Low-Load and High-Load Resistance Exercise Completed to Volitional Fatigue Induce Increases in Postexercise Metabolic Responses With More Prolonged Responses With the Low-Load Protocol.

ABSTRACT: Grisebach, D, Bornath, DPD, McCarthy, SF, Jarosz, C, and Hazell, TJ. Low-load and high-load resistance exercise completed to volitional fatigue induce increases in post-exercise metabolic responses with more prolonged responses with the low-load protocol. J Strength Cond Res XX(X): 000-000, 2024-Comparisons of high-load with low-load resistance training (RT) exercise have demonstrated no differences in postexercise metabolism when volume is matched. This important limitation of matching or equating volume diminishes benefits of the low-load RT protocol. Therefore, the purpose of this study was to determine the effects of acute low-load high volume and high-load low volume RT protocols completed to volitional fatigue on postexercise metabolism. Eleven recreationally active resistance-trained male subjects (24 ± 2 years; BMI: 25.3 ± 1.5 kg·m-2) completed 3 experimental sessions: (a) no-exercise control (CTRL); (b) RT at 30% 1 repetition maximum (1RM; 30% 1RM); and (c) RT at 90% 1RM (90% 1RM) with oxygen consumption (V̇o2) measurements 2 hours postexercise. The RT sessions consisted of 3 sets of back squats, bench press, straight-leg deadlift, military press, and bent-over rows to volitional fatigue completed sequentially with 90 seconds of rest between sets and exercises. Changes were considered important if p < 0.100 with a ≥medium effect size. V̇o2 1 hour postexercise was elevated following 30% 1RM (25%; p = 0.003, d = 1.40) and 90% 1RM (14%; p = 0.010, d = 1.15) vs. CTRL and remained elevated 2 hours postexercise following 30% 1RM (16%; p = 0.010, d = 1.15) vs. CTRL. Total O2 consumed postexercise increased following 30% 1RM and 90% 1RM (∼17%; p < 0.044, d > 0.91) vs. CTRL. Fat oxidation was elevated 1 hour postexercise following 30% 1RM and 90% 1RM (∼155%; p < 0.001, d > 2.97) and remained elevated 2 hours postexercise following 30% 1RM compared with CTRL and 90% 1RM (∼69%; p < 0.030, d > 1.03). These data demonstrate beneficial changes to postexercise metabolism following high- and low-load RT sessions, with more prolonged effects following the low-load RT protocol completed to volitional fatigue.

Differential changes in appetite hormones post-prandially based on menstrual cycle phase and oral contraceptive use: A preliminary study.

This was a preliminary study that examined whether appetite regulation is altered during the menstrual cycle or with oral contraceptives. Ten naturally cycling females (NON-USERS) and nine tri-phasic oral contraceptive using females (USERS) completed experimental sessions during each menstrual phase (follicular phase: FP; ovulatory phase: OP; luteal phase: LP). Appetite perceptions and blood samples were obtained fasted, 30, 60, and 90 min post-prandial to measure acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and total peptide tyrosine tyrosine (PYY). Changes were considered important if p < 0.100 and the effect size was ≥medium. There appeared to be a three-way (group x phase x time) interaction for acylated ghrelin where concentrations appeared to be greater in USERS versus NON-USERS during the OP 90-min post-prandial and during the LP fasted, and 90-min post-prandial. In USERS, ghrelin appeared to be greater 90-min post-prandial in the OP versus the FP with no other apparent differences between phases. There were no apparent differences between phases in NON-USERS. There appeared to be a three-way interaction for PYY where concentrations appeared to be greater in USERS during the FP 60-min post-prandial and during the OP 30-min post-prandial. In USERS PYY appeared to be greater 60-min post-prandial during the OP versus the LP with no other apparent differences. There were no apparent differences between phases in NON-USERS. There appeared to be no effect of group or phase on GLP-1, or appetite perceptions. These data demonstrate small effects of menstrual cycle phase and oral contraceptive use on the acylated ghrelin and total PYY response to a standardized meal, with no effects on active GLP-1 or perceived appetite, though more work with a large sample size is necessary.

Low- and high-load resistance training exercise to volitional fatigue generate exercise-induced appetite suppression.

Research on exercise-induced appetite suppression often does not include resistance training (RT) exercise and only compared matched volumes. PURPOSE: To compare the effects of low-load and high-load RT exercise completed to volitional fatigue on appetite-regulation. METHODS: 11 resistance-trained males (24 ± 2 y) completed 3 sessions in a crossover experimental design: 1) control (CTRL); 2) RT exercise at 30% 1-repetition maximum (RM); and 3) RT exercise at 90% 1-RM. RT sessions consisted of 3 sets of 5 exercises completed to volitional fatigue. Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), active peptide tyrosine (PYY), lactate, and subjective appetite perceptions were measured pre-exercise, 0-, 60-, and 120-min post-exercise. Energy intake was recorded the day before, of, and after each session. RESULTS: Lactate was elevated following both 30% (0-, 60-, 120-min post-exercise) and 90% (0-, 60-min post-exercise; P < 0.001, d > 3.92) versus CTRL, with 30% greater than 90% (0-min post-exercise; P = 0.011, d = 1.14). Acylated ghrelin was suppressed by 30% (P < 0.007, d > 1.22) and 90% (P < 0.028, d > 0.096) post-exercise versus CTRL, and 30% suppressed concentrations versus 90% (60-min post-exercise; P = 0.032, d = 0.95). There was no effect on PYY (P > 0.171, ηp2 <0.149) though GLP-1 was greater at 60-min post-exercise in 90% (P = 0.052, d = 0.86) versus CTRL. Overall appetite was suppressed 0-min post-exercise following 30% and 90% versus CTRL (P < 0.013, d > 1.10) with no other differences (P > 0.279, d < 0.56). There were no differences in energy intake (P > 0.101, ηp2 <0.319). CONCLUSIONS: RT at low- and high-loads to volitional fatigue induced appetite suppression coinciding with changes in acylated ghrelin though limited effects on anorexigenic hormones or free-living energy intake were present.

Intense interval exercise induces greater changes in post-exercise metabolism compared to submaximal exercise in middle-aged adults.

INTRODUCTION: High-intensity interval training (HIIT) and sprint interval training (SIT) consistently elevate post-exercise metabolism compared to moderate-intensity continuous training (MICT) in young adults (18-25 years), however few studies have investigated this in middle-aged adults. PURPOSE: To assess the effect of exercise intensity on post-exercise metabolism following submaximal, near-maximal, and supramaximal exercise protocols in middle-aged adults. METHODS: 12 participants (8 females; age: 44 ± 10 years; V ˙ O2max: 35.73 ± 9.97 mL·kg-1 min-1) had their oxygen consumption ( V ˙ O2) measured during and for 2 h following 4 experimental sessions: (1) no-exercise control (CTRL); (2) MICT exercise (30 min at 65% V ˙ O2max); (3) HIIT exercise (10 × 1 min at 90% maximum heart rate with 1 min rest); and (4) modified-SIT exercise (8 × 15 s "all-out" efforts with 2 min rest). Between session differences for V ˙ O2 and fat oxidation were compared. RESULTS: O2 consumed post-exercise was elevated during the 1st h and 2nd h following HIIT (15.9 ± 2.6, 14.7 ± 2.3 L; P < 0.036, d > 0.98) and modified-SIT exercise (16.9 ± 3.3, 15.30 ± 3.4 L; P < 0.041, d > 0.96) compared to CTRL (13.3 ± 1.9, 12.0 ± 2.5 L) while modified-SIT was also elevated vs HIIT in the 1st h (P < 0.041, d > 0.96). Total post-exercise O2 consumption was elevated following all exercise sessions (MICT: 27.7 ± 4.1, HIIT: 30.6 ± 4.8, SIT: 32.2 ± 6.6 L; P < 0.027, d > 1.03) compared to CTRL (24.9 ± 4.1 L). Modified-SIT exercise increased fat oxidation (0.103 ± 0.019 g min-1) compared to all sessions post-exercise (CTRL: 0.059 ± 0.025, MICT: 0.075 ± 0.022, HIIT: 0.081 ± 0.021 g·min-1; P < 0.007, d > 1.30) and HIIT exercise increased compared to CTRL (P = 0.046, d = 0.87). CONCLUSION: Exercise intensity has an important effect on post-exercise metabolism in middle-aged adults.

Leptin and energy balance: exploring Leptin's role in the regulation of energy intake and energy expenditure.

Leptin is a tonic appetite-regulating hormone, which is integral for the long-term regulation of energy balance. The current evidence suggests that the typical orexigenic or anorexigenic response of many of these appetite-regulating hormones, most notably ghrelin and cholecystokinin (CCK), require leptin to function whereas glucagon-like peptide-1 (GLP-1) is required for leptin to function, and these responses are altered when leptin injection or gene therapy is administered in combination with these same hormones or respective agonists. The appetite-regulatory pathway is complex, thus peptide tyrosine tyrosine (PYY), brain-derived neurotrophic factor (BDNF), orexin-A (OXA), and amylin also maintain ties to leptin, however these are less well understood. While reviews to date have focused on the existing relationships between leptin and the various neuropeptide modulators of appetite within the central nervous system (CNS) or it's role in thermogenesis, no review paper has synthesised the information regarding the interactions between appetite-regulating hormones and how leptin as a chronic regulator of energy balance can influence the acute appetite-regulatory response. Current evidence suggests that potential relationships exist between leptin and the circulating peripheral appetite hormones ghrelin, GLP-1, CCK, OXA and amylin to exhibit either synergistic or opposing effects on appetite inhibition. Though more research is warranted, leptin appears to be integral in both energy intake and energy expenditure. More specifically, functional leptin receptors appear to play an essential role in these processes.

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.

Intense interval exercise induces lactate accumulation and a greater suppression of acylated ghrelin compared with submaximal exercise in middle-aged adults.

Exercise in young adults (18-25 yr) suppresses appetite in a dose-response relationship with exercise intensity. Although several mechanisms have been proposed to explain this response, lactate is the most well established. To date, no study has investigated this specifically in middle-aged adults where the appetite response to a meal is different. To explore the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Nine participants (age: 45 ± 10 yr) completed four experimental sessions: 1) no-exercise control (CTRL); 2) moderate-intensity continuous training [MICT; 30 min, 65% maximal oxygen consumption (V̇o2max)]; 3) high-intensity interval training (HIIT; 10 × 1 min efforts, 90% heart rate maximum, 1 min recovery); and 4) sprint interval training (SIT; 8 × 15 s "all-out" efforts, 2 min recovery). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), active peptide tyrosine tyrosine (PYY), lactate, and subjective appetite perceptions were measured pre-exercise, 0-, 30-, and 90-min postexercise. Energy intake was recorded the day before and day of each session. Acylated ghrelin was suppressed (P < 0.001, [Formula: see text] = 0.474) by HIIT (0-min and 30-min postexercise; P < 0.091, d > 1.84) and SIT (0-min, 30-min, and 90-min postexercise; P < 0.037, d > 1.72) compared with CTRL, and SIT suppressed concentrations compared with MICT (0-min and 30-min postexercise; P < 0.91, d > 1.19). There were no effects of exercise on active PYY, active GLP-1, appetite perceptions, or free-living energy intake (P > 0.126, [Formula: see text] < 0.200). Intense interval exercise that generates lactate accumulation suppresses acylated ghrelin with little effect on anorexigenic hormones, overall appetite, or free-living energy intake.NEW & NOTEWORTHY We explored the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Our data support the intensity-dependent effect of exercise on acylated ghrelin suppression that is closely related to lactate accumulation, though there appears to be little effect on anorexigenic hormones [active peptide tyrosine tyrosine (PYY), active glucagon-like peptide-1 (GLP-1)], overall appetite, or free-living energy intake. These data support previous results in younger adults where lactate was implicated in the exercise-induced suppression of acylated ghrelin.

Classroom Activity Breaks Improve On-Task Behavior and Physical Activity Levels Regardless of Time of Day.

Classroom physical activity breaks (CAB) are beneficial for increasing children's physical activity (PA) levels as well as the amount of time spent being on-task within the classroom. Purpose: To examine the effect of CAB at different times within the school day on on-task behavior and PA levels in primary school (grade 1-3) children. Methods: Thirty-five children (6 ± 1 y, 22 = male, 13 = female) participated in four conditions in a randomized order: morning (AM), afternoon (PM), morning and afternoon (BOTH), and no CAB (CTRL). CAB followed a traditional Tabata format of 20 s work and 10 s rest repeated 8 times for a total of 4 min. PA levels were monitored (accelerometry). On-task behavior and three types of off-task (motor, verbal, passive) were recorded following each CAB (mobile application). Results: When compared to control, AM, PM, and BOTH increased on-task behavior AM: Δ10.4%, PM: Δ10.5%, BOTH: Δ14%; p < .001). AM was most beneficial for reducing off-task motor (Δ-6.5%) and off-task verbal (Δ-3%) behavior, while PM was most beneficial for reducing off-task passive (Δ-9%) behavior. These effects were greatest in those students demonstrating higher amounts off-task behavior during CTRL (r > 0.67, p < .001). Students achieved an additional 8.4 (p = .070; d = 0.93), 12.2 (p < .001, d = 0.49), and 6.3 min (p = .09, d = 0.47) of moderate-vigorous physical activity (MVPA) over 24 h following a CAB vs CTRL in AM, PM, and BOTH, respectively. Additionally, performing any of the CAB conditions increased the number of steps taken during the school day by an average of 2007 steps (p < .009). Conclusion: Overall, these results demonstrate that CAB improve both on-task behavior and PA levels, regardless of time of day. However, performing two CAB (BOTH) is recommended to derive the greatest improvements in on-task behavior across the school day.

The exercise-induced suppression of acylated ghrelin is blunted in the luteal phase of the menstrual cycle compared to the follicular phase following vigorous-intensity exercise.

Limited work examining woman's appetite-regulatory response to exercise has been focused on the follicular phase (FP) of the menstrual cycle. This is an important limitation as estradiol (E2) and progesterone (P4) fluctuate across phases with greater concentrations in the luteal phase (LP). OBJECTIVE: To examine the appetite-regulatory response to vigorous-intensity continuous exercise (VICT) in the FP and LP. METHODS: Twelve women completed 30 min of VICT at 80% V˙O2max in the FP and LP. E2, P4, acylated ghrelin, active peptide tyrosine-tyrosine (PYY), active glucagon-like peptide-1 (GLP-1), and appetite perceptions were measured pre-exercise, 0-, 30-, and 90-min post-exercise. Energy intake was recorded for a 2-day period (day before and of each session). A series of two-way repeated measure ANOVA were used to compare all dependent variables. RESULTS: Pre-exercise E2 (P = 0.005, d = 1.00) and P4 (P < 0.001, d = 1.41) concentrations were greater in the LP than the FP and exercise increased both at 0- and 30-min post-exercise (E2: P < 0.009; P4: P < 0.001, d = 0.63). Acylated ghrelin was lower in the FP versus LP at pre-exercise as well as 0-min (P = 0.006, d = 0.97) and 90-min (P = 0.029, d = 0.72) post-exercise. There were no differences of menstrual phase on PYY (P = 0.359, ηp2 = 0.092), GLP-1 (P = 0.226, ηp2 = 0.130), or overall appetite (P = 0.514, ηp2 = 0.066). Energy intake was greater on the day of in the LP versus the FP (P = 0.003, d = 1.2). CONCLUSION: Acylated ghrelin was lower in the FP compared to the LP and though there were no differences in anorexigenic hormones or subjective appetite, energy intake was greater on the day of the session in the LP suggesting important differences across the menstrual cycle where greater concentrations of ovarian hormones in the LP may blunt the exercise response.

Similar Postexercise Hypotension After MICT, HIIT, and SIT Exercises in Middle-Age Adults.

INTRODUCTION: Acute bouts of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) transiently lower systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the hours after termed postexercise hypotension (PEH); however, the effects of sprint interval training (SIT) exercise have yet to be explored in middle-age adults. Although previous work has found no effect of exercise intensity on PEH, no study has compared submaximal, near maximal, and supramaximal intensities, specifically in middle-age adults where blood pressure (BP) management strategies may be of greater importance. PURPOSE: This study examined the effects of MICT, HIIT, and SIT exercises on PEH in the immediate (≤2 h) and 24 h after exercise specifically in middle-age adults. METHODS: Fourteen participants (10 female; age, 46 ± 9 yr; SBP, 116 ± 11 mm Hg; DBP, 67 ± 6 mm Hg; one hypertensive, four prehypertensive, nine normotensive) had their BP measured before, immediately (15, 30, 60, 120 min), and over 24 h after four experimental sessions: 1) 30-min MICT exercise (65% maximal oxygen consumption), 2) 20-min HIIT exercise (10 × 1 min at 90% maximum heart rate with 1-min rest), 3) 16-min SIT exercise (8 × 15 s all-out sprints with 2-min rest), and 4) no-exercise control. Postexercise BP was compared with no-exercise control. RESULTS: PEH was similar for all exercise sessions for SBP ( P = 0.388, = 0.075) and DBP ( P = 0.206, = 0.108). Twenty-four-hour average SBP was similar for all sessions P = 0.453, = 0.069), and DBP was similar over 24 h except after MICT exercise compared with HIIT exercise ( P = 0.018, d = 1.04). CONCLUSIONS: In middle-age adults, MICT, HIIT, and SIT exercises are effective at reducing SBP; however, the effects on DBP are smaller, and neither reductions are sustained over 24 h.

Menstrual Cycle Related Fluctuations in Circulating Markers of Bone Metabolism at Rest and in Response to Running in Eumenorrheic Females.

This study examined potential fluctuations in bone metabolic markers across the menstrual cycle both at rest and after a 30-min bout of continuous running at 80% of V̇O2max. Resting and post-exercise (0, 30, 90 min) sclerostin, parathyroid hormone (PTH), carboxy-terminal cross-linking telopeptide of type I collagen (ß-CTXI), and procollagen type 1 N propeptide (PINP) were assessed in 10 eumenorrheic women (age: 21 ± 3 y, BMI: 23.2 ± 3.0 kg.m2) during the mid- to late-follicular (FP: day 8.0 ± 1.4) and mid-luteal (LP: day 22.0 ± 2.5) phases of the menstrual cycle. Ovulation was determined using ovulation kits and daily measurement of oral body temperature upon awakening. Menstrual cycle phase was subsequently confirmed by measurement of plasma estradiol and progesterone. On average, resting estradiol concentrations increased from 46.3 ± 8.9 pg·mL-1 in the FP to 67.3 ± 23.4 pg·mL-1 in the LP (p = 0.015), and resting progesterone increased from 4.12 ± 2.36 ng·mL-1 in the FP to 11.86 ± 4.49 ng·mL-1 in the LP (p < 0.001). At rest, there were no differences between menstrual cycle phases in sclerostin (FP: 260.1 ± 135.0 pg·mL-1; LP: 303.5 ± 99.9 pg·mL-1; p = 0.765), PTH (FP: 0.96 ± 0.64 pmol·L-1; LP: 0.79 ± 0.44 pmol·L-1; p = 0.568), ß-CTXI (FP: 243.1 ± 158.0 ng·L-1; LP: 202.4 ± 92.3 ng·L-1; p = 0.198), and PINP (FP: 53.6 ± 8.9 µg·L-1; LP: 66.2 ± 20.2 µg·L-1; p = 0.093). Main effects for time (p < 0.05) were shown in sclerostin, PTH, ß-CTXI and PINP, without phase or interaction effects. Sclerostin increased from pre- to immediately post-exercise (45%; p = 0.007), and so did PTH (43%; p = 0.011), both returning to resting concentrations 30 min post-exercise. ß-CTXI decreased from pre- to post-exercise (20%; p = 0.027) and was still below its pre-exercise concentrations at 90 min post-exercise (17%; p = 0.013). PINP increased immediately post-exercise (29%; p < 0.001), returning to resting concentrations at 30 min post-exercise. These results demonstrate no effect of menstrual cycle phase on resting bone marker concentrations or on the bone metabolic marker response to intense exercise.

Is a verification phase needed to determine [Formula: see text]O2max across fitness levels?

INTRODUCTION: Current methods (plateau/secondary criteria) to determine maximal oxygen consumption ([Formula: see text]O2max) are inconsistently achieved leading some to suggest the use of a verification phase (VP) to confirm [Formula: see text]O2max. PURPOSE: To provide further evidence for the inclusion of a VP to confirm [Formula: see text]O2max in different fitness levels. METHODS: Forty-nine participants (22 females; 21.9 ± 2.6 years, 24.3 ± 2.8 kg m-2, 45.27 ± 7.68 mL kg-1 min-1) had their [Formula: see text]O2 and heart rate measured during three graded exercise tests (GXT) on separate days each followed by a VP of differing intensity (85%, 95%, 105% final workload). Participants were divided into groups using norms adapted from American College of Sports Medicine [Formula: see text]O2max guidelines (30.47-61.47 mL kg-1 min-1). [Formula: see text]O2max was confirmed if the [Formula: see text]O2peak on the VP or an additional GXT was within ± 2 × typical error of the [Formula: see text]O2peak attained on the first GXT. There was no effect of test number so the third GXT was not included in comparison with VP. RESULTS: The [Formula: see text]O2peak from the first GXT was not different than either value attained following the VP at 95 or 105% workload or a second GXT (p > 0.999). The 85% VP [Formula: see text]O2peak was lower than the first GXT [Formula: see text]O2peak (p = 0.002). The VP confirmed the GXT [Formula: see text]O2peak on 73% of VP (no differences among fitness levels). Submaximal VP (85 and 95%) was less effective as 65% and 51% of participants achieved a higher [Formula: see text]O2peak on one of the GXT. CONCLUSION: The use of a VP at 105% or a second GXT was able to confirm the [Formula: see text]O2max value attained across a range of fitness levels.

Individual patterns of response to traditional and modified sprint interval training.

We compared the incidence of response between a traditional sprint interval training (SIT) protocol (30:240: 4-6 x 30-s, 240-s recovery) and 2 modified SIT protocols (15:120: 8-12 x 15-s, 120-s recovery; 5:40: 24-36 x 5-s, 40-s recovery) over 4 weeks of training in 84 recreationally active individuals (n = 23 per SIT group/15 control participants). Pre- and post-testing measures included V. O2max, 5-km time trial, and anaerobic capacity. Responders were classified using 2x typical error and seven other approaches to explore the impact of classification method on response rates. There was no difference in the proportion (2x typical error) of V.O2max responders across groups (30:240: 64%; 15:120: 39%; 5:40: 41%; CTRL: 33%; P= 0.190). The 30:240 group had more responders (P< 0.05) for time trial performance (70%) and peak speed during the 30 s running test (48%) compared to CTRL (21% and 0%, respectively). There were no other between-group differences (P> 0.112). Approaches with the largest response thresholds resulted in the fewest responders highlighting response rates are influenced by the method used. Additionally, we observed intra-individual differences in responsiveness across outcomes. This is the first study to empirically test the difference in the incidence of response and demonstrate individual patterns of response across different SIT protocols.

The emerging role of lactate as a mediator of exercise-induced appetite suppression.

Lactate, a molecule originally considered metabolic waste, is now associated with a number of important physiological functions. Although the roles of lactate as a signaling molecule, fuel source, and gluconeogenic substrate have garnered significant attention in recent reviews, a relatively underexplored and emerging role of lactate is its control of energy intake (EI). To expand our understanding of the physiological roles of lactate, we present evidence from early infusion studies demonstrating the ability of lactate to suppress EI in both rodents and humans. We then discuss findings from recent human studies that have utilized exercise intensity and/or sodium bicarbonate supplementation to modulate endogenous lactate and examine its impact on appetite regulation. These studies consistently demonstrate that greater blood lactate accumulation is associated with greater suppression of the hunger hormone ghrelin and subjective appetite, thereby supporting a role of lactate in the control of EI. To stimulate future research investigating the role of lactate as an appetite-regulatory molecule, we also highlight potential underlying mechanisms explaining the appetite-suppressive effects of lactate using evidence from rodent and in vitro cellular models. Specifically, we discuss the ability of lactate to 1) inhibit the secretory function of ghrelin producing gastric cells, 2) modulate the signaling cascades that control hypothalamic neuropeptide expression/release, and 3) inhibit signaling through the ghrelin receptor in the hypothalamus. Unravelling the role of lactate as an appetite-regulatory molecule can shed important insight into the regulation of EI, thereby contributing to the development of interventions aimed at combatting overweight and obesity.