Congestive heart failure: differential adaptation of the diaphragm and latissimus dorsi

1995 ◽  
Vol 79 (2) ◽  
pp. 389-397 ◽  
Author(s):  
S. Howell ◽  
J. M. Maarek ◽  
M. Fournier ◽  
K. Sullivan ◽  
W. Z. Zhan ◽  
...  

Diaphragm and latissimus dorsi muscle functions, histochemistries, and morphometries were studied in anesthetized male Yucatan minipigs with congestive heart failure (CHF) induced by supraventricular tachycardia (n = 5). Sham-operated animals served as a control group (n = 5). In CHF animals, transdiaphragmatic pressure measured during supramaximal phrenic stimulation was reduced by 40% at low frequencies (< or = 20 Hz) and by 60% at higher frequencies. Twitch amplitude and half-relaxation time were also decreased. The cross-sectional areas of type I, IIa, and IIb fibers were reduced in the diaphragm. The proportion of type I fibers increased, whereas type IIa fibers decreased. Succinate dehydrogenase activity was elevated in type IIa and IIb fibers, but diaphragmatic fatigability was not altered. CHF reduced latissimus dorsi isometric force by 40% for stimulation frequencies > or = 30 Hz. The cross-sectional area of latissimus dorsi type IIb fibers was decreased, but twitch characteristics, fiber type composition, succinate dehydrogenase activity, and fatigability were unchanged. Experimental CHF appears to cause greater intrinsic adaptive changes in the diaphragm compared with those in the latissimus dorsi in the minipig. For both muscles, reduced contractile function was associated with atrophy. Impaired performance of the diaphragm may also be attributed to an increase in the relative contribution of type I fibers to the total tension-generating capacity of the muscle and to the pathophysiological mechanisms underlying the shortened relaxation time of the twitch response.

1994 ◽  
Vol 77 (2) ◽  
pp. 947-955 ◽  
Author(s):  
M. I. Lewis ◽  
S. A. Monn ◽  
W. Z. Zhan ◽  
G. C. Sieck

Interactive effects of emphysema (EMP) and prolonged nutritional deprivation (ND) on contractile, morphometric, and metabolic properties of hamster diaphragm muscle (DIA) were examined. Six months after induction of EMP (intratracheal elastase), saline-treated controls (CTL) and EMP hamsters of similar body weights were subjected to ND over 6 wk. Isometric contractile and fatigue properties of costal DIA were determined in vitro. DIA fibers were histochemically classified as type I or II, and fiber succinate dehydrogenase activity and cross-sectional area were determined using quantitative microscopic procedures. From histochemical sections, the number of capillaries per fiber (C/F) and per fiber cross-sectional area (C/A) were determined. ND resulted in progressive loss of body weight (ND-CTL, 23.8%; ND-EMP, 28.4%; P = NS). ND did not affect reduction in optimal length (Lo) of DIA fibers in EMP compared with CTL and ND-CTL hamsters. Maximum specific force (i.e., force/unit area) was reduced by approximately 25% in EMP animals compared with CTL. ND did not improve or exacerbate the reduction in specific force with EMP. ND attenuated improved fatigue resistance of DIA in EMP animals. No differences in fiber type proportions were noted among experimental groups. Significant atrophy of type I and II DIA fibers was noted after ND. Atrophy was proportionately greater in type II fibers of ND-EMP when referenced to EMP animals. Thus adaptive hypertrophy of type II DIA fibers in EMP animals was abolished. Fiber succinate dehydrogenase activity was significantly increased in type I and II fibers in EMP DIA. ND did not affect this metabolic adaptation of DIA fibers to persistent loads imposed by EMP.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 128 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Matthew J. Fogarty ◽  
Natalia Marin Mathieu ◽  
Carlos B. Mantilla ◽  
Gary C. Sieck

In aged rats, diaphragm muscle (DIAm) reduced specific force and fiber cross-sectional area, sarcopenia, is selective for vulnerable type IIx and/or IIb DIAm fibers, with type I and IIa fibers being resilient. In humans, the oxidative capacity [as measured by maximum succinate dehydrogenase (SDHmax) activity] of fast-type muscle is reduced with aging, with slow-type muscle being unaffected. We hypothesized that in aged Fischer rat DIAm exhibiting sarcopenia, reduced SDHmax activity would occur in type IIx and/or IIb fibers. Rats obtained from the NIA colony (6, 18, and 24 mo old) were euthanized, and ~2-mm-wide DIAm strips were obtained. For SDHmax and fiber type assessments, DIAm strips were stretched (approximately optimal length), fresh frozen in isopentane, and sectioned on a cryostat at 6 μm. SDHmax, quantified by intensity of nitroblue tetrazolium diformazan precipitation, was assessed in a fiber type-specific manner by comparing serial sections labeled with myosin heavy chain (MyHC) antibodies differentiating type I (MyHCSlow), IIa (MyHC2A), and IIx and/or IIb fibers. Isometric DIAm force and fatigue were assessed in DIAm strips by muscle stimulation with supramaximal pulses at a variety of frequencies (5–100 Hz) delivered in 1-s trains. By 24 mo, DIAm sarcopenia was apparent and SDHmax in type IIx and/or IIb fibers activity was reduced ~35% compared with 6-mo-old control DIAm. These results underscore the remarkable fiber type selectivity of type IIx and/or IIb fibers to age-associated perturbations and suggest that reduced mitochondrial oxidative capacity is associated with DIAm sarcopenia. NEW & NOTEWORTHY We examined the oxidative capacity as measured by maximum succinate dehydrogenase activity in older (18 or 24 mo old) Fischer 344 rat diaphragm muscle (DIAm) compared with young rats (6 mo old). In 24-mo-old rats, SDH activity was reduced in type IIx/b DIAm fibers. These SDH changes were concomitant with sarcopenia (reduced specific force and atrophy of type IIx/b DIAm fibers) at 24 mo old. At 18 mo old, there was no change in SDH activity and no evidence of sarcopenia.


1978 ◽  
Vol 44 (3) ◽  
pp. 431-437 ◽  
Author(s):  
L. C. Maxwell ◽  
J. A. Faulkner ◽  
S. A. Mufti ◽  
A. M. Turowski

Fifty extensor digitorium longus muscles of 25 cats were autografted, 33 with and 17 without prior denervation. After 50 days, no significant differences were observed between predenervated and nonpredenervated autografts. Autografted muscles weighed 48% of the weight of control muscles. Few original muscle fibers survived and within 2 wk autografts contained regenerating muscle fibers. The mean cross-sectional area of muscle fibers in the autografts reached 125% of the value for control nontransplanted muscles. The mean percentage of fibers classified high oxidative in autografted muscles was 67% of values for control muscles. SDH activity of autografted muscle homogenates reached 55% of control values. Up to 60 days after surgery autografts had only fast-twitch fibers. At 170 days autografts remained 95% fast twitch in composition. Revascularization began within 4 days, but the capillary to fiber ratio of long term autografts reached only 60% of control values. Although fiber hypertrophy suggests that cats use autografted muscles, lower than control succinate dehydrogenase activity may result from altered recruitment.


1992 ◽  
Vol 72 (4) ◽  
pp. 1401-1406 ◽  
Author(s):  
T. P. Martin ◽  
R. B. Stein ◽  
P. H. Hoeppner ◽  
D. C. Reid

Selected morphological and metabolic properties of single fibers were studied in biopsy samples from the tibialis anterior of normal control and spinal cord-injured (SCI) subjects. In the SCI subjects, one muscle was electrically stimulated progressively over 24 wk, in 6-wk blocks for less than or equal to 8 h/day, while the contralateral muscle remained untreated. The percentage of fibers classified as type I [qualitative alkaline preincubation myofibrillar adenosinetriphosphatase (ATPase)] was significantly less in the unstimulated paralyzed muscles than in the muscles of normal control subjects. Electrical stimulation increased the proportion of type I fibers in the SCI subjects. For both type I and type II fibers, the cross-sectional area, activities of myofibrillar ATPase and succinate dehydrogenase, and the capillary-to-fiber ratio were also significantly less in the paralyzed muscles than in the normal control muscles. Electrical stimulation increased only the activity of succinate dehydrogenase in both fiber types of the SCI subjects. These data are discussed in relation to the electromechanical properties of the respective muscles described in an accompanying paper (J. Appl. Physiol. 72: 1393–1400, 1992). In general, the electrical stimulation protocol used in this study enhanced the oxidative capacity and endurance properties of the paralyzed muscles but had no effect on fiber size and strength.


1995 ◽  
Vol 78 (6) ◽  
pp. 2115-2120 ◽  
Author(s):  
V. K. Sullivan ◽  
S. K. Powers ◽  
D. S. Criswell ◽  
N. Tumer ◽  
J. S. Larochelle ◽  
...  

The objective of this study was to determine the effects of age and exercise on the myosin heavy chain (MHC) composition of skeletal muscle. Young (3 mo) and old (22 mo) female specific pathogen-free barrier-reared Fischer 344 rats were randomly assigned to young untrained or young trained and old untrained or old trained groups, respectively. Young trained and old trained animals performed endurance exercise training on a motorized treadmill for 8 wk. Succinate dehydrogenase activity and MHC isoforms were measured in the plantaris (Plan), lateral and medial gastrocnemius (Gast), and soleus (Sol) muscles. In sedentary animals, aging resulted in a decrease (P < 0.05) in type IIb MHC and an increase (P < 0.05) in type IIa MHC in both the Gast and Plan muscles. Also, aging resulted in a small but significant increase (approximately 4%; P < 0.05) in type I MHC in the Sol. Exercise training resulted in significant (P < 0.05) increases in Gast, Plan, and Sol succinate dehydrogenase activity in both young and old animals. Furthermore, exercise training resulted in a decrease (P < 0.05) in the percentage of type IIb MHC and an increase (P < 0.05) in the percentage of type IIa MHC in the Plan in both young and old animals. These data suggest that there is an age-related shift in locomotor muscle MHC isoforms from a faster to a slower isoform.


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