Efficacy and feasibility of HIIT training for university students: The Uni-HIIT RCT.

OBJECTIVES: The primary aim of this study was to evaluate the preliminary efficacy and feasibility of an 8-week high-intensity interval training program (Uni-HIIT) for young adult students in a university setting. DESIGN: Randomised controlled trial. METHOD: Uni-HIIT was conducted at the University of Newcastle, Australia (February-June, 2017). Participants were university students 18-25yrs (n=53; 20.38±1.88yrs) randomized into the Uni HIIT program (n=26) or wait-list control (n=27) condition. Participants were required to attend up to three HIIT sessions/week for 8-weeks which included a variety of aerobic and muscular fitness exercise combinations lasting 8-12minutes (using 30:30sec rest:work intervals). The primary outcome was cardio-respiratory fitness (CRF) (20mSRT), and secondary outcomes included muscular fitness (standing jump, push-ups), body composition (InBody), executive function (Trail Making Test), anxiety levels (State Trait Anxiety Inventory) and perceived stress (Perceived Stress Scale). Linear mixed models were used to analyse outcomes and Cohen's d effect sizes were calculated. Process evaluation measures of recruitment, retention, attendance and satisfaction were conducted. RESULTS: A large significant group-by-time effect resulted for CRF [8.4 shuttles (95% CI(2.9-13.9), P=0.004,d=1.08] and muscular fitness [4.0 repetitions (95% CI(1.2-6.8), P=0.006,d=0.99], and moderate effect size was observed for Trail B [-5.9seconds (95% CI(-11.8-0.1.0), P=0.052, d=0.63]. No significant intervention effects were found for body composition, standing jump, anxiety or perceived stress (P >0.05). High ratings of participant satisfaction (4.73), enjoyment (4.54) and perceived value (4.54) were observed. CONCLUSION: This study demonstrates the efficacy and feasibility of delivering a novel HIIT program in the university setting.

Sustained Inhibition of Proliferative Response After Transient FGF Stimulation Is Mediated by Interleukin 1 Signaling.

Transient FGF stimulation of various cell types results in FGF memory--a sustained blockage of efficient proliferative response to FGF and other growth factors. FGF memory establishment requires HDAC activity, indicating its epigenetic character. FGF treatment stimulates proinflammatory NFκB signaling, which is also critical for FGF memory formation. The search for FGF-induced mediators of FGF memory revealed that FGF stimulates HDAC-dependent expression of the inflammatory cytokine IL1α. Similarly to FGF, transient cell treatment with recombinant IL1α inhibits the proliferative response to further FGF and EGF stimulation, but does not prevent FGF receptor-mediated signaling. Interestingly, like cells pretreated with FGF1, cells pretreated with IL1α exhibit enhanced restructuring of actin cytoskeleton and increased migration in response to FGF stimulation. IRAP, a specific inhibitor of IL 1 receptor, and a neutralizing anti-IL1α antibody prevent the formation of FGF memory and rescue an efficient proliferative response to FGF restimulation. A similar effect results following treatment with the anti-inflammatory agents aspirin and dexamethasone. Thus, FGF memory is mediated by proinflammatory IL1 signaling. It may play a role in the limitation of proliferative response to tissue damage and prevention of wound-induced hyperplasia.

Transitory FGF treatment results in the long-lasting suppression of the proliferative response to repeated FGF stimulation.

FGF applied as a single growth factor to quiescent mouse fibroblasts induces a round of DNA replication, however continuous stimulation results in arrest in the G1 phase of the next cell cycle. We hypothesized that FGF stimulation induces the establishment of cell memory, which prevents the proliferative response to repeated or continuous FGF application. When a 2-5 days quiescence period was introduced between primary and repeated FGF treatments, fibroblasts failed to efficiently replicate in response to secondary FGF application. The establishment of "FGF memory" during the first FGF stimulation did not require DNA synthesis, but was dependent on the activity of FGF receptors, MEK, p38 MAPK and NFκB signaling, and protein synthesis. While secondary stimulation resulted in strongly decreased replication rate, we did not observe any attenuation of morphological changes, Erk1/2 phosphorylation and cyclin D1 induction. However, secondary FGF stimulation failed to induce the expression of cyclin A, which is critical for the progression from G1 to S phase. Treatment of cells with a broad range histone deacetylase inhibitor during the primary FGF stimulation rescued the proliferative response to the secondary FGF treatment suggesting that the establishment of "FGF memory" may be based on epigenetic changes. We suggest that "FGF memory" can prevent the hyperplastic response to cell damage and inflammation, which are associated with an enhanced FGF production and secretion. "FGF memory" may present a natural obstacle to the efficient application of recombinant FGFs for the treatment of ulcers, ischemias, and wounds.