Philip S. Clifford

The Paradox of Sympathetic Vasoconstriction in Exercising Skeletal Muscle

BUCKWALTER, J.B., and P.S. CLIFFORD. The paradox of sympathetic vasoconstriction in exercising skeletal muscle. Exerc. Sport Sci. Rev., Vol. 29, No. 4, pp. 159–163, 2001. 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.

Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries

To date, no satisfactory explanation has been provided for the immediate increase in blood flow to skeletal muscles at the onset of exercise. We hypothesized that rapid vasodilatation is a consequence of release of a vasoactive substance from the endothelium owing to mechanical deformation of the vasculature during contraction. Rat soleus feed arteries were isolated, removed and mounted on micropipettes in a sealed chamber. Arteries were pressurized to 68 mmHg, and luminal diameter was measured using an inverted microscope. Pressure pulses of 600 mmHg were delivered for 1 s, 5 s, and as a series of five repeated 1 s pulses with 1 s between pulses. During application of external pressure the lumen of the artery was completely closed, but immediately following release of pressure the diameter was significantly increased. In intact arteries (series 1, n= 6) for the 1 s pulse, 5 s pulse and series of five 1 s pulses, the peak increases in diameter were, respectively, (mean ±s.e.m.) 16 ± 2, 14 ± 2 and 27 ± 3%, with respective times from release of pressure to peak diameter of 4.1 ± 0.3, 4.6 ± 0.7 and 2.8 ± 0.4 s. In series 2 (n= 9) the arteries increased diameter by 15 ± 2, 15 ± 2 and 30 ± 3% before and by 8 ± 1, 8 ± 1 and 21 ± 2% after removal of the endothelium with air. The important new finding in these experiments is that mechanical compression caused dilatation of skeletal muscle feed arteries with a time course similar to the change in blood flow after a brief muscle contraction. The magnitude of dilatation was not affected by increasing the duration of compression but was enhanced by increasing the number of compressions. Since removal of the endothelium reduced but did not abolish the dilatation in response to mechanical compression, it appears that the dilatation is mediated by both endothelium‐dependent and ‐independent signalling pathways.

Effect of head-out water immersion on cardiorespiratory response to dynamic exercise

Head-out water immersion is known to produce several cardiopulmonary adjustments at rest due to a cephalad shift in blood volume. The purpose of this study was to determine the effect of head-out water immersion on the cardiorespiratory response to graded dynamic exercise. Nineteen healthy middle-aged men performed upright cycling exercise at 40, 60 and 80% of maximal oxygen consumption on land and in water (31.0 +/- 1.0 degrees C) to the shoulders. Cardiac output (measured by the carbon dioxide rebreathing technique) was significantly greater in water at 40 and 80% maximal oxygen consumption. Stroke volume was significantly elevated at all stages of exercise. Heart rate did not differ significantly at 40 and 60% maximal oxygen consumption but was significantly lower in water at 80% maximal oxygen consumption. Total ventilation did not differ significantly in water and on land at any stage of exercise. The results suggest that the central redistribution of blood volume with head-out water immersion leads to an increase in stroke volume. Because there is not a proportional decrease in heart rate with the elevated stroke volume, cardiac output is regulated at a higher level during upright exercise in water compared with that on land. In conclusion, there are serious limitations of available, prerecorded rhythm data bases for designing and testing of automatic external defibrillators. Performance can be adequately assessed only by extensive clinical tests, which seem mandatory for this new and important type of defibrillator.

The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.

Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimentally induced pain perception is acutely reduced by aerobic exercise in people with chronic low back pain

This study examined whether subjects with chronic low back pain demonstrate exercise-induced analgesia to experimentally induced pressure pain. We employed a repeated measures design to study eight subjects with chronic low back pain (mean +/- standard deviation age = 40 +/- 10, duration of pain = 7 +/- 4 years). Pain ratings were measured immediately before and 2 minutes and 32 minutes after 25 minutes of cycle ergometry (5 minutes at 50% peak oxygen uptake, then 20 minutes at 70% peak oxygen uptake). We based the pain ratings on subject input on a visual analog scale at 10-second intervals during the 2-minute pressure pain stimulus to the nondominant index finger. Compared with preexercise values, pain ratings were significantly (p < 0.05) decreased after exercise at both 2 and 32 minutes postexercise. We conclude that pressure pain perception can be reduced for more than 30 minutes following aerobic exercise from leg cycling among people with chronic low back pain.

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.

Poling forces during roller skiing: effects of technique and speed

PURPOSE Although it has been reported that the majority of propulsive forces are generated through the poles with ski skating, no study has systematically examined poling forces among different skating techniques. The objective of the present study was to examine poling forces and timing during roller skiing on a 2.1% uphill. METHODS Nine highly skilled cross-country skiers roller skied at three paced speeds and maximal speed using the V1 skate (V1), V2-alternate (V2A), V2 skate (V2), and double pole (DP) techniques while poling forces and timing were measured with piezoelectric transducers. RESULTS Peak force (PF) values with the skating techniques were significantly lower than with DP and ranged from 18.9 +/- 3.1% of body weight (BW) to 31.5 +/- 5.6% BW across the speeds of the study. Average force over the entire cycle (ACF) increased with speed with DP, V2A and V1 (P < 0.01) but not with V2. PF and ACF were higher (P < 0.01) with V2 than V1 and V2A. Poling time was longer (P < 0.01) with V2A compared with V1 and V2. CONCLUSIONS The results of this study suggest that 1) the use of the upper body is greater with V2 than with other skating techniques while there is a relatively greater reliance on the lower body for generation of the additional propulsive forces required to increase velocity, and (2) poling forces do not appear to be as effectively applied with V2 as with V2A.

Maximal inspiratory pressure following maximal exercise in trained and untrained subjects.

Previous investigators have demonstrated that 5-10 min of fatiguing exercise would lead to respiratory muscle fatigue in normal subjects. The purpose of this study was to determine if there was a differential inspiratory pressure response to maximal cycle ergometer exercise in trained and untrained subjects. Six highly trained cross country skiers and five untrained college students were studied prior to and 10, 60, and 120 s postexercise (incremental VO2max to exhaustion). On each occasion, maximal inspiratory pressure (MIP) was measured at the mouth from residual volume. Prior to exercise, the two groups had similar MIP values. After exercise, the sedentary subjects experienced significant decreases in MIP compared to the preexercise values. These decreases averaged 10%, 17%, and 13% at 10, 60, and 120 s postexercise, respectively. The skiers, on the other hand, showed no evidence of a decrease in MIP postexercise, with the postexercise values being slightly, but not significantly, higher than the preexercise values. From these results, we conclude that maximal exercise results in inspiratory muscle dysfunction in normal subjects but not in athletes training at or near elite levels. Thus, it appears that endurance exercise training induces an adaptive change in the inspiratory muscles that protects them from the acute loss of strength seen following exercise in normal subjects.

Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle

There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis we examined the blood flow response to a brief tetanic contraction in which potassium (K+) was infused intra‐arterially to elevate the [K+]o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs control contractions increased hindlimb blood flow by 97 ± 14 ml min−1. During K+ infusion the hyperaemic response to contraction was 8 ± 3 ml min−1. Since the hindlimb blood flow was reduced during K+ infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion the hyperaemic response to contraction was preserved (89 ± 23 ml min−1). Recovery contractions performed after the discontinuation of the K+ infusion elicited blood flow responses similar to control (100 ± 11 ml min−1). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs (n= 6) K+ infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation, there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible for the initial contraction‐induced hyperaemia. We conclude that the increase in blood flow immediately following a single muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.

α-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 α1-adrenergic antagonists. The purpose of this study was to examine the existence of α1- and α2-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 α1- (prazosin) or a selective α2-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 α1- and α2-adrenergic receptor-mediated vasoconstriction in exercising skeletal muscles even at heavy workloads and that the magnitude of vasoconstriction decreases as exercise intensity increases.