Interaction between the central motor command and muscle metaboreflex for the regulation of pulmonary ventilation during exercise in humans

• Grant number: 22/10295-7
• Support Opportunities: Scholarships in Brazil - Master
• Start date: November 01, 2022
• End date: October 31, 2023
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Bruno Moreira Silva
• Grantee: Felipe Silva Gomes
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Pulmonary ventilation increases during exercise as the metabolic demand imposed by muscle contractions increases, allowing maintenance of arterial gas homeostasis at moderate (i.e., below the lactate threshold) and heavy (i.e., between the lactate threshold and critical power) exercise intensity. Several humoral and neural mechanisms are capable of regulating lung ventilation. However, in isolation, none of the known mechanisms can explain the huge increase in lung ventilation that can occur during exercise in healthy humans (” = 15 to 20x vs. rest). Even more importantly, the sum of the isolated effects of these mechanisms is also not able to explain exercise hyperpnoea. Therefore, it is assumed that the involved mechanisms interact synergistically so that ventilation increases precisely during exercise. In this sense, this project aims to investigate the interaction between two of the mechanisms known to increase ventilation, these being efferent signals, triggered in higher brain areas involved in skeletal striated muscles motor control (i.e., central motor command), and afferent signals, originated in skeletal striated muscles by the accumulation of metabolites related to muscle contractions (i.e., muscle metaboreflex). Therefore, young healthy adults will perform handgrip exercise with the hands, succeeded by circulatory occlusion of the arms, to trap metabolites produced during handgrip, which will maintain the activation of the muscle metaboreflex. This condition will be compared to a control condition where the handgrip exercise will be succeeded by free blood flow in the arms to remove the metabolites produced, consequently inactivating the muscle metaboreflex. In addition, participants will perform voluntary plantar flexion exercise, i.e., with the participation of the central motor command, or involuntary exercise, i.e., without the participation of the central motor command. Involuntary exercise will be induced by external electrical impulses, transmitted to the calf muscles by electrodes placed on the skin. Finally, the described protocols will be combined to simultaneously activate the central motor command for the calf muscles and the muscle metaboreflex in the muscles involved with handgrip exercise. During the protocols, lung ventilation (pneumotachograph) and respiratory gas exchange (O2 and CO2 sensors), contraction strength (dynamometers), muscle electrical activity (surface electromyography), muscle oxygenation (near-infrared spectroscopy), and sensations related to breathing and exercise (Borg scale) will be measured. A rebreathing system will be used to maintain the partial pressure of CO2 at the end of expiration at a relatively constant level (i.e., isocapnia) in all protocols. When calculating the isolated responses to activation of the central motor control and the muscle metaboreflex, and the response to co-activation of the two mechanisms, co-activation is expected to generate a ventilatory response superior to the sum of the isolated responses (i.e., synergistic effect), supporting the presence of interaction between the mechanisms addressed above for the control of ventilation during exercise. Such a result would be similar to the synergistic interaction already reported between other mechanisms that participate in the control of ventilation in humans, which would therefore strengthen the theoretical model that proposes that the precise adjustment of ventilation during exercise depends on synergistic, and possibly redundant, interactions between multiple neural and humoral mechanisms.