Greater lactate accumulation does not alter peripheral concentrations of key appetite-regulating neuropeptides.

The potential mechanisms involved in lactate's role in exercise-induced appetite suppression requires further examination. We used sodium bicarbonate (NaHCO3) supplementation in a double-blind, placebo controlled, randomized crossover design to explore lactate's role on neuropeptide Y (NPY), agouti-related peptide (AgRP), and alpha-melanocyte stimulating hormone (α-MSH) concentrations. Twelve adults (7 males; 24.2±3.4 kg‧m-2; 42.18±8.56 mL‧kg-1‧min-1) completed two identical high-intensity interval training sessions following ingestion of NaHCO3 (BICARB) or sodium chloride (PLACEBO) pre-exercise. Blood lactate, acylated ghrelin, NPY, AgRP, α-MSH, and appetite perceptions were measured pre-exercise, 0-, 30-, 60-, and 90-min post-exercise. Free-living energy intake (electronic food diaries) was measured the day before, of, and after each experimental session. In BICARB, blood lactate was greater post-exercise (p<0.002, d>0.70) though acylated ghrelin was similar (p=0.075, =0.206) at all time-points post-exercise (p>0.034, d<0.22). NPY (p=0.006, >0.509) and AgRP (p<0.001, >0.488) had main effects of time increasing following exercise and returning to baseline, with no differences between sessions (NPY: p=0.0.192, =0.149; AgRP: p=0.422, =0.060). α-MSH had no main effect of time (p=0.573, =0.063) or session (p=0.269, =0.110). Appetite perceptions were similar during BICARB and PLACEBO (p=0.007, d=0.28) increasing in both sessions post-exercise (p<0.088, d>0.57). Energy intake had a main effect of day (p=0.025, =0.825), where the experimental session day was greater than the day before (p=0.010, d=0.59) with no other differences between days (p>0.260, d<0.38). The lower accumulation of lactate than our previous work did not generate exercise-induced appetite suppression as there were no differences in acylated ghrelin, appetite perceptions, or peripheral concentrations of neuropeptides.

Physiologically relevant lactate accumulation from exercise or peripheral injection does not alter central or peripheral appetite signaling in mice.

Lactate has been implicated in exercise-induced appetite suppression though little work has explored the mechanisms underpinning its role. Recent work suggests lactate accumulation via exercise and intracerebroventricular injection can alter central appetite regulating pathways, though a supraphysiological dose of lactate was administered centrally and there was no assessment of peripheral appetite markers. Therefore, we examined how physiologically relevant lactate accumulation via exercise or intraperitoneal injection altered central and peripheral appetite signaling pathways and whether the lactate dehydrogenase inhibitor oxamate could blunt any exercise effect. Forty 10-week-old C57BL/6 J male mice (n = 10/group) were assigned to either: 1) sedentary (SED + SAL; saline); 2) exercise (EX+SAL; saline); 3) exercise with oxamate (EX+OX; 750 mg‧kg-1 body mass); or 4) lactate (SED + LAC; 1.0 g‧kg-1 body mass). Blood, stomach, and hypothalamus samples were collected ∼2 h post-exercise/injection. Though oxamate blunted exercise-induced lactate accumulation compared to the EX+SAL condition (P = 0.044, d = 0.73), there were no differences in circulating acylated ghrelin or stomach ghrelin O-acyltransferase content between groups (P > 0.213, ηp2<0.125). There were also no differences in hypothalamic content for neuropeptide Y, proopiomelanocortin, agouti-related peptide, and alpha melanocyte-stimulating hormone (P > 0.150, ηp2<0.170). Exercise did increase phosphorylated-total signal transducer and activator of transcription 3 (pSTAT3) compared to EX+OX (p = 0.065, d = 1.23) but there were no differences in other markers of lactate signaling: phosphorylated-total adenosine monophosphate activated protein kinase, and protein kinase b (P > 0.121, ηp2<0.160). Our results suggest that lactate accumulation due to exercise or peripheral injection does not alter central or peripheral appetite signaling when measured 2 h post-exercise/injection, though pSTAT3 was blunted with oxamate.

Lactate increases ADAM10 activity and reduces BACE1 activity in mouse brain.

The accumulation and aggregation of beta-amyloid (Aß) peptides contributes to neuronal dysfunction and death. These Aß peptides originate from a transmembrane protein known as amyloid precursor protein (APP), which can be processed via two competing pathways. Alpha-secretase (ADAM10) cleavage is thought to be neuroprotective while beta-secretase (BACE1) cleavage results in the production of Aß. Aerobic exercise reduces BACE1 activity, but the mechanisms involved are unknown though several exercise-induced mediators such as lactate may be involved. The current study examined whether systemic lactate can alter APP processing and BACE1 and ADAM10 activity. Mice were randomly assigned to one of four groups (n = 10 per group): (1) sedentary; (2) lactate-injection (1.0 g kg-1 body mass); (3) exercise; and (4) exercise and oxamate (lactate dehydrogenase inhibitor; 750 mg kg-1 body mass). Two hours following intervention, the hippocampus and prefrontal cortex (PFC) were collected. In the PFC lactate-injection and exercise resulted in higher ADAM10 activity compared to sedentary (exercise P = 0.0215, lactate P = 0.0038), in the hippocampus lactate-injection was higher compared to sedentary (lactate P = 0.011), and this was absent in the presence of oxamate. Hippocampal BACE1 activity was lower in the lactate group compared to the exercise group (P = 0.01). Oxamate resulted in higher BACE1 protein content compared to sedentary in the PFC (vs. sedentary P = 0.048). These findings suggest that lactate is important for regulating ADAM10 activity and thereby shifts APP processing away from Aß production. KEY POINTS: Exercise is known to alter the processing of amyloid precursor protein by reducing the activity of the rate-limiting enzyme BACE1 and increasing the activity of ADAM10. It is thought that exercise-induced factors are responsible for these enzymatic changes. This study examined if lactate accumulation plays a role in this process. Mice were assigned to one of four groups: sedentary, lactate, exercise and exercise + lactate. The findings demonstrate that lactate accumulation alters brain BACE1 and ADAM10 and shifts amyloid precursor protein processing away from beta-amyloid production.

Oral sodium lactate ingestion does not increase blood lactate concentrations and is accompanied by moderate to severe gastrointestinal side effects.

Lactate has diverse roles in biology and has been implicated in the control of energy intake. A variety of methods (i.e., exercise, ingestion, infusion) have been used to study its effects on different metabolic outcomes and the original intent of this project was to explore the effect of oral sodium lactate (Na-Lactate) ingestion on appetite regulation. During piloting we were unable to show that Na-Lactate could increase blood lactate concentrations, thus the purpose of the brief manuscript is to highlight that oral Na-Lactate ingestion is not an effective method to study lactate metabolism. Five male participants (26 ± 3 y, 82.4 ± 3.8 kg, 25.4 ± 1.6 kg∙m-2) completed 15 experimental sessions where Na-Lactate solutions were consumed with assessment of blood lactate pre-ingestion, 30 min, 45 min, and 60 min post-ingestion. Oral Na-Lactate ingestion did not increase blood lactate concentrations (Pre: 0.9±0.2; 30 min: 1.2±0.7; 45 min: 1.0±0.5; 60 min: 0.9±0.4 mmol∙L-1). Additionally, there were moderate-severe gastrointestinal (GI) side effects (e.g., vomiting, diarrhea) following ingestion. Taken together our data suggest that oral ingestion of Na-Lactate is not an effective method to study lactate's role on metabolism as it did not increase blood lactate concentrations and was accompanied by problematic GI side effects.

The effects of acute aerobic exercise on appetite-regulating parameters and energy intake in males with obesity.

Objective: To investigate the effects of moderate-intensity aerobic exercise on appetite control parameters, appetite perceptions, and energy intake in sedentary males with obesity. Design: Eleven males with obesity (body fat percentage 36.5 ± 2.5%, body mass index 35.3 ± 4.2 kg/m2, V̇O2peak 29 ± 3.1 mL·kg-1·min-1) completed two experimental sessions: (1) no exercise (CTRL) and (2) 60 min of moderate-intensity cycling exercise at 60% V̇O2peak (MICT) in a crossover design. Blood analysis included growth differentiation factor 15 (GDF-15), total ghrelin, peptide tyrosine tyrosine3-36 (PYY3-36), total glucagon-like peptide-1 (GLP-1), insulin, and glucose, as well as subjective appetite perceptions were measured in specific intervals. A standard breakfast at 0 h and an ad libitum meal postexercise was provided. Result: GDF-15 (95% confidence interval [CI]: [2.48-27.28] ng/L, p = 0.021) increased immediately following MICT compared to CTRL. However, there were no differences for PYY3-36 (p = 0.480, η p 2 = 0.025 ), total ghrelin (p = 0.646, η p 2 = 0.011 ), and total GLP-1 (p = 0.451, η p 2 = 0.029 ) between sessions. Appetite perceptions (95% CI: [(-20.38)-(-6.16)] mm, p = 0.001) were suppressed following MICT though energy intake was not different between the sessions (95% CI: [(-1904.9)-928.1] kJ, p = 0.480). Conclusion: Sixty minutes of MICT increased GDF-15 while suppressing appetite perceptions in individuals with obesity. There was no energy compensation postexercise.

Exercise-induced appetite suppression: An update on potential mechanisms.

The first systematic reviews of the effects of exercise on appetite-regulation and energy intake demonstrated changes in appetite-regulating hormones consistent with appetite suppression and decreases in subsequent relative energy intake over a decade ago. More recently, an intensity-dependent effect and several potential mechanisms were proposed, and this review aims to highlight advances in this field. While exercise-induced appetite suppression clearly involves acylated ghrelin, glucagon-like peptide-1 may also be involved, though recent evidence suggests peptide tyrosine tyrosine may not be relevant. Changes in subjective appetite perceptions and energy intake continue to be equivocal, though these results are likely due to small sample sizes and methodological inconsistencies. Of the proposed mechanisms responsible for exercise-induced appetite suppression, lactate has garnered the most support through in vitro and in vivo rodent studies as well as a growing amount of work in humans. Other potential modulators of exercise-induced appetite suppression may include sex hormones, growth-differentiation factor 15, Lac-Phe, brain-derived neurotrophic factor, and asprosin. Research should focus on the mechanisms responsible for the changes and consider these other modulators (i.e., myokines/exerkines) of appetite to improve our understanding of the role of exercise on appetite regulation.

The Effect of the Menstrual Cycle on Energy Intake: A Systematic Review and Meta-analysis.

CONTEXT: Energy intake may differ across the menstrual cycle, with some studies identifying greater energy intake in the luteal phase (LP) compared with the follicular phase (FP) and others finding no clear differences. To date, no study has systematically synthesized the available data to draw more definite conclusions while considering any methodological inconsistencies between studies. OBJECTIVE: The aim was to conduct a systematic review/meta-analysis in an effort to determine if there are differences in energy intake between the FP and LP. DATA SOURCES: A systematic search strategy was developed and the search was conducted in 5 databases for studies that investigated any changes in energy intake across menstrual phases. DATA EXTRACTION: Using Covidence, studies were identified and included if they contained individuals between the ages of 18 and 45 years, maintained an average body mass index (BMI) of 18.5-25 kg/m2, had no history of disordered eating, and included energy intake and menstrual cycle measurements in the FP and LP. DATA ANALYSIS: Effect sizes were calculated for each study and a random-effects model was used to pool the results of each study. RESULTS: Fifteen datasets were included consisting of 330 female participants with a mean age of 26 ± 4 years and mean BMI of 22.4 ± 2.3 kg/m2. Overall, there was a statistically significant difference (standardized mean difference = 0.69; P = .039) with increased energy intake in the LP compared with the FP (crude 168 kcal⋅d-1 average difference between phases). CONCLUSION: Energy intake was found to be greater in the LP compared with the FP, providing insight into the effect of the menstrual cycle on energy intake. However, there were repeated methodological inconsistencies and future work should strive to utilize best practices for both energy intake measurement and menstrual phase specification.

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 38(8): 1386-1393, 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 (V̇ o2 ) 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. V̇ o2 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 O 2 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.

Maternal and Fetal Cardiovascular Responses to Acute High-Intensity Interval and Moderate-Intensity Continuous Training Exercise During Pregnancy: A Randomized Crossover Trial.

OBJECTIVE: We aimed to compare maternal and fetal cardiovascular responses to an acute bout of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) during pregnancy. METHODS: Fifteen women with a singleton pregnancy (27.3 ± 3.5 weeks of gestation, 33 ± 4 years of age) were recruited. Following a peak fitness test, participants engaged in a session of HIIT (10 × 1-min intervals ≥ 90% maximum heart rate [HRmax]) interspersed with 1 min of active recovery) and MICT (30 min at 64-76% HRmax) 48 h apart in random order. Maternal HR, blood pressure, middle (MCAv), and posterior cerebral artery blood velocity (PCAv), as well as respiratory measures were monitored continuously throughout HIIT/MICT. Fetal heart rate, as well as umbilical systolic/diastolic (S/D) ratio, resistive index (RI), and pulsatility index (PI) were assessed immediately before and after exercise. RESULTS: Average maternal heart rate was higher for HIIT (82 ± 5% HRmax) compared with MICT (74 ± 4% HRmax; p < 0.001). During the HIIT session, participants achieved a peak heart rate of 96 ± 5% HRmax (range of 87-105% HRmax). Maternal cerebral blood velocities increased with exercise but was not different between HIIT and MICT for MCAv (p = 0.340) and PCAv (p = 0.142). Fetal heart rate increased during exercise (p = 0.244) but was not different between sessions (HIIT: Δ + 14 ± 7 bpm; MICT: Δ + 10 ± 10 bpm). Metrics of umbilical blood flow decreased with exercise and were not different between exercise sessions (PI: p = 0.707; S/D ratio: p = 0.671; RI: p = 0.792). Fetal bradycardia was not observed, and S/D ratio, RI, and PI remained within normal ranges both before and immediately after all exercise sessions. CONCLUSIONS: An acute bout of HIIT exercise consisting of repeated 1-min near-maximal to maximal exertions, as well as MICT exercise is well tolerated by both mother and fetus. CLINICAL TRIAL REGISTRATION: NCT05369247.

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.

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.

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.