PubMed · 15395930
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
H E WILSON. 1949. Lip exercises.. https://pubmed.ncbi.nlm.nih.gov/15395930/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The near-immediate increase in breathing that accompanies the onset of constant load, dynamic exercise has remained a topic of interest to respiratory physiologists for the better part of a century. During this time, several theories have been proposed and tested in an attempt to explain what has been called the phase I response of exercise hyperpnoea, or the fast neural drive to breathe, and much controversy still remains as to what mediates this response. 'Central motor command' and 'afferent feedback' mechanisms, as described in animal models, have been centre stage in the debate, with much supportive evidence for their involvement. This review presents three relatively recent and controversial mechanisms and examines the increasing evidence for their involvement in the initial phase of exercise hyperpnoea: (1) the vascular distension hypothesis, (2) the vestibular feedback hypothesis and (3) the behavioral state hypothesis. Some outstanding fundamental questions and directions for future research are presented throughout, always with a focus on mechanistic efficacy in the integrated system response.
This study intended to find simple parameters that were able to determine the increase in physical performance as a result of sport in a group of patients with COPD (lung sport). We regularly investigated pulse, oxygenation and peak expiratory flow in participants with COPD of a "lung sport group", who participated in a structured weekly training program under professional supervision. Ten volunteers (7 females, 3 males, median of age = 69) with COPD (grade II-III) took part in the study. - The relative changes after 3 and 6 months were compared with the values of the first month of exercise. Measurements were carried out before exercise, after stamina training and at the end of the program. - Pulse and oxygenation did not show any changes. However, there was a significant improvement of peak flow after 6 months. - These peak flow changes represent further evidence of positive effects of sport in COPD and provide a parameter which allows the patients themselves to measure and evaluate the success of their physical activity.
The purpose of this review is to summarise the latest literature on the signalling pathways involved in transcriptional modulations of genes that encode contractile and metabolic proteins in response to endurance exercise. A special attention has been paid to the cooperation between signalling pathways and coordinated expression of protein families that establish myofibre phenotype. Calcium acts as a second messenger in skeletal muscle during exercise, conveying neuromuscular activity into changes in the transcription of specific genes. Three main calcium-triggered regulatory pathways acting through calcineurin, Ca(2+)-calmodulin-dependent protein kinases (CaMK) and Ca(2+)-dependent protein kinase C, transduce alterations in cytosolic calcium concentration to target genes. Calcineurin signalling, the most important of these Ca(2+)-dependent pathways, stimulates the activation of many slow-fibre gene expression, including genes encoding proteins involved in contractile process, Ca(2+) uptake and energy metabolism. It involves the interaction between multiple transcription factors and the collaboration of other Ca(2+)-dependent CaMKs. Although members of mitogen-activated protein kinase (MAPK) pathways are activated during exercise, their integration into other signalling pathways remains largely unknown. The peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator-1alpha (PGC-1alpha) constitutes a pivotal factor of the circuitry which coordinates mitochondrial biogenesis and which couples to the expression of contractile and metabolic genes with prolonged exercise.