Interleukin-6 is not involved in appetite regulation following moderate-intensity exercise in males with normal weight and obesity.

OBJECTIVE: In obesogenic states and after exercise, interleukin (IL)-6 elevations are established, and IL-6 is speculated to be an appetite-regulating mechanism. This study examined the role of IL-6 on exercise-induced appetite regulation in sedentary normal weight (NW) males and those with obesity (OB). METHODS: Nine NW participants and eight participants with OB completed one non-exercise control (CTRL) and one moderate-intensity continuous training (MICT; 60 minutes, 65% V̇O2max ) session. IL-6, acylated ghrelin, active peptide tyrosine-tyrosine3-36 , active glucagon-like peptide-1, and overall appetite perceptions were measured fasted, pre exercise, and 30, 90, and 150 minutes post exercise. RESULTS: Fasted IL-6 concentrations were elevated in OB (p = 0.005, η p 2 = 0.419); however, increases following exercise were similar between groups (p = 0.934, η p 2 = 0.000). Acylated ghrelin was lower in OB versus NW (p < 0.017, d > 0.84), and OB did not respond to MICT (p > 0.512, d < 0.44) although NW had a decrease versus CTRL (p < 0.034, d > 0.61). IL-6 did not moderate/mediate acylated ghrelin release after exercise (p > 0.251). There were no observable effects of MICT on tyrosine-tyrosine3-36 , glucagon-like peptide-1, or overall appetite (p > 0.334, η p 2 < 0.062). CONCLUSIONS: These results suggest that IL-6 is not involved in exercise-induced appetite suppression. Despite blunted appetite-regulatory peptide responses to MICT in participants with OB, NW participants exhibited decreased acylated ghrelin; however, no differences in appetite perceptions existed between CTRL and MICT or NW and OB.

High Load With Lower Repetitions vs. Low Load With Higher Repetitions: The Impact on Asymmetry in Weight Distribution During Deadlifting.

This study investigated weight distribution between the lower limbs using a symmetry index (SI) score of the vertical ground reaction forces (GRF) and measures of postural stability in high load/low repetition (termed "heavy") and low load/high repetition (termed "light") deadlifting. Ten participants performed two deadlift protocols with equal cumulative external load. These protocols were designed to represent standard high load/low repetition and low load/high repetition workouts; order was random and separated by 7 days. An effect of lifting condition (p = 0.023) and set number (p = 0.011) was observed such that lifts in the heavy condition were less symmetrical than those in the light condition and lifts became more symmetrical as set number increased. There was no effect of lift number on symmetry of force production (p = 0.127). Additional analysis revealed that center of pressure (COP) path length was greater during heavy lifts (p = 0.002) however COP range was unaffected suggesting controlled point of force application within the same boundaries regardless of lifting condition. As asymmetries have been previously associated with increased injury risk, greater training emphasis on the symmetrical performance of sub-maximal deadlifts should be considered to try to minimize the development of asymmetries.

Greater lactate accumulation following an acute bout of high-intensity exercise in males suppresses acylated ghrelin and appetite postexercise.

High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given lactate may mediate these effects, we used sodium bicarbonate (NaHCO3) supplementation in a double-blind, placebo-controlled, crossover design to investigate lactate's purported role in exercise-induced appetite suppression. Eleven males completed two identical high-intensity interval training sessions (10 × 1 min cycling bouts at ~90% heart rate maximum interspersed with 1-min recovery), where they ingested either NaHCO3 (BICARB) or sodium chloride (NaCl) as a placebo (PLACEBO) preexercise. Blood lactate, acylated ghrelin, GLP-1, and PYY concentrations, as well as overall appetite were assessed preexercise and 0, 30, 60, and 90 min postexercise. Blood lactate was greater immediately (P < 0.001) and 30 min postexercise (P = 0.049) in the BICARB session with an increased (P = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 (P = 0.014) and 90 min postexercise (P = 0.016), with a decreased AUC (P = 0.039). The BICARB session had increased PYY (P = 0.034) with an increased AUC (P = 0.031). The BICARB session also tended (P = 0.060) to have increased GLP-1 at 30 (P = 0.003) and 60 min postexercise (P < 0.001), with an increased AUC (P = 0.030). The BICARB session tended (P = 0.059) to reduce overall appetite, although there was no difference in AUC (P = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression.NEW & NOTEWORTHY We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression, given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.

The effects of a pre-exercise meal on postexercise metabolism following a session of sprint interval training.

Sprint interval training (SIT) has demonstrated reductions in fat mass through potential alterations in postexercise metabolism. This study examined whether exercising in the fasted or fed state affects postexercise metabolism following acute SIT. Ten active males performed a bout of modified SIT (8 × 15-s sprints; 120 s recovery) in both a fasted (FAST) and fed (FED) state. Gas exchange was collected through 3 h postexercise, appetite perceptions were measured using a visual analog scale, and energy intake was recorded using dietary food logs. There was no difference in energy expenditure between conditions at any time point (p > 0.329) or in total session energy expenditure (FED: 514.8 ± 54.9 kcal, FAST: 504.0 ± 74.3 kcal; p = 0.982). Fat oxidation at 3 h after exercise was higher in FED (0.110 ± 0.04 g·min-1) versus FAST (0.069 ± 0.02 g·min-1; p = 0.013) though not different between conditions across time (p > 0.340) or in total postexercise fat oxidation (FED: 0.125 ± 0.04 g·min-1, FAST: 0.105 ± 0.02 g·min-1; p = 0.154). Appetite perceptions were lower in FED (-4815.0 ± 4098.7 mm) versus FAST (-707.5 ± 2010.4 mm, p = 0.022); however, energy intake did not differ between conditions (p = 0.429). These results demonstrate the fasted or fed state does not augment postexercise metabolism following acute SIT in a way that would favour fat loss following training. Novelty Energy expenditure was similar between conditions, while fat oxidation was significantly greater in FED at 3 h after exercise. Appetite perceptions were significantly lower in FED; however, energy intake was not different between conditions. Current findings suggest that performing SIT in the fed or fasted state would not affect fat loss following training.