Sprint-interval training (SIT) is a viable method to improve health and fitness. However, researchers have questioned the utility of SIT because of its strenuous nature. The current study aimed to determine if manipulating the sprint and recovery duration, while maintaining the 1:8 work to rest ratio, could uncover a more favourable SIT protocol. Nine healthy active males (age, 23.3 ± 3.0 years; body mass index, 22.4 ± 2.2 kg·m −2 ; maximal oxygen consumption, 48.9 ± 5.
This study examines the involvement of two potential mechanisms (lactate and IL-6) that may explain the intensity-dependent effects of acute exercise on appetite-related parameters. Our findings support a clear intensity-dependent paradigm for appetite-regulation following exercise, as highlighted by the change in acylated ghrelin and the suppression of appetite and energy intake after vigorous exercise (continuous and intermittent). Further, our findings extend previous work in animal/cell models by providing evidence for the potential role of lactate and IL-6 in mediating changes in appetite-related parameters following exercise in humans.
Mice are commonly housed at room temperatures below their thermoneutral zone meaning they are exposed to chronic thermal stress. r Endurance exercise induces browning and mitochondrial biogenesis in white adipose tissue of rodents, but there are conflicting reports of this phenomenon in humans. r We hypothesized that the ambient room temperature at which mice are housed could partially explain these discrepant reports between humans and rodents. r We housed mice at room temperature or thermoneutrality and studied their physiological responses to acute and chronic exercise. We found that thermoneutral housing altered running behaviour and glucose homeostasis, and further, that exercise-induced markers of mitochondrial biogenesis and the browning of white adipose tissue were reduced in mice housed at thermoneutrality.
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