The pulmonary vascular response to combined activation of the muscle metaboreflex and mechanoreflex.

Muscle metabo- and mechanoreflexes are known to influence systemic cardiovascular responses to exercise. Whether interplay between these reflexes is operant in the control of the pulmonary vascular response to exercise is unknown. The aim of this study was to assess the pulmonary vascular response to the combined activation of the two muscle reflexes. Nine healthy subjects performed a bout of isometric calf plantarflexion exercise during local circulatory occlusion, which was continued for 9 min postexercise (PECO). At 5 min into PECO the calf muscle was passively stretched for 180 s. A control (no exercise) protocol was also undertaken. Heart rate, blood pressure measurements and echocardiographically determined estimates of systolic pulmonary artery pressure (SPAP) and cardiac output ( ) were obtained at intervals throughout the two protocols. Elevations in SPAP (by 22.51 ± 2.61%), (by 26.92 ± 2.99%) and mean arterial pressure (by 15.38 ± 2.29%) were noted during isometric exercise in comparison to baseline (all P < 0.05). Increases in SPAP and mean arterial pressure persisted during PECO (All P < 0.05), whereas returned to resting levels. These increases in mean arterial pressure and SPAP were sustained during stretch which significantly elevated (All P < 0.05). These data suggest that activation of the muscle mechanoreflex attenuated the increases in pulmonary vascular resistance caused by metaboreflex activation. This finding has important implications for the regulation of pulmonary haemodynamics during human exercise.

A respiratory response to the activation of the muscle metaboreflex during concurrent hypercapnia in man.

In this study, we aimed to assess the ventilatory and cardiovascular responses to the combined activation of the muscle metaboreflex and the ventilatory chemoreflex, achieved by postexercise circulatory occlusion (PECO) and euoxic hypercapnia (end-tidal partial pressure of CO2 7 mmHg above normal), respectively. Eleven healthy subjects (4 women and 7 men; 29 +/- 4.4 years old; mean +/- S.D.) undertook the following four trials, in random order: 2 min of isometric handgrip exercise followed by 2 min of PECO with hypercapnia; 2 min of isometric handgrip exercise followed by 2 min of PECO while breathing room air; 4 min of rest with hypercapnia; and 4 min of rest while breathing room air. Ventilation was significantly increased during exercise in both the hypercapnic (+3.17 +/- 0.82 l min(-1)) and the room air breathing trials (+2.90 +/- 0.26 l min(-1); all P < 0.05). During PECO, ventilation returned to pre-exercise levels when breathing room air (+0.52 +/- 0.37 l min(-1); P > 0.05), but it remained elevated during hypercapnia (+3.77 +/- 0.23 l min(-1); P < 0.05). The results indicate that the muscle metaboreflex stimulates ventilation with concurrent chemoreflex activation. These findings have implications for disease states where effort intolerance and breathlessness are linked.

The pulmonary vascular response to the sustained activation of the muscle metaboreflex in man.

The pulmonary circulation is influenced by the autonomic nervous system, yet whether this is physiologically important during exercise in man is not known. The aim of this study was to assess the pulmonary vascular response to sympathoexcitation induced by the maintained activation of the muscle metaboreflex in the postexercise period. Nine healthy subjects performed isometric handgrip exercise at 50% of their maximal voluntary contraction force for 2 min. Exercise was followed by circulatory occlusion so as to maintain the muscle metaboreflex activated for 2 min (postexercise circulatory occlusion; PECO). Blood pressure measurements and echocardiographically determined estimates of systolic pulmonary artery pressure (SPAP) and cardiac output were obtained at various intervals throughout the two protocols. Compared with baseline values, elevations in SPAP (by 20.06 +/- 2.08%), cardiac output (by 36.04 +/- 4.97%) and mean arterial pressure (MAP; by 25.62 +/- 3.54%) were noted during isometric exercise (means +/- s.e.m., all P < 0.05). Increases in SPAP and MAP persisted during PECO (all P < 0.05), whereas cardiac output returned to resting levels. Our findings suggest that the sympathoexcitation induced by isometric exercise affects the pulmonary circulation, possibly by inducing vasoconstriction and/or stiffening the large conduit arteries. The exaggerated activation of the sympathetic nervous system that has been evidenced in cardiopulmonary patients could therefore be implicated in their abnormal pulmonary haemodynamic responses and intolerance of exercise.