Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Many hypotheses have been advanced to explain the hyperpnea of exercise and its close relations to the level of metabolic work, expressed as oxygen uptake (VO2) and carbon dioxide production (VCO2). Evidence is presented that a neural central command mechanism from the hypothalamus is important in the driving of both respiration and circulatory adjustments during locomotion or exercise, and that short-term potentiation of neurons in the medulla makes an important contribution. Both are probably augmented by receptors in working muscle and by the effects of increased [K+] acting on the carotid bodies. Feedback from "respiratory" mechanisms, including CO2 and O2 mediated mechanisms and inputs from the lungs, are important in stabilizing ventilation at the level primarily dictated by the major neural mechanisms.
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