Muscle Metaboreceptors Research Articles

Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure.

Resting sympathetic nervous system activity is increased in heart failure. Whether sympathetic nervous system responses during exercise are increased is controversial. Furthermore, the role of muscle metaboreceptors and central command in regulating sympathetic outflow has been largely unexplored. Muscle sympathetic nerve activity (MSNA, peroneal nerve) was measured in nine heart failure subjects and eight age-matched control subjects during static exercise (30% maximal voluntary contraction) for 2 minutes and during a period of posthandgrip regional circulatory arrest. This maneuver isolates the metaboreceptor contribution to sympathetic nervous system responses. MSNA responses were similar during static exercise in the two groups. During posthandgrip regional circulatory arrest we observed a marked attenuation in MSNA responses in the heart failure subjects (15% increase in heart failure versus 57% increase in control subjects). A cold pressor test demonstrated a normal MSNA response to a potent nonspecific stimulus in the heart failure subjects (heart failure subjects, 141% increase; control subjects, 215% increase; NS). Nuclear magnetic resonance spectroscopy studies in five separate heart failure subjects and five control subjects suggested that the attenuated metaboreceptor response in heart failure was not due to reduced H+ production. Skeletal muscle metaboreceptor responses are impaired in heart failure. Because MSNA responses during static exercise are similar in the two groups, mechanisms aside from metaboreceptor stimulation must be important in increasing sympathetic nervous system activity.

Dichloroacetate reduces sympathetic nerve responses to static exercise

Lactic acid is thought to be a stimulant of muscle metaboreceptors. The goal of the present study was to determine if inhibition of lactic acid production by dichloroacetate (DCA) would attenuate muscle sympathetic nerve activity (MSNA) during static forearm exercise. DCA increases pyruvate dehydrogenase levels. Thus, for a given amount of pyruvate produced, less lactic acid is formed. Seven subjects performed static forearm exercise at 20% maximal voluntary contraction until fatigue followed by posthandgrip circulatory arrest (PHG-CA) (trial.1). Subjects then received DCA (35 mg/kg) and repeated the exercise protocol (trial 2). We observed an attenuated rise in forearm venous lactate and MSNA. The trial 2 MSNA value during PHG-CA was 51 +/- 11% less than the value during trial 1 (P less than 0.01). In seven control subjects, two bouts of static forearm exercise were performed with an intervening saline infusion. This intervention had no effect on lactate or MSNA responses to exercise. We conclude that DCA attenuates lactate responses to static exercise, and this is associated with a blunted MSNA response.

Reflex responses of renal nerve activity during isometric muscle contraction in cats

Renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), and heart rate (HR) were measured during isometric muscle contraction of a hindlimb in chloralose-anesthetized cats. In 14 cats RSNA, AP, and HR increased during a 1-min contraction by 45%, 39 mmHg, and 11 beats/min, respectively; however, in three cats there was a brief initial decrease in RSNA followed by an increase. In 11 cats isometric contraction was maintained for 5 min by alternate stimulation of the L7 and S1 ventral roots. In the first 1 min of sustained contraction, there was a positive correlation (gamma = 0.58, P less than 0.005) between RSNA and tension development. Thereafter RSNA remained elevated despite a tension decrease, and there was no significant correlation between these changes. The RSNA response to contraction of both hindlimbs was greater than that to contraction of either hindlimb alone. Passive stretch of the hindlimb muscle significantly increased RSNA. Thus the initial increase in RSNA during sustained contraction is likely due to activation of muscle mechanoreceptors, whereas the later increase is probably caused by activation of the muscle metaboreceptors.

Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans.

The total blood flow requirements of a large muscle mass can exceed the maximal cardiac output generated by the heart during exercise. Therefore, to maintain blood pressure, muscle vasodilation must be opposed by sympathetic vasoconstriction. The primary neural signal that increases sympathetic outflow is unclear. In an effort to isolate the vasoconstricting mechanism that opposes vasodilation, we measured the peak forearm vascular conductance response after the release of 10 minutes of forearm circulatory arrest under five separate study conditions: 1) no leg exercise, 2) low-level supine leg exercise, 3) low-level supine leg exercise with leg circulatory arrest after exercise, 4) high-level supine leg exercise, and 5) high-level supine leg exercise with leg circulatory arrest after exercise. We found that both high-workload conditions reduced peak forearm conductance below the no-leg exercise condition (a 34% reduction during leg exercise and a 52% reduction during leg exercise followed by leg circulatory arrest). In addition, at each workload, leg circulatory arrest after exercise, which isolated the skeletal muscle metaboreceptor contribution to vasoconstriction, reduced forearm conductance by approximately 20% below the values noted for leg exercise alone (combined central command and metaboreceptor stimulation). In a separate group of subjects, peak forearm blood flow was measured during lower-body negative pressure to levels up to -40 mm Hg, a maneuver that unloads high- and low-pressure baroreceptors. This intervention did not affect peak forearm blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of the skin blood flow-body temperature relationship by upright exercise.

Modification of the skin blood flow-body temperature relationship by upright exercise.

Competition between cutaneous vasodilator and vasoconstrictor reflexes in man.

A two-part experiment was carried out on seven men to determine whether skin will respond to increased neurogenic vasoconstrictor activity during heating. The latter was induced by lower body negative pressure of -50 mm Hg applied for 5 of each 15 min in 12 studies with constant, neutral skin temperature (32.2-34.4 C) in a 40-min control period and with skin temperature held at 38 C for 40-70 min. We conclude that during heating, skin retains the ability to vasoconstrict but that this vasoconstriction cannot completely override heat-induced vasodilatation.

Neural processes in thermoregulation.

Neural processes in thermoregulation.

Sustained human skin and muscle vasoconstriction with reduced baroreceptor activity.

Sustained human skin and muscle vasoconstriction with reduced baroreceptor activity.

Absence of appreciable cardiovascular and respiratory responses to muscle vibration.

Absence of appreciable cardiovascular and respiratory responses to muscle vibration.

Splanchnic vasoconstriction in hyperthermic man--role of falling blood pressure.

Results of a study in which six supine resting subjects, wearing water-perfused suits, had body skin temperature controlled at 35 C for 30 min (control period), then rapidly increased to 40.5 C for 43 to 50 min (heating period) in a two-part experiment. In the first part of the experiment arterial mean pressure (MP) in three men was increased back to, or above control levels at the 30 to 35th min of heating by total occlusion of both legs for 8 to 10 min. Splanchnic blood flow (SBF), which had fallen from 1.4 to 0.9 L/min at occlusion, rose only 0.05 L/min during occlusion. Splanchnic vascular resistance (SVR) rose throughout heating and occlusion. In the second part of the experiment (three men) SBF fell despite a spontaneous rise in MP and aortic pulse pressure prior to leg occlusion. Cardiac output (CO) was measured just before, during and after occlusion. Occlusion raised MP 10 to 15 mm Hg and reduced CO only slightly. It is concluded that falling MP or aortic pulse pressure are not major causes of the splanchnic vasoconstriction in response to heating man.

Importance of skin temperature in the regulation of sweating.

Human sweating regulation at rest, evaluating thermal inputs effects on thermoregulatory center and internal hypothalamic and skin temperatures

Partitional calorimetric studies of responses of man to thermal transients.

Partitional calorimetric studies of responses of man to thermal transients.