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Biomedical subjects

L C Maxwell

Publications and source records attributed to L C Maxwell.

At least 19 recordsLinked to original sources
PubMed2001

Constancy of masseter muscle structure and function with age in F344 rats.

Senile muscle atrophy is a characteristic feature of advancing age. Despite the growing body of knowledge about weight-bearing muscles in rodents and man, there is relatively little such information on the muscles of mastication. Therefore, the primary goal here was to develop a masseter muscle preparation from male Fischer 344 rats suitable for studying contractile characteristics in vitro. And, secondarily, the goal was to examine this preparation for evidence of age-related changes in muscle composition and function in rats aged 4--24 months. Histochemical analysis of the composition of the four anatomical regions (branches) of the masseter revealed a mixture of rapidly contracting, fatiguable and fatigue-resistant muscle fibres with no significant differences between branches. Fibre type and size were determined with myosin ATPase, NADH-TR and toluidine blue staining of quick- frozen muscle sections. No significant changes in fibre type or fibre area were found with increasing age. One branch of the masseter, the anterior deep masseter, is sufficiently thin (less than 0.8 mm thickness) for adequate diffusion of oxygen and nutrients in studies of isometric contractile properties in vitro. Contraction time, half-relaxation time, dry weight:wet weight ratio and maximum force per unit area were found to be similar in muscles of young and old rats. Our results demonstrate that the anterior deep masseter of the rat is a suitable preparation for investigating masseter function in vitro. The surprising absence of age-related changes in composition and function is consistent with some, but not all, data on ageing rodent limb muscles. The results suggest that masticatory muscle performance is preserved with age in rats.

Aging↗
PubMed1998

Effect of nitric oxide synthase inhibitor on diaphragmatic function after resistive loading.

We studied the effect of a nitric oxide synthase inhibitor, Nomega-Nitro-L-arginine-methyl-ester (L-NAME), on in vitro diphragmatic function both at rest (control) or after inspiratory resistive loading (IRL). Sprague-Dawley rats were anesthetized, instrumented, and then the following experimental groups: (1) controls; (2) L-NAME (100 mg/kg/body weight intravenously alone); (3) IRL alone; and (4) L-NAME + IRL. The IRL protocol consisted of applying a variable resistor to the inspiratory limb of a two-way valve at 70% of maximal airway pressure until apnea. After the experiment, the animals were sacrificed and diaphragmatic strips were obtained for activity of constitutive nitric oxide synthase (cNOS) and measurements of in vitro contractile properties: tetanic (Po) and twitch tensions (Pt). cNOS activity was significantly decreased in the L-NAME and L-NAME + IRL groups (P < or = 0.05) as compared with control and IRL groups. L-NAME alone did not affect Po or Pt. However, in both IRL groups, with and without was a significant decrease in Po and Pt. This reduction was comparable in both groups. In summary, our data showed that L-NAME resulted in a significant decrease cNOS activity, but in vitro contractility was impaired.

Animals↗
PubMed1998

Effects of selenium deficiency on diaphragmatic function after resistive loading.

Diaphragmatic fatigue has been associated with increased production of reactive oxygen species. Among the defenses against reactive oxygen species is the glutathione redox system. The selenium-dependent enzyme glutathione peroxidase is an important component of this system. Thus, we hypothesized that selenium deficiency would lower glutathione peroxidase activity and render the diaphragm more susceptible to a mild exertional protocol. Sprague-Dawley rats were fed a selenium-deficient or control diet for 12 weeks then divided into four experimental groups: (1) unloaded, basic diet with selenium supplementation (control); (2) unloaded, selenium-deficient diet; (3) loaded, basic diet with selenium supplementation; and (4) loaded, selenium-deficient diet. Diaphragmatic in vitro contractile properties, glutathione peroxidase activity and glutathione content were measured. During inspiratory resistive loading, the animals breathed against an inspiratory resistor at 70% of maximal airway pressure until the target pressure was not achieved for five consecutive breaths. Selenium deficiency resulted in a significant decrease in diaphragmatic glutathione peroxidase activity, without changes in total glutathione content. Neither selenium deficiency nor inspiratory resistive loading alone impaired diaphragmatic contractility. Selenium deficiency in conjunction with inspiratory resistive loading resulted in a significant decrease in diaphragmatic twitch and tetanic force, with a downward shift in the force/frequency curve. These data suggest that selenium deficiency lowers diaphragmatic glutathione peroxidase activity, and when these animals are subjected to the oxidative stress of resistive loading, there is an impairment in muscle function. We conclude that a functional glutathione peroxidase is necessary to protect the diaphragm against the effects of resistive loading.

Animals↗
PubMed1996

Alterations in skeletal muscle related to short-term impaired physical mobility.

The purpose of this investigation was to describe and compare two methods of recovery of atrophied skeletal muscle following short-term impaired physical mobility. An animal model was used to study morphologic adaptations of atrophied soleus and plantaris muscles to the effects of 7 days of hind-limb suspension (HS) followed by either sedentary recovery or run training during a 28-day recovery period. Significant atrophy, demonstrated by decreased mean fiber area (MFA, in square micrometers), occurred during the 7-day period of HS. During recovery, MFA returned to control values 14 days earlier in the sedentary compared with the trained groups. Runs training following short-term atrophy induced by HS did not result in the high levels of frank muscle damage and type IIC fibers previously reported following long-term (28-day) atrophy.

Analysis of Variance↗
PubMed1994

Total parenteral nutrition does not improve diaphragm development in premature baboons.

We hypothesized that total parenteral nutrition accelerates growth and development of diaphragm muscle (DPH) in prematurely delivered baboons (140 days gestation). For 10 days after delivery by cesarean section, we administered parenteral nutrition containing glucose, electrolytes, and water or total parenteral nutrition containing lipids, amino acids, glucose, vitamins, and electrolytes. After 10 days of care, dorsolateral and ventrolateral (VL) costal DPH were sampled for histochemically determined mean fiber area (MFA) and fiber type percentages. We determined isolated bundle isometric tension (normalized for cross-sectional area), time to peak tension, half-relaxation time, force-frequency relationship, and fatigability. Neither sex nor nutritional treatment affected contractile properties. Differences among sexes and muscle sites, but not among nutritional treatments, were observed for histochemical characteristics. In females, the VL DPH had a lower percentage of type IIo fibers and a greater MFA of type IIc fibers than the dorsolateral DPH and a lower percentage of type IIo fibers and greater MFA of type IIc and IIo fibers than the VL DPH in males. Mean fiber cross-sectional area of VL DPH was significantly greater in females than males. The larger fibers in females than males suggest a stronger DPH in females. Earlier growth of type II fibers in females could contribute to a better outcome for female than male premature infants with hyaline membrane disease.

Animals↗
PubMed1994

Effects of hyperoxia on rat diaphragm function.

The association of oxygen radical generation with impaired diaphragm performance has previously been reported after inspiratory resistive loading (IRL). We hypothesized that exposure of rats to normobaric hyperoxia (O2) could produce impaired diaphragm function because of free radical production. Sprague-Dawley rats were divided into four groups: 1) room air (control), 2) > 95% O2 for 24 h, 3) > 95% O2 for 48 h, and 4) > 95% O2 for 60 h. Each group was studied at rest after the O2 exposure and then after IRL. During IRL, the animals breathed through an inspiratory resistor until they were unable to sustain > 70% of the maximum airway pressure. Diaphragm samples were obtained for analysis of glutathione (GSH) and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile properties were also determined, including maximal tetanic tension (Po) and maximal twitch tension (Pt), in GSSG content and in GSSG-to-GSH ratios. Hyperoxia for > 48 h resulted in significant decreases in Po and Pt and an increase in GSSG content and in GSSG-to-GSH ratios compared with other groups. Those same animals subjected to IRL showed a further decrease in Po and Pt. These data suggest that free radical generation may occur in the diaphragm during a hyperoxia exposure associated with activation of the GSH redox cycle and impairment of diaphragm function.

Airway Resistance↗
PubMed1994

Buthionine sulfoximine treatment impairs rat diaphragm function.

Activation of the glutathione (GSH) redox cycle with production of glutathione disulfide (GSSG) has been shown to occur in the diaphragm during inspiratory resistive loading (RB). Buthionine sulfoximine (BSO) lowers tissue GSH by irreversibly inhibiting the rate-limiting synthesis enzyme gamma-glutamylcysteine synthetase. We investigated the effects of BSO on rat diaphragm function, both at rest and after a period of RB. Rats in the RB groups underwent inspiratory RB until they were unable to sustain 70% of their maximal airway pressure. A portion of the diaphragm was analyzed for GSH and GSSG levels, and measurements of in vitro contractile properties included contraction times, maximal tetanic tension (Po), maximal twitch tension (Pt), and force frequency curves. BSO treatment produced a profound depletion of diaphragmatic GSH. Neither BSO nor RB alone significantly altered diaphragm contractile properties at this load of RB. But, in BSO-RB rats, there was a significant decrease in Pt, Po, and tetanic tension at all frequencies of stimulation compared with those in other groups. These data reveal that animals treated with BSO followed by inspiratory resistive loading exhibit marked diaphragm impairment, suggesting that GSH may play an important role in protecting the diaphragm from the stress induced by this resistive breathing protocol.

Analysis of Variance↗
PubMed1993

Diaphragmatic function after resistive breathing in vitamin E-deficient rats.

The effects of vitamin E deficiency on diaphragm function were studied at rest and after resistive breathing (RB) in Sprague-Dawley rats (wt 300-400 g). The animals were pair fed a vitamin E-deficient diet (E-def) or a matched vitamin E-sufficient diet (E-suf). Each diet group was then further subdivided into a group that breathed unimpeded (control) and a second group that breathed through an inspiratory resistor until the animals were unable to sustain 70% of their maximum airway pressure. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances, glutathione (GSH) concentrations, and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile studies were also performed and included twitch (Pt) and maximum tetanic (Po) tensions, force-frequency curves, fatigue index, and recovery index. Pt was significantly reduced in the E-suf RB group as well as both of the E-def groups. Po was also significantly reduced in both E-def groups. The E-def rats subjected to RB showed a significant decrease in tension at both high and low frequencies compared with the E-suf rats. Concentrations of diaphragm thiobarbituric acid-reactive substances were significantly increased in both E-def groups. RB in both E-suf and E-def rats resulted in increases in diaphragm concentrations of GSSG and decreases in the GSH/GSSG ratios. We conclude that reduction of contractile function, lipid peroxidation, and activation of the GSH redox cycle occur with RB and that these effects are significantly increased in the presence of vitamin E deficiency.

Animals↗
PubMed1993

Diethylmaleate produces diaphragmatic impairment after resistive breathing.

Formation of oxygen-derived free radicals and activation of the glutathione (GSH) redox cycle has been associated with impaired rat diaphragm performance. Diethylmaleate (DEM) given intraperitoneally irreversibly conjugates with GSH, resulting in marked decreases in tissue concentrations of GSH. We have investigated the effects of acute GSH depletion by DEM on diaphragmatic function during resistive breathing (RB) in the rat. The experimental groups were 1) control, 2) DEM alone, 3) RB, and 4) DEM with RB (DEM + RB). RB was obtained by inspiratory RB until the rats were unable to sustain 70% of maximum airway opening pressure. A portion of the diaphragm was frozen for biochemical assays, and the rest of the diaphragm was prepared for measurement of in vitro contractile properties, including maximum tetanic tension, twitch tension, force-frequency curves, and contraction times. DEM treatment produced a profound depletion of GSH in the DEM and DEM + RB groups. Neither DEM nor RB alone significantly altered diaphragm contractile properties. In DEM + RB rats, however, there was a significant decrease in maximum tetanic tension, twitch tension, and tetanic tension. These data reveal that DEM produced an acute depletion of GSH in the diaphragm without impairment of the muscle in nonstressed rats. In the presence of DEM-induced GSH depletion, RB did result in marked diaphragm impairment. The depletion of GSH and the subsequent impairment in diaphragm contractility after RB suggest that GSH may play an important role in protecting the diaphragm against oxidative stress associated with RB.

Animals↗
PubMed1992

Muscle atrophy continues after early cast removal following tendon repair.

We studied soleus (SOL), plantaris (PLN), and gastrocnemius (GST) muscles to determine whether early cast removal minimizes muscle atrophy or permits recovery from atrophy after tendon repair. After right tendocalcaneus (Achilles tendon) was transected and repaired, rabbit right hindlimbs were immobilized with the ankle plantar flexed and the knee flexed to 90 degrees. Rabbits were maintained in the cast and sacrificed at 5, 15, or 21 days postoperatively or the cast was removed on day 5 and the animals sacrificed at day 15 or 21. SOL, PLN, and GST muscles of both limbs were removed and weighed, and then histochemical analyses were performed on SOL and PLN muscles. Immobilization decreased SOL muscle wet weights, mean fiber cross-sectional area, and percentage of Type I fibers and increased the percentage of Type IIc fibers. Ten days after cast removal (i.e., postoperative day 15), SOL muscle atrophy and fiber composition did not differ significantly from continuously immobilized controls. However, 16 days after cast removal (i.e., postoperative day 21), SOL muscle fiber cross-sectional area and fiber composition were near normal, differing significantly from continuously casted controls. At each of the time intervals studied, PLN (containing many glycolytic fibers) did not atrophy as much as SOL (containing mainly oxidative fibers). Our results indicate that 1) early cast removal prevents atrophy of PLN glycolytic fibers, but not oxidative fibers in either PLN or SOL, and 2) early cast removal promotes recovery from atrophy of both oxidative and glycolytic fibers. In spite of the many differences between rabbits and humans, these findings suggest that, although early cast removal may not prevent oxidative muscle fiber atrophy after postoperative immobilization, it may facilitate recovery from atrophy.

Achilles Tendon↗
PubMed1992

Immobilization-induced muscle atrophy is not reversed by lengthening the muscle.

In clinical practice, repaired tendocalcaneus (Achilles tendon) ruptures are often protected in immobilization casts for 4 weeks in the fully plantar flexed position and for up to another 4 weeks after returning the ankle to joint neutral. Moderate to severe muscle atrophy occurs within 4 weeks of immobilization in plantar flexion, but it is not known if this atrophy is minimized or reversed following restoration of joint neutral position. We tested the hypothesis that the extent of atrophy could be reduced by returning the ankle to joint neutral after 4 weeks of immobilization. Eighteen rabbits were anesthetized, and their right hind-limbs were casted with the knee flexed 90 degrees and the ankle fully plantar flexed. Three animals each were studied after 3, 4, 6, or 8 weeks of immobilization. After 4 weeks of immobilization, the immobilization casts of the remaining six rabbits were modified to return the ankle to joint neutral for another 2 or 4 weeks. For muscle studies, the animals were anesthetized, and the soleus (SOL), plantaris (PLN), and gastrocnemius (GST) muscles were removed and weighed; the SOL and PLN were quick frozen and processed for histochemical fiber typing and fiber cross-sectional area measurement. All three muscles showed significantly reduced muscle weight to body weight ratios after 3 weeks of immobilization. SOL was the most affected, and GST was least affected. There was no significant further atrophy through 8 weeks of immobilization. The atrophy correlated with a significant reduction of mean fiber area (MFA) for Types I, IIo, and IIc fibers in SOL and PLN. In PLN, Type IIg fiber area was not significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of exercise and food restriction on rat skeletal muscles.

Studies were undertaken to compare the effects of exercise and food restriction on body weight (BW), muscle weight (MW), muscle fiber size, and proportion of muscle fiber types. 20 male Fischer 344 rats were randomly assigned to four equal groups: ad libitum-fed control (AC), ad libitum-fed exercise (AE), food restricted control (RC) and food restricted exercise (RE). From 6 weeks of age, RC and RE rats received 60% of the daily food intake of AC and AE rats, respectively. At 7 months of age, AE and RE rats began 40-50 min of daily treadmill exercise. Running speed increased from 1.2 to 1.6 miles/hour and the grade increased to 15% during the first 2 weeks of training. After 10 weeks of training, rats were weighed, sacrificed, and the soleus (SOL), plantaris (PLN) and extensor digitorum longus (EDL) muscles were removed at in situ rest length, weighed, and quick-frozen. Standard histochemical assays were performed, and muscle fiber cross-sectional area was determined planimetrically. Training had little effect on MW or BW, but food restriction greatly reduced BW. This resulted in greater MW/BW ratio in RC and RE than AC and AE rats, respectively. Exercise also increased SOL muscle fiber area in ad libitum-fed but not food restricted rats resulting in smaller fibers in SOL of RE than AE. No changes in percentage of SOL fiber types occurred with food restriction or exercise. In PLN, the percentage of fast-twitch oxidative fibers of AE and RE was greater than in AC and RC, but there was no effect of food restriction or exercise on fiber area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1992

Ultrastructural morphometry of matrical changes induced by exercise and food restriction in the rat calcaneal tendon.

The ultrastructural morphometry of collagen fibril populations in 24 calcaneal tendons obtained from 12 Fischer 344 rats were studied to elucidate matrical changes induced by food restriction and/or endurance exercise. Rats were randomly assigned to four equal groups: ad libitum control (AC), ad libitum exercise (AE), restricted diet control (RC) and restricted diet exercise (RE) groups. Beginning from 6 weeks of age, animals in the two food restriction groups were fed 60% of the mean food consumption of ad libitum fed rats. Then, starting from 6-7 months of age, the rats in the two exercise groups performed 40-50 min of treadmill running at 1.2-1.6 miles h-1 every day for a total of 10 weeks. Endurance training did not significantly alter body weight, but food restriction with or without exercise resulted in a significant loss of body weight. In ad libitum fed controls, food restriction alone did not significantly alter the mean collagen fibril CSA, but predisposed a preponderance of small-sized collagen fibrils. Endurance training per se induced a significant (32%) increase in mean fibril CSA (P less than 0.05), but this adaptive response to exercise was prevented by food restriction, as indicated by a 33% decline in fibril CSA (P less than 0.05). These findings demonstrate that dietary restriction modifies the adaptation of tendon collagen morphometry in response to endurance training, and that weight loss is better achieved with food restriction than endurance exercise.

Animal Nutritional Physiological Phenomena↗
PubMed1992

Resistive breathing activates the glutathione redox cycle and impairs performance of rat diaphragm.

Free radical activation and lipid peroxidation have been described in skeletal muscle during strenuous exercise. We hypothesized that oxygen radicals could also be formed in the diaphragm muscle during strenuous resistive breathing and that these radicals might affect diaphragm function. Seven control and 12 experimental male Sprague-Dawley rats were studied. Six experimental animals were subjected to resistive breathing (RB) alone and six animals received 15 min of mechanical ventilatory support (MV) after the resistive breathing period. Inspiratory resistance was adjusted to maintain airway opening pressure at 70% maximum in both groups until exhaustion. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances (TBAR), reduced glutathione (GSH), and glutathione disulfide (GSSG). In vitro isometric contraction times, twitch (Pt) tension and maximum tetanic (Po) tension, force-frequency curves, fatigue index, and recovery index were measured. In RB and MV compared with controls, there were significant decreases in Pt and Po. Diaphragm TBAR concentrations were increased in MV compared with controls or RB. GSSG-to-total glutathione ratio was increased in RB and MV compared with controls. Production of free radicals during RB and MV may represent an important mechanism of diaphragmatic injury that could contribute to the decline in contractility.

Airway Resistance↗
PubMed1990

Running during recovery from hindlimb suspension induces transient muscle injury.

The objectives were to study morphological adaptations of soleus muscle to decreased loading induced by hindlimb suspension and the effect of run training during the subsequent recovery period. Adult female Wistar rats were kept for 28 days with hindlimbs suspended. For the next 28 days, rats were assigned to a cage-sedentary or daily running group. Compared with control soleus muscles, 28 days of hindlimb suspension reduced the mass and fiber cross-sectional area to 58 and 53% of control values, respectively, and decreased type I fibers from 92 +/- 2 to 81 +/- 2%. During recovery, clusters of damaged fibers were observed in the soleus muscle, and this observation was more pronounced in trained animals. Type IIc fibers appeared transiently during recovery, and their presence was exacerbated with training, as IIc fibers increased to approximately 20% of the total by day 14 of recovery and were no longer evident at day 28. Although muscle wet mass does not differ as a result of mode of recovery at day 14, training transiently decreased the overall fiber area compared with sedentary recovery at this point. By day 28 of recovery the morphological characteristics of soleus muscle in the trained group did not differ from control muscle, whereas in the sedentary group muscle mass and overall fiber cross-sectional area were approximately 14% less than control values.

Animals↗
PubMed1989

Regional distribution of fiber types in developing baboon diaphragm muscles.

Fiber type distribution and mean fiber area were determined for seven sites in diaphragm muscles of premature (140 days gestation), full-term (180 days gestation), and adult baboons. Within a group, data did not differ significantly amongst the seven sites. The diaphragm of premature animals had a large proportion [56(+/- 2)%] of type IIc fibers, smaller proportions of type I, IIo, and IIh fibers [16(+/- 2), 21(+/- 1), and 7(+/- 2)%, respectively], and no type IIg fibers. Full-term animals had fewer type IIc [2(+/- 1)%] fibers, greater proportions of type I [46(+/- 2)%], IIh [23(+/- 1)%], and IIg [11(+/- 1)%] fibers, and a similar proportion of type IIo fibers [17(+/- 1)%]. Diaphragm from adult baboons had similar proportions of type IIh, IIg, and IIc fibers in females [39(+/- 4), 20(+/- 2), 1(+/- 1), 41(+/- 5), and 1(+/- 1)%] and males [48(+/- 2), 16 (+/- 1), 0(+/- 0), 36(+/- 2), and 3(+/- 2)%]. Fiber area for premature [143(+/- 9), 210(+/- 15), 231(+/- 15), and 156(+/- 16) microns2 for type I, IIo, IIh, and IIc fibers], newborn [317(+/- 32), 374(+/- 36), 468(+/- 42), 498(+/- 43), and 322(+/- 37) microns2 for type I, IIo, IIh, IIg, and IIc fibers], and for type I, IIo, IIg, and IIc fibers from adult female [1,759(+/- 130), 2,365(+/- 284), 5,026(+/- 742), and 1,843(+/- 111) microns2] and adult male [2,513(+/- 221), 3,987(+/- 267), 6,102(+/- 376), and 2,833(+/- 151) microns2] baboons indicated growth which correlated with body weight. Our results also show that metabolic and contractile enzymes develop normally, but growth of respiratory muscle fibers is arrested, during 10 days following premature birth.

Animals↗
PubMed1987

Analysis of contractile properties of muscles from rats immunized with purified acetylcholine receptor.

Experimental autoimmune myasthenia gravis (EAMG) was induced in rats by injection of purified acetylcholine receptor (AChR). In addition to detecting elevated serum titers of anti-AChR antibodies, we observed decreased twitch-tension at submaximal stimulation voltages and increased curare sensitivity by muscles obtained from immunized rats when compared to muscles obtained from nonimmune control rats. Furthermore, antibody-induced neuromuscular impairment was expressed to differing extents dependent on whether the diaphragm, soleus, or extensor digitorum longus muscle was examined. Thus, we conclude that potential antibody perturbation of AChR function will depend not only on the nature of the antibody, but also on the complex structure-function relationships that exist in individual muscles. This may partially explain the variable impairment of different muscle groups in patients with myasthenia.

Animals↗