No abstract

No abstract

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.

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.

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.

Introduction Brain-derived neurotrophic factor (BDNF) is an exercise-induced neurotropin mediating neuroprotection and synaptic plasticity. Although exercise intensity is implicated as a potentially important mediator of BNDF release after exercise, the optimal exercise stimulus (interval vs continuous) and intensity (submaximal vs supramaximal) for augmenting circulating BDNF levels remains unknown. Irisin, an exercise-driven myokine, may also contribute to neuroprotection by upregulating BDNF. Purpose To examine the response and recovery of plasma BDNF and irisin after acute exercise of differing intensities. Methods Eight males (23.1 ± 3.0 yr of age; V˙O2max 51.2 ± 4.4 mL·kg−1·min−1) completed four acute exercise sessions: 1) moderate-intensity continuous training (MICT, 65% V˙O2max); 2) vigorous-intensity continuous training (VICT, 85% V˙O2max); 3) sprint interval training (SIT, “all out”); and 4) no exercise (CTRL). Blood was collected preexercise as well as immediately, 30 min, and 90 min postexercise. Plasma BDNF and irisin were assessed with commercially available enzyme-linked immunosorbent assay kits. Results Plasma BDNF levels increased immediately after exercise in the SIT group (P < 0.0001) with plasma concentrations recovering 30 and 90 min postexercise. The BDNF levels after MICT were reduced 30 min postexercise compared with immediately postexercise (P = 0.0189), with no other changes across time points in MICT and VICT groups. Plasma BDNF area under the curve in SIT was significantly higher compared with CTRL, MICT, and VICT (P = 0.0020). No changes in plasma irisin across exercise groups and time points were found (P > 0.9999). Conclusions Plasma BDNF levels increased in an intensity-dependent manner with SIT eliciting the highest BDNF concentration immediately postexercise. These results identify SIT as a time-efficient exercise modality to promote brain health through BDNF release.

Exercise training has robust effects on subcutaneous inguinal white adipose tissue (iWAT), characterized by a shift to a brown adipose tissue (BAT)-like phenotype. Consistent with this, transplantation of exercise-trained iWAT into sedentary rodents activates thermogenesis and improves glucose homeostasis, suggesting that iWAT metabolism may contribute to the beneficial effects of exercise. However, it is yet to be determined if adaptations in iWAT are necessary for the beneficial systemic effects of exercise. To test this, male C57BL/6 mice were provided access to voluntary wheel running (VWR) or remained as a cage control (SED) for 11 nights after iWAT removal via lipectomy (LIPX) or SHAM surgery. We found that SHAM and LIPX mice with access to VWR ran similar distances and had comparable reductions in body mass, increased food intake, and increased respiratory exchange ratio (RER). Further, VWR improved indexes of glucose homeostasis and insulin tolerance in both SHAM and LIPX mice. The lack of effect of LIPX in the response to VWR was not explained by compensatory increases in markers of mitochondrial biogenesis and thermogenesis in skeletal muscle, epididymal white adipose tissue, or interscapular brown adipose tissue. Together, these data demonstrate that mice with and without iWAT have comparable adaptations to VWR, suggesting that iWAT may be dispensable for the metabolic health benefits of exercise.

Adaptations to sprint interval training (SIT) are observed with brief (≤15-s) work bouts highlighting peak power generation as an important metabolic stimulus. This study examined the effects of manipulating SIT work bout and recovery period duration on energy expenditure (EE) during and postexercise, as well as postexercise fat oxidation rates. Nine active males completed a resting control session (CTRL) and 3 SIT sessions in randomized order: (i) 30:240 (4 × 30-s bouts, 240-s recovery); (ii) 15:120 (8 × 15-s bouts, 120-s recovery); (3) 5:40 (24 × 5-s bouts, 40-s recovery). Protocols were matched for the total duration of work (2 min) and recovery (16 min), as well as the work-to-recovery ratio (1:8 s). EE and fat oxidation rates were derived from gas exchange measured before, during, and for 3 h postexercise. All protocols increased EE versus CTRL (P < 0.001). Exercise EE was greater (P < 0.001) with 5:40 (209 kcal) versus both 15:120 (163 kcal) and 30:240 (138 kcal), while 15:120 was also greater (P < 0.001) than 30:240. Postexercise EE was greater (P = 0.014) with 15:120 (313 kcal) versus 5:40 (294 kcal), though both were similar (P > 0.077) to 30:240 (309 kcal). Postexercise fat oxidation was similar (P = 0.650) after 15:120 (0.104 g·min −1 ) and 30:240 (0.116 g·min −1 ) and both were greater (P < 0.030) than 5:40 (0.072 g·min −1 ) and CTRL (0.049 g·min −1 ). In conclusion, shorter SIT work bouts that target peak power generation increase exercise EE without compromising postexercise EE, though longer bouts promote greater postexercise fat utilization.Key words: high-intensity interval training, energy expenditure, excess postexercise oxygen consumption, fat oxidation, repeated sprint exercise, peak power generation. Mots-clés : entraînement par intervalle d'intensité élevée, dépense énergétique, consommation d'oxygène postexercice en surplus, oxydation des graisses, exercice de sprint répété, production de puissance de pointe.