Exertional dyspnea is present across the spectrum of chronic obstructive pulmonary disease (COPD) severity. However, without realizing it themselves, patients may decrease daily physical activity to avoid distressing respiratory sensations. Dyspnea also may be associated with deconditioning. Cardiopulmonary exercise testing can uncover exertional dyspnea and its physiological determinants in patients with preserved or only mildly reduced FEV1. Dyspnea in mild COPD can largely be explained by increased “wasted” ventilation in the physiological dead space, which heightens the drive to breathe and worsens the inspiratory mechanical constraints. During incremental exercise testing, this is readily identified as an excessive ventilation-to-metabolic demand, that is, a high ventilation (V.e) to carbon dioxide output (V.co2) relationship. Linking increases in V.e/V.co2 to exertional dyspnea may provide objective evidence that a patient’s poor exercise tolerance is not just a consequence of deconditioning. This information should prompt a proactive therapeutic approach to increase the available ventilatory reserve by, for example, giving inhaled bronchodilators. Considering that the structural determinants of ventilatory inefficiency (early emphysema, ventilation–perfusion mismatching, and microvascular disease) may progress despite only modest changes in FEV1, serial V.e/V.co2 measurements might also prove valuable to track disease progression in these symptomatic patients.

The study investigated the influence of β-alanine supplementation during a high-intensity interval training (HIIT) program on repeated sprint ability (RSA) performance. This study was randomized, double-blinded, and placebo controlled. Eighteen men performed an incremental running test until exhaustion (T_INC) at baseline and followed by 4-wk HIIT (10 × 1-min runs 90% maximal T_INCvelocity [1-min recovery]). Then, participants were randomized into two groups and performed a 6-wk HIIT associated with supplementation of 6.4 g/day of β-alanine (Gβ) or dextrose (placebo group; GP). Pre- and post-6-wk HIIT + supplementation, participants performed the following tests: 1) T_INC; 2) supramaximal running test; and 3) 2 × 6 × 35-m sprints (RSA). Before and immediately after RSA, neuromuscular function was assessed by vertical jumps, maximal isometric voluntary contractions of knee extension, and neuromuscular electrical stimulations. Muscle biopsies were performed to determine muscle carnosine content, muscle buffering capacity in vitro (βm_{in vitro}), and content of phosphofructokinase (PFK), monocarboxylate transporter 4 (MCT4), and hypoxia-inducible factor-1α (HIF-1α). Both groups showed a significant time effect for maximal oxygen uptake (Gβ: 6.2 ± 3.6% and GP: 6.5 ± 4.2%; P > 0.01); only Gβ showed a time effect for total (−3.0 ± 2.0%; P = 0.001) and best (−3.3 ± 3.0%; P = 0.03) RSA times. A group-by-time interaction was shown after HIIT + Supplementation for muscle carnosine (Gβ: 34.4 ± 2.3 mmol·kg⁻¹·dm⁻¹and GP: 20.7 ± 3.0 mmol·kg⁻¹·dm⁻¹; P = 0.003) and neuromuscular voluntary activation after RSA (Gβ: 87.2 ± 3.3% and GP: 78.9 ± 12.4%; P = 0.02). No time effect or group-by-time interaction was shown for supramaximal running test performance, βm, and content of PFK, MCT4, and HIF-1α. In summary, β-alanine supplementation during HIIT increased muscle carnosine and attenuated neuromuscular fatigue, which may contribute to an enhancement of RSA performance.NEW & NOTEWORTHY β-Alanine supplementation during a high-intensity interval training program increased repeated sprint performance. The improvement of muscle carnosine content induced by β-alanine supplementation may have contributed to an attenuation of central fatigue during repeated sprint. Overall, β-alanine supplementation may be a useful dietary intervention to prevent fatigue.

Ventilatory inefficiency in non-COPD smokers is associated with lower exercise capacityhttp://ow.ly/Mf7n308Qm5M

D acidosis induction on lactate minimum intensity (LMI). Twenty recreationally trained males who were experienced in cycling (15 cyclists and 5 triathletes) participated in this study. The athletes underwent 3 lactate minimum tests on an electromagnetic cycle ergometer. The hyperlactemia induction methods used were graded exercise test (GXT), Wingate test (WAnT), and 2 consecutive Wingate tests (2 × WAnTs). The LMI at 2 × WAnTs (200.3 ± 25.8 W) was statistically higher than the LMI at GXT (187.3 ± 31.9 W) and WAnT (189.8 ± 26.0 W), with similar findings for blood lactate, oxygen uptake, and pulmonary ventilation at LMI. The venous pH after 2 × WAnTs was lower (7.04 ± 0.24) than in (p ≤ 0.05) the GXT (7.19 ± 0.05) and WAnT (7.19 ± 0.05), whereas the blood lactate response was higher. In addition, similar findings were observed for bicarbonate concentration [HCO3] (2 × WAnTs lower than WAnT; 15.3 ± 2.6 mmol·L−1 and 18.2 ± 2.7 mmol·L−1, respectively) (p ≤ 0.05). However, the maximal aerobic power and total time measured during the incremental phase also did not differ. Therefore, we can conclude that the induction mode significantly affects pH, blood lactate, and [HCO3] and consequently they alter the LMI and physiological parameters at LMI....