High-resistance training and muscle metabolism during prolonged exercise.

To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance training (HRT), active but untrained males (age 20 +/- 0.7 yr; mean +/- SE) performed lower-limb weight training 3 days/wk for 12 wk using three sets of 6-8 repetitions maximal (RM)/day. Muscle metabolism was examined at different stages of training (4, 7, and 12 wk) using a two-stage continuous cycle test performed at the same absolute power output and duration (56.4 +/- 2.9 min) and representing 57 and 72% of pretraining peak aerobic power (VO2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher (P < 0.05) phosphocreatine (PCr; 27.4 +/- 6. 7 vs. 38.0 +/- 1.9 mmol/kg dry wt), a lower lactate (38.9 +/- 8.5 vs. 24.4 +/- 6.1 mmol/kg dry wt), and a higher (P < 0.05) glycogen content (132 +/- 11 vs. 181 +/- 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72% VO2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found on VO2 peak with training (41.2 +/- 2.9 vs. 41.0 +/- 2.1 ml. kg-1. min-1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy.

Serial effects of high-resistance and prolonged endurance training on Na+-K+ pump concentration and enzymatic activities in human vastus lateralis.

The purpose of this study was to compare two contrasting training models, namely high-resistance training and prolonged submaximal training on the expression of Na+-K+ ATPase and changes in the potential of pathways involved in energy production in human vastus lateralis. The high-resistance training group (VO2peak = 45.3 +/- 1.9 mL kg(-1) min(-1), mean +/- SE, n = 9) performed three sets of six to eight repetitions maximal, each of squats, leg presses and leg extensions, three times per week for 12 weeks, while the prolonged submaximal training group (VO2peak = 44.4 +/- 6.6 mL kg(-1) min(-1), n = 7) cycled 5-6 times per week for 2 h day(-1) at 68% VO2peak for 11 weeks. In the HRT group, Na+-K+ ATPase (pmol g(-1) wet wt), measured with the 3H-ouabain binding technique, showed no change from 0 (289 +/- 22) to 4 weeks (283 +/- 15), increased (P < 0.05) by 16% at 7 weeks and remained stable until 12 weeks (319 +/- 19). For prolonged submaximal training, a 22% increase (P < 0.05) was observed from 0 (278 +/- 31) until 3 weeks (339 +/- 29) with no further changes observed at either 9 weeks (345 +/- 25) or 11 weeks (359 +/- 34). In contrast to high-resistance training, where a 15% increase (P < 0.05) was observed, only in the maximal activity of phosphorylase, prolonged submaximal training resulted in increases in malate dehydrogenase, beta-hydroxyl-CoA dehydrogenase, hexokinase and phosphofructokinase. In contrast to high-resistance training which failed to result in an increase in VO2peak, prolonged submaximal training increased VO2peak by approximately 15%. Only for prolonged exercise training was a relationship observed for VO2peak and Na+-K+-ATPase (r = 0.59; P < 0.05). Correlations between VO2peak and mitochondrial enzyme activities were not significant (P > 0.05) for either training programme. It is concluded that although both training programmes stimulate an up-regulation in Na+-K+ ATPase concentration, only the prolonged submaximal training programme enhances the potential for beta-oxidation, oxidative phosphorylation and glucose phosphorylation.

Regulation of fiber size, oxidative potential, and capillarization in human muscle by resistance exercise.

To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 +/- 2.3 ml. kg-1. min-1; mean +/- SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions (P < 0.05) in type IIB fibers (15.1 +/- 2.1% vs. 7.2 +/- 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase (P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.

Glucose tolerance is improved after low- and high-intensity exercise in middle-age men and women.

We compared the effects of low- and high-intensity exercise on oral glucose tolerance immediately and 24 hr after each exercise bout. Participants were 5 male and 5 female individuals (age 40-48). A fasted, oral glucose tolerance test (OGTT) was conducted several days before the first exercise bout. Glucose and insulin concentrations were determined every 15 min throughout a 2 hr, 75 g OGTT. Immediately after low-intensity exercise, the incremental glucose area under the curve was reduced by 16%, compared to the fasting OGTT (p < .05). This was reduced further (-30%) 24 hr postexercise (p < .05). After high-intensity exercise, similar results were observed, with the incremental glucose area reduced by 14 and 35% immediately and 24 hr postexercise, respectively (p < .05). In conclusion, exercise improves glucose tolerance, this effect is more pronounced 24 hr postexercise, and low- and high-intensity exercise provide similar beneficial effects on glucose tolerance.

Relationships between fluid and electrolyte hormones and plasma volume during exercise with training and detraining.

PURPOSE: The purpose of this study was to investigate the relationship between training-induced alterations in plasma volume (PV) and changes in fluid and electrolyte regulatory hormones during prolonged exercise. METHODS: Seven male subjects (VO2peak 49.2 +/- 2.4 mL.kg-1.min-1, X +/- SE) performed a cycling test before (C) and after (T) 6 d of training and after 6 d of detraining (DT). Training was conducted for 2 h.d-1 at 68% VO2peak at a room temperature between 26-28 degrees C. The 60-min exercise challenge included 20 min at 50%, 65%, and 75% VO2peak workloads. RESULTS: Training resulted in a calculated 13.8 +/- 1.6% PV expansion (P < 0.05) which recovered to C levels with DT (1.8 +/- 2.3%, P > 0.05). Compared with that at C, training resulted in a reduction of aldosterone (ALDO) concentration at all exercise intensities (P < 0.05) which normalized to C levels with DT. With T, epinephrine (EPI) concentrations were reduced at the highest power output only (365 +/- 51 vs 113 +/- 22 pg.mL-1; P < 0.05) and returned to C levels with DT. Arginine vasopressin (AVP) concentrations were also reduced at the highest workload only (20.2 +/- 3.2 pg.mL-1 vs 10.4 +/- 0.7 pg.mL-1; P < 0.05) and remained depressed after DT (11.8 +/- 1.3 pg.mL-1; P < 0.05). Atrial natriuretic factor (ANF) and norepinephrine (NOREPI) were not affected by T or DT. CONCLUSIONS: The results suggest that concentrations of ALDO, and to a lesser extent EPI, during exercise are related to PV levels, whereas ANF and NOREPI concentrations are not. AVP concentrations are related to other adaptive factors, the effects of which persist for a longer time course than do PV changes.

Short-term training, muscle glycogen, and cycle endurance.

The objective of this study was to test the hypothesis that the increased glycogen concentration found in the working muscles following short-term training would result in an increase in endurance performance. Endurance performance was examined in 8 active but untrained males who cycled until fatigue at 65% VO2max prior to and following 3 consecutive days of training. Training consisted of cycling for 2 hrs a day at the same power output used in the prolonged fatigue trials. A 39% increase in cycle time, from 103 +/- 7.7 to 143 +/- 14 min (p < 0.05), was observed following training. At fatigue prior to training, glycogen concentration in the vastus lateralis muscle was depleted by 75% (317 +/- 17 to 78.8 +/- 32 mmol.glucosyl units .kg-1 d.w). Following training, glycogen concentration at a comparable work time was 2.3 times higher. The elevated glycogen level following training was due both to higher glycogen at rest and during exercise. The energy cost of the activity as measured by the VO2 at selected intervals was unchanged with training. No change (p > 0.05) in exercise time was observed in a control group who were subjected to similar exercise protocols approximately 1 to 2 weeks apart. It is concluded that short-term training at least in untrained individuals (VO2max averaging 43.6 +/- 2.9 ml.kg-1.min-1) substantially elevates submaximal exercise tolerance and that the increase in resistance to fatigue is related to the elevated availability of glycogen.

Metabolic adaptations to short-term training are expressed early in submaximal exercise.

In previous studies we have been able to demonstrate tighter metabolic control of muscle metabolism during prolonged steady-state exercise 5 to 6 days after the initiation of training and well before changes in oxidative potential. To examine whether the metabolic adaptations are manifested during the non-steady-state adjustment to submaximal exercise, 11 male subjects (Vo2 peak, 45 +/- 2.4 mL.kg(-1). min(-1), X +/- SE) performed 98 min of cycle exercise at 67% of Vo2 peak prior to and following 3 to 4 days of training for 2 h per day. Analysis of lactate concentration (mmol/kg dry weight) in samples rapidly extracted from vastus lateralis indicated reductions (p < 0.05) of 44% at 3 min ( 42.1 +/- 7.1 vs. 23.6 +/- 7.7), 29% at 15 min (35.4 +/- 6.4 vs. 25.0 +/- 6.0), and 32% at 98 min (22.9 +/- 6.9 vs. 15.6 +/- 3.2) with training. Training also resulted in higher phosphocreatine and lower creatine and P(i) values that were not specific to any exercise time point. In addition, Vo2 was not altered either during the non-steady state or during the steady-state phases of exercise. These results suggest that at least part of the tightening of the metabolic control and the apparent reduction in glycogenolysis and glycolysis in response to short-term training occurs during the adjustment phase to steady-state exercise.

Adaptations in muscle metabolism to prolonged voluntary exercise and training.

In previous research we established using a short-term (5-7 days) training model that increases in muscle oxidative potential are not a prerequisite for the characteristic energy metabolic adaptations (lower lactate, glycogen depletion, and phosphocreatine hydrolysis) observed during prolonged exercise. To investigate whether increased muscle aerobic potential further potentiates the metabolic adaptive response, seven healthy male volunteers [maximal O2 uptake (VO2max) = 45.1 +/- 1.1 (SE) ml.kg-1.min-1] engaged in an 8-wk training program consisting of 2 h of cycle exercise at 62% of pretraining VO2max 5-6 times/wk. Analysis of tissue samples obtained from the vastus lateralis after 60 min of exercise revealed that by 4 wk of training muscle lactate concentration, phosphocreatine hydrolysis, and glycogen depletion were depressed (all P < 0.05). Further training for 4 wk had no additional effect (P < 0.05). The ratio of fructose 6-phosphate to fructose 1,6-phosphate, an index of phosphofructokinase activity, was not altered with training. Muscle oxidative potential as estimated from the maximal activity of succinic dehydrogenase increased by 31% by 4 wk of training (P < 0.05) before plateauing during the final 4 wk of training. The increase in VO2max of 15.6% (P < 0.05) noted with training was also primarily expressed during the initial 4 wk. O2 uptake during submaximal exercise was unchanged. Because the metabolic response was similar in magnitude to that previously observed with short-term training, we conclude that, at least for the conditions of this study, the development of increased muscle aerobic potential is of minimal consequence on the magnitude of the energy metabolic adaptations examined.

Coupling of muscle phosphorylation potential to glycolysis during work after short-term training.

To examine whether the metabolic adaptations to short-term training are expressed over a range of submaximal levels of mitochondrial respiration, seven untrained male subjects [maximal O2 uptake (VO2max) = 45.9 +/- 1.9 (SE) ml.kg-1.min-1] performed a progressive three-stage protocol of cycle exercise at 60% (20 min), 79% (20 min), and 92% (11 min) of pretraining VO2max before and after training. Training consisted of 5-6 days of cycling for 2 h/day at 65% VO2max. Muscle tissue rapidly obtained from the vastus lateralis by needle biopsy indicated that training blunted (P < 0.05) the increase in lactate observed at 60% (23.4 +/- 6.5 vs. 12.4 +/- 2.9 mmol/kg dry wt), 79% (48.9 +/- 5.1 vs. 25.6 +/- 5.2 mmol/kg dry wt), and 92% (68.3 +/- 6.4 vs. 41.5 +/- 6.5 mmol/kg dry wt) of VO2max. Training also resulted in a higher phosphocreatine and lower creatine and P(i) concentrations at both 79% (P < 0.05) and 92% (P < 0.05) of VO2max and higher muscle glycogen levels (P < 0.05). These changes were accompanied by small but significant reductions (P < 0.05) in O2 uptake at the two higher exercise intensities. Given that the lactate-to-pyruvate ratio and the calculated free ADP and AMP were also reduced (P < 0.05), it would appear that short-term training results in a tighter metabolic control over a range of mitochondrial respiratory rates.

Increases in human skeletal muscle Na(+)-K(+)-ATPase concentration with short-term training.

To investigate the effect of short-term training on Na(+)-K(+)-adenosine triphosphatase (ATPase) concentration in skeletal muscle and on plasma K+ homeostasis during exercise, 9 subjects performed cycle exercise for 2 h per day for 6 consecutive days at 65% of maximal aerobic power (VO2 max). Na(+)-K(+)-ATPase concentration determined from biopsies obtained from the vastus lateralis muscle using the [3H]ouabain-binding technique increased 13.6% (P < 0.05) as a result of the training (339 +/- 16 vs. 385 +/- 19 pmol/g wet wt, means +/- SE). Increases in Na(+)-K(+)-ATPase concentration were accompanied by a small but significant increase in VO2 max (3.36 +/- 0.16 vs. 3.58 +/- 0.13 l/min). The increase in arterialized plasma K+ concentration and plasma K+ content determined during continuous exercise at three different intensities (60, 79, and 94% VO2 max) was depressed (P < 0.05) following training. These results indicate that not only is training capable of inducing an upregulation in sarcolemmal Na(+)-K(+)-ATPase concentration in humans, but provided that the exercise is of sufficient intensity and duration, the upregulation can occur within the first week of training. Moreover, our findings are consistent with the notion that the increase in Na(+)-K(+)-ATPase pump concentration attenuates the loss of K+ from the working muscle.

Time-dependent increases in Na+,K(+)-ATPase content of low-frequency-stimulated rabbit muscle.

Chronic low-frequency stimulation of rabbit fast-twitch muscle induced time-dependent increases in the concentration of the sarcolemmal Na+,K(+)-ATPase and in mitochondrial citrate synthase activity. The almost twofold increase in Na+,K(+)-ATPase preceded the rise in citrate synthase and was complete after 10 days of stimulation. We suggest that the increase in Na+,K(+)-ATPase enhances resistance to fatigue of low-frequency-stimulated muscle prior to elevations in aerobic-oxidative capacity.

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.

Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man.

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects (VO2max = 53.0 +/- 2.0 mL.kg-1.min-1, mean +/- SE) for 10-12 days with each exercise session lasting for 2 h at an average intensity of 59% of VO2max. This training protocol resulted in reductions (p less than 0.05) in blood lactate concentration (mM) at 15 min (2.96 +/- 0.46 vs. 1.73 +/- 0.23), 30 min (2.92 +/- 0.46 vs. 1.70 +/- 0.22), 60 min (2.96 +/- 0.53 vs. 1.72 +/- 0.29), and 90 min (2.58 +/- 1.3 vs. 1.62 +/- 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p less than 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p less than 0.05) were observed for blood beta-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p less than 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p less than 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.

Energy metabolism in human slow and fast twitch fibres during prolonged cycle exercise.

1. The effects of prolonged exercise on energy metabolism in type I and type II muscle fibres in the vastus lateralis muscle were investigated in six male subjects (20.0 +/- 0.5 years, mean +/- S.E.M.) who performed one-legged cycling at 61% of maximum O2 consumption (VO2,max; determined with one leg) until fatigue or for a maximum of 2 h. 2. Analysis of pools of freeze-dried fibres obtained by needle biopsy and separated into specific types by the myofibrillar ATPase histochemical procedure indicated higher (P less than 0.05) lactate concentrations in type II fibres compared to type I fibres at 15 min (43.9 +/- 9.7 and 51.2 +/- 9.8 mmol (kg dry wt)-1) and at 60 min (18.2 +/- 4.7 and 25.9 +/- 6.5 mmol (kg dry wt)-1). No differences existed in lactate concentration between fibre types for pre-exercise (10.0 +/- 1.6 and 13.3 +/- 2.8 mmol (kg dry wt)-1) or post-exercise. 3. Glycogen degradation was most pronounced in type I fibres. By the end of exercise, glycogen concentration was 82.4 +/- 45 mmol glucosyl units (kg dry wt)-1 in type I fibres and 175 +/- 62 mmol glucosyl units (kg dry wt)-1 in type II fibres. 4. No significant changes in ATP and creatine phosphate (CrP) were found in either fibre type with exercise. 5. It is concluded that, at least for lactate and glycogen, fibre-specific differences are evident in prolonged submaximal exercise. The cause of the difference probably relates both to the unique energy metabolic characteristics of each fibre type and to the manner in which they are utilized during the exercise. 6. The failure to find a reduction in ATP concentration in either fibre type during prolonged exercise in the face of a progressive increase in the number of fibres showing little or no glycogen concentration suggests that protective mechanisms exist that prevent an energy crisis. The nature of these protective mechanisms remains to be elucidated.

Early muscular and metabolic adaptations to prolonged exercise training in humans.

A short-term training program involving 2 h of daily exercise at 59% of peak O2 uptake (VO2max) repeated for 10-12 consecutive days was employed to determine the significance of adaptations in energy metabolic potential on alterations in energy metabolism and substrate utilization in working muscle. The initial VO2max determined before training on the eight male subjects was 53.0 +/- 2.0 (SE) ml.kg-1.min-1. Analysis of samples obtained by needle biopsy from the vastus lateralis muscle before exercise (0 min) and at 15, 60, and 99 min of exercise indicated that on the average training resulted (P less than 0.05) in a 6.5% higher concentration of creatine phosphate, a 9.9% lower concentration of creatine, and a 39% lower concentration of lactate. Training had no effect on ATP concentration. These adaptations were also accompanied by a reduction in the utilization in glycogen such that by the end of exercise glycogen concentration was 47.1% higher in the trained muscle. Analysis of the maximal activities of representative enzymes of different metabolic pathways and segments indicated no change in potential in the citric acid cycle (succinate dehydrogenase, citrate synthase), beta-oxidation (3-hydroxyacyl CoA dehydrogenase), glucose phosphorylation (hexokinase), or potential for glycogenolysis (phosphorylase) and glycolysis (pyruvate kinase, phosphofructokinase, alpha-glycerophosphate dehydrogenase, lactate dehydrogenase). With the exception of increases in the capillary-to-fiber area ratio in type IIa fibers, no change was found in any fiber type (types I, IIa, and IIb) for area, number of capillaries, capillary-to-fiber area ratio, or oxidative potential with training.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle energetics during prolonged cycling after exercise hypervolemia.

This study examined the question of whether increases in plasma volume (hypervolemia) induced through exercise affect muscle substrate utilization and muscle bioenergetics during prolonged heavy effort. Six untrained males (19-24 yr) were studied before and after 3 consecutive days of cycling (2 h/day at 65% of peak O2 consumption) performed in a cool environment (22-23 degrees C, 25-35% relative humidity). This protocol resulted in a 21.2% increase in plasma volume (P less than 0.05). During exercise no difference was found in the blood concentrations of glucose, lactate, and plasma free fatty acids at either 30, 60, 90, or 120 min of exercise before and after the hypervolemia. In contrast, blood alanine was higher (P less than 0.05) during both rest and exercise with hypervolemia. Measurement of muscle samples extracted by biopsy from the vastus lateralis muscle at rest and at 60 and 120 min of exercise indicated no effect of training on high-energy phosphate metabolism (ATP, ADP, creatine phosphate, creatine) or on selected glycolytic intermediate concentrations (glucose 1-phosphate, glucose 6-phosphate, fructose 6-phosphate, lactate). In contrast, training resulted in higher (P less than 0.05) muscle glucose and muscle glycogen concentrations. These changes were accompanied by blunting of the exercise-induced increase (P less than 0.05) in both blood epinephrine and norepinephrine concentrations. Plasma glucagon and serum insulin were not affected by the training. The results indicate that exercise-induced hypervolemia did not alter muscle energy homeostasis. The reduction in muscle glycogen utilization appears to be an early adaptive response to training mediated either by an increase in blood glucose utilization or a decrease in anaerobic glycolysis.

Glycogen utilization in rat respiratory muscles during intense running.

Glycogen concentration in the adult rat diaphragm and intercostal muscles has been examined following heavy treadmill exercise to determine the recruitment strategy and the significance of glycogen as a substrate to satisfy the elevated energy requirements accompanying hyperpnea. Short-term continuous running at 60 m/min and a 12 degree grade resulted in a reduction (p less than 0.05) in the concentration of glycogen (39%) in the costal region of the rat diaphragm. Similarly, glycogen concentration was significantly reduced (p less than 0.05) with this exercise protocol in all respiratory muscles studied, with the exception of the sternal region of the diaphragm. With the less intense running protocols, glycogen degradation continued to be pronounced (p less than 0.05) in the majority of the respiratory muscles sampled. The significance of muscle glycogen as a substrate for energy metabolism in the respiratory muscles was not affected by the procedure used to prepare the animal for tissue sampling (Somnitol, diethyl ether, decapitation). Examination of selected locomotor muscles revealed extensive glycogen loss in muscles composed of essentially slow oxidative fibres (soleus), fast oxidative glycolytic fibres (vastus lateralis red), and fast glycolytic fibres (vastus lateralis white). It is concluded that during heavy exercise in the rat, recruitment of motor units occurs in all regions of the diaphragm and in the intercostal muscles. At least for the costal region of the diaphragm and as evidenced by the modest (two- to four-fold) but significant (p less than 0.05) increases in lactate concentration, the increased ATP requirements in these muscles are met to a large degree by increases in aerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Fiber type specific glycogen utilization in rat diaphragm during treadmill exercise.

To examine the significance of endogenous stores of glycogen in specific fiber types (I, IIa, IIb) of the costal region of the diaphragm, adult male Wistar rats performed continuous running (25 m/min, 8 degrees grade) exercise for either 30 min or until fatigue. At 30 min of exercise, glycogen loss, as measured microphotometrically using the periodic acid-Schiff technique averaged between 73 and 80% (P less than 0.05) in the different fiber types. When exercise was performed to exhaustion, representing an additional 94 min, no further reduction in glycogen was observed in any fiber type. Biochemical determinations of glycogen from the diaphragm confirmed the extensive reduction in glycogen concentration with exercise. Large reductions (P less than 0.05) in glycogen were also noted in the soleus, plantaris, and vastus lateralis red. Although significant depletion (P less than 0.05) occurred in the vastus lateralis white, it was not as pronounced as in these other muscles. Repletion to preexercise glycogen concentration was complete by 4 h of recovery in all muscles except the vastus lateralis white. It is concluded that endogenous glycogen is a significant substrate in all muscles sampled regardless of fiber composition. In the case of the costal region of the diaphragm, the increased work of breathing resulting from heavy exercise leads to the recruitment of all fiber types, and each fiber type depends on glycogen as a substrate at least early in the exercise.