Effects of dietary inorganic nitrate on static and dynamic breath-holding in humans.

Inorganic nitrate has been shown to reduce oxygen cost during exercise. Since the nitrate-nitrite-NO pathway is facilitated during hypoxia, we investigated the effects of dietary nitrate on oxygen consumption and cardiovascular responses during apnea. These variables were measured in two randomized, double-blind, placebo-controlled, crossover protocols at rest and ergometer exercise in competitive breath-hold divers. Subjects held their breath for predetermined times along with maximum effort apneas after two separate 3-day periods with supplementation of potassium nitrate/placebo. In contrast to our hypothesis, nitrate supplementation led to lower arterial oxygen saturation (SaO(2), 77 ± 3%) compared to placebo (80 ± 2%) during static apnea, along with lower end-tidal fraction of oxygen (FETO(2)) after 4 min of apnea (nitrate 6.9 ± 0.4% vs. placebo 7.6 ± 0.4%). Maximum apnea duration was shorter after nitrate (329 ± 13 s) compared to placebo (344 ± 13 s). During cycle ergometry nitrate had no effect on SaO(2), FETO(2) or maximum apnea duration. The negative effects of inorganic nitrate during static apnea may be explained by an attenuated diving response.

Acute dietary nitrate supplementation improves dry static apnea performance.

Acute dietary nitrate (NO3⁻) supplementation has been reported to lower resting blood pressure, reduce the oxygen (O2) cost of sub-maximal exercise, and improve exercise tolerance. Given the proposed effects of NO3⁻ on tissue oxygenation and metabolic rate, it is possible that NO3⁻ supplementation might enhance the duration of resting apnea. If so, this might have important applications both in medicine and sport. We investigated the effects of acute NO3⁻ supplementation on pre-apnea blood pressure, apneic duration, and the heart rate (HR) and arterial O2 saturation (SaO2) responses to sub-maximal and maximal apneas in twelve well-trained apnea divers. Subjects were assigned in a randomized, double blind, crossover design to receive 70 ml of beetroot juice (BR; containing ∼5.0 mmol of nitrate) and placebo juice (PL; ∼0.003 mmol of nitrate) treatments. At 2.5 h post-ingestion, the subjects completed a series of two 2-min (sub-maximal) static apneas separated by 3 min of rest, followed by a maximal effort apnea. Relative to PL, BR reduced resting mean arterial pressure by 2% (PL: 86±7 vs. BR: 84 ± 6 mmHg; P=0.04). The mean nadir for SaO2 after the two sub-maximal apneas was 97.2±1.6% in PL and 98.5±0.9% in BR (P=0.03) while the reduction in HR from baseline was not significantly different between PL and BR. Importantly, BR increased maximal apneic duration by 11% (PL: 250 ± 58 vs. BR: 278±64s; P=0.04). In the longer maximal apneas in BR, the magnitude of the reductions in HR and SaO2 were greater than in PL (P ≤ 0.05). The results suggest that acute dietary NO3⁻ supplementation may increase apneic duration by reducing metabolic costs.

Sleep apnea in a child with the pickwickian syndrome.

A 3-year-old girl with a history of excessive weight gain from birth presented with obesity, somnolence, and cyanosis, characteristic of the Pickwickian syndrome. Obesity was familial and exogenous without endocrine or neurologic anomaly. Respiratory center sensitivity to carbon dioxide was normal. Excessive somnolence was due to the obesity, which during sleep caused airway obstruction, apnea, and awakening, finally resulting in sleep deprivation. The sleep apneas and the daytime somnolence disappeared with weight reduction, showing that obesity alone had been responsible for the disorder.