Compensation for obesity-induced insulin resistance in dogs: Causal web analysis of the associations of leptin and GLP-1.

Obesity affects aspects of glucose homeostasis such as insulin secretion and insulin sensitivity. Hormones secreted by adipocytes like leptin mediate the metabolic consequences of obesity. Incretin hormones like glucagon-like peptide-1 (GLP-1) increase insulin secretion in response to changes in blood glucose concentration and have been proposed to regulate insulin secretion in fasting, overweight dogs. The aim of this study was to examine hormonal mechanisms by which adiposity alters glucose homeostasis, plasma insulin concentration, and insulin sensitivity in spontaneously overweight dogs.

Ramp and constant power trials produce equivalent critical power estimates

The standard critical power test protocol on the cycle prescribes a series of trials to exhaustion, each at a different but constant power setting. Recently the protocol has been modified and applied to a series of trials to exhaustion each at a different ramp incremental rate. This study was undertaken to compare critical power and anaerobic work capacity estimates in the same group of subjects when derived from the two protocols. Ten male subjects of mixed athletic ability cycled to exhaustion on eight occasions in randomized order over a 3-wk period. Four trials were performed at differing constant power settings and four trials on differing ramp incremental rates. Both critical power and anaerobic work capacity were estimated for each subject by curve fitting of the ramp model and of three versions of the constant power model. After adjusting for inter-subject variability, no significant differences were detected between critical power estimates or between anaerobic work capacity estimates from any model formulation or from the two protocols. It is concluded that both the ramp and constant power protocols produce equivalent estimates for critical power and anaerobic work capacity.