Reflex Responses in Plasma Catecholamines Caused by Static Contraction of Skeletal Muscle.

Abstract

Muscle contraction activates small muscular afferents (myelinated group III and unmyelinated group IV fibers), which is believed to initiate autonomic reflex adjustment of the cardiovascular system. It was demonstrated that sympathetic outflows to the heart and the kidneys increase during static muscle contraction induced by electrical stimulation of the ventral roots in anesthetized cats [1][2][3][4]. The increase in cardiac sympathetic nerve activity correlates with an increase in heart rate [3], and the increase in renal sympathetic nerve activity correlates with reduced renal blood flow [2], suggesting that the reflex changes in postganglionic sympathetic nerve activities caused by skeletal muscle contraction contribute to cardiovascular adjustments, such as increases in cardiac output and arterial blood pressure and a redistribution of car-591Japanese Journal of Physiology, 51, 591-597, 2001 Key words: norepinephrine, epinephrine, adrenal medulla, adrenal sympathetic nerve activity, mechanical stretch of muscle. Abstract:To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L 7 and S 1 ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23Ϯ3.1 mmHg and 19Ϯ4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18Ϯ0.072 ng/ml over the control of 0.14Ϯ0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47Ϯ0.087 ng/ml over the control of 0.71Ϯ 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012Ϯ0.001 ng/ml) and the baseline NEp was lowered to 0.52Ϯ0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.

Deciphering the metabolic and mechanical contributions to the exercise-induced circulatory response: insights from eccentric cycling

“…Large muscle tensions are likely to activate peripheral mechanoreceptors, which constitute about 10% of the myelinated nerve fibers in leg muscles (20), leading to sympathetic activation (17). The specific increase in plasma epinephrine in heavy ECC vs. light CON, with no change in plasma norepinephrine supports a mechanically induced sympathetic activation, as previously reported in animals and humans (32,36,44). The small, but remaining mechanical effect, on SV (16%) may be related to exercise-induced intramuscular pressure oscillations (3), possibly facilitating venous return to the heart (i.e., muscle pump) (30).…”

Progressive arteriolar vasoconstriction and fatigue during tetanic contractions of rat skeletal muscle are inhibited by α-receptor blockade

“…Static or isometric locomotor muscle contractions elicit the exercise pressor response, and MAP and HR are increase immediately after the onset of exercise [16,23]. In this study, however, MAP and HR did not change significantly in the temporal proximity of the stimulations.…”

Increase in serum growth hormone induced by electrical stimulation of muscle combined with blood flow restriction

“…In this study, however, plasma noradrenaline concentration increased in a similar manner in the ST BFR and NT BFR conditions, and the magnitude of the increase was much smaller than that reported for voluntary exercise (Madarame et al 2008;Takarada et al 2000a). Thus, in contrast to GH, it is likely that the exercise-induced noradrenaline secretion appears to be mainly depending on the central motor activity but not on the metabolic stress, and signiWcant but slight increase observed in the present study might be attributable to mechanical stress (Matsukawa et al 2001) induced by the EMS and/or cuV occlusion. We should note several limitations of this study.…”