Biomedical subjects

J B Buckwalter

Publications and source records attributed to J B Buckwalter.

14 recordsLinked to original sources

PubMed2001

The paradox of sympathetic vasoconstriction in exercising skeletal muscle.

Is there sympathetic vasoconstriction in exercising skeletal muscle? Although convincing evidence exists that demonstrates vasoconstriction in active muscle, the proposition that the sympathetic nervous system constricts skeletal muscle during exercise poses a paradox, given the robust vasodilation that occurs in muscle during exercise. Ultimately, muscle perfusion is a balance between metabolic vasodilation and sympathetic vasoconstriction.

Blood Pressure↗

PubMed2001

Exercise attenuates alpha-adrenergic-receptor responsiveness in skeletal muscle vasculature.

Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. A potential mechanism is a reduction in alpha-adrenergic-receptor responsiveness. The purpose of this study was to examine alpha(1)- and alpha(2)-adrenergic-receptor-mediated vasoconstriction in resting and exercising skeletal muscle using intra-arterial infusions of selective agonists. Thirteen mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective alpha(1)-adrenergic agonist (phenylephrine) or the selective alpha(2)-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of 76 +/- 4, 71 +/- 5, and 31 +/- 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by 81 +/- 5, 49 +/- 4, and 14 +/- 2%, respectively. The response to intra-arterial infusion of clonidine was unaffected by surgical sympathetic denervation. Agonist infusion did not affect either systemic blood pressure, heart rate, or blood flow in the contralateral iliac artery. alpha(1)-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, alpha(2)-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. These results suggest that the mechanism of exercise sympatholysis may involve reductions in postsynaptic alpha-adrenergic-receptor responsiveness.

Adrenergic alpha-Agonists↗

PubMed2001

Parasympathetic innervation of canine tracheal smooth muscle.

To investigate whether efferent parasympathetic fibers to the tracheal smooth muscle course through the pararecurrent nerve rather than the recurrent or the superior laryngeal nerve, we stimulated all three nerves in anesthetized dogs. We also recorded the pararecurrent nerve activity response to bronchoconstrictor stimuli and compared it with pressure changes inside a saline-filled cuff of an endotracheal tube. Electrical stimulation (30 s, 100 Hz, 0.1 ms, 10 mA) increased tracheal cuff pressure by 21.0 +/- 3.2 and 1.3 +/- 0.7 cmH(2)O for the pararecurrent and the recurrent laryngeal nerve, respectively. Stimulation of the superior laryngeal nerve increased tracheal cuff pressure before, but not after, sectioning of the ramus anastomoticus, which connects it to the pararecurrent nerve. Intravenous administration of sodium cyanide increased pararecurrent nerve activity by 208 +/- 51% and tracheal cuff pressure by 14.4 +/- 3.5 cmH(2)O. Elevation of end-tidal PCO(2) to 50 Torr increased pararecurrent nerve activity by 49 +/- 19% and tracheal cuff pressure by 8.4 +/- 3.6 cmH(2)O. Further elevation to 60 Torr increased pararecurrent nerve activity by 101 +/- 33% and tracheal cuff pressure by 11.3 +/- 2.9 cmH(2)O. These results lead us to the conclusion that parasympathetic efferent fibers reach the smooth muscle of the canine trachea via the pararecurrent nerve.

Animals↗

PubMed2000

Dynamic exercise attenuates sympathetic responsiveness of canine vascular smooth muscle.

The phenomenon of reduced responsiveness of the skeletal muscle arterial vasculature to sympathetic activation during exercise (sympatholysis) remains controversial. The purpose of this study was to examine the vascular effects of sympathoactivation in dynamically exercising skeletal muscle. Mongrel dogs (19-24 kg) were instrumented chronically with transit-time ultrasonic flow probes on the external iliac arteries. After pretreatment with atropine (0.2 mg/kg), an intravenous bolus (4 microg/kg) of a nicotinic ganglion stimulant [1,1-dimethyl-4-phenylpiperazinium iodide (DMPP)] was given at rest and during treadmill exercise at graded intensities. Administration of DMPP was associated with prompt reductions in iliac blood flow and increases in arterial pressure under all conditions. There were significant reductions (P < 0.05) in iliac vascular conductance of 58 +/- 4 (SE), 48 +/- 3, 36 +/- 5, and 16 +/- 3% at rest, 3 miles/h and 0% grade, 6 miles/h and 0% grade, and 6 miles/h and 15% grade, respectively. These data demonstrate that activation of postganglionic sympathetic nerves with DMPP caused vasoconstriction in the skeletal muscle vasculature at rest and during exercise. Additionally, the magnitude of vasoconstriction was inversely related to exercise intensity. These results support the concept of exercise sympatholysis.

Animals↗

PubMed1999

alpha-adrenergic vasoconstriction in active skeletal muscles during dynamic exercise.

Sympathetic vasoconstriction in working muscles during dynamic exercise has been demonstrated by intra-arterial administration of alpha(1)-adrenergic antagonists. The purpose of this study was to examine the existence of alpha(1)- and alpha(2)-adrenergic receptor-mediated vasoconstriction in active skeletal muscles during exercise. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs, and a catheter was inserted in one femoral artery. All dogs ran on a motorized treadmill at three exercise intensities (3 miles/h, 6 miles/h, and 6 miles/h at 10% grade) on separate days. After 5 min of exercise, a selective alpha(1)- (prazosin) or a selective alpha(2)-adrenergic antagonist (rauwolscine) was infused as a bolus into the femoral arterial catheter (only one drug per day). The doses of the antagonists were adjusted to maintain the same effective concentration at each exercise intensity. At the mild, moderate, and heavy workloads prazosin infusion produced immediate increases in iliac conductance of 65 +/- 9, 35 +/- 6, and 18 +/- 4% (means +/- SE), respectively, and increases in blood flow of 290 +/- 24, 216 +/- 23, and 172 +/- 18 ml/min, respectively. Rauwolscine infusion produced increases in conductance of 52 +/- 5%, 36 +/- 5%, and 26 +/- 3%, respectively, and blood flow increases of 250 +/- 34, 244 +/- 39, and 259 +/- 35 ml/min at the three workloads. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by any of the antagonist infusions. These results demonstrate that there is ongoing alpha(1)- and alpha(2)-adrenergic receptor-mediated vasoconstriction in exercising skeletal muscles even at heavy workloads and that the magnitude of vasoconstriction decreases as exercise intensity increases.

Adrenergic alpha-Antagonists↗

PubMed1999

Autonomic control of skeletal muscle blood flow at the onset of exercise.

The purpose of this study was to determine whether the autonomic nervous system is involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs (n = 7) were instrumented with flow probes on both external iliac arteries. Before treadmill exercise at 3 miles/h, 0% grade, hexamethonium (10 mg/kg) and atropine (0.2 mg/kg) or saline was infused intravenously. Ganglionic blockade increased resting heart rate from 87 +/- 5 to 145 +/- 8 beats/min (P < 0.01) and reduced mean arterial pressure from 100 +/- 4 to 88 +/- 5 mmHg (P < 0.01). During steady-state exercise, heart rate was unaffected by ganglionic blockade (from 145 +/- 8 to 152 +/- 5 beats/min), whereas mean arterial pressure was reduced (from 115 +/- 4 to 72 +/- 4 mmHg; P < 0.01). Immediate and rapid increases in iliac blood flow and conductance occurred with initiation of exercise with or without ganglionic blockade. Statistical analyses of hindlimb conductance at 5-s intervals over the first 30 s of exercise revealed a statistically significant difference between the control and ganglionic blockade conditions at 20, 25, and 30 s (P < 0.01) but not at 5, 10, and 15 s of exercise. Hindlimb conductance at 1 min of exercise was 9.21 +/- 0.68 and 11.82 +/- 1.32 ml. min(-1). mmHg(-1) for the control and ganglionic blockade conditions, respectively. Because ganglionic blockade did not affect the initial rise in iliac conductance, we concluded that the autonomic nervous system is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs. Autonomic control of skeletal muscle blood flow during exercise is manifested through vasoconstriction and not vasodilation.

Animals↗

PubMed1999

Rapid vasodilation in response to a brief tetanic muscle contraction.

To test the hypothesis that vasodilation occurs because of the release of a vasoactive substance after a brief muscle contraction and to determine whether acetylcholine spillover from the motor nerve is involved in contraction-induced hyperemia, tetanic muscle contractions were produced by sciatic nerve stimulation in anesthetized dogs (n = 16), instrumented with flow probes on both external iliac arteries. A 1-s stimulation of the sciatic nerve at 1. 5, 3, and 10 times motor threshold increased blood flow above baseline (P < 0.01) for 20, 25, and 30 s, respectively. Blood flow was significantly greater 1 s after the contraction ended for 3 and 10 x motor threshold (P < 0.01) and did not peak until 6-7 s after the contraction. The elevations in blood flow to a 1-s stimulation of the sciatic nerve and a 30-s train of stimulations were abolished by neuromuscular blockade (vecuronium). The delayed peak blood flow response and the prolonged hyperemia suggest that a vasoactive substance is rapidly released from the contracting skeletal muscle and can affect blood flow with removal of the mechanical constraint imposed by the contraction. In addition, acetylcholine spillover from the motor nerve is not responsible for the increase in blood flow in response to muscle contraction.

Acetylcholine↗

PubMed1998

Cycle rate variations in roller ski skating: effects on oxygen uptake and poling forces.

The purpose of this study was to examine the effect of cycle rate (CR) variations on the metabolic cost and upper body forces during roller skiing with the V2-alternate technique on flat terrain. Nine highly skilled cross-country skiers roller skied at a paced speed of 18.0+/-0.1 km x h(-1) using their chosen CR, and CRs that were 10% slower and 20% faster. Oxygen uptake (VO2) was determined through collection of expired gases into a meterological balloon and poling forces were measured with piezoelectric transducers during the last 30 s of each four minute trial of roller skiing. One-way repeated measures ANOVA revealed that VO2 varied significantly with CR (p=0.02) with the chosen CR being significantly lower than the higher CR (p < 0.05). Poling forces and poling time were not significantly different among the CR conditions. The present results demonstrate that 1) an alteration in cycle rate affects metabolic cost of roller ski skating, 2) skiers tend to naturally select the most economical cycle rate, and 3) moderate variations in cycle rate do not appear to affect propulsive force generation through the poles in roller skiing.

Adult↗

PubMed1998

Effect of rolling resistance on poling forces and metabolic demands of roller skiing.

OBJECTIVE: To examine the effect of an increase in roller ski rolling resistance on the physiological and upper body demands of roller skiing with the V2-alternate technique. METHODS: Nine highly skilled cross-country skiers roller skied at three paced speeds on a flat oval loop using roller skis with high (HiR) and low (LowR) rolling resistance. Oxygen uptake (VO2), heart rate, and poling forces were measured during the last 30 s and rating of perceived exertion (RPE) was requested immediately after each 4-min bout of roller skiing. RESULTS: VO2 and all force-related variables increased significantly with speed and were higher (P < 0.01) for HiR at given speeds. Poling time was similar between HiR and LowR, whereas poling recovery time was shorter (P = 0.0002) and cycle rate was higher (P = 0.002) for HiR. For given VO2 levels, peak and average forces, heart rates, and RPE values were similar between HiR and LowR, whereas average poling force across the cycle was greater (P = 0.006) and duty cycle (i.e., percentage of cycle when poling forces were applied) was higher (P = 0.0001) with HiR. CONCLUSIONS: 1) The decrease in poling recovery time and increase in cycle rate associated with an increase in roller ski rolling resistance is comparable to the effect previously observed from increasing grade and probably occurs as a means of limiting deceleration. 2) Since changes in rolling resistance do not alter the relationships of RPE and heart rate with VO2, the central cardiovascular adaptations from roller ski training should not be affected by the rolling resistance of the roller skis. 3) Higher resistance roller skis are likely to induce greater upper body aerobic adaptations than lower resistance roller skis.

Adult↗

PubMed1998

Renal hemodynamic responses to dynamic exercise in rabbits.

Cardiovascular hemodynamics, including renal blood flow, were measured in rabbits with one intact and one denervated kidney during various intensities of treadmill exercise. Within the first 10 s of exercise, there was rapid vasoconstriction in the innervated kidney associated with decreases in renal blood flow (range -10 to -17%). The vasoconstriction in the innervated kidney was evident at all workloads and was intensity dependent. There was no significant vasoconstriction or change in renal blood flow (range 0.5 to -3.1%) in the denervated kidney at the onset of exercise. However, a slowly developing vasoconstriction occurred in the denervated kidney as exercise progressed to 2 min at all workloads. Examination of responses to exercise performed under alpha-adrenergic blockade with phentolamine (5 mg/kg iv) revealed that the vasoconstriction in the innervated kidney at the onset of exercise and the delayed vasoconstriction in the denervated kidney were due primarily to activation of alpha-adrenergic receptors. In addition, a residual vasoconstriction was also present in the innervated kidney after alpha-adrenergic blockade, suggesting that, during exercise, activation of other renal vasoconstrictor mechanisms occurs which is dependent on the presence of renal nerves.

Adrenergic alpha-Agonists↗

PubMed1998

Skeletal muscle vasodilation at the onset of exercise.

The purpose of this study was to determine whether beta-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs (n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 microgram), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 +/- 35, 646 +/- 49, 637 +/- 68, and 705 +/- 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of beta-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

Adrenergic beta-Antagonists↗

PubMed1998

alpha1-adrenergic-receptor responsiveness in skeletal muscle during dynamic exercise.

Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. One potential mechanism is a reduction in alpha1-adrenergic-receptor responsiveness. The purpose of this study was to examine alpha1-adrenergic-receptor-mediated vasoconstriction in resting and working skeletal muscles by using intra-arterial infusions of a selective agonist. Seven mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. A selective alpha1-adrenergic-receptor agonist (phenylephrine) was infused as a bolus into the femoral artery catheter at rest and during exercise. All dogs ran on a motorized treadmill at two exercise intensities (3 and 6 miles/h). Intra-arterial infusions of the same effective concentration of phenylephrine elicited reductions in vascular conductance of 76 +/- 4, 76 +/- 6, and 67 +/- 5% (P > 0.05) at rest, 3 miles/h, and 6 miles/h, respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected by phenylephrine. These results do not demonstrate an attenuation of vasoconstriction to a selective alpha1-agonist during exercise and do not support the concept of sympatholysis.

Adrenergic alpha-Agonists↗

PubMed1997

Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise.

Studies utilizing systemic administration of alpha-adrenergic antagonists have failed to demonstrate sympathetic vasoconstriction in working muscles during dynamic exercise. The purpose of this study was to examine the existence of active sympathetic vasoconstriction in working skeletal muscles by using selective intra-arterial blockade. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and with a catheter in one femoral artery. All dogs ran on a motorized treadmill at three intensities on separate days. After 2 min, the selective alpha 1-adrenergic antagonist prazosin (0.1 mg) was infused as a bolus into the femoral artery catheter. At mild, moderate, and heavy workloads, there were immediate increases in iliac conductance of 76 +/- 7, 54 +/- 11, and 22 +/- 6% (mean +/- SE), respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected. These results demonstrate that there is sympathetic vasoconstriction in active skeletal muscles even at high exercise intensities.

Adrenergic alpha-Antagonists↗

PubMed1997

Autonomic control of skeletal muscle vasodilation during exercise.

Despite extensive investigation, the control of blood flow during dynamic exercise is not fully understood. The purpose of this study was to determine whether beta-adrenergic or muscarinic receptors are involved in the vasodilation in exercising skeletal muscle. Six mongrel dogs were instrumented with ultrasonic flow probes on both external iliac arteries and with a catheter in a branch of one femoral artery. The dogs exercised on a treadmill at 6 miles/h while drugs were injected intra-arterially into one hindlimb. Isoproterenol (0.2 microg) or acetylcholine (1 microg) elicited increases in iliac blood flow of 89.8 +/- 14.4 and 95.6 +/- 17.4%, respectively, without affecting systemic blood pressure or blood flow in the contralateral iliac artery. Intra-arterial propranolol (1 mg) or atropine (500 microg) had no effect on iliac blood flow, although they abolished the isoproterenol and acetylcholine-induced increases in iliac blood flow. These data indicate that exogenous activation of beta-adrenergic or muscarinic receptors in the hindlimb vasculature increases blood flow to dynamically exercising muscle. More importantly, because neither propranolol nor atropine affected iliac blood flow, we conclude that beta-adrenergic and muscarinic receptors are not involved in the control of blood flow to skeletal muscle during moderate steady-state dynamic exercise in dogs.

Adrenergic beta-Agonists↗