61 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
Ketorolac Attenuates the Blood Pressure Response to Plantar Flexion Exercise in Peripheral Arterial Disease Patients
No full textMuller, M., Drew R., Heffernan, M., Blaha C., Sinoway, L. Penn State Hershey Heart and Vascular Institute, Penn State College of Medicine, Hershey, PA
Prostaglandins are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex (EPR). Humans with peripheral arterial disease (PAD) have an augmented EPR but the metabolite(s) responsible for this augmented response are not known. Purpose: We tested the hypothesis that intravenous infusion of ketorolac (a non-selective cyclooxygenase inhibitor that reduces prostaglandins) would attenuate the rise in mean arterial blood pressure (MAP) and heart rate (HR) in response to low-intensity plantar flexion exercise in humans with PAD. Methods: Six PAD patients underwent four minutes of one-legged rhythmic plantar flexion (30 contractions/min) in the supine posture. The workload began at 0.5 kg and progressed by 0.5 kg each minute. The leg with more severe PAD was always tested first, followed by a rest period and then the opposite leg. MAP and HR were measured on a beat-by-beat basis; changes from baseline in response to exercise were determined. Rating of perceived exertion (6-20) and leg pain (0-10) were also obtained. Results: Ketorolac did not affect resting MAP (97 ± 3 versus 94 ± 4 mmHg) or HR (58 ± 2 versus 55 ± 2 bpm). During the first 20 seconds of exercise with the most diseased leg, ΔMAP was significantly attenuated with ketorolac (2 ± 2 mmHg) as compared to control (8 ± 2 mmHg, P = 0.017) but ΔHR was similar (7 ± 2 versus 6 ± 1 bpm). During the second and third minutes of exercise, ΔMAP was also significantly attenuated under ketorolac. The less diseased leg displayed similar results. Importantly, subjects rated the exercise bout as “very light” to “fairly light” and average pain ratings were 1 out of 10. Neither perceived exertion nor pain ratings were altered by ketorolac. Conclusions: These data indicate that prostaglandins contribute to the augmented EPR in patients with PAD. Because this response occurred at very low workloads, we speculate that muscle mechanoreceptors are sensitized by cycolooxyegnase products under conditions of chronic limb ischemia.
Supported by NIH P01 HL096570 and UL1 TR00012
Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms
No full text MacLean, D. A., B. Saltin, G. Rådegran, and L. Sinoway. Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms. J. Appl. Physiol. 83(4): 1045–1053, 1997.—The purpose of the present study was to examine the effects of femoral arterial injections of adenosine on muscle sympathetic nerve activity (MSNA) under three different conditions. These conditions were adenosine injection alone, adenosine injection after phenylephrine infusion, and adenosine injection distal to a thigh cuff inflated to arrest the circulation. The arterial injection of adenosine alone resulted in a fourfold (255 ± 18 U/min) increase above baseline (73 ± 12 U/min; P< 0.05) in MSNA with an onset latency of 15.8 ± 0.8 s from the time of injection. The systemic infusion of phenylephrine resulted in an increase ( P < 0.05) in mean arterial pressure of ∼10 mmHg and a decrease ( P < 0.05) in heart rate of 8–10 beats/min compared with baseline values before phenylephrine infusion. After adenosine injection, the onset latency for the increase in MSNA was delayed to 19.2 ± 2.1 s and the magnitude of increase was attenuated by ∼50% (123 ± 20 U/min) compared with adenosine injection alone ( P < 0.05). When a cuff was inflated to 220 mmHg to arrest the circulation and adenosine was injected into the leg distal to the inflated cuff, there were no significant changes in MSNA or any of the other measured variables. However, on deflation of the cuff, there was a rapid increase ( P < 0.05) in MSNA, with an onset latency of 9.1 ± 0.9 s, and the magnitude of increase (276 ± 28 U/min) was similar to that observed for adenosine alone. These data suggest that ∼50% of the effects of exogenously administered adenosine are a result of baroreceptor unloading due to a drop in blood pressure. Furthermore, the finding that adenosine did not directly result in an increase in MSNA while it was trapped in the leg but that it needed to be released into the circulation suggests that adenosine does not directly stimulate thin fiber muscle afferents in the leg of humans. In contrast, it would appear that adenosine exerts its effects via some other chemically sensitive pool of afferents. </jats:p
Inventing the world grant university: Chinese international students' mobilities, literacies, and identities
No full textIncludes bibliographical references.In English with passages in Chinese with English translationCulturally responsive pedagogies developed for undergraduate Chinese international students, who have enrolled in Western institutions in increasing numbers in recent years. Focusing on the literacy practices of these students at Michigan State University and at Sinoway International Educational Summer School in China, Fraiberg.--Provided by publisher.Friction in the educational marketplace -- Geographies of difference: underground knotworks and transnational social fields -- Relationship webs in academic lives -- Learning lords and scumbags: underground literacies and learning economies -- Study abroad at home -- Assembling the cosmopolitan -- Gaming life like outlaws
Effect of Beta-Adrenergic Blockade on Coronary Blood Flow during Isometric Exercise in Older Adults
No full textRoss A., Gao Z., Heffernan M., Leuenberger U., Sinoway L., Muller M. Penn State Hershey Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, PA
The rise in heart rate (HR) and cardiac contractility during exercise is due to activation of myocardial b-adrenergic receptors. b-receptors are also located on coronary blood vessels and are thought to participate in exercise hyperemia, thereby helping to preserve the balance between myocardial oxygen supply and demand. However, experimental data in human subjects are lacking. Purpose: We hypothesized that intravenous b-adrenergic blockade would attenuate the reflex tachycardia and coronary hyperemia in response to isometric handgrip (i.e., a stimulus known to increase both cardiac metabolism and coronary blood flow). Methods: Six men (66 ± 2 yrs) performed isometric handgrip exercise at 40% of maximal voluntary contraction for 2 minutes after receiving intravenous propranolol; control trials occurred on separate days. HR and blood pressure were monitored continuously and rate-pressure product (RPP) was calculated as an index of myocardial oxygen demand. Coronary blood flow velocity (CBFV) was measured by transthoracic Doppler echocardiography (left anterior descending coronary artery) and coronary vascular resistance (CVR) was calculated. The ratio of RPP/CVR was used as an index of myocardial oxygen supply. Physiological parameters were statistically compared at baseline and in response to exercise between conditions. Results: Refer to Table. Conclusion: The novel finding of this study is that under resting conditions propranolol raises coronary resistance (impaired oxygen supply) despite also lowering cardiac metabolism (reduced oxygen demand). These data support the concept that coronary b-adrenergic receptors contribute to myocardial blood flow regulation both at rest and during exercise in humans.
Supported by NIH P01 HL096570 and UL1 TR00012
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
Skeletal muscle metaboreceptor stimulation opposes peak metabolic vasodilation in humans
No full textReversible 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
Leg exercise conditioning increases peak forearm blood flow
No full text To examine whether forearm vascular adaptations could occur after upright-leg exercise training, the reactive hyperemic blood flow after 10 min of forearm circulatory arrest (RHBF10) was studied. RHBF10 was examined in seven subjects before, at 2 wk, and after the completion of 4 wk of bicycle ergometer training. Maximal O2 consumption (VO2max) for leg ergometer work increased 13% (P less than 0.05) over 4 wk. Over that period of time RHBF10 in the forearm increased 50% (P less than 0.05), with a reciprocal drop in minimum vascular resistance. Resting heart rate decreased 15% (P less than 0.05) during the same period. Changes in RHBF10 and VO2max were noted after 2 wk of training. Mean arterial pressure did not change. We conclude that vascular adaptations can occur in the forearm muscle beds, even though the training regimen is designed to condition the lower extremities. </jats:p
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