37 research outputs found
Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise
No full text Sinoway, Lawrence, Jeffrey Shenberger, Gretchen Leaman, Robert Zelis, Kristen Gray, Robert Baily, and Urs Leuenberger.Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise. J. Appl. Physiol. 81(4): 1778–1784, 1996.—We previously demonstrated that nonfatiguing rhythmic forearm exercise at 25% maximal voluntary contraction (12 2-s contractions/min) evokes sympathoexcitation without significant engagement of metabolite-sensitive muscle afferents (B. A. Batman, J. C. Hardy, U. A. Leuenberger, M. B. Smith, Q. X. Yang, and L. I. Sinoway. J. Appl. Physiol. 76: 1077–1081, 1994). This is in contrast to the sympathetic nervous system responses observed during fatiguing static forearm exercise where metabolite-sensitive afferents are the key determinants of sympathetic activation. In this report we examined whether forearm exercise training would attenuate sympathetic nervous system responses to rhythmic forearm exercise. We measured heart rate, mean arterial blood pressure (MAP), muscle sympathetic nerve activity (microneurography), plasma norepinephrine (NE), and NE spillover and clearance (tritiated NE kinetics) during nonfatiguing rhythmic forearm exercise before and after a 4-wk unilateral forearm training paradigm. Training had no effect on forearm mass, maximal voluntary contraction, or heart rate but did attenuate the increase in MAP (increase in MAP: from 15.2 ± 1.8 before training to 11.4 ± 1.4 mmHg after training; P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 ± 1.4 before training to 6.2 ± 1.1 bursts/min after training; P < 0.030), and the NE spillover (increase in arterial spillover: from 1.3 ± 0.2 before training to 0.6 ± 0.2 nmol ⋅ min−1 ⋅ m−2after training, P < 0.014; increase in venous spillover: from 2.0 ± 0.6 before training to 1.0 ± 0.5 nmol ⋅ min−1 ⋅ m−2after training, P < 0.037) seen in response to exercise performed by the trained forearm. Thus forearm training reduces sympathetic responses during a nonfatiguing rhythmic handgrip paradigm that does not engage muscle metaboreceptors. We speculate that this effect is due to a conditioning-induced reduction in mechanically sensitive muscle afferent discharge. </jats:p
Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip
No full text Mostoufi-Moab, Sogol, Eric J. Widmaier, Jacob A. Cornett, Kristen Gray, and Lawrence I. Sinoway. Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip. J. Appl. Physiol. 84(1): 277–283, 1998.—We examined the effects of unilateral, nondominant forearm training (4 wk) on blood pressure and forearm metabolites during ischemic and nonischemic rhythmic handgrip (30 1-s contractions/min at 25% maximal voluntary contraction). Contractions were performed by 10 subjects with the forearm enclosed in a pressurized Plexiglas tank to induce ischemic conditions. Training increased the endurance time in the nondominant arm by 102% ( protocol 1). In protocol 2, tank pressure was increased in increments of 10 mmHg/min to +50 mmHg. Training raised the positive-pressure threshold necessary to engage the pressor response. In protocol 3, handgrip was performed at +50 mmHg and venous blood samples were analyzed. Training attenuated mean arterial pressure (109 ± 5 and 98 ± 4 mmHg pre- and posttraining, respectively, P < 0.01), venous lactate (2.9 ± 0.4 and 1.8 ± 0.3 mmol/l pre- and posttraining, respectively, P < 0.01), and the pH response (7.21 ± 0.02 and 7.25 ± 0.01, pre- and posttraining, respectively, P < 0.01). However, deep venous O2 saturation was unchanged. Training increased the positive-pressure threshold for metaboreceptor engagement, reduced metabolite concentrations, and reduced mean arterial pressure during ischemic exercise. </jats:p
Reversible impairment of forearm vasodilation after forearm casting
No full text To examine whether the resumption of normal physical activity after forearm immobilization would reverse impaired vasodilation, the minimal vascular resistance was examined in six subjects who had forearm casts placed for broken forearm bones. Each subject was examined twice, once within 48 h after forearm cast removal and again approximately 29 days later. The formerly casted forearm and the opposite forearm (noncasted) were examined. Minimal vascular resistance decreased in the casted forearm from 3.0 +/- 0.4 to 2.6 +/- 0.5 mmHg.ml-1.min.100 ml (P less than 0.014). There was no change in the noncasted forearm: 2.5 +/- 0.3 vs. 2.5 +/- 0.3 mmHg.ml-1.min.100 ml. This study shows that maximal vasodilation improves with the resumption of normal physical activity and therefore demonstrates that immobilization is associated with a reduced forearm vasodilator capacity. </jats:p
Interstitial pH, K<sup>+</sup>, lactate, and phosphate determined with MSNA during exercise in humans
No full text The purpose of the present study was to use the microdialysis technique to simultaneously measure the interstitial concentrations of several putative stimulators of the exercise pressor reflex during 5 min of intermittent static quadriceps exercise in humans ( n = 7). Exercise resulted in approximately a threefold ( P < 0.05) increase in muscle sympathetic nerve activity (MSNA) and 13 ± 3 beats/min ( P < 0.05) and 20 ± 2 mmHg ( P < 0.05) increases in heart rate and blood pressure, respectively. During recovery, all reflex responses quickly returned to baseline. Interstitial lactate levels were increased ( P < 0.05) from rest (1.1 ± 0.1 mM) to exercise (1.6 ± 0.2 mM) and were further increased ( P < 0.05) during recovery (2.0 ± 0.2 mM). Dialysate phosphate concentrations were 0.55 ± 0.04, 0.71 ± 0.05, and 0.48 ± 0.03 mM during rest, exercise, and recovery, respectively, and were significantly elevated during exercise. At the onset of exercise, dialysate K+ levels rose rapidly above resting values (4.2 ± 0.1 meq/l) and continued to increase during the exercise bout. After 5 min of contractions, dialysate K+ levels had peaked with an increase ( P < 0.05) of 0.6 ± 0.1 meq/l and subsequently decreased during recovery, not being different from rest after 3 min. In contrast, H+ concentrations rapidly decreased ( P < 0.05) from resting levels (69.4 ± 3.7 nM) during quadriceps exercise and continued to decrease with a mean decline ( P < 0.05) of 16.7 ± 3.8 nM being achieved after 5 min. During recovery, H+ concentrations rapidly increased and were not significantly different from baseline after 1 min. This study represents the first time that skeletal muscle interstitial pH, K+, lactate, and phosphate have been measured in conjunction with MSNA, heart rate, and blood pressure during intermittent static quadriceps exercise in humans. These data suggest that interstitial K+ and phosphate, but not lactate and H+, may contribute to the stimulation of the exercise pressor reflex. </jats:p
Forearm compression during exercise increases sympathetic nerve traffic
No full text Previously, we showed that forearm venous congestion augmented muscle sympathetic nerve activity (MSNA) during static exercise. We postulated that venous congestion increased interstitial pressure, sensitizing mechanoreceptor afferents that led to a greater sympathoexcitation during exercise. In this study, we tested the hypothesis that forearm compression (FC) would increase interstitial pressure and selectively stimulate mechanically sensitive afferents. We measured MSNA during 2 min of ischemic static exercise (40% maximal voluntary contraction) and 2 min of posthandgrip circulatory arrest. Exercise was performed again after 5 min of FC induced by inflation of a forearm cuff to 90 mmHg (n = 6) and 110 mmHg (n = 7). FC without exercise had no effect on any of the hemodynamic variables. MSNA and mean arterial blood pressure responses were not augmented when exercise was performed with FC at 90 mmHg. However, static exercise coupled with FC at 110 mmHg did augment the reflex responses to static exercise (changes in MSNA before and after FC were 277 +/- 58 and 503 +/- 82 arbitrary units, respectively, P < 0.02; changes in mean arterial pressure before and after FC were 35 +/- 4 and 41 +/- 5 mmHg, respectively, P < 0.003). These responses were probably not due to greater metaboreceptor stimulation, since posthandgrip circulatory arrest responses were unaffected by FC. We postulate that FC sensitizes mechanoreceptors, leading to greater sympathoexcitation during exercise. </jats:p
Contributions of MSNA and stroke volume to orthostatic intolerance following bed rest
No full text We examined whether the altered orthostatic tolerance following 14 days of head-down tilt bed rest (HDBR) was related to inadequate sympathetic outflow or to excessive reductions in cardiac output during a 10- to 15-min head-up tilt (HUT) test. Heart rate, blood pressure (BP, Finapres), muscle sympathetic nerve activity (MSNA, microneurography), and stroke volume blood velocity (SVV, Doppler ultrasound) were assessed during supine 30° (5 min) and 60° (5–10 min) HUT positions in 15 individuals who successfully completed the pre-HDBR test without evidence of orthostatic intolerance. Subjects were classified as being orthostatically tolerant (OT, n = 9) or intolerant (OI, n = 6) following the post-HDBR test. MSNA, BP, and SVV during supine and HUT postures were not altered in the OT group. Hypotension during 60° HUT in the post-bed rest test for the OI group ( P < 0.05) was associated with a blunted increase in MSNA ( P < 0.05). SVV was reduced following HDBR in the OI group (main effect of HDBR, P < 0.02). The data support the hypothesis that bed rest-induced orthostatic intolerance is related to an inadequate increase in sympathetic discharge that cannot compensate for a greater postural reduction in stroke volume. </jats:p
Determination of muscle-specific glucose flux using radioactive stereoisomers and microdialysis
No full text The purpose of the present study was to evaluate a novel approach for determining skeletal muscle-specific glucose flux using radioactive stereoisomers and the microdialysis technique. Microdialysis probes were inserted into the vastus lateralis muscle of human subjects and perfused (4 μl/min) with a Ringer solution containing small amounts of radioactived- and l-glucose as the internal reference markers for determining probe recovery as well as varying concentrations of insulin (0–10 μM). The rationale behind this approach was that both stereoisomers would be equally affected by the factors that determine probe recovery, with the exception ofl-glucose, which is nonmetabolizable and would not be influenced by tissue uptake. Therefore, any differences in the probe recovery ratios between the d- andl-stereoisomers represent changes in skeletal muscle glucose uptake directly at the tissue level. There were no differences in probe recovery between the d- (42.3 ± 3.5%) andl- (41.2 ± 3.5) stereoisomers during the control period (no insulin), which resulted in a D/L ratio of 1.04 ± 0.03. However, during insulin perfusion (1 μM), The D/L ratio increased to 1.62 ± 0.08 and 1.58 ± 0.07 ( P< 0.05) during the two collection (0–15 and 15–30 min) periods, respectively. This was accomplished solely by an increase ( P < 0.05) in d-glucose probe recovery, asl-glucose probe recovery remained unchanged. In a second set of experiments, the perfusion of 10 μM insulin did not increase the D/L ratio (1.40 ± 0.11) above that observed during 1.0 μM (1.41 ± 0.07) insulin perfusion. These data suggest that this method is sufficiently sensitive to detect differences in insulin-stimulated glucose uptake; thus the use of radioactive stereoisomers in conjunction with the microdialysis technique provides a novel and useful technique for determining tissue-specific glucose flux and insulin sensitivity. </jats:p
Effects of hindlimb contraction on pressor and muscle interstitial metabolite responses in the cat
No full text We used the microdialysis technique to measure the interstitial concentration of several putative metabolic stimulants of the exercise pressor reflex during 3- and 5-Hz twitch contractions in the decerebrate cat. The peak increases in heart rate and mean arterial pressure during contraction were 20 ± 5 beats/min and 21 ± 8 mmHg and 27 ± 9 beats/min and 37 ± 12 mmHg for the 3- and 5-Hz stimulation protocols, respectively. All variables returned to baseline after 10 min of recovery. Interstitial lactate rose ( P < 0.05) by 0.41 ± 0.15 and 0.56 ± 0.16 mM for the 3- and 5-Hz stimulation protocols, respectively, and were not statistically different from one another. Interstitial lactate levels remained above ( P < 0.05) baseline during recovery in the 5-Hz group. Dialysate phosphate concentrations (corrected for shifts in probe recovery) rose with stimulation ( P < 0.05) by 0.19 ± 0.08 and 0.11 ± 0.03 mM for the 3- and 5-Hz protocols. There were no differences between groups. The resting dialysate K+ concentrations for the 3- and 5-Hz conditions were 4.0 ± 0.1 and 3.9 ± 0.1 meq/l, respectively. During stimulation the dialysate K+ concentrations rose steadily for both conditions, and the increase from rest to stimulation ( P < 0.05) was 0.57 ± 0.19 and 0.81 ± 0.06 meq/l for the 3- and 5-Hz conditions, respectively, with no differences between groups. Resting dialysate pH was 6.915 ± 0.055 and 6.981 ± 0.032 and rose to 7.013 ( P < 0.05) and 7.053 ( P < 0.05) for the 3- and 5-Hz conditions, respectively, and then became acidotic (6.905, P < 0.05) during recovery (5 Hz only). This study represents the first time simultaneous measurements of multiple skeletal muscle interstitial metabolites and pressor responses to twitch contractions have been made in the cat. These data suggest that interstitial K+ and phosphate, but not lactate and H+, may contribute to the stimulation of thin fiber muscle afferents during contraction. </jats:p
Enhanced maximal metabolic vasodilatation in the dominant forearms of tennis players
No full text In an effort to evaluate potential peripheral adaptations to training, maximal metabolic vasodilation was studied in the dominant and nondominant forearms of six tennis players and six control subjects. Maximal metabolic vasodilation was defined as the peak forearm blood flow measured after release of arterial occlusion, the reactive hyperemic blood flow (RHBF). Two ischemic stimuli were employed in each subject: 5 min of arterial occlusion (RHBF5) and 5 min of arterial occlusion coupled with 1 min of ischemic exercise (RHBF5ex). RHBF and resting forearm blood flows were measured using venous occlusion strain-gauge plethysmography (ml X min-1 X 100 ml-1). Resting forearm blood flows were similar in both arms of both groups. RHBF5ex was similar in both arms of our control group (dominant, 40.8 +/- 1.2 vs. nondominant, 40.9 +/- 2.1). However, RHBF5ex was 42% higher in the dominant than in the nondominant forearms of our tennis player population (dominant, 48.7 +/- 4.0 vs. nondominant, 34.4 +/- 3.4; P less than 0.05). This intraindividual difference in peak forearm blood flows was not secondary to improved systemic conditioning since the maximal O2 consumptions in the two study groups were similar (controls, 45.4 +/- 3.9 vs. tennis players, 46.1 +/- 1.7). These findings suggest a primary peripheral cardiovascular adaptation to exercise training in the dominant forearms of the tennis players resulting in a greater maximal vasodilatation. </jats:p
Hydrogen ion concentration is not the sole determinant of muscle metaboreceptor responses in humans.
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