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Scientific Programme

Physiology & Nutrition

CP-PN13 - Endocrine regulation

Date: 09.07.2026, Time: 18:30 - 19:30, Session Room: SG 0213 (EPFL)

Description

Chair TBA

Chair

TBA
TBA
TBA

ECSS Paris 2023: CP-PN13

Speaker A Marco Lista

Speaker A

Marco Lista
eCampus University, Department of Theoretical and Applied Sciences
Italy
"How physical exercise modulate the release of Kisspeptin"

INTRODUCTION: Kisspeptin is a neuropeptide that plays an important role in the regulation of the hypothalamic–pituitary–gonadal (HPG) axis. Kisspeptin hypothalamic expression stimulates Gonadotropin Releasing Hormone (GnRH) production and modulates the pulsatile secretion of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). LH and FSH regulate reproductive function in males and females. In males, LH stimulates testosterone production. In females, LH stimulates ovarian androgen secretion. In endurance sport, athletes show a lot of reproductive dysfunctions. In men, hypogonadotropic hypogonadism and lower testosterone levels are observed; in women, hypothalamic amenorrhea is observed. These dysfunctions have been associated with altered GnRH pulsatility, potentially linked to altered kisspeptin activity. Literature evidence suggests an inverse relationship between chronic endurance training and hypothalamic kisspeptin expression. Training load and energy availability can influence kisspeptin regulation. The aim of this pilot study was to evaluate the acute effect of maximal aerobic exercise on serum kisspeptin concentrations in well trained males. METHODS: Six healthy, well trained male university students were recruited to perform a maximal incremental test on cycle ergometer. (60 rpm, every 3 minutes, until exhaustion, workload increased by 30 Watts) blood samples were collected at baseline before the exercise (Pre), immediately post exercise (Post), and at 15 and 30 minutes post exercise. Serum kisspeptin concentration were measured and changes from baseline (Pre) were calculated. RESULTS: Kisspeptin increased immediately post exercise (changes Post – Pre: +1.3). At 15 minutes post exercise values remained slightly above baseline (changes Post 15 – Pre: +0.4) At 30 minutes post exercise concentration returned to pre-exercise baseline (changes Post 30 – Pre: -0.2). CONCLUSION: Maximal aerobic exercise stimulates an acute increase in circulating kisspeptin in well trained male university students. Although limited by the small sample size, these findings indicate that kisspeptin is responsive to high intensity exercise. Further research is needed to clarify the influence of exercise modality, training load, intensity and energy availability on kisspeptin regulation and its potential role in related with chronic hormonal regulation and reproductive dysfunction.

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ECSS Paris 2023: CP-PN13

Speaker B Xhuljano Vukaj

Speaker B

Xhuljano Vukaj
Catholic University of the Sacred Heart of Milan, Laboratory of Cellular Biochemistry and Molecular Biology, CRIBENS, Department of Psychology, Università Cattolica Del Sacro Cuore, Milan, Italy
Italy
"NEUROMUSCULAR ELECTRICAL STIMULATION CYCLING EXERCISE SIGNIFICANTLY INCREASES PLASMATIC ADIPONECTIN RELEASE"

INTRODUCTION: Exercise is a key factor for health and prevention of metabolic disorders (1), partially mediated by the secretion of exerkines such as adiponectin. This hormone displays key anti-hyperglycemic, anti-atherogenic, and anti-inflammatory properties (2). Neuromuscular electrical stimulation (NMES) has been shown to amplify an acute metabolic and hormonal response by increasing motor unit recruitment (3). Although the effects of NMES during cycling have been studied, its specific impact on adiponectin levels remains unexplored. Therefore, this study aimed to investigate the acute and chronic effects of cycling with and without synchronous superimposed NMES on plasma adiponectin expression levels. METHODS: Sixteen active male participants (age 39 ±10 years, V̇O2peak 47.9 ±4.6 mL·kg-1·min-1) were randomly assigned to the control (CTRL) or the electrically stimulated (EXP) group. Both groups performed a 4x5min interval at 60% peak power output (PPO), interspersed with 3min recovery at 40% PPO (14 training sessions over 6 weeks). Adaptive Functional Electrical Stimulation Kinesitherapy (AFESK), delivered through the VIK8 device, was adopted to trigger NMES in synchrony with voluntary contraction of the lower limb muscles during all the training sessions for the EXP group. Plasma adiponectin, analysed by ELISA assay, was evaluated at baseline, 15min, 24h, and 48h after the first (S1) and last (S14) training sessions. Friedman and Mann-Whitney tests were used for statistical analyses. RESULTS: After the S1, a slight increase in plasma adiponectin was detected in both the CRTL (+8.6%) and EXP groups (+9.6%). At S14, both groups showed a significant rise in adiponectin levels at 15min, and 24h post-exercise, returning to basal levels after 48h. However, within-group analysis showed that the EXP group exhibited a greater increase from baseline (+15.6% and +15.0%; p<0.005) in comparison to the CTRL group (+8.8% and +8.4%; p<0.005). Moreover, after 13 training sessions, the analysis between-groups revealed that EXP displayed significantly higher adiponectin levels than CTRL at baseline (p<0.05), as well as after 15min (p<0.005), and 24h (p<0.005). CONCLUSION: While both protocols induced acute adiponectin release, the EXP group exhibited higher chronic effects at basal levels and a greater transient response. Such data suggest that the synchronous recruitment of additional motor units via AFESK may potentiate the adipose tissue response by increasing adiponectin secretion, offering superior metabolic health outcomes than cycling alone.

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ECSS Paris 2023: CP-PN13

Speaker C Teruo Miyazaki

Speaker C

Teruo Miyazaki
Tokyo Medical University, Ibaraki Medical Center
Japan
"Myokine-like Effects of the Valine Intermediate 3-Hydroxyisobutyric Acid on Hepatic Gluconeogenesis via the Sympathetic Nervous System"

INTRODUCTION: During prolonged endurance exercise, branched-chain amino acids (BCAAs)—valine, leucine, and isoleucine—are catabolized in skeletal muscle as alternative energy substrates to compensate for reduced glucose supply. 3-hydroxyisobutyric acid (3HIB), a mitochondrial intermediate of valine catabolism, is released from muscle into the systemic circulation. We previously demonstrated that intraperitoneal administration of 3HIB rapidly and transiently elevates blood glucose levels in rats. In this study, we investigated the mechanisms by which 3HIB influences blood glucose levels, focusing on sympathetic nerve activity and hepatic gluconeogenesis. METHODS: Ten-week-old male ICR mice were intraperitoneally injected with 3HIB (60 mg/kg body weight) alone or in combination with the α-adrenergic blocker prazosin (5 mg/kg body weight). Hepatocyte cell lines (HepG2 and AML12) were incubated with gluconeogenic precursors (10 mM 3HIB, 1 mM lactate, 10 mM alanine, and 10 mM glutamate) and/or noradrenaline (NE) for 18 h. Ligand activities of 3HIB toward G-protein–coupled free fatty acid receptors (GPR41 and GPR43) and the γ-aminobutyric acid type B receptor (GABABR) were assessed using GPCR ligand-binding assays. RESULTS: In mice injected with 3HIB, blood glucose and NE levels were significantly increased 15 min after injection compared with baseline and returned to basal levels by 60 min. These effects were abolished by prazosin administration. Correspondingly, hepatic concentrations of glucose, fumarate, and malate, as well as mRNA expression of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, were significantly elevated at 15 min. In cultured hepatocytes, glucose production was robustly stimulated by lactate, whereas 3HIB and other amino acid precursors induced only weak glucose production, even in the presence of NE. 3HIB exhibited agonistic activity toward GPR41 at concentrations as low as approximately 70 μM and toward GPR43 at approximately 600 μM, but showed no activity toward GABA𝐵R. CONCLUSION: These findings suggest that the blood glucose–elevating effect of 3HIB is mediated by activation of hepatic gluconeogenesis through stimulation of the sympathetic nervous system, likely via its agonistic action on GPR41. In contrast, 3HIB itself does not appear to be an efficient substrate for gluconeogenesis. During extreme endurance exercise, 3HIB may function as a myokine-like signaling molecule that rapidly enhances hepatic glucose output to meet the metabolic demands of skeletal muscle.

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ECSS Paris 2023: CP-PN13