Respiratory muscle training and exercise ventilation while diving at altitude

Introduction: Pre-dive altitude exposure may increase respiratory fatigue and subsequently augment exercise ventilation at depth. This study examined pre-dive altitude exposure and the efficacy of resistance respiratory muscle training (RMT) on respiratory fatigue while diving at altitude. Methods: Ten men (26±5 years; V̇O2peak: 39.8±3.3 mL•kg-1•min-1) performed three dives; one control (ground level) and two simulated altitude dives (3,658 m) to 17 msw, relative to ground level, before and after four weeks of resistance RMT. Subjects performed pulmonary function testing (e.g., inspiratory [PI] and expiratory [PE] pressure testing) pre- and post-RMT and during dive visits. During each dive, subjects exercised for 18 minutes at 55% V̇O2peak, and ventilation (V̇ E), breathing frequency (ƒb,), tidal volume (VT) and rating of perceived exertion (RPE) were measured. Results: Pre-dive altitude exposure reduced PI before diving (p=0.03), but had no effect on exercise V̇E, ƒb, or VT at depth. At the end of the dive in the pre-RMT condition, RPE was lower (p=0.01) compared to control. RMT increased PI and PE (p<0.01). PE was reduced from baseline after diving at altitude (p<0.03) and this was abated after RMT. RMT did not improve V̇E or VT at depth, but decreased ƒb (p=0.01) and RPE (p=0.048) during the final minutes of exercise. Conclusion: Acute altitude exposure pre- and post-dive induces decrements in PI and PE before and after diving, but does not seem to influence ventilation at depth. RMT reduced ƒb and RPE during exercise at depth, and may be useful to reduce work of breathing and respiratory fatigue during dives at altitude.

Variations in exercise ventilation in hypoxia will affect oxygen uptake

Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and VE were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42–87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The VE was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (Wb). The greater VE at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for Wb from a VE–VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in VE among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

Exertional Dyspnea in Childhood: Is There an Iceberg Beneath the Apex?

This essay expounds on fundamental, quantitative elements of the exercise ventilation in children, which was the subject of the Tom Rowland Lecture given at the NASPEM 2018 Conference. Our knowledge about how much ventilation rises during aerobic exercise is reasonably solid; our understanding of its governance is a work in progress, but our grasp of dyspnea and ventilatory limitation in children (if it occurs) remains embryonic. This manuscript summarizes ventilatory mechanics during dynamic exercise, then proceeds to outline our current understanding of mechanisms of dyspnea, particularly during exercise (exertional dyspnea). Most research in this field has been done in adults, and the vast majority of these studies in patients with chronic obstructive pulmonary disease. To what extent conclusions drawn from this literature apply to children and adolescents—both healthy and those with cardiopulmonary disease—will be discussed. The few, recent, pertinent, pediatric studies will be reviewed in an attempt to provide an empirical basis for proposing a hypothetical model to study exertional dyspnea in youth. Just as somatic growth will have consequences for ventilatory and exercise capacity, so too will neural developmental plasticity and experience affect perception of dyspnea. Our path to understand how these evolving inputs and influences summate during a child’s life will be Columbus’ India.