Effect of increased inspiratory muscle work on blood flow to inactive and active limbs during submaximal dynamic exercise.

NEW FINDINGS: What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle metaboreflex. Does increased sympathetic vasoconstriction originating from the respiratory musculature elicit a reduction in blood flow to an inactive limb in order to maintain blood flow to an active limb? What is the main finding and its importance? Arm blood flow was reduced whereas leg blood flow was preserved during mild leg exercise with inspiratory resistance. Blood flow to the active limb is maintained via sympathetic control of blood flow redistribution when the respiratory muscle-induced metaboreflex is activated. ABSTRACT: The purpose of this study was to elucidate the effect of increasing inspiratory muscle work on blood flow to inactive and active limbs. Healthy young men (n = 10, 20 ± 2 years of age) performed two bilateral dynamic knee-extension and knee-flexion exercise tests at 40% peak oxygen uptake for 10 min. The trials consisted of spontaneous breathing for 5 min followed by voluntary hyperventilation either with or without inspiratory resistance for 5 min (40% of maximal inspiratory mouth pressure, inspiratory duty cycle of 50% and a breathing frequency of 40 breaths min-1 ). Mean arterial blood pressure was acquired using finger photoplethysmography. Blood flow in the brachial artery (inactive limb) and in the femoral artery (active limb) were monitored using Doppler ultrasound. Mean arterial blood pressure during exercise was higher (P < 0.05) with inspiratory resistance (121 ± 7 mmHg) than without resistance (99 ± 5 mmHg). Brachial artery blood flow increased during exercise without inspiratory resistance (120 ± 31 ml min-1 ) compared with the resting level, whereas it was attenuated with inspiratory resistance (65 ± 43 ml min-1 ). Femoral artery blood flow increased at the onset of exercise and was maintained throughout exercise without inspiratory resistance (2576 ± 640 ml min-1 ) and was unchanged when inspiratory resistance was added (2634 ± 659 ml min-1 ; P > 0.05). These results suggest that sympathetic control of blood redistribution to active limbs is facilitated, in part, by the respiratory muscle-induced metaboreflex.

Relationship between respiratory muscle endurance and dyspnea during high-intensity exercise in trained distance runners.

We hypothesized that the trained distance runners, who have a relatively high respiratory muscle endurance, but not high respiratory muscle strength, have lower dyspneic sensations during submaximal running. Twenty-one male collegiate distance runners participated. Incremental respiratory endurance tests (IRET) and maximal inspiratory mouth pressure (PImax) measurements were performed under resting conditions. A submaximal exercise test was also performed on a treadmill at two different speeds (16 and 18 km/h) for 4 min each, and the subjects reported the rate of dyspnea (range: 0-10). The time to endpoint during the IRET, an index of respiratory muscle endurance, ranged from 9.4 to 18.8 min, and PImax, as an index of inspiratory muscle strength, ranged from 74.1 to 137.0 cmH2O. The dyspnea rating during running at 16 and 18 km/h ranged from 1 to 6 and from 4 to 8, respectively. The relative exercise intensity was approximately 80 % of peak oxygen uptake (VO2peak) at 16 km/h and 90 %VO2peak at 18 km/h. The time to endpoint during the IRET was significantly negatively correlated with dyspnea during running at 18 km/h (r = -0.459, P = 0.040), but not at 16 km/h (r = -0.161, P = 0.470). There was no significant correlation between PImax and dyspnea during running at 16 km/h (r = -0.003, P = 0.989) or 18 km/h (r = 0.070, P = 0.755). These results suggest that dyspneic sensations during high-intensity running are related to respiratory muscle endurance, but not inspiratory muscle strength, in trained distance runners.