J Appl Physiol 95: 330-335, 2003.
First published March 14, 2003; doi:10.1152/japplphysiol.00040.2003
8750-7587/03 $5.00
Insulin does not mediate the attenuation of fatigue associated with glucose infusion in rat plantaris muscle
Antony D. Karelis,
François Péronnet, and
Phillip F. Gardiner
Département de Kinésiologie, Université de Montréal, Montréal, Québec, Canada H3C 3J7
Submitted 15 January 2003
; accepted in final form 5 March 2003
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ABSTRACT
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Glucose infusion attenuates fatigue in rat plantaris muscle stimulated in situ, and this is associated with a better maintenance of electrical properties of the fiber membrane (Karelis AD, Péronnet F, and Gardiner PF. Exp Physiol 87: 585–592, 2002). The purpose of the present study was to test the hypothesis that elevated plasma insulin concentration due to glucose infusion (
900 pmol/l), rather than high plasma glucose concentration (10–11 mmol/l), could be responsible for this phenomenon, because insulin has been shown to stimulate the Na+-K+ pump. The plantaris muscle was indirectly stimulated (50 Hz, for 200 ms, 5 V, every 2.7 s) via the sciatic nerve to perform concentric contractions for 60 min, while insulin (8 mU · kg-1 · min-1: plasma insulin 900 pmol/l) and glucose were infused to maintain plasma glucose concentration between 4 and 6 [6.2 ± 0.4 mg · kg-1 · min-1: hyperinsulinemic-euglycemic (HE)] or 10 and 12 mmol/l [21.7 ± 1.1 mg · kg-1 · min-1: hyperinsulinemic-hyperglycemic clamps (HH)] (6 rats/group). The reduction in submaximal dynamic force was significantly (P < 0.05) less with HH (-53%) than with HE and saline only (-66 and -70%, respectively). M-wave characteristics were also better maintained in the HH than in HE and control groups. These results demonstrate that the increase in insulin concentration is not responsible for the increase in muscle performance observed after the elevation of circulating glucose.
muscle force; M wave; hyperinsulinemic-euglycemic clamp; hyperinsulinemic-hyperglycemic clamp
WE HAVE RECENTLY SHOWN THAT glucose infusion attenuates fatigue in rat plantaris muscle stimulated indirectly for 60 min in situ (15). This was associated with a better maintenance of the electrical properties of the membrane of the muscle fiber as shown by the characteristics of M wave (peak-to-peak amplitude, duration, and total area). The electrical properties of the membrane depend largely on gradients of Na+ and K+, which are maintained by the activity of the ATP-dependent Na+-K+ pump (20, 22). Glucose infusion and the associated increase in plasma glucose concentration could have favored the maintenance of these gradients by providing glycolytic ATP, which could preferentially fuel the Na+-K+ pump (1, 21). However, in our experiment, glucose infusion and the resultant high plasma glucose concentration (11 mmol/l) also resulted in a marked increase in plasma insulin concentration (900 pmol/l). In addition to increasing glucose uptake, insulin directly favors K+ uptake and Na+ efflux through the stimulation of the Na+-K+ pump (24, 25). This effect could, at least in part, explain the maintenance of electrical properties of the membrane and the attenuation of muscle fatigue when glucose was infused. The effect of insulin on Na+-K+ homeostasis and on the electrical properties of the muscle fiber membrane has been shown, for example, by Clausen et al. (3). In that study, the reduction in isometric twitch and tetanic force observed when the muscle was exposed to high K+ concentrations (10–12.5 mmol/l) was partially reversed by insulin, and this was associated with an efflux of Na+ from the cell and an increase in the resting membrane potential.
The purpose of the present study was to test the hypothesis that elevated plasma insulin concentration due to glucose infusion rather than high plasma glucose concentration per se could attenuate muscle fatigue during prolonged indirect electrical stimulation in situ. For this purpose, submaximal dynamic force of the plantaris muscle along with changes in M-wave characteristics were measured in anesthetized rats during prolonged nerve electrical stimulation in situ, in a control situation, and when plasma insulin concentration was raised markedly (900 pmol/l) by infusion of insulin, with glucose maintained between 4 and 6 mmol/l (hyperinsulinemic-euglycemic clamp) or between 10 and 12 mmol/l (hyperinsulinemic-hyperglycemic clamp). Maximum dynamic and isometric forces, twitch force, and half-relaxation time were also measured before and after the stimulation period.
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METHODS
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Animal care and anesthesia of animals. Adult female Sprague-Dawley rats weighing 250 g were obtained from Charles River (St. Constant, PQ, Canada). The animals were housed by pairs in grid cages in a room maintained at 20–23°C and 25% relative humidity, with a 12:12-h light-dark cycle. The animals were provided with commercially available laboratory rat chow and water ad libitum from the time of reception until the day of the experiment. The care and treatments of animals were conducted according to the directives of the Canadian Council on Animal Care. The animals were anesthetized by intraperitoneal injections of an initial dose of ketamine and xylazine (61.5 mg/kg ketamine and 7.7 mg/kg xylazine). Two supplemental doses were given in the middle of preparation (45 min) and immediately after the beginning of stimulation (12.3 mg/kg ketamine and 1.5 mg/kg xylazine ip) to maintain deep anesthesia.
Animal preparation. The experiments were conducted on the plantaris muscle, which contains a mixture of fiber types (7) and motor units (10) and is resistant to fatigue during submaximal prolonged stimulation. As previously described (15) the plantaris muscle and sciatic nerve were surgically isolated, and the plantaris tendon was attached to the lever arm of a muscle puller servomotor (Cambridge LR 305B, Aurora Scientific, Aurora, ON, Canada). The rectal temperature was monitored throughout the experiment and kept at 36°C by using a heating pad.
The animals were divided randomly into three groups of six and studied before, during, and after a 60-min period of electrical stimulation of the sciatic nerve with infusion of either saline (10 ml · kg-1
· h-1) or insulin (8 mU · kg-1 · min-1; administered with saline 10 ml · kg-1
· h-1) (pump: Harvard Apparatus, St-Laurent, PQ, Canada; human insulin: Sigma Chemical, Oakville, ON, Canada). On the basis of a series of preliminary experiments, infusion of insulin was started 30 min before the beginning of the stimulation to attain a plateau at 900 pmol/l of plasma, which was maintained throughout the experiment (Fig. 1). To limit blood loss, plasma insulin concentration at the beginning and in the middle of the stimulation period (t = 0 and t = 30 min) was measured in additional groups of rats. Plasma glucose was monitored at 5-min intervals and was maintained either between 4.0 and 6.0 mmol/l (hyperinsulinemic-euglycemic clamp) or between 10 and 12 mmol/l (hyperinsulinemic-hyperglycemic clamp) by infusing glucose as needed. The total amounts of glucose infused were 6.2 ± 0.4 and 21.7 ± 1.1 mg · kg-1 · min-1 for the hyperinsulinemic-euglycemic and hyperinsulinemic-hyperglycemic clamps, respectively. The insulin and glucose were infused through a catheter in the left jugular vein. In the control group, the infusion of saline alone was started 30 min before the beginning of stimulation.
Experimental protocol. After determination of optimal muscle length, as previously described (15), twitch forces were recorded by using supramaximal (5 V) single square pulses of 0.05 ms in duration delivered once every 3 s (Grass S88 stimulator; Quincy, MA). The muscle was then subjected to a single maximum dynamic contraction (200-ms train, at 200 Hz and 5 V) and was allowed to rest for 5 min before the 60-min period of stimulation began.
Figure 2 shows the pattern of stretch, stimulation, and contraction used, which was identical to that in the previous experiment (15). Submaximal dynamic force and surface electromyogram from a ball electrode mounted on a spring were continuously monitored on an oscilloscope (Hewlett-Packard 1741A, Mississauga, ON, Canada) and recorded throughout the 60-min period of stimulation. At the end of the 60-min stimulation period, twitch force and maximum dynamic force were recorded again. A bipolar electrode was then inserted in the belly of the muscle, and the muscle was alternately stimulated indirectly (200 ms, 200 Hz, 5 V) and directly (200 ms, 200 Hz, 150 V) maximally while muscle length was kept constant. After the experiment, animals were killed by an overdose of ketamine and xylazine.
Measurements. Twitch force and half-relaxation time together with maximum dynamic force were measured before and after the 60-min period of stimulation. Submaximal dynamic muscle force was measured throughout the 60-min period of stimulation. Maximum isometric forces in response to indirect and direct muscle stimulation were measured after the 60-min period of stimulation. Comparisons were made with maximum isometric force developed through indirect and direct stimulation in a separate group of rats (n = 6) at the end of a 60-min period of saline infusion without stimulation. Finally, the first evoked M wave during each concentric contraction was analyzed after full-wave rectification for the measurement of peak-to-peak amplitude, duration, and total area throughout the 60-min period of stimulation. Custom-designed software was used to perform all of the above measurements.
Plasma glucose concentrations were determined in blood droplets sampled by incision of the tail (Glucometer Elite, Toronto, ON, Canada). For the measurement of plasma insulin concentration (automated radioimmunoassay: Medicorp, Montreal, PQ, Canada), 1-ml blood samples were withdrawn from a catheter placed in the right femoral vein and centrifuged at 16,000 g
for 4 min at 4°C, and the plasma was stored at -80°C for subsequent analysis. Both plantaris muscles were excised and frozen into liquid nitrogen immediately after the end of each experiment and stored at -80°C until analysis. Muscle glycogen levels were measured by using the technique of Lo et al. (17).
Statistical analysis. Data are expressed as means ± SD. Comparisons were made by using a two-way ANOVA. When significant differences were revealed, a Scheffé's post hoc test was performed. The level of statistical significance was set at P < 0.05.
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RESULTS
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In the control group, with infusion of saline only, submaximal dynamic force significantly decreased over the first 5 min of stimulation and remained constant thereafter (Fig. 3). Compared with the initial value, over the last 55 min of stimulation the average reduction of force developed was 70.4 ± 3.8%. Maximum dynamic force (Fig. 4), isometric force (Fig. 5), and twitch force (Table 1) were also significantly reduced after the period of stimulation. The pattern of changes in submaximal dynamic force was similar in the animals infused with insulin (Fig. 3). In the euglycemic group, the average reduction in submaximal force over the last 55 min of stimulation (66.3 ± 3.2%), as well as the reduction in maximum dynamic (0.85 ± 0.04 N), twitch (0.42 ± 0.03 N), and maximal isometric force developed in response to indirect stimulation (1.5 ± 0.08 N), were not significantly different from those observed in the control group. In contrast, in animals infused with insulin but with a high plasma glucose concentration, the reduction in submaximal dynamic force (53.1 ± 2.9%) (Fig. 3), maximal dynamic force (0.21 ± 0.01 N) (Fig. 4), and maximal isometric force developed in response to indirect stimulation (0.78 ± 0.04 N) (Fig. 5) were lower. The reduction in twitch force was similar to those observed in the control group and in the euglycemic group (Table 1), and no significant change was observed for half-relaxation time in any of the three groups after the stimulation period (Table 1). No significant difference was observed between the maximum isometric force developed in response to indirect and direct stimulation in the group of rats that were not submitted to the fatigue protocol (Fig. 5). In contrast, the maximum isometric force developed in response to direct stimulation after the end of the experiment was significantly higher than that developed in response to indirect stimulation. However, the differences were not significantly different in rats infused with saline (19.2 ± 0.9%) and with insulin (21.1 ± 1.0 and 18.4 ± 0.8% in the euglycemic and hyperglycemic group, respectively).
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Fig. 4. Initial and final maximum dynamic force in the control (solid), hyperinsulinemic-euglycemic (open), and hyperinsulinemic-hyperglycemic (hatched) groups. Values are means ± SD (n = 6). *Significantly different from initial values (P < 0.05).  Significantly different from other groups (P < 0.05).
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Figure 6 shows changes in M-wave peak-to-peak amplitude, duration, and total area during the 60-min period of stimulation. The reduction in peak-to-peak amplitude (60%) and in total area (from 0.08 to 0.059–0.062 V · s) and the increase in duration (from 5.0 to 10.1–9.6 ms) were similar in rats infused with saline and in rats infused with insulin but maintained euglycemic. The reduction in peak-to-peak amplitude (35%) and the increase in duration (from 5.0 to 7.6 ms) were significantly lower in rats infused with insulin but with a very high plasma glucose concentration, whereas M-wave total area was not significantly modified.
The 60-min period of stimulation significantly decreased muscle glycogen content in the three groups (Table 1), with no significant difference in the initial and final values, respectively, among the three groups.
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DISCUSSION
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Ingestion of carbohydrates during prolonged exercise has been shown to increase exercise time to exhaustion in humans (4–6, 12, 19) and animals (2, 8, 23) and could also increase the ability to perform resistance exercise (11, 16). In a recent experiment, we have shown that the beneficial effect of infused glucose on exercise performance could be in part due to a direct effect on the neuromuscular function (15). In this study, the plantaris muscle was stimulated indirectly in anesthetized rats over a 60-min period while either saline or glucose was infused. When glucose was infused (17 mg · kg-1 · min-1), plasma glucose concentration was maintained between 10 and 11 mmol/l (vs. 5 mmol/l in rats infused with saline), and this was associated with a significant attenuation of muscle fatigue, as shown by the lower reduction in submaximal dynamic force during the period of stimulation (55% decrease vs. 70% in control rats) and a lower reduction in maximum dynamic and isometric force after the period of stimulation. In addition, in rats infused with saline for 30 min, submaximal dynamic force was partially restored when glucose was administered for the subsequent 30 min. Thus not only did glucose infusion from the beginning of muscle contraction attenuate muscle fatigue but also it partly reversed muscle fatigue later in the period of stimulation. Comparison between maximal isometric force developed with indirect and massive direct muscle stimulation showed that the attenuation of fatigue was not due to a better maintenance of the neuromuscular junction. In contrast, M-wave characteristics indicated that glucose infusion helped alleviate deterioration of the electrical properties of the muscle fiber membrane. This phenomenon could be due to the effect of a high plasma glucose concentration per se, which could increase the supply of glycolytic ATP to the Na+-K+ pump (1, 21). However, the high plasma insulin concentration observed, in this situation, in response to glucose infusion, and high plasma glucose concentration, could also be involved in the better maintenance of the electrical properties of the muscle fiber membrane. Indeed, as shown by Hundal et al. (13) and Marette et al. (18), insulin increases the activity of Na+-K+-ATPase in the membrane of the muscle fiber. Data from Clausen et al. (3) indicate that insulin could have a beneficial effect on muscle force. In that experiment, when extracellular potassium concentration was increased from the control value of 4 to 12.5 mmol/l, the tetanic force of the soleus muscle was reduced by 96%. Insulin administration (100 mU/ml) produced a 38% recovery of force within 20 min, and this was associated with a 21% increase in efflux of Na+
from the cell and a 14% increase in K+ uptake. The purpose of the present experiment was, thus, to test the hypothesis that the beneficial effect of glucose infusion on muscle fatigue observed in our previous experiment could be due to the associated high plasma insulin concentration rather than to the high plasma glucose concentration and delivery to the muscle per se. It should be recognized, however, that carbohydrate ingestion during prolonged exercise in humans is not associated with high plasma insulin concentrations (9, 14). As a consequence, although the high plasma insulin concentration could explain our previous findings, it is unlikely to be responsible for the improvement in performance in endurance events when carbohydrates are ingested.
The above hypothesis was not confirmed by the results obtained. When saline was infused, with plasma glucose and plasma insulin concentrations averaging 5 mmol/l and 265 pmol/l throughout the experiment, submaximal dynamic force as well as maximal dynamic and isometric forces were significantly reduced after the 60-min stimulation period. Similar reductions were observed when plasma insulin concentration was increased to 900 pmol/l but with plasma glucose concentration maintained between 4 and 6 mmol/l by infusing only a small amount of glucose (93 mg over 60 min) (hyperinsulinemic-euglycemic clamp). In contrast, when plasma glucose concentration was raised between 10 and 12 mmol/l by infusing a larger amount of glucose (325 mg over 60 min) while maintaining plasma insulin concentration at 900 pmol/l (hyperinsulinemic-hyperglycemic clamp), the reduction in submaximal dynamic force as well as maximal dynamic and isometric forces were much lower. These observations indicate that increased plasma glucose concentration and/or glucose delivery to the muscle, and not the associated increase in plasma insulin concentration, was responsible for the attenuation of muscle fatigue when glucose was administered.
The mechanisms by which increased plasma glucose concentration and/or glucose delivery to the muscle attenuates muscle fatigue remain to be determined. However, as observed in the previous experiment (15), this was not related to difference in muscle glycogen utilization, which was similar in the three groups, nor to a better maintenance of the properties of the neuromuscular junction, as shown by differences between direct and indirect stimulation of the muscle at the end of the experiment. In contrast, as also observed in the previous experiment (15), the reduction in muscle force when saline was infused, as well as with the hyperinsulinemic-euglycemic clamp, was associated with a concomitant reduction in M-wave peak-to-peak amplitude and total area and an increase in M-wave duration. The larger submaximal and maximal dynamic forces and maximal isometric forces observed with the hyperinsulinemic-hyperglycemic clamp were associated with a better maintenance of M-wave characteristics. These observations confirm that muscle fatigue was at least partly due to impairments of action potential generation and/or propagation along the muscle fiber membrane and that high plasma glucose concentration and/or delivery to the muscle helps alleviate these impairments. This phenomenon could be due in part to the fact that infused glucose could provide glycolytic ATP, which appears to preferentially fuel the Na+-K+ pump, as shown by data from Okamoto et al. (21). An alternative or complementary explanation is that glycolytic ATP from infused glucose could also preferentially fuel the Ca2+ pump in the sarcoplasmic reticulum, as shown by Xu et al. (27), and could, thus, help attenuate muscle fatigue related to change in Ca2+ handling, which also develops under prolonged stimulation in situ (26).
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ACKNOWLEDGMENTS
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We thank Gérard Ouellet, Paul Martin, and Mariannick Marcil for technical assistance.
This work was supported by grants from the Natural Science and Engineering Research Council of Canada.
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FOOTNOTES
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Address for reprint requests and other correspondence: F. Péronnet, Université de Montréal, Dept. of Kinesiology, P.O. Box 6128 Centre-Ville, Montreal, Quebec, Canada H3C 3J7 (E-mail: francois.peronnet{at}umontreal.ca).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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Copyright © 2003 by the American Physiological Society.
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ABSTRACT
METHODS
), hyperinsulinemic-euglycemic (
), and hyperinsulinemic-hyperglycemic (
) groups. Values are means ± SD; n = 6. *Significantly different from initial value, P < 0.05.
Significantly different from the control group (P < 0.05).