The Ventilatory Response to Muscle Metaboreflex Activation During Concurrent Hypercapnia is Attenuated by Local Muscle Training
Authors: AlGhaith Jassim , White Michael 
Published: June 2021

Increased ventilation during post‐exercise circulatory occlusion (PECO) with concurrent hypercapnia suggests a synergistic interaction between muscle metaboreflex activation and chemoreflex stimulation. The exercise pressor reflex (EPR) response to contraction of a human calf muscle and subsequent PECO can be attenuated by training, indicating a decreased activation of muscle metaboreceptive afferents driving the EPR. We hypothesised that 6 weeks of one legged calf raise training would attenuate metaboreceptor activity, the EPR and if these afferents provide a drive to breathe, the ventilatory response seen during PECO when combined with mild hypercapnia. In the contralateral limb there would be no effect on muscle afferent input to the cardiovascular or respiratory control systems so no change in EPR or breathing would be expected during PECO.

Eleven male subjects aged 19.5 ± 0.8 years (mean±SD) gave informed consent to participate in the study, approved by the local ethics committee. A standardized test of the cardiovascular and respiratory responses to isometric contraction of the calf muscle at 50% of maximum voluntary force (MVC) for 2 min was followed by 3 min of PECO. In random order left and right legs were tested separately under two conditions, 1) breathing room air 2) hypercapnia, 5% CO2 above end tidal level. A dynamic end tidal forcing system controlled the inspired gas composition and monitored ventilation. Heart rate (HR) and blood pressure (MAP) were measured by ECG and Portapres respectively. Right leg training consisted of 120 calf raises to maximum height in 4 sets of 30, one heel raise and lower per second, one minute rest between sets. Whenever 4 sets could be achieved loading of 10%, then increments of 5% body mass was added. After 6 weeks of training the initial tests were repeated.

MVC did not change after training in either leg. During exercise of the trained leg during hypercapnia, average MAP rise from baseline was reduced from 18.1± 1.4, to 15.6±1.4 mmHg (mean±SEM), p<0.05 after, training. Ventilation change from the hypercapnic baseline was also reduced from 17.5± 2.8 to 12.1±2.6 l.min−1, p<0.05 after training.

Table 1 shows the data from each leg in the PECO phase of the trials, performed before and after the training. In the room air and hypercapnia trials, the EPR was significantly reduced from control values in the trained leg. The increase in ventilation from baseline was reduced, by ~45%, in the trained limb during the hypercapnia trial. There were no alterations in the cardiovascular or ventilatory responses to PECO, during hypercapnia or room air breathing trials in the untrained limb, ruling out any central or peripheral adaptation in this leg, induced by the training period. In the trained leg the MAP data shows clear evidence of a decrease in the EPR after training, indicating reduced muscle metaboreflex activation during PECO. This is despite generating the same force‐time integral during the exercise period as before training. We conclude that in the trained limb the marked decrease in ventilation during PECO in the hypercapnia condition must be due to a decreased drive to breathe arising from metabosensitive muscle afferents.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.