Force development and metabolism in skeletal muscle of euthyroid and hypothyroid rats

1981 ◽  
Vol 97 (2) ◽  
pp. 221-225 ◽  
Author(s):  
M. E. Everts ◽  
C. van Hardeveld ◽  
H. E. D. J. Ter Keurs ◽  
A. A. H. Kassenaar
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Muscle Metabolism ◽  
Glucose Consumption ◽  
Triceps Surae ◽  
Active Force ◽  
Muscle Preparation ◽  
Force Development ◽  
Contraction Process ◽  
Triceps Surae Muscles

Abstract. The effects of thyroid hormone depletion on skeletal muscle metabolism in relation to force development were studied. For this purpose, the triceps surae muscles were perfused and stimulated at 5 Hz. The basal oxygen consumption of the skeletal muscle preparation was 50% lower in hypothyroid rats as compared with euthyroid rats. The results show that: 1. Active force development was the same in euthyroid and hypothyroid rats during 30 min of stimulation. 2. The increase in oxygen consumption during contraction was twice as high in the euthyroid group compared with the hypothyroid group. 3. Lactate release and glucose consumption were considerably higher in the euthyroid group than in the hypothyroid group during the last 15 min of stimulation. The data show that force development is not impaired in hypothyroid rats but, on the contrary, indicate that the contraction process proceeds more economically in hypothyroid rats than in euthyroid rats.

EFFECTS OF EXPERIMENTAL HYPOTHYROIDISM ON SKELETAL MUSCLE METABOLISM IN THE RAT

1978 ◽  
Vol 87 (1) ◽  
pp. 114-124 ◽  
Author(s):  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Initial Level ◽  
Control Level ◽  
Lactate Production ◽  
Muscle Metabolism ◽  
Glucose Consumption ◽  
Glycerol Production ◽  
Base Level ◽  
Limb Perfusion

ABSTRACT Hind-limb perfusion was used to study the effect of thyroidectomy on some metabolic parameters in the skeletal muscle of the rat. A week after thyroidectomy obtained by one dose of 3/4 mCi 131I, neither T4 nor T3 was detected in the blood. Lactate production and glycerol production were already decreased a week after the treatment and reached a base level at two weeks. At that time, the oxygen consumption was significantly lower (70 % of initial level) than in the control animals and decreased further in the third week to nearly 50 % of the control level. Glucose consumption and alanine release were decreased three weeks after thyroidectomy. One dose of T3 (10 μg/100 g b. w.), administered to animals two weeks after the injection of 131I, restored the oxygen consumption, lactate production, and glycerol production to normal levels in 24 h. After 48 h, the glucose consumption was normal. Glycerol production was already significantly increased 6 h after T3 injection in animals one week after thyroidectomy, and in another group of animals two weeks after thyroidectomy. Apparently the diminished oxygen consumption in the latter group does not retard the lipolytic response to T3. No direct relationship could be found between the activity of lipolytic process and the thyroid hormone controlled oxygen consumption.

INFLUENCE OF EXPERIMENTAL HYPERTHYROIDISM ON SKELETAL MUSCLE METABOLISM IN THE RAT

1977 ◽  
Vol 85 (1) ◽  
pp. 71-83 ◽  
Author(s):  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Dose Range ◽  
Nervous Activity ◽  
Lactate Production ◽  
Muscle Metabolism ◽  
Glucose Consumption ◽  
Daily Injection ◽  
Limb Perfusion ◽  
Energy Consuming

ABSTRACT In this study hind-limb perfusion was used to investigate the influence of thyroid hormones on some metabolic parameters in the skeletal muscle of the rat. Daily injection of 20 μg L-thyroxine (T4) per 100 g b. w. for a week caused a 25 % increase in oxygen consumption. Further enlargement of the T4 dose had little additive effect. In the dose range 20–80 μg T4/100 g b. w., no important changes occurred in lactate production or glucose consumption. Only at the highest T4 dose did the glucose consumption increase significantly. The most profound effect of T4 was on lipolysis. A daily dose of 20 μg T4/100 g b. w. gave a doubling of glycerol production rate, the maximum occurring at a dose of 40 μg T4/100 g b. w Inactivation of the nervous system was without influence on the T4-induced increase in oxygen consumption. However, the T4-induced elevation of lipolysis disappeared after abolition of the nervous activity. This raises the possibility that the T4 effect on lipolysis in skeletal muscle is a potentiation of catecholamine effects. The T4-induced oxygen consumption increase might be dependent not on the lipolytic process but rather on other energy-consuming cell processes.

Production of hydroxyl radicals in contracting skeletal muscle of cats

1996 ◽  
Vol 81 (3) ◽  
pp. 1197-1206 ◽  
Author(s):  
C. A. O'Neill ◽  
C. L. Stebbins ◽  
S. Bonigut ◽  
B. Halliwell ◽  
J. C. Longhurst
Keyword(s):  
Skeletal Muscle ◽  
Triceps Surae ◽  
Oxygen Species ◽  
Static Contraction ◽  
Maximal Tension ◽  
Cumulative Production ◽  
Triceps Surae Muscles ◽  
Specific Species

Reactive oxygen species increase during exhaustive contraction of skeletal muscle, but characterization of the specific species involved and their rates of production during nonexhaustive muscle contraction have not been investigated. We hypothesized that the production rate of hydroxyl radical (.OH) increases in contracting muscle and that this rate is attenuated by pretreatment with deferoxamine (Def) or dimethylthiourea (DMTU). We measured the rate of production of .OH before, during, and after 5 min of intermittent static contraction of the triceps surae muscles in cats (n = 6) using the formation of p-, m-, and o-tyrosines by hydroxylation of phenylalanine. L-Phenylalanine (30 mg/kg i.v.) was administered to each animal 3 min before contraction. Blood samples were collected from the popliteal vein 1 min before contraction; 1, 3, and 4.5 min during contraction; and 1 min after contraction. During and after contraction, the cumulative production rates of p-, m-, and o-tyrosines were elevated by 42.84 +/- 5.41, 0.25 +/- 0.04, and 0.21 +/- 0.03 nmol.min-1.g-1, respectively, compared with noncontracting triceps surae muscles. Pretreatment with Def (10 mg/kg i.v.; n = 5) or DMTU (10 mg/kg i.v.; n = 4) decreased the cumulative rates of production of p-, m-, and o-tyrosines during and after contraction. Additionally, the rate of tyrosine production increased in proportion to the percentage of maximal tension developed by the triceps surae muscles. These results directly demonstrate that .OH is produced in vivo in the skeletal muscle of cats during intermittent static contraction and that production can occur before the onset of fatigue.

scholarly journals IMP2 Increases Mouse Skeletal Muscle Mass and Voluntary Activity by Enhancing Autocrine Insulin-Like Growth Factor 2 Production and Optimizing Muscle Metabolism

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Laura Regué ◽  
Fei Ji ◽  
Daniel Flicker ◽  
Dana Kramer ◽  
William Pierce ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Growth Factor ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Wheel Running ◽  
Muscle Metabolism ◽  
Insulin Like Growth Factor ◽  
Voluntary Activity ◽  
Mouse Muscle

ABSTRACT Insulin-like growth factor 2 (IGF2) mRNA binding protein 2 (IMP2) was selectively deleted from adult mouse muscle; two phenotypes were observed: decreased accrual of skeletal muscle mass after weaning and reduced wheel-running activity but normal forced treadmill performance. Reduced wheel running occurs when mice are fed a high-fat diet but is normalized when mice consume standard chow. The two phenotypes are due to altered output from different IMP2 client mRNAs. The reduced fiber size of IMP2-deficient muscle is attributable, in part, to diminished autocrine Igf2 production; basal tyrosine phosphorylation of the insulin and IGF1 receptors is diminished, and Akt1 activation is selectively reduced. Gsk3α is disinhibited, and S536-phosphorylated ε subunit of eukaryotic initiation factor 2B [eIF2Bε(S536)] is hyperphosphorylated. Protein synthesis is reduced despite unaltered mTOR complex 1 activity. The diet-dependent reduction in voluntary exercise is likely due to altered muscle metabolism, as contractile function is normal. IMP2-deficient muscle exhibits reduced fatty acid oxidation, due to a reduced abundance of mRNA of peroxisome proliferator-activated receptor α (PPARα), an IMP2 client, and PPARα protein. IMP2-deficient muscle fibers treated with a mitochondrial uncoupler to increase electron flux, as occurs with exercise, exhibit reduced oxygen consumption from fatty acids, with higher oxygen consumption from glucose. The greater dependence on muscle glucose metabolism during increased oxygen demand may promote central fatigue and thereby diminish voluntary activity.

Muscle reflex stimulates sympathetic postganglionic efferents innervating triceps surae muscles of cats

1996 ◽  
Vol 271 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
J. M. Hill ◽  
C. M. Adreani ◽  
M. P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Cardiovascular Function ◽  
Triceps Surae ◽  
Sympathetic Outflow ◽  
Central Command ◽  
Muscle Reflex ◽  
Triceps Surae Muscles ◽  
Nerve Recordings ◽  
Stimulation Of

Two neural mechanisms contribute to the cardiovascular responses to exercise. The first, central command, proposes a parallel activation of central locomotor and brain stem circuits controlling cardiovascular function. The second, the muscle reflex, proposes that contraction-activated group III and IV afferents increase cardiovascular function. In humans, whole nerve recordings of sympathetic discharge suggest that central command increases sympathetic outflow to skin but not to skeletal muscle and that the muscle reflex increases sympathetic outflow to skeletal muscle but not to skin. We therefore tested the hypothesis that the muscle reflex, but not central command, increases the discharge of single sympathetic postganglionic efferents innervating the triceps surae muscles of decerebrate unanesthetized cats. Central command was evoked by electrical stimulation of the mesencephalic locomotor region. The reflex was evoked by electrical stimulation of the tibial nerve, which in turn contracted the triceps surae muscles. Hexamethonium abolished spontaneous and evoked activity, verifying that the recordings were from sympathetic postganglionic fibers. The discharge of 13 efferents was increased by static contraction (from 0.6 +/- 0.2 to 1.0 +/- 0.3 imp/s; P < 0.05) but was not increased by central command (from 0.6 +/- 0.2 to 0.8 +/- 0.2 imp/s; P > 0.05). Nevertheless, the discharge of nine efferents, not increased by central command before alpha-adrenergic blockade (from 0.5 +/- 0.2 to 0.9 +/- 0.4 imp/s; P > 0.05), was increased after blockade (from 1.3 +/- 0.2 to 3.2 +/- 0.8 imp/s; P < 0.05). We conclude that the muscle reflex stimulates sympathetic postganglionic efferents innervating the vasculature of skeletal muscle. Furthermore, baroreceptors appear to buffer the central command-induced increases in the discharge of these efferents.

scholarly journals Effects of previous activity on the energetics of activation in frog skeletal muscle.

1980 ◽  
Vol 75 (6) ◽  
pp. 617-631 ◽  
Author(s):  
J A Rall
Keyword(s):  
Skeletal Muscle ◽  
Time Delay ◽  
Time Course ◽  
Frog Skeletal Muscle ◽  
Active Force ◽  
Force Development ◽  
Uptake Sites ◽  
Contractile Activation ◽  
Terminal Cisternae ◽  
Activation Heat

Effects of previous activity on the ability of frog skeletal muscle at 0 degrees C to liberate energy associated with contractile activation, i.e., activation heat (AH), have been examined. Earlier work suggests that activation heat amplitude (as measured from muscles stretched to lengths where active force development is nearly abolished) is related to the amount of Ca2+ released upon stimulation. After a twitch, greater than 2 s is required before a second stimulus (AHt) can liberate the same activation heat as a first stimulus (AH infinity), i.e., (AHt)/(AH infinity) = 1 -0.83 e-1.40t, where t is time in seconds. Caffeine introduces a time delay in the recovery of the ability to generate activation heat after a twitch. After a tetanus, the activation heat is depressed to a greater extent at any time than after a twitch. The activation heat elicited by a stimulus 1 s after a tetanus is depressed progressively with respect to tetanus duration up to 3 s. For tetani of 3, 40, and 80 s duration the postetanus activation heat is comparably depressed. The time-course of the recovery of the ability of the muscle to produce activation heat after a tetanus can be described as (AHt)/(AH infinity) = 1 -0.80 e-0.95t -0.20 e-0.02t. Greater than 90 s is required before the posttetanus activation heat is equal to the pretetanus value. The faster phase of recovery is similar to recovery after the twitch and the slower phase may be associated with the return of calcium to the terminal cisternae from uptake sites in the longitudinal sarcoplasmic reticulum.

Reflex effect of skeletal muscle mechanoreceptor stimulation on the cardiovascular system

1988 ◽  
Vol 65 (4) ◽  
pp. 1539-1547 ◽  
Author(s):  
C. L. Stebbins ◽  
B. Brown ◽  
D. Levin ◽  
J. C. Longhurst
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
External Pressure ◽  
Triceps Surae ◽  
Static Contraction ◽  
Muscle Mechanoreceptor ◽  
Triceps Surae Muscles ◽  
Passive Stretch

To determine the potential for mechanical stimulation of skeletal muscle to contribute to the reflex cardiovascular response to static contraction (exercise reflex), we examined the cardiovascular effects caused by either passive stretch or external pressure applied to the triceps surae muscles. First, the triceps surae were stretched to an average developed tension of 4.8 +/- 0.3 kg. This resulted in increases in mean arterial pressure (MAP) of 28 +/- 7 mmHg, dP/dt of 1,060 +/- 676 mmHg/s, and heart rate (HR) of 6 +/- 2 beats/min (P less than 0.05). Additionally, increments of 0.3, 0.5, 1.0, 2.0, 4.0, and 8.0 kg of tension produced by passive stretch elicited pressor responses of -6 +/- 1, 7 +/- 1, 16 +/- 3, 21 +/- 8, 28 +/- 6, and 54 +/- 9 mmHg, respectively. External pressure, applied with a cuff to the triceps surae to produce intramuscular pressures (125-300 mmHg) that were similar to those seen during static contraction, also elicited small increases in MAP (4 +/- 1 to 10 +/- 1 mmHg) but did not alter HR. Transection of dorsal roots L5-L7 and S1 abolished the responses to passive stretch and external pressure. Moreover, when the triceps surae were stretched passively to produce a pattern and amount of tension similar to that seen during static hindlimb contraction, a significant reflex cardiovascular response occurred. During this maneuver, the pressor response averaged 51% of that seen during contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Acid-sensing ion channels contribute to the metaboreceptor component of the exercise pressor reflex

2009 ◽  
Vol 297 (1) ◽  
pp. H443-H449 ◽  
Author(s):  
Jennifer L. McCord ◽  
Hirotsugu Tsuchimochi ◽  
Marc P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Pressor Response ◽  
Triceps Surae ◽  
Exercise Pressor Reflex ◽  
Acid Sensing Ion Channels ◽  
Pressor Responses ◽  
Static Contraction ◽  
Pressor Reflex ◽  
Triceps Surae Muscles

The exercise pressor reflex is evoked by both mechanical and metabolic stimuli arising in contracting skeletal muscle. Recently, the blockade of acid-sensing ion channels (ASICs) with amiloride and A-316567 attenuated the reflex. Moreover, amiloride had no effect on the mechanoreceptor component of the reflex, prompting us to determine whether ASICs contributed to the metaboreceptor component of the exercise pressor reflex. The metaboreceptor component can be assessed by measuring mean arterial pressure during postcontraction circulatory occlusion when only the metaboreceptors are stimulated. We examined the effects of amiloride (0.5 μg/kg), A-317567 (10 mM, 0.5 ml), and saline (0.5 ml) on the pressor response to and after static contraction while the circulation was occluded in 30 decerebrated cats. Amiloride ( n = 11) and A-317567 ( n = 7), injected into the arterial supply of the triceps surae muscles, attenuated the pressor responses both to contraction while the circulation was occluded and to postcontraction circulatory occlusion (all, P < 0.05). Saline ( n = 11), however, had no effect on the pressor responses to contraction while the circulation was occluded or to postcontraction circulatory occlusion (both, P > 0.79). Our findings led us to conclude that ASICs contribute to the metaboreceptor component of the exercise pressor reflex.

scholarly journals No effect of acute beetroot juice ingestion on oxygen consumption, glucose kinetics, or skeletal muscle metabolism during submaximal exercise in males

2016 ◽  
Vol 120 (4) ◽  
pp. 391-398 ◽  
Author(s):  
Scott Betteridge ◽  
Raúl Bescós ◽  
Miquel Martorell ◽  
Antoni Pons ◽  
Andrew P. Garnham ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Muscle Metabolism ◽  
Glucose Disposal ◽  
Beetroot Juice ◽  
Glucose Kinetics ◽  
Nonesterified Fatty Acids ◽  
Skeletal Muscle Metabolism ◽  
Acute Ingestion ◽  
Plasma Nitrite

Beetroot juice, which is rich in nitrate (NO3−), has been shown in some studies to decrease oxygen consumption (V̇o2) for a given exercise workload, i.e., increasing efficiency and exercise tolerance. Few studies have examined the effect of beetroot juice or nitrate supplementation on exercise metabolism. Eight healthy recreationally active males participated in three trials involving ingestion of either beetroot juice (Beet; ∼8 mmol NO3−), Placebo (nitrate-depleted Beet), or Beet + mouthwash (Beet+MW), all of which were performed in a randomized single-blind crossover design. Two-and-a-half hours later, participants cycled for 60 min on an ergometer at 65% of V̇o2 peak. [6,6-2H]glucose was infused to determine glucose kinetics, blood samples obtained throughout exercise, and skeletal muscle biopsies that were obtained pre- and postexercise. Plasma nitrite [NO2−] increased significantly (∼130%) with Beet, and this was attenuated in MW+Beet. Beet and Beet+MW had no significant effect on oxygen consumption, blood glucose, blood lactate, plasma nonesterified fatty acids, or plasma insulin during exercise. Beet and Beet+MW also had no significant effect on the increase in glucose disposal during exercise. In addition, Beet and Beet+MW had no significant effect on the decrease in muscle glycogen and phosphocreatine and the increase in muscle creatine, lactate, and phosphorylated acetyl CoA carboxylase during exercise. In conclusion, at the dose used, acute ingestion of beetroot juice had little effect on skeletal muscle metabolism during exercise.

Bradykinin release from contracting skeletal muscle of the cat

1990 ◽  
Vol 69 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
C. L. Stebbins ◽  
O. A. Carretero ◽  
T. Mindroiu ◽  
J. C. Longhurst
Keyword(s):  
Skeletal Muscle ◽  
Arterial Occlusion ◽  
Triceps Surae ◽  
Strongly Correlated ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Before And After ◽  
Pressor Reflex ◽  
Triceps Surae Muscles ◽  
Induced Changes

Results of previous studies from our laboratory suggest that bradykinin has a role in the exercise pressor reflex elicited by static muscle contraction. The purpose of this study was to quantify the release of bradykinin from contracting skeletal muscle. In 18 cats, blood samples were withdrawn directly from the venous effluent of the triceps surae muscles immediately before and after 30 s of static contraction producing peak muscle tensions of 33, 50, and 100% of maximum electrically stimulated contraction. Contractions producing muscle tensions of 50 and 100% of maximum increased muscle venous bradykinin levels by 27 +/- 9 and 19 +/- 10 pg/ml, respectively. Conversely, 33% maximum contraction did not alter muscle venous bradykinin concentrations. However, when captopril was administered to slow the degradation of bradykinin, muscle venous bradykinin increased from 68 +/- 15 pg/ml at rest to 106 +/- 18 after contractions of 33% of maximum. When muscle ischemia was induced by 2 min of arterial occlusion before and during 30 s of 33% of maximum contraction, muscle venous bradykinin increased by 15 +/- 5 pg/ml. In addition, contraction-induced changes in muscle venous pH and lactate strongly correlated with bradykinin concentrations (r = 0.80 and 0.83, respectively). These data demonstrate that static contraction of relatively high intensity evokes the release of bradykinin from skeletal muscle and that ischemia, decreased pH, and increased lactate are strongly correlated with this release.

Sign in / Sign up

Export Citation Format

Share Document