Ventilatory and gas exchange response during walking in severe peripheral vascular disease

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Abstract

It has long been recognized that at the onset of a dynamic muscular exercise the ventilatory and the circulatory (blood flow) responses appear to be matched, thereby maintaining arterial blood gas homeostasis. Such a coupling has recently been suggested to rely upon ventilatory reflex triggered by mechanoreceptors encoding changes in muscle blood flow or, more likely, blood volume. The aim of this study was to investigate whether patients with severe peripheral blood flow limitation to the lower extremities have a normal ventilatory response during a light intensity exercise. The ventilatory and gas exchange temporal response characteristics were studied during a 6 min walking test in seven patients with severe ischemic peripheral vascular disease and in six normal age-matched subjects. The magnitude of the overall ventilatory and V̇O2 increment at the end of the tests was similar in both groups. However, in contrast to the control subjects, who presented an almost rectangular response, the patients had a considerably slowed response dynamics (t50=33±4 vs. 9±3 sec for V̇O2 and 37±5 vs. 10±8 sec for V̇e) with a dramatic reduction in the magnitude of the initial 20 sec of the responses. Although the slow V̇O2 dynamics in patients presumably reflected the impeded perfusion of the working muscles, the accompanying sluggishness of the V̇e course implies that either muscular ischemia actually inhibits ventilatory response to exercise or, more likely, that this response is strongly linked to the magnitude of the hyperemia in the exercising muscles.

Introduction

The characteristics of the ventilatory and circulatory responses to a muscular exercise depend on both the absolute level of work rate (see Whipp and Ward, 1991 for review) and the level of fitness of the subject performing the work (Hagberg et al., 1980; Babcock et al., 1994). Indeed, the long acknowledged dynamic characteristics of the ventilatory as well as the heart rate (HR) and V̇O2 responses to a constant load exercise, i.e. abrupt rise (phase I) followed, after a brief plateau, by an exponential climb (phase II) to a new steady state (phase III), are only observed for mild to moderate intensity exercise and an average level of fitness (see Dejours, 1967; Whipp and Ward, 1991 for review). High intensity exercise, which may correspond to a very low work rate level in subjects with deteriorating fitness or in patients with circulatory disorders (Sietsema et al., 1986, Sietsema et al., 1988, Whipp and Ward, 1991) often precludes reaching a new steady state of ventilatory and HR responses before exhaustion. On the other hand, in subjects with a high level of fitness or during very low intensity tasks, like slow walking or loadless pedalling in sedentary subjects, the time course of all the responses appears to be speeded up (Hagberg et al., 1980; Babcock et al., 1994), and can virtually be reduced to a squarewave-like phase I pattern (Dejours, 1967; Sietsema et al., 1988). The traditional demarcation drawn by the lactate threshold, creating a sub and suprathreshold domain is, however, incapable of providing a satisfactory explanation for the above observations, since unfit and very fit subjects do respond differently even during a subthreshold exercise (Hagberg et al., 1980; Babcock et al., 1994). Worthy of mention is that a severe training program can dramatically affect the characteristics of the cardio-respiratory and gas exchange response to a given exercise of mild intensity, i.e. below the lactate threshold, to such an extent that a prolonged rise of V̇e in an unfit subject was replaced by a fast response typical of very light exercise after 6 months of training (Babcock et al., 1994).

One of the most enduring concepts of cardio-respiratory control during exercise postulates a prominent role for the type III and IV contraction-specific muscle afferents, which simultaneously activates the cardiovascular and respiratory systems in order to satisfy the increased peripheral gas exchange (McCloskey and Mitchell, 1972; Tibes, 1977). In addition, high metabolic chemical by-products (e.g. H+, La, K+) further stimulate these afferents in certain experimental conditions in animals (see Kaufman, 1995 for review) and are thought to act likewise in humans. This model implies that any mismatching between O2 supply and demand in the muscles will be signalled by slow conducting afferent fibers to the central nervous system and stimulate ventilation and HR. However, such a control mechanism cannot account for the promptness of the cardio-respiratory responses in fit subjects and, perhaps more importantly, there have been persistent reports that trapping metabolites in the exercising (Huszczuk et al., 1993) or recovering muscles (Dejours et al., 1957; Innes et al., 1989; Huszczuk et al., 1993; Haouzi et al., 1993) by means of vascular occlusion actually reduces ventilatory and HR responses. A hypothesis has recently been proposed arguing that the group III and IV intramuscular nerve endings possess multimodal transduction properties which, in addition to those mentioned above, are primarily equipped to detect the degree of muscular hyperemia (Huszczuk et al., 1993; Haouzi et al., 1995) and, via feedforward mechanism, match ventilation to the flow of metabolically loaded blood leaving the exercising muscles. The faster the circulatory adaptation in the muscles, the shorter the Ve response time course.

In this study, we report the ventilatory and gas exchange response at the onset of a constant work rate exercise of light intensity in seven subjects with severe peripheral ischemic vascular disease. Patients with peripheral blood flow limitation have been shown to have significantly slower than normal V̇O2 kinetics, when exercising their below pain threshold (Auchincloss et al., 1980), reflecting their peripheral circulatory disorder. Studying their V̇e response is therefore relevant in understanding the effect of severe muscle blood flow limitation on ventilatory control in humans. The hypothesis is that blood flow impediment is associated with a low level of stimulation of group III and IV muscle afferent located in the vicinity of the microvascular network, thereby leading to a lower than normal ventilatory response. Conversely, a normal or higher early V̇e response is expected if muscle afferent fibers responding to movement and/or local chemical changes play a significant role in triggering the ventilatory response to light intensity exercise.

Section snippets

Patients

Seven patients with peripheral ischemic vascular disease of the lower extremities were studied. All patients had severe bilateral disease. They could walk at a speed of 2–3 km/h but had pain limitation after 200–300 m or as soon as their walking velocity was above 3 km/h. Six normal age-matched subjects (56.6±2.8 vs. 57.7±3.2 years old) served as controls but had body weight that was however significantly higher than those of the patients (73.3±5.4 vs. 64.7±4.7 kg). Table 1 gives the physical

Gas exchange response

The increase in O2 uptake at the end of the test was slightly but not significantly lower in patients (+335±27 ml/min) than in control subjects (+433±50 ml/min, NS). This difference, although not significant, persisted after correction for body weight (+5.9 vs. +5.1 ml/min per kg) reflecting the small difference in the actual work rate performed by both groups or anaerobic supplement in patients. The dynamics of the response were, however, dramatically affected in subjects with peripheral

Discussion

We observed an almost four-fold increase in the half time of the V̇O2, V̇e, and HR responses to very light exercise in patients with severe impediment of the arterial supply to the hindlimbs in comparison to normal, age-matched subjects whose responses were typical of this light task (Dejours, 1967; Sietsema et al., 1988).

The slow V̇O2 rise in patients was not unexpected. Auchincloss et al. (1980) reported lower than normal values of V̇O2 40–60 sec into a constant work rate exercise in patients

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    Present address: VACUMED, 4483 McGrath St, Ventura, CA 93 003, USA.

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