Search

Cao, Yinhang, Naoto Fujii, Tomomi Fujimoto, Yin-Feng Lai, Takeshi Ogawa, Tsutomu Hiroyama, Yasushi Enomoto, and Takeshi Nishiyasu. CO

Physical activity could improve the muscle fitness of youth, but the systematic analysis of physical activity elements and muscle fitness was limited. This systematic review and meta-analysis aim to explore the influence of physical activity elements on muscle fitness in children and adolescents. We analyzed literature in Embase, EBSCO, Web of Science, and PubMed databases from January 2000 to September 2020. Only randomized controlled studies with an active control group, which examined at least 1 muscle fitness evaluation index in individuals aged 5–18 years were included. Articles were evaluated using the Jaded scale. Weighted-mean standardized mean differences (SMDs) were calculated using random-effects models. Twenty-one studies and 2267 subjects were included. Physical activity had moderate effects on improving muscle fitness (SMD: 0.58–0.96, p < 0.05). Physical activity element subgroup analysis showed that high-intensity (SMD 0.68–0.99, p < 0.05) physical activity

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.

We tested whether expiratory flow limitation (EFL) occurs in endurance athletes in a moderately hypobaric hypoxic environment equivalent to 2500 m above sea level and, if so, whether EFL inhibits peak ventilation (urn:x-wiley:2051817X:media:phy213996:phy213996-math-0001Epeak), thereby exacerbating the hypoxia‐induced reduction in peak oxygen uptake (urn:x-wiley:2051817X:media:phy213996:phy213996-math-0002O2peak). Seventeen young male endurance runners performed incremental exhaustive running on separate days under hypobaric hypoxic (560 mmHg) and normobaric normoxic (760 mmHg) conditions. Oxygen uptake (urn:x-wiley:2051817X:media:phy213996:phy213996-math-0003O2), minute ventilation (urn:x-wiley:2051817X:media:phy213996:phy213996-math-0004E), arterial O2 saturation (SpO2), and operating lung volume were measured throughout the incremental exercise. Among the runners tested, 35% exhibited EFL (EFL group, n = 6) in the hypobaric hypoxic condition, whereas the rest did not (Non‐EFL group, n = 11). There were no differences between the EFL and Non‐EFL groups for urn:x-wiley:2051817X:media:phy213996:phy213996-math-0005Epeak and urn:x-wiley:2051817X:media:phy213996:phy213996-math-0006O2peak under either condition. Percent changes in urn:x-wiley:2051817X:media:phy213996:phy213996-math-0007Epeak (4 ± 4 vs. 2 ± 4%) and urn:x-wiley:2051817X:media:phy213996:phy213996-math-0008O2peak (−18 ± 6 vs. −16 ± 6%) from normobaric normoxia to hypobaric hypoxia also did not differ between the EFL and Non‐EFL groups (all P > 0.05). No differences in maximal running velocity, SpO2, or operating lung volume were detected between the two groups under either condition. These results suggest that under the moderate hypobaric hypoxia (2500 m above sea level) frequently used for high‐attitude training, ~35% of endurance athletes may exhibit EFL, but their ventilatory and metabolic responses during maximal exercise are similar to those who do not exhibit EFL.