other substances such as the protons, nitric oxide and prostaglandins could be involved (ChwalbinskaMoneta et al, 1989;Koller et al, 1990;Dyke et al, 1995;Bangsbo and Hellsten, 1998;Shoemaker et al, 1999). This hyperemic response is probably due to the accumulation and subsequent washout of vasodilatory metabolites and is dependent on the adequacy of forearm perfusion (Angelides et al, 1978). Finally, the post-exercise hyperemic response could be connected to the exercise duration in the ischemic state.…”

Section: Hyperemia With/without Ischemia At Different Exercise Intensmentioning

confidence: 99%

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

Osada

Katsumura

Murase

et al. 2003

J. Physiol. Anthropol.

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Post-exercise related time course of muscle oxygenation during recovery provides valuable information on peripheral vascular disease. The purpose of the present study was to examine post-exercise hyperemia (forearm blood flow; FBF, Doppler ultrasound) assessed by peak FBF, excess FBF and the time constant for FBF (FBF Tc ) following isometric handgrip exercise (IHE). Post-exercise hyperemia was assessed in an ischemic and non-ischemic state at different exercise intensities and durations. Peak FBF and excess FBF were defined as the maximum FBF during recovery, and the total amount of FBF volume, respectively. FBF Tc represents the time to reach approximately 37% of the change in FBF between peak FBF and resting FBF (delta peak FBF). Ten subjects performed IHE at "10% and 30% maximum voluntary contraction (MVC)" for 2 min with or without arterial occlusion (AO), followed by 2 min of AO alone (Study I). In Study II, six subjects performed 30%MVC-IHE with AO for "100%, 66%, 33% and 10% of the exhausted exercise duration" (time to exhaustion). In Study I, although peak FBF and excess FBF were significantly higher in ischemic than non-ischemic IHE for both 10% and 30%MVC (pϽ0.05), FBF Tc was similar in the ischemic and non-ischemic conditions. The peak FBF, excess FBF and FBF Tc were all significantly higher at 30% than at 10%MVC (pϽ0.05). In Study II, the peak FBF and excess FBF increased linearly compared to the absolute and relative exercise durations for ischemic IHE. FBF Tc increased exponentially when compared to the absolute and relative exercise durations. These data suggest the ischemic exercise has a larger hyperemic response compared to the non-ischemic exercise. In conclusion, the peak FBF, excess FBF and FBF Tc seen during post-exercise hyperemia are closely correlated with exercise intensity and duration, not only in non-ischemic, but also in the ischemic exercise. In combination with the ischemic exercise, these parameters could potentially prove to be valuable indicators of peripheral vascular disease.

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The mechanism of calf claudication: Studies of simultaneous clearance of 99Tcm from the calf and thigh

Cited by 29 publications

References 14 publications

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

Effect of type 2 diabetes mellitus on exercise intolerance and the physiological responses to exercise in peripheral arterial disease

Post-exercise Hyperemia after Ischemic and Non-ischemic Isometric Handgrip Exercise

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