The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

We investigated the effect of a 12-week physical training programme on the sleep of nine unfit women. Data were collected at 0, 4, 8 and 12 weeks of the training programme. Changes in fitness were assessed by changes in maximal oxygen consumption (VO2max) and onset of blood lactate turn point (LTP). Lean body mass (LBM) was calculated from total body potassium measurements. The all-night sleep recordings were made following days during which the subjects carried out their normal daily routines and did no extra exercise. Although cardiorespiratory fitness improved significantly as indicated by an increase in both VO2max and LTP, there was no change in LBM. The improvement in cardiorespiratory fitness did not result in any changes in the sleep parameters measured. Other workers have reported an improvement in sleep quality in eight army recruits during their basic training. The male recruits showed improved cardiorespiratory fitness and an increase in muscle bulk. These results suggest that increased fitness only facilitates sleep when there is an associated increase in LBM. Alternatively it may be that the response of sleep to improved fitness is sex-linked.

Effects of central administration of a cholinesterase inhibitor, physostigmine, on cardiovascular responses to static contraction and passive stretch of the triceps surae were studied using anesthetized cats. Contraction increased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) by 44 +/- 5 mmHg, 18 +/- 1 beats/min, and 86 +/- 6%, respectively. MAP, HR, and RSNA increased during stretch by 44 +/- 5 mmHg, 15 +/- 1 beats/min, and 61 +/- 4%, respectively. Administration of physostigmine (100 micrograms; 5 microliters) into the third ventricle decreased resting MAP by 22 +/- 3 mmHg and RSNA by 32 +/- 4%, with no effect on HR. Physostigmine attenuated the contraction-evoked responses as MAP, HR, and RSNA increased by 17 +/- 2 mmHg, 3 +/- 1 beats/min, and 31 +/- 6%, respectively. Also, physostigmine blunted MAP, HR, and RSNA responses to stretch (16 +/- 2 mmHg, 4 +/- 1 beats/min, and 9 +/- 6%, respectively). Posterior hypothalamic stimulation increased MAP by 39 +/- 3 mmHg, which was unaffected by physostigmine, despite a lower baseline. Cardiovascular and RSNA responses to contraction and stretch returned to control 90-120 min after physostigmine. Preadministration of the muscarinic antagonist, atropine sulfate (100 micrograms; 5 microliters), blocked the effects of physostigmine. Results suggest central cholinergic stimulation can inhibit the exercise pressor reflex in anesthetized cats.

This study investigated whether activation of serotonin1A [5-hydroxytryptamine (5-HT)1A] receptors in the dorsal horn of the spinal cord attenuates the reflex pressor response to static contraction and passive muscle stretch. In addition, we determined if the attenuation of the response to contraction is mediated by inhibiting substance P (SP) release in the dorsal horn. Static contractions of the triceps surae muscle of chloralose-anesthetized cats were induced by stimulating the cut L7 and S1 ventral roots. Microdialysis (10 mM) of a selective 5-HT1A agonist [8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT)] into the L7 dorsal horn region produced a reversible attenuation of the reflex pressor response to a 1-min contraction (in mmHg: control = 36 +/- 3; 8-OH-DPAT = 17 +/- 3; recovery = 31 +/- 8; P = 0.013; n = 6) or passive stretch (in mmHg: control = 36 +/- 6; 8-OH-DPAT = 15 +/- 2; recovery = 32 +/- 6; P = 0.002; n = 6). However, a 5-HT1B agonist, 1-[3-(trifluoromethyl)-phenyl]piperazine, had no effect on the reflex pressor response. During 5-min contractions (n = 8), 8-OH-DPAT (10 mM) also blunted the pressor response but had no effect on the levels of SP-like immunoreactivity (in fmol/100 microliters: control = 0.492 +/- 0.026; 8-OH-DPAT = 0.501 +/- 0.034). These results suggest that activation of 5-HT1A receptors in the dorsal horn attenuates the reflex pressor response to contraction through a mechanism other than inhibition of SP release.

The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48+6 mm Hg, 18+2 beats per minute, and 66±5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51±6 mm Hg, 17+2 beats per minute, and 50+3%, respectively. . These results demonstrate that stimulation of a2-adrenergic receptors in the L-7 dorsal horn attenuates the cardiovascular responses and RSNA changes to static contraction and passive stretch. This attenuation by clonidine appears not to be mediated through presynaptic inhibition of SP release. (Circ Res. 1994;75:567-575.) Key Words * exercise pressor reflex * passive stretchsympathetic nerve activity * a2-adrenergic receptor .yohimbine Static muscle contraction evokes increases in arterial pressure (AP), heart rate (HR), cardiac contractility, and renal sympathetic nerve activity (RSNA) in anesthetized cats.1-6 These changes are a reflex arising from the contracting muscle, which is commonly known as the "exercise pressor reflex."4 The reflex cardiovascular and sympathetic nerve activity responses are initiated by a contraction-induced activation of thinly myelinated (group III) and unmyelinated (group IV) muscle afferents. The majority of the group III afferents display mechanosensitivity; ie, their endings respond to mechanical stimuli, whereas the majority of the group IV afferents respond to metabolic changes.7,8 The dorsal horn of the spinal cord is the site of the first synapse of the majority of group III and group IV muscle afferents.9'10 Thus, this region may play an important role in the reflex cardiovascular changes observed during muscle contraction. A variety of neurotransmitters and/or neuromodulators of group III and group IV afferents have been identified in the dorsal