Exercise with End-expiratory Breath Holding Induces Large Increase in Stroke Volume.

Eight well-trained male cyclists participated in two testing sessions each including two sets of 10 cycle exercise bouts at 150% of maximal aerobic power. In the first session, subjects performed the exercise bouts with end-expiratory breath holding (EEBH) of maximal duration. Each exercise bout started at the onset of EEBH and ended at its release (mean duration: 9.6±0.9 s; range: 8.6-11.1 s). At the second testing session, subjects performed the exercise bouts (same duration as in the first session) with normal breathing. Heart rate, left ventricular stroke volume (LVSV), and cardiac output were continuously measured through bio-impedancemetry. Data were analysed for the 4 s preceding and following the end of each exercise bout. LVSV (peak values: 163±33 vs. 124±17 mL, p<0.01) was higher and heart rate lower both in the end phase and in the early recovery of the exercise bouts with EEBH as compared with exercise with normal breathing. Cardiac output was generally not different between exercise conditions. This study showed that performing maximal EEBH during high-intensity exercise led to a large increase in LVSV. This phenomenon is likely explained by greater left ventricular filling as a result of an augmented filling time and decreased right ventricular volume at peak EEBH.

Exercise with hypoventilation induces lower muscle oxygenation and higher blood lactate concentration: role of hypoxia and hypercapnia.

Eight men performed three series of 5-min exercise on a cycle ergometer at 65% of normoxic maximal O(2) consumption in four conditions: (1) voluntary hypoventilation (VH) in normoxia (VH(0.21)), (2) VH in hyperoxia (inducing hypercapnia) (inspired oxygen fraction [F(I)O(2)] = 0.29; VH(0.29)), (3) normal breathing (NB) in hypoxia (F(I)O(2) = 0.157; NB(0.157)), (4) NB in normoxia (NB(0.21)). Using near-infrared spectroscopy, changes in concentration of oxy-(Delta[O(2)Hb]) and deoxyhemoglobin (Delta[HHb]) were measured in the vastus lateralis muscle. Delta[O(2)Hb - HHb] and Delta[O(2)Hb + HHb] were calculated and used as oxygenation index and change in regional blood volume, respectively. Earlobe blood samples were taken throughout the exercise. Both VH(0.21) and NB(0.157) induced a severe and similar hypoxemia (arterial oxygen saturation [SaO(2)] < 88%) whereas SaO(2) remained above 94% and was not different between VH(0.29) and NB(0.21). Arterialized O(2) and CO(2) pressures as well as P50 were higher and pH lower in VH(0.21) than in NB(0.157), and in VH(0.29) than in NB(0.21). Delta[O(2)Hb] and Delta[O(2)Hb - HHb] were lower and Delta[HHb] higher at the end of each series in both VH(0.21) and NB(0.157) than in NB(0.21) and VH(0.29). There was no difference in Delta[O(2)Hb + HHb] between testing conditions. [La] in VH(0.21) was greater than both in NB(0.21) and VH(0.29) but not different from NB(0.157). This study demonstrated that exercise with VH induced a lower tissue oxygenation and a higher [La] than exercise with NB. This was caused by a severe arterial O(2) desaturation induced by both hypoxic and hypercapnic effects.