METHODS: We reviewed 22 previous studies that (1) empirically manipulated social support in a stressful situation, (2) measured CVR, and (3) tested a moderator of social support effects on CVR.
RESULTS: Although a majority of studies reported a CVR-mitigating effect of social support resulting in an overall significant combined p-value, we found that there were different effects of social support on CVR when we considered high- and low-engagement contexts. That is, compared to control conditions, social support lowered CVR in more engaging situations but had no significant effect on CVR in less engaging situations.
CONCLUSION: Our results suggest that a dual-effect model of social support effects on CVR may better capture the nature of social support, CVR, and health associations than the buffering hypothesis and emphasize a need to better understand the health implications of physiological reactivity in various contexts. Statement of contribution What is already known on this subject? According to the stress-buffering hypothesis (Cohen & McKay, ), one pathway social support benefits health is through mitigating the physiological arousal caused by stress. However, previous studies that examined the effects of social support on blood pressure and heart rate changes were not consistently supporting the hypothesis. Some studies reported that social support causes elevations in cardiovascular reactivity (CVR) to stress (Anthony & O'Brien, ; Hilmert, Christenfeld, & Kulik, ; Hilmert, Kulik, & Christenfeld, ) and others showed no effect of social support on CVR (Christian & Stoney, ; Craig & Deichert, ; Gallo, Smith, & Kircher, ). What does this study add? When participants were in more engaging conditions, social support decreased CVR relative to no support. When participants were in less engaging conditions, social support did not have a significant effect on CVR. Provide an alternative way to explain the ways social support affects cardiac health.
METHODS: Twenty-five young and healthy university students performed a triceps push-down exercise at 45% one repetition maximum (1RM) with and without CS until task failure, and the rate of fatigue (ROF), endurance time (ET) and number of repetitions (NR) for both exercises were analyzed. In addition, the first and last six repetitions of each exercise were considered non-fatiguing (NF) and fatiguing (Fa), respectively, and the root mean square (RMS), mean power frequency (MPF) and median frequency (MDF) for each exercise repetition were evaluated.
RESULTS: The lateral and long head showed significant differences (P<0.05) in the ROF between the two exercises, and all the heads showed significant (P<0.05) differences in the RMS between the two exercises under NF conditions. Only the long head showed a significant difference (P<0.05) in the MPF and MDF between the two exercises. CS increases the ET (24.74%) and NR (27%) of the exercise. The three heads showed significant differences (P<0.05) in the RMS, MPF and MDF under all exercise conditions.
CONCLUSION: A lower ROF was obtained with CS. In addition, the RMS was found to be better approximator of CS, whereas MPF and MDF were more resistant to the effect of CS. The results showed that the three heads worked independently under all conditions, and the non-synergist and synergist head pairs showed similar behavior under Fa conditions. The findings from this study provide additional insights regarding the functioning of each TB head.
METHODS: Male C57BL/6 mice of 8-12 week-old were subjected to intra-cerebroventricular (i.c.v.) and/or intra-vlPAG (i.pag.) microinjection of NPS, orexin-A or substance P alone or in combination with selective antagonists of NPS receptors (NPSRs), OX1 receptors (OX1Rs), NK1 receptors (NK1Rs), mGlu5 receptors (mGlu5Rs) and CB1 receptors (CB1Rs), respectively. Antinociceptive effects of these mediators were evaluated via the hot-plate test. SIA in mice was induced by a 30-min restraint stress. NPS levels in the LH and substance P levels in vlPAG homogenates were compared in restrained and unrestrained mice.
RESULTS: NPS (i.c.v., but not i.pag.) induced antinociception. This effect was prevented by i.c.v. blockade of NPSRs. Substance P (i.pag.) and orexin-A (i.pag.) also induced antinociception. Substance P (i.pag.)-induced antinociception was prevented by i.pag. Blockade of NK1Rs, mGlu5Rs or CB1Rs. Orexin-A (i.pag.)-induced antinociception has been shown previously to be prevented by i.pag. blockade of OX1Rs or CB1Rs, and here was prevented by NK1R or mGlu5R antagonist (i.pag.). NPS (i.c.v.)-induced antinociception was prevented by i.pag. blockade of OX1Rs, NK1Rs, mGlu5Rs or CB1Rs. SIA has been previously shown to be prevented by i.pag. blockade of OX1Rs or CB1Rs. Here, we found that SIA was also prevented by i.c.v. blockade of NPSRs or i.pag. blockade of NK1Rs or mGlu5Rs. Restrained mice had higher levels of NPS in the LH and substance P in the vlPAG than unrestrained mice.
CONCLUSIONS: These results suggest that, during stress, NPS is released and activates LH orexin neurons via NPSRs, releasing orexins in the vlPAG. Orexins then activate OX1Rs on substance P-containing neurons in the vlPAG to release substance P that subsequently. Activates NK1Rs on glutamatergic neurons to release glutamate. Glutamate then activates perisynaptic mGlu5Rs to initiate the endocannabinoid retrograde inhibition of GABAergic transmission in the vlPAG, leading to analgesia.