BACKGROUND

Heart rate variability (HRV) is a common tool for assessing autonomic nervous system activity and monitoring training load in athletes. However, limited research has explored how HRV responds to different forms of resistance training, particularly in high-intensity intermittent sports like basketball and football.

This study aims to compare the acute HRV responses between neuromuscular and metabolic training in collegiate athletes involved in high-intensity intermittent sports.

A comparative cross-sectional study with a quasi-experimental crossover design will be employed.

Collegiate athletes will be randomly assigned to undergo both neuromuscular and metabolic training sessions with a one-week wash-out period in between. HRV data will be recorded using the Polar H10 chest strap during each session.

Descriptive statistics will summarize salient participant characteristics and HRV measurements. Inferential analysis will use paired t-tests or Wilcoxon signed-rank tests based on normality, assessed via the Kolmogorov-Smirnov test. All statistical analyses will be conducted using the IBM SPSS (ver.25) with a confidence interval set. at 95% and a critical α equal to 0.05.

Neuromuscular training is expected to elicit higher low-frequency (LF) power and an increased LF/HF ratio, reflecting greater sympathetic activation, while metabolic training is expected to show lower LF power and a decreased LF/HF ratio, indicating a more balanced autonomic response. These findings will offer insights into the differential autonomic impacts of these training modalities.

The nucleus tractus solitarius (NTS) is the primary brain region for receiving and integrating cardiovascular afferent signals. It plays a crucial role in maintaining balance of autonomic nervous system and regulating blood pressure through cardiovascular reflexes. Neurons within the NTS form complex synaptic connections and interact reciprocally with other brain regions. The NTS regulates autonomic nervous system activity and arterial blood pressure through modulating baroreflex, sympathetic nerve activity, renin-angiotensin-aldosterone system, and oxidative stress. Dysfunctions in NTS activity may contribute to hypertension. Understanding the NTS' role in centrally regulating blood pressure and alterations of neurotransmission or signaling pathways in the NTS may provide rationale for new therapeutic strategies of prevention and treatment. This review summarizes the research findings on autonomic nervous system regulation and arterial blood pressure control by NTS, as well as unresolved questions, in order to provide reference for future investigation.
Solitary Nucleus/physiopathology* ; Hypertension/physiopathology* ; Humans ; Animals ; Autonomic Nervous System/physiopathology* ; Blood Pressure/physiology* ; Baroreflex/physiology* ; Renin-Angiotensin System/physiology* ; Sympathetic Nervous System/physiology*

Temporomandibular joint osteoarthritis (TMJ-OA) is a common disease often accompanied by pain, seriously affecting physical and mental health of patients. Abnormal innervation at the osteochondral junction has been considered as a predominant origin of arthralgia, while the specific mechanism mediating pain remains unclear. To investigate the underlying mechanism of TMJ-OA pain, an abnormal joint loading model was used to induce TMJ-OA pain. We found that during the development of TMJ-OA, the increased innervation of sympathetic nerve of subchondral bone precedes that of sensory nerves. Furthermore, these two types of nerves are spatially closely associated. Additionally, it was discovered that activation of sympathetic neural signals promotes osteoarthritic pain in mice, whereas blocking these signals effectively alleviates pain. In vitro experiments also confirmed that norepinephrine released by sympathetic neurons promotes the activation and axonal growth of sensory neurons. Moreover, we also discovered that through releasing norepinephrine, regional sympathetic nerves of subchondral bone were found to regulate growth and activation of local sensory nerves synergistically with other pain regulators. This study identified the role of regional sympathetic nerves in mediating pain in TMJ-OA. It sheds light on a new mechanism of abnormal innervation at the osteochondral junction and the regional crosstalk between peripheral nerves, providing a potential target for treating TMJ-OA pain.
Animals ; Osteoarthritis/physiopathology* ; Mice ; Sympathetic Nervous System/physiopathology* ; Temporomandibular Joint Disorders/physiopathology* ; Arthralgia ; Sensory Receptor Cells ; Disease Models, Animal ; Norepinephrine ; Male ; Temporomandibular Joint/physiopathology* ; Pain Measurement

It is well established that increased excitability of the presympathetic neurons in the hypothalamic paraventricular nucleus (PVN) during hypertension leads to heightened sympathetic outflow and hypertension. However, the mechanism underlying the overactivation of PVN presympathetic neurons remains unclear. This study aimed to investigate the role of endogenous corticotropin-releasing factor (CRF) on the excitability of presympathetic neurons in PVN using Western blot, arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA) recording, CRISPR/Cas9 technique and patch-clamp technique. The results showed that CRF protein expression in PVN was significantly upregulated in spontaneously hypertensive rats (SHRs) compared with normotensive Wistar-Kyoto (WKY) rats. Besides, PVN administration of exogenous CRF significantly increased RSNA, heart rate and ABP in WKY rats. In contrast, knockdown of upregulated CRF in PVN of SHRs inhibited CRF expression, led to membrane potential hyperpolarization, and decreased the frequency of current-evoked firings of PVN presympathetic neurons, which were reversed by incubation of exogenous CRF. Perfusion of rat brain slices with artificial cerebrospinal fluid containing CRF receptor 1 (CRFR1) blocker, NBI-35965, or CRF receptor 2 (CRFR2) blocker, Antisauvagine-30, showed that blocking CRFR1, but not CRFR2, hyperpolarized the membrane potential and inhibited the current-evoked firing of PVN presympathetic neurons in SHRs. However, blocking CRFR1 or CRFR2 did not affect the membrane potential and current-evoked firing of presympathetic neurons in WKY rats. Overall, these findings indicate that increased endogenous CRF release from PVN CRF neurons enhances the excitability of presympathetic neurons via activation of CRFR1 in SHRs.
Rats ; Animals ; Rats, Inbred SHR ; Paraventricular Hypothalamic Nucleus/physiology* ; Receptors, Corticotropin-Releasing Hormone/metabolism* ; Rats, Inbred WKY ; Corticotropin-Releasing Hormone/metabolism* ; Neurons/physiology* ; Hypertension ; Sympathetic Nervous System

Humans ; Lymphoma, T-Cell, Cutaneous/complications* ; Neuroglia ; Pruritus/pathology* ; Skin Neoplasms/complications* ; Spinal Cord/pathology* ; Sympathetic Nervous System

Myocardial ischemia (MI) causes somatic referred pain and sympathetic hyperactivity, and the role of sensory inputs from referred areas in cardiac function and sympathetic hyperactivity remain unclear. Here, in a rat model, we showed that MI not only led to referred mechanical hypersensitivity on the forelimbs and upper back, but also elicited sympathetic sprouting in the skin of the referred area and C8-T6 dorsal root ganglia, and increased cardiac sympathetic tone, indicating sympathetic-sensory coupling. Moreover, intensifying referred hyperalgesic inputs with noxious mechanical, thermal, and electro-stimulation (ES) of the forearm augmented sympathetic hyperactivity and regulated cardiac function, whereas deafferentation of the left brachial plexus diminished sympathoexcitation. Intradermal injection of the α₂ adrenoceptor (α₂AR) antagonist yohimbine and agonist dexmedetomidine in the forearm attenuated the cardiac adjustment by ES. Overall, these findings suggest that sensory inputs from the referred pain area contribute to cardiac functional adjustment via peripheral α₂AR-mediated sympathetic-sensory coupling.
Animals ; Ganglia, Spinal ; Hyperalgesia/etiology* ; Myocardial Ischemia/complications* ; Pain, Referred/complications* ; Rats ; Sympathetic Nervous System

Autonomic Pathways ; Humans ; Parasympathetic Nervous System ; Stomach Neoplasms ; Sympathetic Nervous System

High salt intake increases blood pressure, and dietary salt intake has been clearly demonstrated to be associated with hypertension incidence. Japanese people consume higher amounts of salt than Westerners. It has been reported that miso soup was one of the major sources of daily salt intake in Japanese people. Adding salt is indispensable to make miso, and therefore, in some cases, refraining from miso soup is recommended to reduce dietary salt intake. However, recent studies using salt-sensitive hypertensive models have revealed that miso lessens the effects of salt on blood pressure. In other word, the intake of miso dose not increase the blood pressure compared to the equivalent intake of salt. In addition, many clinical observational studies have demonstrated the absence of a relationship between the frequency of miso soup intake and blood pressure levels or hypertension incidence. The mechanism of this phenomenon seen in the subjects with miso soup intake has not been fully elucidated yet. However, in basic studies, it was found that the ingredients of miso attenuate sympathetic nerve activity, resulting in lowered blood pressure and heart rate. Therefore, this review focused on the differences between the effects of miso intake and those of the equivalent salt intake on sympathetic nerve activity, blood pressure, and heart rate.
Blood Pressure ; drug effects ; physiology ; Heart Rate ; drug effects ; physiology ; Humans ; Soy Foods ; adverse effects ; Sympathetic Nervous System ; drug effects ; physiology

Objective: To explore the effects of the mu-opioid receptor (MOR) in the paraventricular nucleus (PVN) on the ejaculatory behaviors of male rats and its potential mechanisms. METHODS: Male SD rats with normal ejaculation ability were mated with female ones in hormone-induced estrus. After bilateral PVN microinjection of D-Ala-2-Me-Phe-4-Gly-ol enkephalin (DAGO) or D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) with an inserted catheter, the male animals were observed for mount latency (ML), mount frequency (MF), intromission latency (IL), intromission frequency (IF), ejaculation latency (EL), ejaculation frequency (EF), post-ejaculation interval (PEI), and intromission ratio (IR). The lumbar sympathetic nerve activity (LSNA) of the rats was recorded using the PowerLab data acquisition hardware device, and the levels of norepinephrine (NE) in the peripheral plasma were measured by ELISA following microinjection of saline or different doses of DAGO or CTAP. RESULTS: Neither CTAP nor DGAO significantly affected the ML of the male rats (P > 0.05). DGAO remarkably increased IF (P < 0.01) and MF (P < 0.01), prolonged IL (P < 0.01), EL (P < 0.01) and PEI (P < 0.01), and reduced EF (P <0.01) and IR (P < 0.05). On the contrary, CTAP markedly decreased IF (P < 0.01) and MF (P < 0.01), shortened IL (P < 0.01), EL (P < 0.01) and PFI (P < 0.01), and elevated EF (P < 0.01) and IR (P < 0.01). Additionally, DAGO decreased LSNA in a dose-dependent manner and reduced the NE level in the peripheral plasma. CTAP, however, not only offset the effects of DAGO on LSNA, but also significantly increased LSNA. CONCLUSIONS MOR in PVN inhibits ejaculatory behaviors in male rats by weakening LSNA, which has provided some theoretical evidence for the use of highly selective opioids in the treatment of premature ejaculation.
Animals ; Ejaculation ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology* ; Female ; Male ; Paraventricular Hypothalamic Nucleus/physiology* ; Peptide Fragments/pharmacology* ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, mu/physiology* ; Somatostatin/pharmacology* ; Sympathetic Nervous System/physiology*

The nineteenth century neuroscience studied the instinct of animal to understand the human mind. In particular, it has been found that the inheritance of unconscious behavior like instinct is mediated through ganglion chains, such as the spinal cord or sympathetic nervous system, which control unconscious reflexes. At the same time, the theory of Inheritance of Acquired Characteristics (hereafter ‘IAC’) widely known as Lamarck's evolutionary theory provided the theoretical frame on the origin of instinct and the heredity of action that the parental generation's habits were converted into the nature of the offspring generation. Contrary to conventional knowledge, this theory was not originally invented by Lamarck, and Darwin also did not discard this theory even after discovering the theory of natural selection in 1838 and maintained it throughout his intellectual life. Above all, in the field of epigenetics, the theory of ‘IAC’ has gained attention as a reliable scientific theory today. Darwin discovered crucial errors in the late 1830s that the Lamarck version's theory of ‘IAC’ did not adequately account for the principle of the inheritance of unconscious behavior like instinct. Lamarck's theory regarded habits as conscious and willful acts and saw that those habits are transmitted through the brain to control conscious actions. Lamarck's theory could not account for the complex and elaborate instincts of invertebrate animals, such as brainless ants. Contrary to Lamarck's view, Darwin established the new theory of ‘IAC’ that could be combined with contemporary neurological theory, which explains the heredity of unconscious behavior. Based on the knowledge of neurology, Darwin was able to translate the ‘principle of habit’ into a neurological term called ‘principle of reflex’. This article focuses on how Darwin join the theory of ‘IAC’ with nineteenth century neuroscience and how the neurological knowledge from the nineteenth century contributed to Darwin's overcoming of Lamarck's ‘IAC’. The significance of this study is to elucidate Darwin's notion of ‘IAC’ theory rather than natural selection theory as a principle of heredity of behavior. The theory of ‘IAC’ was able to account for the rapid variation of instincts in a relatively short period of time, unlike natural selection, which operates slowly in geological time spans of tens of millions of years. The nineteenth century neurological theory also provided neurological principles for ‘plasticity of instinct,’ empirically supporting the fact that all nervous systems responsible for reflexes respond sensitively to very fine stimuli. However, researchers of neo-Darwinian tendencies, such as Richard Dawkins and evolutionary psychologists advocating the ‘selfish gene’ hypothesis, which today claim to be Darwin's descendants, are characterized by human nature embedded in biological information, such as the brain and genes, so that it cannot change at all. This study aims to contribute to reconstructing the evolutionary discourse by illuminating Darwin's insights into the “plasticity of nature” that instincts can change relatively easily even at the level of invertebrates such as earthworms.
Animals ; Ants ; Brain ; Epigenomics ; Ganglion Cysts ; Heredity ; Human Characteristics ; Humans ; Instinct ; Invertebrates ; Nervous System ; Neurology ; Neurosciences ; Oligochaeta ; Parents ; Psychology ; Reflex ; Selection, Genetic ; Spinal Cord ; Sympathetic Nervous System ; Transcutaneous Electric Nerve Stimulation ; Wills