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Postexercise nutrient intake timing in humans is critical to recovery of leg glucose and protein homeostasis.

Although the importance of postexercise nutrient ingestion timing has been investigated for glycogen metabolism, little is known about similar effects for protein dynamics. Each subject (n = 10) was studied twice, with the same oral supplement (10 g protein, 8 g carbohydrate, 3 g fat) being administered either immediately (EARLY) or 3 h (LATE) after 60 min of moderate-intensity exercise. Leg blood flow and circulating concentrations of glucose, amino acids, and insulin were similar for EARLY and LATE. Leg glucose uptake and whole body glucose utilization (D-[6,6-2H(2)]glucose) were stimulated threefold and 44%, respectively, for EARLY vs. LATE. Although essential and nonessential amino acids were taken up by the leg in EARLY, they were released in LATE. Although proteolysis was unaffected, leg (L-[ring-2H(5)]phenylalanine) and whole body (L-[1-13C]leucine) protein synthesis were elevated threefold and 12%, respectively, for EARLY vs. LATE, resulting in a net gain of leg and whole body protein. Therefore, similar to carbohydrate homeostasis, EARLY postexercise ingestion of a nutrient supplement enhances accretion of whole body and leg protein, suggesting a common mechanism of exercise-induced insulin action.

Adult↗

Exercise-induced muscle injury augments forearm vascular resistance during leg exercise.

The purpose of the present investigation was to examine the effect of exercise-induced muscle injury on hemodynamic responses during exercise. Ten subjects performed unilateral isometric knee extensions (IKE) at 30% of preinjury maximum voluntary contraction to fatigue and for 3 min before and 48 h after muscle injury. Muscle injury was elicited by performing 8 sets of 10 repetitions of eccentric muscle actions of the knee extensor muscles (i.e., quadriceps muscles) by lowering a weight equivalent to 75% of eccentric maximum load. Exercise time to fatigue for IKE at 30% of maximum voluntary contraction in the injured leg was significantly decreased from preinjury to postinjury IKE (257 +/- 21 to 203 +/- 23 s; n = 10), but was unchanged in the control leg (244 +/- 16 to 254 +/- 20 s; n = 7). With the use of a 10-cm visual analog scale, ratings of muscle soreness in the injured leg increased from 0 to 5. 1 +/- 0.7 cm (P < 0.001) but were not changed in the control leg (0 both times). Both heart rate and mean arterial pressure responses to exercise were unchanged following muscle injury. Forearm blood flow and forearm vascular resistance were not different at rest and during the first minute of exercise before and after muscle injury. However, after muscle injury, forearm blood flow was significantly lower and forearm vascular resistance was significantly higher (P < 0.03) during the second and third minutes of exercise. There were no significant changes in any variables with the contralateral control leg. In four subjects, resting magnetic resonance images demonstrated a 23% greater relative cross-sectional area of the knee extensor muscles with an elevated transverse relaxation time in the injured versus control leg. The results indicate that forearm vascular resistance is augmented during isometric knee extension following muscle injury of the knee extensor muscles. The data suggest that muscle injury alters vascular control to non-exercising skeletal muscle during exercise.

Adult↗

Bed rest attenuates sympathetic and pressor responses to isometric exercise in antigravity leg muscles in humans.

Although spaceflight and bed rest are known to cause muscular atrophy in the antigravity muscles of the legs, the changes in sympathetic and cardiovascular responses to exercises using the atrophied muscles remain unknown. We hypothesized that bed rest would augment sympathetic responses to isometric exercise using antigravity leg muscles in humans. Ten healthy male volunteers were subjected to 14-day 6 degrees head-down bed rest. Before and after bed rest, they performed isometric exercises using leg (plantar flexion) and forearm (handgrip) muscles, followed by 2-min postexercise muscle ischemia (PEMI) that continues to stimulate the muscle metaboreflex. These exercises were sustained to fatigue. We measured muscle sympathetic nerve activity (MSNA) in the contralateral resting leg by microneurography. In both pre- and post-bed-rest exercise tests, exercise intensities were set at 30 and 70% of the maximum voluntary force measured before bed rest. Bed rest attenuated the increase in MSNA in response to fatiguing plantar flexion by approximately 70% at both exercise intensities (both P < 0.05 vs. before bed rest) and reduced the maximal voluntary force of plantar flexion by 15%. In contrast, bed rest did not alter the increase in MSNA response to fatiguing handgrip and had no effects on the maximal voluntary force of handgrip. Although PEMI sustained MSNA activation before bed rest in all trials, bed rest entirely eliminated the PEMI-induced increase in MSNA in leg exercises but partially attenuated it in forearm exercises. These results do not support our hypothesis but indicate that bed rest causes a reduction in isometric exercise-induced sympathetic activation in (probably atrophied) antigravity leg muscles.

Adult↗

Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Muscle sympathetic nerve responses to static leg exercise.

Previous studies of muscle sympathetic nerve activity (MSNA) during static exercise have employed predominantly the arms. These studies have revealed striking increases in arm and leg MSNA during static handgrip (SHG) and postexercise circulatory arrest (PECA). The purpose of this study was to examine MSNA during static leg exercise (SLE) at intensities and duration commonly used during SHG followed by PECA. During 2 min of SLE (static knee extension) at 10% of maximal voluntary contraction (MVC; n = 18) in the sitting position, mean arterial pressure and heart rate increased significantly. Surprisingly, MSNA in the contralateral leg did not increase above control levels during SLE but rather decreased (23 +/- 5%; P < 0.05) during the 1st min of SLE at 10% MVC. We compared MSNA responses to SHG and SLE (n = 8) at 30% MVC. SHG and SLE elicited comparable increases (P < 0.05) in arterial pressure and heart rate, but SHG elicited significant increases in MSNA, whereas SLE did not. During PECA after SHG and SLE, mean arterial pressure remained significantly above control. However, MSNA was unchanged during PECA after SLE but was significantly greater than control during PECA after SHG. Because previous studies have indicated differences in MSNA responses to the arm and leg, we measured arm and leg MSNA simultaneously in six subjects during SLE at 20% MVC and PECA. During SLE and PECA, MSNA in the contralateral arm and leg did not differ significantly from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

Reduced leg blood flow during dynamic exercise in older endurance-trained men.

It is currently unclear whether aging alters the perfusion of active muscles during large-muscle dynamic exercise in humans. To study this issue, direct measurements of leg blood flow (femoral vein thermodilution) and systemic arterial pressure during submaximal cycle ergometry (70, 140, and 210 W) were compared between six younger (Y; 22-30 yr) and six older (O; 55-68 yr) chronically endurance-trained men. Whole body O2 uptake, ventilation, and arterial and femoral venous samples for blood-gas, catecholamine, and lactate determinations were also obtained. Training duration (min/day), estimated leg muscle mass (dual-energy X-ray absorptiometry; Y, 21.5 +/- 1.2 vs. O, 19.9 +/- 0.9 kg), and blood hemoglobin concentration (Y, 14.9 +/- 0.4 vs. O, 14.7 +/- 0.2 g/dl) did not significantly differ (P > 0.05) between groups. Leg blood flow, leg vascular conductance, and femoral venous O2 saturation were approximately 20-30% lower in the older men at each work rate (all P < 0.05), despite similar levels of whole body O2 uptake. At 210 W, leg norepinephrine spillover rates and femoral venous lactate concentrations were more than twofold higher in the older men. Pulmonary ventilation was also higher in the older men at 140 (+24%) and 210 (+39%) W. These results indicate that leg blood flow and vascular conductance during cycle ergometer exercise are significantly lower in older endurance-trained men in comparison to their younger counterparts. The mechanisms responsible for this phenomenon and the extent to which they operate in other groups of older subjects deserve further attention.

Adult↗

Leg mass and lower body negative pressure tolerance in men and women.

To explore the hypothesis that lower body muscle mass correlates with orthostatic tolerance, 18 healthy volunteers (age 18-48 yr; 10 men, 8 women) underwent a graded lower body negative pressure (LBNP) protocol consisting of six, 5-min stages of suction up to 60 mmHg in 10-mmHg increments. Forearm blood flow, heart rate, and blood pressure were measured, and forearm vascular resistance was calculated. Leg muscle mass was assessed by dual-energy X-ray absorptiometry. All subjects received standard intravenous hydration for at least 8 h before the study. Six men and four women completed all stages of LBNP. Four men and four women developed presyncopal symptoms, including marked bradycardia and/or hypotension, at LBNP levels of 30 mmHg (n = 2;1 man, 1 woman), 40 mmHg (n = 2;1 man, 1 woman), and 50 mmHg (n = 4;2 men, 2 women). The presyncopal subjects had leg muscle masses ranging from 19.5 to 25.2 kg in men and from 11.7 to 16.6 kg in women. In subjects who completed all stages of LBNP, leg muscle mass ranged from 17.5 to 24.1 kg in men and from 10.4 to 18.0 kg in women. Leg muscle mass did not differ between presyncopal subjects and those who completed the protocol. Furthermore, there were no differences in the hemodynamic responses to LBNP between subjects with low vs. high leg mass. These data suggest that leg muscle mass is not a critical determinant of LBNP tolerance in otherwise healthy men and women.

Absorptiometry, Photon↗

Muscle quality. I. Age-associated differences between arm and leg muscle groups.

To determine the differences between arm and leg muscle quality (MQ) across the adult life span in men and women, concentric (Con) and eccentric (Ecc) peak torque (PT) were measured in 703 subjects (364 men and 339 women, age range 19-93 yr) and appendicular skeletal muscle mass (MM) was determined in the arm and leg in a subgroup of 502 of these subjects (224 men and 278 women). Regression analysis showed that MQ, defined as PT per unit of MM, was significantly higher in the arm ( approximately 30%) than in the leg across age in both genders (P < 0.01). Arm and leg MQ declined at a similar rate with age in men, whereas leg MQ declined approximately 20% more than arm MQ with increasing age in women (P </= 0.01 and P < 0.05 for Con and Ecc PT, respectively). Moreover, the age-associated decrease in arm MQ was steeper in men than in women whether Con or Ecc PT was used (both P < 0.05). Arm MQ as determined by Con PT showed a linear age-related decline in men and women (28 and 20%, respectively, P < 0.001), whereas arm MQ as determined by Ecc PT showed a linear age-related decline in men (25%, P < 0.001) but not in women (not significant). In contrast, both genders exhibited an age-related quadratic decline in leg MQ as determined by Con PT ( approximately 40%) and Ecc PT ( approximately 25%; both P < 0.001), and the rate of decline was similar for men and women. Thus MQ is affected by age and gender, but the magnitude of this effect depends on the muscle group studied and the type of muscle action (Con vs. Ecc) used to assess strength.

Adult↗

Sympathetic adaptations to one-legged training.

The purpose of the present study was to determine the effect of leg exercise training on sympathetic nerve responses at rest and during dynamic exercise. Six men were trained by using high-intensity interval and prolonged continuous one-legged cycling 4 day/wk, 40 min/day, for 6 wk. Heart rate, mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA; peroneal nerve) were measured during 3 min of upright dynamic one-legged knee extensions at 40 W before and after training. After training, peak oxygen uptake in the trained leg increased 19 +/- 2% (P < 0.01). At rest, heart rate decreased from 77 +/- 3 to 71 +/- 6 beats/min (P < 0.01) with no significant changes in MAP (91 +/- 7 to 91 +/- 11 mmHg) and MSNA (29 +/- 3 to 28 +/- 1 bursts/min). During exercise, both heart rate and MAP were lower after training (108 +/- 5 to 96 +/- 5 beats/min and 132 +/- 8 to 119 +/- 4 mmHg, respectively, during the third minute of exercise; P < 0.01). MSNA decreased similarly from rest during the first 2 min of exercise both before and after training. However, MSNA was significantly less during the third minute of exercise after training (32 +/- 2 to 22 +/- 3 bursts/min; P < 0.01). This training effect on MSNA remained when MSNA was expressed as bursts per 100 heartbeats. Responses to exercise in five untrained control subjects were not different at 0 and 6 wk. These results demonstrate that exercise training prolongs the decrease in MSNA during upright leg exercise and indicates that attenuation of MSNA to exercise reported with forearm training also occurs with leg training.

Adult↗

Carotid baroreflex control of leg vascular conductance at rest and during exercise.

We sought to test the hypothesis that the carotid baroreflex (CBR) alters mean leg blood flow (LBF) and leg vascular conductance (LVC) at rest and during exercise. In seven men and one woman, 25 +/- 2 (SE) yr of age, CBR control of LBF and LVC was determined at rest and during steady-state one-legged knee extension exercise at approximately 65% peak O(2) uptake. The application of 5-s pulses of +40 Torr neck pressure and -60 Torr neck suction significantly altered mean arterial pressure (MAP) and LVC both at rest and during exercise. CBR-mediated changes in MAP were similar between rest and exercise (P > 0.05). However, CBR-mediated decreases in LVC (%change) to neck pressure were attenuated in the exercising leg (16.4 +/- 1.6%) compared with rest (33 +/- 2.1%) and the nonexercising leg (23.7 +/- 1.9%) (P < 0.01). These data suggest CBR control of blood pressure is partially mediated by changes in leg vascular tone both at rest and during exercise. Furthermore, despite alterations in CBR-induced changes in LVC during exercise, CBR control of blood pressure was well maintained.

Adult↗

Effects of 18 days of bed rest on leg and arm venous properties.

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6 degrees head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 +/- 0.007 ml x 100 ml(-1) x mmHg(-1), post: 0.033 +/- 0.007 ml x 100 ml(-1) x mmHg(-1); P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 +/- 1.08 mmHg x ml(-1) x 100 ml x min, post: 3.10 +/- 1.00 mmHg x ml(-1) x 100 ml x min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure x time), decreased in all subjects after bed rest (pre: 932 mmHg x min, post: 747 mmHg x min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.

Adolescent↗

Leg ulcers in patients with myeloproliferative disorders: disease- or treatment-related?

Leg ulcers are a relatively frequent problem in patients with myeloproliferative disorders under treatment with hydroxyurea (HU). The pathogenesis is currently unknown and may be multifactorial. Concomitant arterial or venous disease may play a contributing role in the development of these wounds. Vasculitis, cryoglobulinemia and pyoderma gangrenosum should be considered if typical clinical signs are present. We report on 3 patients with myeloproliferative disorders who developed HU-induced leg ulcers and review the literature. HU-induced leg ulcers share clinical features which can help to differentiate them from leg ulcers of other etiologies: occurrence under long-term treatment with HU at a dose of at least 1 g/day, localization in the malleolar region and spontaneous healing when HU is discontinued. We conclude that differentiation between disease-related and treatment-induced leg ulcers can be difficult and may not always be possible. In HU-induced leg ulcers, cessation of the drug typically leads to wound healing.

Aged↗

Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, free fatty acids, and amino acids.

Arterial concentrations and substrate exchange across the leg and splanchnic vascular beds were determined for glucose, lactate, pyruvate, glycerol, individual acidic and neutral amino acids, and free fatty acids (FFA) in six subjects at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. FFA turnover and regional exchange were evaluated using (14)C-labeled oleic acid. The arterial glucose concentration was constant for the first 40 min of exercise, but fell progressively thereafter to levels 30% below basal. The arterial insulin level decreased continuously, while the arterial glucagon concentration had risen fivefold after 4 h of exercise. Uptake of glucose and FFA by the legs was markedly augmented during exercise, the increase in FFA uptake being a consequence of augmented arterial levels rather than increased fractional extraction. As exercise was continued beyond 40 min, the relative contribution of FFA to total oxygen metabolism rose progressively to 62%. In contrast, the contribution from glucose fell from 40% to 30% between 90 and 240 min. Leg output of alanine increased as exercise progressed. Splanchnic glucose production, which rose 100% above basal levels and remained so throughout exercise, exceeded glucose uptake by the legs for the first 40 min but thereafter failed to keep pace with peripheral glucose utilization. Total estimated splanchnic glucose output was 75 g in 4 h, sufficient to deplete approximately 75% of liver glycogen stores. Splanchnic uptake of gluconeogenic precursors (lactate, pyruvate, glycerol, alanine) had increased 2- to 10-fold after 4 h of exercise, and was sufficient to account for 45% of glucose release at 4 h as compared to 20-25% at rest and at 40 min of exercise. In the case of alanine and lactate, the increase in precursor uptake was a consequence of a rise in splanchnic fractional extraction. It is concluded that during prolonged exercise at a low work intensity (a) blood glucose levels fall because hepatic glucose output fails to keep up with augmented glucose utilization by the exercising legs; (b) a large portion of hepatic glycogen stores is mobilized and an increasing fraction of the splanchnic glucose output is derived from gluconeogenesis; (c) blood-borne substrates in the form of glucose and FFA account for a major part of leg muscle metabolism, the relative contribution from FFA increasing progressively; and (d) augmented secretion of glucagon may play an important role in the metabolic adaptation to prolonged exercise by its stimulatory influence on hepatic glycogenolysis and gluconeogenesis.

Abdomen↗

Splanchnic and leg exchange of glucose, amino acids, and free fatty acids during exercise in diabetes mellitus.

The influence of exercise on leg and splanchnic exchange of substrates was examined in eight insulin-dependent diabetics 24 h after withdrawal of insulin and in eight healthy controls studied at rest and after 40 min of bicycle ergometer exercise at 55-60% of maximal capacity. In four of the diabetic subjects, basal arterial ketone acid levels were 3-4 mmol/ liter (ketotic diabetics) and in the remainder, below 1 mmol/liter (nonketotic diabetics). ,ree fatty acid (FFA) turnover and regional exchange were evaluated with 14-C- labeled oleic acid. Leg uptake of blood glucose rose 13-18 fold during exercise in both the diabetics and controls and accounted for a similar proportion of the total oxygen uptake by leg muscles (25-28%) in the two groups. In contrast, leg uptake of FFA corresponded to 39% of leg oxygen consumption in the diabetic group but only 27% in controls. Systemic turnover of oleic acid was similar in the two groups. Splanchnic glucose output increased during exercise 3-4 fold above resting levels in both groups. In the diabetics, splanchnic uptake of lactate, pyruvate, glycerol, and glycogenic amino acids rose more than twofold above resting levels and was fourfold greater than in exercising controls. Total precursor uptake could account for 30% of the splanchnic glucose output in the diabetic group. In contrast, in the controls, total splanchnic uptake of glucose precursors was no greater during exercise than in the resting state and could account for no more than 11% of splanchnic glucose output. The augmented precursor uptake during exercise in the diabetics was a consequence of increased splanchnic fractional extraction as well as increased peripheral production of gluconeogenic substrates. The arterial glucagon concentration was unchanged by exercise in both groups, but was higher in the diabetics. In the diabetic subjects with ketosis in the resting state, exercise elicited a rise in arterial glucose and FFA, an augmented splanchnic uptake of FFA, and a 2-3 fold increase in splanchnic output of 3-hydroxybutyrate. Uptake of 3-hydroxybutyrate by the exercising leg rose more rapidly than splanchnic production, resulting in a fall in arterial levels of 3-hydroxybutyrate. It is concluded that (a) glucose uptake by exercising muscle in hyperglycemic diabetics is no different from that of controls; (b) splanchnic glucose output rises during exercise to a similar extent in diabetics and controls, while uptake of gluconeogenic substrates is markedly higher in diabetics and accounts for a greater proportion of total splanchnic glucose output; (c) exercise in diabetic patients with mild ketosis is associated with a rise in blood glucose and FFA levels as well as augmented splanchnic production and peripheral uptake of ketone bodies.

Abdomen↗

Quantitative evaluation of the skin circulation in ischemic legs by transcutaneous measurement of oxygen tension.

We tried to apply transcutaneous oxygen tension (tcPo2) in evaluating the ischemic leg quantitatively from the standpoint of the skin circulation. The tcPo2 measurement was performed on the pretibial and dorsal skin at rest, on exercise loading, and during oxygen inhalation; tcPo2 on the chest wall was measured as a standard value. The subjects consisted of 47 patients with ischemic legs and 20 normal healthy males without ischemic legs. tcPo2 in the pretibial skin had a tendency to decrease with aging. There was a correlation between pretibial tcPo2 and ankle pressure (r = 0.51, p less than 0.02). In the affected leg, each mean pretibial tcPo2 under 3 different conditions was much lower than that of control. Pretibial tcPo2 of patients also correlated well with the Fontaine classification of clinical severity of ischemic legs. We concluded that transcutaneous measurements of oxygen tension at the pretibial region are useful in evaluating the ischemic leg quantitatively.

Adult↗

Chronic exertional compartment syndrome: the controversial "fifth" compartment of the leg.

BACKGROUND: The existence of a "fifth" compartment in the leg capable of developing distinct chronic exertional compartment syndrome remains a subject of controversy. HYPOTHESIS: Specific pressure recordings and dissection will confirm or disprove the existence of a fifth compartment. STUDY DESIGN: Empirical anatomic study. METHODS: Radiopaque dye was injected directly into the tibialis posterior muscle of 25 embalmed cadaveric legs while intracompartmental pressure was monitored. Radiographs demonstrated dye distribution, and dissection-documented fascial and epimysial layers. RESULTS: Evidence was found that the fibular origin of the flexor digitorum longus muscle, when present, could create subcompartments within the deep posterior compartment. The nature of this attachment varied from being absent, to small (<8 cm), to extensive (>8 cm). The attachment partially covered the tibialis posterior muscle in the majority of the 14 legs that developed high pressures, and it was limited or absent in the 11 legs that did not. Radiographs demonstrated that the dye was confined to the tibialis posterior muscle in four legs. CONCLUSIONS: No consistent fifth compartment exists in the leg; however, subcompartments within the deep posterior compartment created by the fibular origin of the flexor digitorum longus muscle may develop pressures congruent with chronic exertional compartment syndrome. CLINICAL RELEVANCE: Potential deep posterior subcompartments demand accurate pressure investigation. A modified technique to decompress the entire deep posterior compartment, including the tibialis posterior muscle, is necessary for successful treatment of chronic exertional compartment syndrome.

Aged↗

Effects of a functional knee brace on leg muscle function.

The effects of a functional knee brace on local intramuscular pressures and on calculated blood perfusion pressure in the tibialis anterior muscle of the legs of six volunteers were determined. Torque generation during dorsiflexion of the ankle joint was measured with a Kinetic Computerized ergometer, and the time to elicit muscle fatigue during exercise was recorded. For each experimental subject studies compared right with left unbraced legs, then right braced with left unbraced legs, and finally right unbraced with left braced legs. In the braced leg, intramuscular pressure at rest and muscle relaxation pressure during exercise were significantly higher, and the time to elicit muscle fatigue was 35% shorter. The calculated local blood perfusion pressure was lower because of the increased muscle relaxation pressure. We conclude that the increased muscle relaxation pressure during exercise caused by a knee brace is a possible explanation for the premature development of muscle fatigue in the braced leg.

Adult↗

Anatomic investigation of the deep posterior compartment of the leg.

The purpose of this study is to critically investigate the anatomy of the deep posterior compartment of the leg. Specifically, the relationship of the deep posterior compartment to the superficial posterior compartment and their insertion onto the posteromedial border of the tibia are assessed. Cross-sectioning of 10 fresh-frozen cadaver legs was performed at 2-cm increments. The inferior surface of each section was photographed. The photographs were visually analyzed, and the fascial separation between the posterior compartments along with their relationship to the posteromedial border of the tibia were recorded for each specimen. Magnetic resonance images in the axial plane of 10 healthy, normal volunteers' lower extremities at 2-cm increments were obtained and analyzed. All specimens and images demonstrated that the medial fascial attachment of the deep posterior compartment was along the posteromedial aspect of the tibia in the proximal third of the leg and was not superficially accessible. In the proximal third of the leg, the superficial posterior compartment fascial attachment overlapped the deep posterior compartment by inserting medial and anterior to the deep posterior compartment fascial attachment. In the middle and distal thirds of the leg, the medial fascial attachment of the deep posterior compartment shifted medially and anteriorly, making the deep posterior compartment superficially accessible. The surgeon must appreciate the change in the anatomic relationships along the medial side of the leg while performing double-incision four-compartment fasciotomy release to obtain a complete release of the muscular portion of the deep posterior compartment.

Cadaver↗