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.

Sprint interval training (SIT) protocols involving brief (≤15 s) work bouts improve aerobic and anaerobic performance, highlighting peak speed generation as a potentially important adaptive stimulus. To determine the physiological and psychological effects of reducing the SIT work bout duration, while maintaining total exercise and recovery time, 43 healthy males (n = 27) and females (n = 16) trained for 4 weeks (3 times/week) using one of the following running SIT protocols: (i) 30:240 (n = 11; 4-6 × 30-s bouts, 4 min rest); (ii) 15:120 (n = 11; 8-12 × 15-s bouts, 2 min rest); (iii) 5:40 (n = 12; 24-36 × 5-s bouts, 40 s rest); or (iv) served as a nonexercising control (n = 9). Protocols were matched for total work (2-3 min) and rest (16-24 min) durations, as well as the work-to-rest ratio (1:8 s). Pre- and post-training measures included a graded maximal oxygen consumption test, a 5-km time trial, and a 30-s maximal sprint test. Self-efficacy, enjoyment, and intentions were assessed following the last training session. Training improved maximal oxygen consumption (5.5%; P = 0.006) and time-trial performance (5.2%; P = 0.039), with a main effect of time for peak speed (1.7%; P = 0.042), time to peak speed (25%; P < 0.001), and body fat percentage (1.4%; P < 0.001) that appeared to be driven by the training. There were no group effects for self-efficacy (P = 0.926), enjoyment (P = 0.249), or intentions to perform SIT 3 (P = 0.533) or 5 (P = 0.951) times/week. This study effectively demonstrated that the repeated generation of peak speed during brief SIT work bouts sufficiently stimulates adaptive mechanisms promoting increases in aerobic and anaerobic capacity.

support-information-section). OLZ Glucagon Blood sugar Ketogenic diet Fasting α cell Centrally mediated effects of OLZ on glucagon Direct effects of OLZ on the pancreasAbstract Antipsychotic (AP) medications, such as olanzapine (OLZ), are used in the treatment of schizophrenia and a growing number of 'off-label' conditions. A single dose of OLZ causes robust increases in blood glucose within minutes of treatment. The purpose of the current study was to investigate whether interventions that increase circulating ketone bodies (fasting, β-hydroxybutyrate (βHB), ketone esters or a ketogenic diet (KD)) would be sufficient to protect against the acute metabolic side effects of OLZ. We demonstrate that fasting or the short-term consumption of a KD Hesham Shamshoum joined Dr David Wright's laboratory to pursue his Doctorate in the

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