Respiratory Muscle Strength and Ventilatory Function Outcome: Differences Between Trained Athletes and Healthy Untrained Persons.

It is known that the maximum mouth inspiratory pressure (MIP) and expiratory pressure (MEP) vary with age, weight, height, and skeletal muscle mass. However, the influence of physical training on ventilatory function outcomes is an area of limited understanding. The aim of this study was to investigate the respiratory muscle strength and its relation to spirometry variables in untrained healthy persons versus trained athletes. MIP and MEP were assessed in 22 power athletes and 28 endurance athletes, and in 24 age- and sex-matched normal healthy subjects (control group). The measurement was done with a mouth pressure meter. We found that respiratory muscle strength and ventilatory function in endurance athletes were outstandingly superior to that in power athletes; the latter's muscle strength was better than that of healthy untrained controls. Both MIP and MEP significantly correlated with the maximum voluntary ventilation (MVV) in both power athletes and controls, but not so in endurance athletes. The corollary is that the intensive endurance training could result in the improvement of respiratory muscle strength, meeting the maximum upper limit of functional reserve of respiratory muscles and the corresponding ventilation. On the other hand, targeted training of respiratory muscle strength may be an effective strategy to increase ventilatory function in power athletes, particularly those having a low maximum inspiratory and expiratory pressure, and in less physically fit healthy persons.

Interleukin-1beta suppresses the ventilatory hypoxic response in rats via prostaglandin-dependent pathways.

We investigated the effect of the major inflammatory cytokine interleukin-1beta (IL-1ß) on the ventilatory response to hypoxia. The goal was to test the hypothesis that IL-1ß impairs the hypoxic ventilatory response in vivo by indirectly inhibiting respiratory neurons in the brainstem via prostaglandins. Thus, IL-1ß was delivered by cerebroventricular injection, and the ventilatory hypoxic response was assessed in anesthetized, spontaneously breathing rats pretreated with or without diclofenac, a nonspecific inhibitor of prostaglandin synthesis. We found that the slope of the ventilatory response to hypoxia decreased almost 2-fold from 10.4 ± 3.02 to 4.06 ± 0.86 mL·min-1·(mm Hg)-1 (-61%) 90 min after administration of IL-1ß (p < 0.05). The slope of tidal volume and mean inspiratory flow also decreased from 0.074 ± 0.02 to 0.039 ± 0.01 mL·(mm Hg)-1 (-45%, p < 0.05), and from 0.36 ± 0.07 to 0.2 ± 0.04 mL·s-1·(mm Hg)-1 (-46%, p < 0.05), respectively. Pretreatment with diclofenac blocked these effects. Thus, the data indicate that IL-1ß degrades the ventilatory hypoxic response by stimulating production of prostaglandin. The increase of cerebral levels of IL-1ß, which is induced by the activation of immune cells in the brain, may impair respiratory chemoreflexes.

Effect of intracerebroventricular injection of interleukin-1-beta on the ventilatory response to hyperoxic hypercapnia.

OBJECTIVE: Oxidative stress developed at several disease states and strenuous resistive breathing lead to the elevation of plasma and cerebral levels of proinflammatory cytokines. We hypothesized that the elevation of the cytokine level in body fluids would modulate breathing pattern and the ventilatory response to stimulation of central chemoreceptors by hypercapnia. - MATERIAL AND METHODS: In experiments on anesthetized, tracheostomized, spontaneously breathing rats, the effects of intracerebroventricular injection of the human recombinant interleukin-1ß (IL-1ß) (0.5 µg/rat) on breathing were studied. - RESULTS: During resting breathing IL-1ß evoked a significant increase in minute ventilation and in mean inspiratory flow. Furthermore, injection of IL-1ß into the cerebral-spinal fluid decreases the responses of ventilation, tidal volume, and of mean inspiratory flow to carbon dioxide. - CONCLUSIONS: The elevation of a proinflammatory cytokine in cerebrospinal fluid intensifies ventilation by modulation of breathing pattern, but weakens the chemoreflex sensitivity to hypercapnia. The results suggest the participation of cytokines in the central control of breathing and in the mechanisms of central chemoreception.