scholarly journals Faculty Opinions recommendation of Inverse relationship of maximal exercise capacity to hospitalization secondary to coronavirus disease 2019.

Author(s):  
David Nieman
2021 ◽  
Vol 96 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Clinton A. Brawner ◽  
Jonathan K. Ehrman ◽  
Shane Bole ◽  
Dennis J. Kerrigan ◽  
Sachin S. Parikh ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 611
Author(s):  
Sihui Ma ◽  
Jiao Yang ◽  
Takaki Tominaga ◽  
Chunhong Liu ◽  
Katsuhiko Suzuki

The low-carbohydrate ketogenic diet (LCKD) is a dietary approach characterized by the intake of high amounts of fat, a balanced amount of protein, and low carbohydrates, which is insufficient for metabolic demands. Previous studies have shown that an LCKD alone may contribute to fatty acid oxidation capacity, along with endurance. In the present study, we combined a 10-week LCKD with an 8-week forced treadmill running program to determine whether training in conjunction with LCKD enhanced fatty acid oxidation capacity, as well as whether the maximal exercise capacity would be affected by an LCKD or training in a mice model. We found that the lipid pool and fatty acid oxidation capacity were both enhanced following the 10-week LCKD. Further, key fatty acid oxidation related genes were upregulated. In contrast, the 8-week training regimen had no effect on fatty acid and ketone body oxidation. Key genes involved in carbohydrate utilization were downregulated in the LCKD groups. However, the improved fatty acid oxidation capacity did not translate into an enhanced maximal exercise capacity. In summary, while favoring the fatty acid oxidation system, an LCKD, alone or combined with training, had no beneficial effects in our intensive exercise-evaluation model. Therefore, an LCKD may be promising to improve endurance in low- to moderate-intensity exercise, and may not be an optimal choice for those partaking in high-intensity exercise.


2021 ◽  
Author(s):  
Lisa M. Wilson ◽  
Matthew J. Ellis ◽  
Rebecca L. Lane ◽  
John W. Wilson ◽  
Dominic T. Keating ◽  
...  

2010 ◽  
Vol 55 (18) ◽  
pp. 1945-1954 ◽  
Author(s):  
Fabio Esposito ◽  
Odile Mathieu-Costello ◽  
Ralph Shabetai ◽  
Peter D. Wagner ◽  
Russell S. Richardson

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Samah A. Moawd ◽  
Alshimaa R. Azab ◽  
Zizi M. Ibrahim ◽  
Anju Verma ◽  
Walid Kamal Abdelbasset

Objectives. Congenital diaphragmatic hernia (CDH) is a birth defect affecting the respiratory functions, functional performance, and quality of life (QOL) in school-aged children. Rarely have studies been conducted to evaluate the impacts of respiratory muscle training on school-aged children with postoperative CDH. The current study was designed to evaluate the impacts of respiratory muscle training on respiratory function, maximal exercise capacity, functional performance, and QOL in these children. Methods. This study is a randomized control study. 40 children with CDH (age: 9-11 years) were assigned randomly into two groups. The first group conducted an incentive spirometer exercise combined with inspiratory muscle training (study group, n=20), whereas the second group conducted only incentive spirometer exercise (control group, n=20), thrice weekly for twelve consecutive weeks. Respiratory functions, maximal exercise capacity, functional performance, and pediatric quality of life inventory (PedsQL) were assessed before and after the treatment program. Results. Regarding the posttreatment analysis, the study group showed significant improvements in all outcome measures (FVC%, p<0.001; FEV1%, p=0.002; VO2max, p=0.008; VE/VCO2 slope, p=0.002; 6-MWT, p<0.001; and PedsQL, p<0.001), whereas the control group did not show significant changes (p>0.05). Conclusion. Respiratory muscle training may improve respiratory functions, maximal exercise capacities, functional performance, and QOL in children with postoperative CDH. Clinical commendations have to be considered to include respiratory muscle training in pulmonary rehabilitation programs in children with a history of CDH.


2020 ◽  
Author(s):  
Caterina Maffeis ◽  
Daniel Armando Morris ◽  
Evgeny Belyavskiy ◽  
Martin Kropf ◽  
Aravind Kumar Radhakrishnan ◽  
...  

2001 ◽  
Vol 90 (5) ◽  
pp. 1707-1713 ◽  
Author(s):  
Shin-Da Lee ◽  
Hitoshi Nakano ◽  
Gaspar A. Farkas

Obesity is often associated with a reduced ventilatory response and a decreased maximal exercise capacity. GABA is a major inhibitory neurotransmitter in the mammalian central nervous system. Altered GABAergic mechanisms have been detected in obese Zucker rats and implicated in their hyperphagic response. Whether altered GABAergic mechanisms also contribute to regulate ventilation and influence exercise capacity in obese Zucker rats is unknown and formed the basis of the present study. Eight lean [317 ± 18 (SD) g] and eight obese (450 ± 27 g) Zucker rats were studied at 12 wk of age. Ventilation at rest and ventilation during hypoxic (10% O2) and hypercapnic (4% CO2) challenges were measured by the barometric method. Peak O2 consumption (V˙o 2 peak) in response to a progressive treadmill test to exhaustion was measured in a metabolic treadmill. Ventilation and V˙o 2 peak were assessed after administration of equal volumes of DMSO (vehicle) and the GABAA receptor antagonist bicuculline (1 mg/kg). In lean animals, bicuculline administration had no effect on ventilation andV˙o 2 peak. In obese rats, bicuculline administration significantly ( P < 0.05) increased resting ventilation (465 ± 53 and 542 ± 72 ml · kg−1 · min−1 for control and bicuculline, respectively), ventilation during exposure to hypoxia (899 ± 148 and 1,038 ± 83 ml · kg−1 · min−1 for control and bicuculline, respectively), andV˙o 2 peak (62 ± 3.7 and 67 ± 3.5 ml · kg−0.75 · min−1 for control and bicuculline, respectively). However, in obese Zucker rats, ventilation in response to hypercapnia did not change after bicuculline administration (608 ± 96 vs. 580 ± 69 ml · kg−1 · min−1). Our findings indicate that endogenous GABA depresses ventilation and limits exercise performance in obese Zucker rats.


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