Increase In Intramuscular Pressure Research Articles

The effects of limb elevation and increased intramuscular pressure on nerve and muscle function in the human leg.

In this study we investigated the effects of increased intramuscular pressure (IMP) on nerve and muscle function in the leg and foot. In study A, muscle pressure was increased by inducing venous stasis in both legs, placed in plaster casts, of eight healthy subjects having a mean age of 29 years. The results from elevated and non-elevated limbs were compared. In study B, two different models for increasing IMP were studied in nine healthy subjects having a mean age of 32 years. The results of increased IMP and decreased blood perfusion pressure on local (= leg) and distal (= foot) function of muscle and nerve induced by venous stasis of a leg in a plaster cast and by external compression of the contralateral leg were compared. Contraction pressure of the tibialis anterior muscle in the leg was recorded. A biphasic compound muscle action potential was measured from the extensor hallucis brevis and the extensor digitorum muscles as an indication of foot muscle function. Muscle contraction pressure was 87 (SD 38) mm Hg in the vein-obstructed leg and 133 (SD 42) mm Hg in the externally compressed leg (P<0.05). In both studies the skin sensibility of the feet was significantly lower in the vein-obstructed elevated leg after 30 min (P<0.05). Vein stasis in an elevated human leg in a plaster cast defines a model for simulating imminent acute compartment syndrome with reversible neuromuscular dysfunction.

Physiological response to submaximal isometric contractions of the paravertebral muscles.

Brief (30-second) isometric trunk extensions at 5%, 20%, 40%, 60%, and 80% of maximal voluntary contraction (MVC) and 3 minutes of prolonged trunk extension (20% MVC) in erect position were studied in nine healthy male subjects. To investigate the intercorrelation between intramuscular pressure and tissue oxygenation of the paravertebral muscles during submaximal isometric contractions and further, to evaluate paravertebral electromyogram and intramuscular pressure as indicators of force development. Local physiologic responses to muscle contraction are incompletely understood. Relative oxygenation was monitored with noninvasive near-infrared spectroscopy, intramuscular pressure was measured with a transducer-tipped catheter, and surface electromyogram was monitored at three recording sites. The root mean square amplitudes of the paravertebral electromyogram (L4, left and right; T12, right) and intramuscular pressure measured in the lumbar multifidus muscle at L4 increased with greater force development in a curvilinear manner. A significant decrease in the oxygenation of the lumbar paravertebral muscle in response to muscle contraction was found at an initial contraction level of 20% MVC. This corresponded to a paravertebral intramuscular pressure of 30-40 mm Hg. However, during prolonged trunk extension, no further decrease in tissue oxygenation was found compared with the tissue oxygenation level at the end of the brief contractions, indicating that homeostatic adjustments (mean blood pressure and heart rate) over time were sufficient to maintain paravertebral muscle oxygen levels. At a threshold intramuscular pressure of 30-40 mm Hg during muscle contraction, oxygenation in the paravertebral muscles is significantly reduced. The effect of further increase in intramuscular pressure on tissue oxygenation over time may be compensated for by an increase in blood pressure and heart rate. Surface electromyogram amplitudes and intramuscular pressure can be used as indicators of paravertebral muscle force.

A CONTINUOUS MEASUREMENT OF OXIDATIVE RATE BY NEAR INFRARED SPECTROSCOPY IN HUMAN MUSCLES

1174 Measurements of muscle oxidative rate by near infrared spectroscopy (NIRS) require repeated brief arterial occlusions. Therefore, disadvantages such as a poor time resolution, occur. In this study, we tried to continuously measure muscle oxidative rate by NIRS. In order to achieve this objective, we used an intermittent isometric exercise at high intensity, which elicits a transient occlusion of the blood flow to the muscle due to an increase in intramuscular pressure. Muscle oxygenation and energetics in the finger flexors (N=5) were measured by NIRS and magnetic resonance spectroscopy (MRS), respectively. The sampling time of the data for NIRS and MRS was 0.1 sec. and 2.0 sec., respectively. Changes in muscle oxygenation and phosphocrealine (PCr) concentration were monitored during an exercise at varying frequencies (3-5 sec. contraction/3-5 sec. relaxation) at 50% of maximum voluntary contraction for 3 minutes each. The oxidative rate was measured from the deoxygenation rate during the last 2 sec. of each contraction. The time resolution for the measurement of oxidative rate and PCr was 6 sec. and 10 sec., respectively. Oxidative rates at the onset of exercise followed an exponential time course with a time constant of 42 sec. on average. This value agreed with the time constant of the decrease in PCr (48 sec.). The oxidative rate during exercise increased 15 to 25 fold of the resting value on average, while the decrease in PCr was 58% on average. We observed a significant correlation between the change in oxidative rate and PCr concentration (r=0.95, p<0.05). This result suggests that the oxidative rate was successfully monitored by NIRS during exercise without arterial occlusion. Supported in part by a Grant-in-Aid for Encouragement of Young Scientists, the Ministry of Education, Science, Sports and Culture in Japan (#09780087).

Effects of limb elevation on abnormally increased intramuscular pressure, blood perfusion pressure, and foot sensation: an experimental study in humans.

To study the effects of limb elevation on abnormally increased intramuscular pressure (IMP) and blood perfusion pressure in the anterior compartment of the leg. An experimental cross-over design. The test leg was elevated and the control leg was kept at heart level. Eight healthy subjects with a mean age of twenty-nine years. IMP was measured in the anterior compartment of the leg, and blood pressures were taken in the left arm and both legs. Four variables were recorded (with or without venous stasis, with or without plaster cast). All measurements were made simultaneously in both legs. When the leg was obstructed by venous stasis and elevated to between thirty-three and thirty-five centimeters, IMP decreased from 16.5 to 9.8 millimeters of mercury. When venous stasis was simulated in a level casted leg, the IMP was thirty-eight (SD = 6.4) millimeters of mercury but showed only a slight decline to thirty-five (SD = 7.8) millimeters of mercury after the leg was elevated. Blood perfusion pressure fell significantly once the leg was elevated, decreasing 53 percent from forty-seven (SD = 7.8) to twenty-five (SD = 8.0) millimeters of mercury (p < 0.001). All subjects experienced loss of foot sensation in the elevated limb. In those cases in which venous stasis increased IMP levels in the anterior compartment of the leg, elevating the limb produced a 40 percent reduction in IMP. However, limb elevation did not significantly reduce increased IMP levels when the venous stasis occurred in a casted leg. Therefore, we believe casted legs in which abnormally increased IMP is attributable to venous stasis should not be elevated above heart level because elevation induces low perfusion pressure and sensory dysfunction.

THE POWER ATHLETE

A number of normal daily and athletic activities require isometric or static exercise. Sports such as weight lifting and other high-resistance activities are used by power athletes to gain strength and skeletal muscle bulk. Static exercise, the predominant activity used in power training, significantly increases blood pressure, heart rate, myocardial contractility, and cardiac output. These changes occur in response to central neural irradiation, called central command, as well as a reflex originating from statically contracting muscle. Studies have demonstrated that blood pressure appears to be the regulated variable, presumably because the increased pressure provides blood flow into muscles whose arterial inflow is reduced as a result of increases in intramuscular pressure created by contraction. Thus, static exercise is characterized by a pressure load on the heart and can be differentiated from the hemodynamic response to dynamic (isotonic) exercise, which involves a volume load to the heart. Physical training with static exercise (i.e., power training) leads to concentric cardiac (particularly left ventricular) hypertrophy, whereas training with dynamic exercise leads to eccentric hypertrophy. The magnitude of cardiac hypertrophy is much less in athletes training with static than dynamic exercise. Neither systolic nor diastolic function is altered by the hypertrophic process associated with static exercise training. Many of the energy requirements for static exercise, particularly during more severe levels of exercise, are met by anaerobic glycolysis because the contracting muscle becomes comes deprived of blood flow. Power athletes, training with repetitive static exercise, derive little benefit from an increase in oxygen transport capacity, so that maximal oxygen consumption is increased only minimally or not at all. Peripheral cardiovascular adaptations also can occur in response to training with static exercise. Although the studies are controversial, these adaptations include modest decreases in resting blood pressure, reduced increases in blood pressure and sympathetic nerve activity during a given workload, enhanced baroreflex function, increases in muscle capillary-to-fiber ratio, possible improvements in lipid and lipoprotein profiles, and increases in glucose and insulin responsiveness. Some of these adaptations can occur in cardiac or hypertensive patients with no concomitant cardiovascular complications. In both healthy individuals and those with cardiovascular disease, the manner in which resistance training is performed may dictate the extent to which these adjustments take place. Specifically, training that involves frequent repetitions of moderate weight (and hence contains dynamic components) seems to produce the most beneficial results.

Pressure-flow relationships in in vitro model of compartment syndrome.

Compartment syndrome is a condition in which an increase in intramuscular pressure decreases blood flow to skeletal muscle. According to the Starling resistor (i.e., vascular waterfall) model of blood flow, the decrease in flow could occur through an increase in arterial resistance (Rart) or an increase in the critical closing pressure (Pcrit). To determine which explains the decrease in flow, we pump perfused a canine gastrocnemius muscle placed within an airtight box, controlled box pressures (Pbox) so that flow ranged from 100 to 50%, and measured Pcrit, Rart, arterial compliance, small venular pressure (measured by the double-occlusion technique), and venous pressure. An increase in Pbox limited flow mainly through an increase in Pcrit (75-85%), with only small changes in Rart (15-25%) and no change in arterial compliance. Increases in Pbox also produced a vascular waterfall in the venous circulation, but small venular transmural pressure always remained less than control levels. We conclude that increases in Pbox mostly limit blood flow through increases in Pcrit and that Rart plays a minor role. Transmural pressure across the small venules decreases with increases in intramuscular pressure, which contradicts the currently held belief that compartment syndrome is due to a cycle of swelling-ischemia-swelling.

Exercise-induced swelling of rat soleus muscle: its relationship with intramuscular pressure

Exercise-induced tissue swelling and its possible consequence for tissue pressure were studied in rat soleus muscle. Rats ran for 75 min on a belt with a 10 degree positive incline. Wet weights of cryofixed soleus muscles were increased at 3 (16%), 6 (28%), 9 (16%), and 24 (16%) h after running compared with those of nonexercised controls. The transient increase in muscle wet weight correlated in time with an increase in muscle volume. Muscle fiber swelling accounted for most of the muscle swelling in absolute terms because of the large proportion (approximately 90%) of the muscle volume composed of fibers, but swelling of the interstitium was about twofold larger than fiber swelling per unit area. Muscle fiber degeneration was most frequently found at the end of the observation period, i.e., 24 h after running. The muscle swelling was not associated with an increase in intramuscular pressure. During the postexercise measuring period (18 min to 24 h after exercise), intramuscular pressures of exercised rats (1.3 +/- 0.3 mm Hg) did not differ significantly from control values (1.0 +/- 0.2 mm Hg). These findings indicate that increased intramuscular pressure is not responsible for the muscle fiber degeneration found in rat soleus muscle 24 h after endurance running.

Intramuscular pressure in the lower leg in deep vein thrombosis and phlegmasia cerulae dolens.

The influence of deep vein thrombosis on intramuscular pressure was evaluated in 22 patients by means of the wick technique. Intramuscular pressure was measured in the anterior tibial and the deep posterior compartments in both legs before and during treatment. The intramuscular pressure was significantly (p less than 0.001) higher in the thrombosed leg than in the contralateral leg (0-16 mmHg). The increase in intramuscular pressure was related to the extension of the thrombus. Iliofemoral thrombosis caused a significantly (p less than 0.001) higher pressure (17-28 mmHg) than calf thrombosis (16-23 mmHg). A compartment syndrome was found to be a part of the entity phlegmasia cerulea dolens (rest pressure 47-56 mmHg). In the treatment of phlegmasia cerulea dolens, fasciotomy is suggested additional to other therapeutic procedures.