Controlled-frequency breath swimming improves swimming performance and running economy.

Respiratory muscle fatigue can negatively impact athletic performance, but swimming has beneficial effects on the respiratory system and may reduce susceptibility to fatigue. Limiting breath frequency during swimming further stresses the respiratory system through hypercapnia and mechanical loading and may lead to appreciable improvements in respiratory muscle strength. This study assessed the effects of controlled-frequency breath (CFB) swimming on pulmonary function. Eighteen subjects (10 men), average (standard deviation) age 25 (6) years, body mass index 24.4 (3.7) kg/m(2), underwent baseline testing to assess pulmonary function, running economy, aerobic capacity, and swimming performance. Subjects were then randomized to either CFB or stroke-matched (SM) condition. Subjects completed 12 training sessions, in which CFB subjects took two breaths per length and SM subjects took seven. Post-training, maximum expiratory pressure improved by 11% (15) for all 18 subjects (P < 0.05) while maximum inspiratory pressure was unchanged. Running economy improved by 6 (9)% in CFB following training (P < 0.05). Forced vital capacity increased by 4% (4) in SM (P < 0.05) and was unchanged in CFB. These findings suggest that limiting breath frequency during swimming may improve muscular oxygen utilization during terrestrial exercise in novice swimmers.

Physiological consequences of a high work of breathing during heavy exercise in humans.

The healthy respiratory system has a remarkable capacity for meeting the metabolic demands placed upon it during strenuous exercise. For example, in order to regulate alveolar partial pressure of oxygen and carbon dioxide during heavy workloads, a 20-fold increase in alveolar ventilation can occur. The high metabolic costs and subsequent increased work of breathing associated with this ventilatory increase can result in a number of limitations to the healthy respiratory system. Two examples of respiratory system limitations that are associated with a high work of breathing are expiratory flow limitation and exercise-induced diaphragmatic fatigue. Expiratory flow limitation can lead to an inability to increase alveolar ventilation (V (A)) in the face of increasing metabolic demands, resulting in gas exchange impairment and diminished endurance exercise performance. Furthermore, the high ventilatory requirements of endurance athletes and the inherent anatomical differences in females could make these groups more susceptible to expiratory flow limitation. Fatigue of the diaphragm has also been documented after strenuous exercise and may be related to a mechanism which increases sympathetic vasoconstrictor outflow and reduces limb blood flow during prolonged exercise. This competition between the muscles of respiration and locomotion for a limited cardiac output may have dramatic consequences for exercise performance. This brief review summarizes the literature as it pertains to the work of breathing, expiratory flow limitation, and exercise-induced diaphragmatic fatigue in healthy humans.

The association between cardiorespiratory fitness and abdominal adiposity in postmenopausal, physically inactive South Asian women.

In South Asians, a unique obesity phenotype of high abdominal fat is associated with increased cardiovascular risk. Low cardiorespiratory fitness (CRF) is associated with abdominal fat and an increased risk of cardiovascular disease. The purpose of this paper is to determine whether CRF as assessed by VO2 peak, in post-menopausal South Asian women, was associated with body fat distribution and abdominal fat. Physically inactive post-menopausal South Asian women (n = 55) from the Greater Vancouver area were recruited and assessed from January to August 2014. At baseline, VO2 peak was measured with the Bruce Protocol, abdominal fat with CT imaging, and body composition with dual energy X-ray absorptiometry. ANOVA was used to assess differences in subcutaneous abdominal adipose tissue (SAAT), visceral adipose tissue (VAT) and total abdominal adipose tissue (TAAT) between tertiles of CRF. Bivariate correlation and multiple linear regression analyses explored the association between VO2 peak with SAAT, VAT, TAAT and body composition. Models were further adjusted for body fat and body mass index (BMI). Compared to women in the lowest tertile of VO2 peak (13.8-21.8 mL/kg/min), women in the highest tertile (25.0-27.7 mL/kg/min) had significantly lower waist circumference, BMI, total body fat, body fat percentage, lean mass, SAAT, VAT and TAAT (p < 0.05). We found VO2 peak to be negatively associated with SAAT, VAT and TAAT, independent of age and body fatness but not independent of BMI. Further research is necessary to assess whether exercise and therefore improvements in CRF would alter SAAT, VAT and TAAT in post-menopausal South Asian women.

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists.

We tested the hypothesis that intense short duration hypoxic exercise would result in an increase in extravascular lung water (EVLW), as evidenced by an increase in lung density. Using computed tomography (CT), baseline lung density was obtained in eight highly trained male cyclists (mean +/- SD: age = 28 +/- 8 years; height = 180 +/- 9 cm; mass = 71.6 +/- 8.2 kg; VO2max= 65.0 +/- 5.2 ml kg min(-1)). Subjects then completed an intense hypoxic exercise challenge on a cycle ergometer and metabolic data, HR and %S(p)O2 were recorded throughout. While breathing 15% O2, subjects performed five 3 km cycling intervals (mean power, 286 +/- 20 W; HR = 91 +/- 4% HRmax) separated by 5 min of recovery. From a resting hypoxic S(p)O2 of 92 +/- 4%, subjects further desaturated during exercise to 76 +/- 3%. CT scans were repeated 76 +/- 10 min (range 63-88 min) following the completion of exercise. There was no change in lung density from pre (0.18 +/- 0.02 g ml(-1)) to post-exercise (0.18 +/- 0.04 g ml(-1)). The substantial reduction in S(p)O2 may be explained by a number of potential mechanisms, including decreased pulmonary diffusion capacity, alveolar hypoventilation, reduced red cell transit time, ventilation/perfusion inequality or a temperature and pH induced rightward-shift in the oxyhaemoglobin dissociation curve. Alternatively, the integrity of the blood gas barrier may have been disrupted without any measurable increase in lung density.