Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure

Lang, Chim C., Don B. Chomsky, Glenn Rayos, T. K. Yeoh, andJohn R. Wilson. Skeletal muscle mass and exercise performance instable ambulatory patients with heart failure. J. Appl. Physiol. 82(1): 257-261, 1997.The purposeof this study was to determine whether skeletal muscle atrophy limitsthe maximal exercise capacity of stable ambulatory patients with heartfailure. Body composition and maximal exercise capacity were measuredin 100 stable ambulatory patients with heart failure. Body compositionwas assessed by using dual-energy X-ray absorption. Peak exerciseoxygen consumption (O_{2 peak}) and theanaerobic threshold were measured by using a Naughton treadmillprotocol and a Medical GraphicsCardioO₂ System.O_{2 peak} averaged 13.4 ± 3.3 ml ^· min^{1 ·} kg¹or 43 ± 12% of normal. Lean body mass averaged 52.9 ± 10.5 kg and leg lean mass 16.5 ± 3.6 kg. Leg lean mass correlated linearly with O_{2 peak}(r= 0.68, P < 0.01), suggesting that exerciseperformance is influenced by skeletal muscle mass. However, lean bodymass was comparable to levels noted in 1,584 normal control subjects, suggesting no decrease in muscle mass. Leg muscle mass was comparable to levels noted in 34 normal control subjects, further supporting thisconclusion. These findings suggest that exercise intolerance in stableambulatory patients with heart failure is not due to skeletal muscleatrophy.

     

Skeletal muscle oxygenation during incremental exercise

The purpose of this study was to investigate the relationship between muscle oxygenation level at exhaustion and maximal oxygen uptake (VO2max) in an incremental cycling exercise. Nine male subjects took part in an incremental exhaustive cycling exercise, and then cuff occlusion was performed. Changes in oxy-(deltaHbO2) and deoxy-(deltaHb) hemoglobin concentrations in the vastus lateralis muscle were measured with a near infrared spectroscopy (NIRS). Muscle oxygenation during incremental exercise was expressed as a percentage (%Moxy) of the maximal range observed during an arterial occlusion as the lower reference point. A systematic decrease was observed in %Moxy with increasing intensity. A significant relationship was observed between %Moxy at exhaustion and VO2max (p < 0.01). We concluded that the one of the limiting factor of VO2max is the muscle oxygen diffusion capacity, and %Moxy during exercise could be one of the indexes of muscle oxygen diffusion capacity.     

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

Oelberg, David A., Allison B. Evans, Mirko I. Hrovat, PaulP. Pappagianopoulos, Samuel Patz, and David M. Systrom. Skeletal muscle chemoreflex and pH_i inexercise ventilatory control. J. Appl.Physiol. 84(2): 676-682, 1998.To determinewhether skeletal muscle hydrogen ion mediates ventilatory drive inhumans during exercise, 12 healthy subjects performed three bouts ofisotonic submaximal quadriceps exercise on each of 2 days in a 1.5-Tmagnet for ³¹P-magnetic resonancespectroscopy(³¹P-MRS). Bilaterallower extremity positive pressure cuffs were inflated to 45 Torr duringexercise (BLPP_ex) or recovery(BLPP_rec) in a randomized orderto accentuate a muscle chemoreflex. Simultaneous measurements were madeof breath-by-breath expired gases and minute ventilation, arterializedvenous blood, and by ³¹P-MRS ofthe vastus medialis, acquired from the average of 12 radio-frequencypulses at a repetition time of 2.5 s. WithBLPP_ex, end-exercise minuteventilation was higher (53.3 ± 3.8 vs. 37.3 ± 2.2 l/min;P < 0.0001), arterializedPCO₂ lower (33 ± 1 vs. 36 ± 1 Torr; P = 0.0009), and quadricepsintracellular pH (pH_i) more acid (6.44 ± 0.07 vs. 6.62 ± 0.07; P = 0.004), compared withBLPP_rec. Bloodlactate was modestly increased withBLPP_ex but without a change inarterialized pH. For each subject, pH_i was linearly relatedto minute ventilation during exercise but not to arterialized pH. Thesedata suggest that skeletal muscle hydrogen ion contributes to theexercise ventilatory response.

     

Skeletal muscle RNA synthesis following endurance and sprint exercise

Two groups of male Wistar endurance- and sprint-acclimatized rats were used to study the time course of uridine uptake into skeletal muscle RNA following acute exercise. Endurance and sprint animals were killed at 0, 2, 18, 24, and 48 hr following 1 hr of either endurance (30 m X min-1) or sprint running (90 m X min-1). Red vastus (RV) and white vastus (WV) muscle samples were incubated for 30 min in a medium containing 1 microCi 5-[14C]uridine. Uridine uptake was determined in the myofibrillar-nuclear, mitochondrial, microsomal, and soluble fractions of skeletal muscle via liquid scintillation counting. A significant decrease in whole muscle uridine uptake into RNA was observed in RV muscles following endurance exercise as well as in WV of sprint-exercised rats. Sprint-exercised RV had significantly greater uridine uptake into RNA in the homogenate and myofibrillar-nuclear fraction 2-18 hr post exercise. Increased mitochondrial uridine incorporation into RNA was observed in endurance- and sprint-exercised muscles between 18 and 48 hr post exercise. A very large increment in microsomal uridine uptake was observed in sprint-exercised WV at 24 hr. These data suggest that while whole muscle RNA synthesis may decline immediately following acute exercise overload, increases are observed in specific muscle fractions. These changes appear to coincide with protein-specific adaptations to sprint and endurance exercise.     

Skeletal muscle enlargement with weight-lifting exercise by rats

A rat model of weight lifting that produces skeletal muscle enlargement utilizing regimens of resistance training similar to those employed in human training programs is described. The model consists of electrically stimulating the lower leg muscles to contract against a weighted pulley bar. Animals were subjected to training protocols employing low-frequency repetitions with high training loads within a training session. Initial maximum loads of between 200 and 800 g were progressively increased during the 16 wk of training. Work done at the end of the training period increased to an average value 66% higher than that performed at the start of training. The gastrocnemius wet weight and protein content increased (P less than 0.001) by 18 and 17%, respectively, in the stimulated loaded leg in all but one training protocol, a program in which rats were exercised more frequently. RNA content, but not concentration, was increased in the trained gastrocnemius muscle from each protocol, resulting in muscle enlargement. These data indicate that the basic model presented here provides a suitable vehicle for future studies into the biochemical events that may cause skeletal muscle enlargement during resistance training but, based on limited data, suggests that an increased frequency of training days may hinder muscle enlargement in this model.     

Skeletal muscle vasodilation at the onset of exercise

The purpose of this study was to determinewhether -adrenergic or muscarinic receptors are involved in skeletalmuscle vasodilation at the onset of exercise. Mongrel dogs(n = 7) were instrumented with flow probes on both externaliliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 µg), both drugs, or saline was infusedintra-arterially immediately before treadmill exercise at 3 miles/h,0% grade. Immediate and rapid increases in iliac blood flow occurredwith initiation of exercise under all conditions. Peak blood flows werenot significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although thedoses of antagonists employed had no effect on heart rate or systemicblood pressure, they were adequate to abolish agonist-induced increasesin iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of -adrenergic andmuscarinic receptors is not essential for the rapid vasodilation inactive skeletal muscle at the onset of exercise in dogs.

     

Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.     

Skeletal muscle plasma membrane glucose transport and glucose transporters after exercise

Recent reports have shown that immediately after an acute bout of exercise the glucose transport system of rat skeletal muscle plasma membranes is characterized by an increase in both glucose transporter number and intrinsic activity. To determine the duration of the exercise response we examined the time course of these changes after completion of a single bout of exercise. Male rats were exercised on a treadmill for 1 h (20 m/min, 10% grade) or allowed to remain sedentary. Rats were killed either immediately or 0.5 or 2 h after exercise, and red gastrocnemius muscle was used for the preparation of plasma membranes. Plasma membrane glucose transporter number was elevated 1.8- and 1.6-fold immediately and 30 min after exercise, although facilitated D-glucose transport in plasma membrane vesicles was elevated 4- and 1.8-fold immediately and 30 min after exercise, respectively. By 2 h after exercise both glucose transporter number and transport activity had returned to nonexercised control values. Additional experiments measuring glucose uptake in perfused hindquarter muscle produced similar results. We conclude that the reversal of the increase in glucose uptake by hindquarter skeletal muscle after exercise is correlated with a reversal of the increase in the glucose transporter number and activity in the plasma membrane. The time course of the transport-to-transporter ratio suggests that the intrinsic activity response reverses more rapidly than that involving transporter number.     

Skeletal muscle metabolism during exercise is influenced by heat acclimation

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.     

Skeletal muscle energy metabolism during prolonged, fatiguing exercise.

A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inosine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O(2) uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 +/- 3% of LT ( approximately 65% peak O(2) uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, approximately 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 +/- 31 min). Glycogen concentration progressively declined (P < 0.01) to very low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when F-40 was compared with F and was only reduced by 40% when F was compared with rest (52. 8 +/- 3.7 vs. 87.8 +/- 2.0 mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r = 0.95; P < 0. 05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.     

Skeletal muscle biochemical adaptations to exercise training in miniature swine

McAllister, Richard M., Brian L. Reiter, John F. Amann, andM. Harold Laughlin. Skeletal muscle biochemical adaptations toexercise training in miniature swine. J. Appl.Physiol. 82(6): 1862-1868, 1997.The primarypurpose of this study was to test the hypothesis that enduranceexercise training induces increased oxidative capacity in porcineskeletal muscle. To test this hypothesis, female miniature swine wereeither trained by treadmill running 5 days/wk over 16-20 wk (Trn;n = 35) or pen confined (Sed;n = 33). Myocardialhypertrophy, lower heart rates during submaximal stages of a maximaltreadmill running test, and increased running time to exhaustion duringthat test were indicative of training efficacy. A variety of skeletalmuscles were sampled and subsequently assayed for the enzymes citratesynthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactatedehydrogenase and for antioxidant enzymes. Fiber type composition of arepresentative muscle was also determined histochemically. The largestincrease in CS activity (62%) was found in the gluteus maximus muscle(Sed, 14.7 ± 1.1 µmol · min¹ · g¹;Trn, 23.9 ± 1.0; P < 0.0005).Muscles exhibiting increased CS activity, however, were locatedprimarily in the forelimb; ankle and knee extensor and respiratorymuscles were unchanged with training. Only two muscles exhibited higher3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed.Lactate dehydrogenase activity was unchanged with training, as wereactivities of antioxidant enzymes. Histochemical analysis of thetriceps brachii muscle (long head) revealed lower type IIB fibernumbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4;P < 0.01) and greater type IID/Xfiber numbers (Sed, 11 ± 2; Trn, 22 ± 3;P < 0.025). These findingsindicate that porcine skeletal muscle adapts to endurance exercisetraining in a manner similar to muscle of humans and other animalmodels, with increased oxidative capacity. Specificmuscles exhibiting these adaptations, however, differ between theminiature swine and other species.

     

Skeletal muscle ECF pH error signal for exercise ventilatory control

Evans, Allison B., Larry W. Tsai, David A. Oelberg, HomayounKazemi, and David M. Systrom. Skeletal muscle ECF pH error signalfor exercise ventilatory control. J. Appl.Physiol. 84(1): 90-96, 1998.An autonomic reflexlinking exercising skeletal muscle metabolism to central ventilatorycontrol is thought to be mediated by neural afferents having freeendings that terminate in the interstitial fluid of muscle. Todetermine whether changes in muscle extracellular fluid pH(pH_e) can provide an errorsignal for exercise ventilatory control,pH_e was measured duringelectrically induced contraction by³¹P-magnetic resonancespectroscopy and the chemical shift of a phosphorylated, pH-sensitivemarker that distributes to the extracellular fluid (phenylphosphonicacid). Seven lightly anesthetized rats underwentunilateral continuous 5-Hz sciatic nerve stimulation in an 8.45-Tnuclear magnetic resonance magnet, which resulted in a mixed lacticacidosis and respiratory alkalosis, with no net change in arterial pH.Skeletal muscle intracellular pH fell from 7.30 ± 0.03 units atrest to 6.72 ± 0.05 units at 2.4 min of stimulation and then roseto 7.05 ± 0.01 units (P < 0.05), despite ongoing stimulation and muscle contraction.Despite arterial hypocapnia, pH_eshowed an immediate drop from its resting baseline of 7.40 ± 0.01 to 7.16 ± 0.04 units (P < 0.05)and remained acidic throughout the stimulation protocol. During the on-and off-transients for 5-Hz stimulation, changes in the pH gradientbetween intracellular and extracellular compartments suggestedtime-dependent recruitment of sarcolemmal ion-transport mechanisms.pH_e of exercising skeletal musclemeets temporal and qualitative criteria necessary for a ventilatorymetaboreflex mediator in a setting where arterial pH doesnot.

     

Skeletal muscle properties and performance in elite female track athletes

Selected biochemical and physiological properties of skeletal muscle were studied in light of performance capabilities in 24 elite female track athletes. The feasibility of quantifying end point histochemistry and relating oxidative staining density (reduced nicotinomide adenine dinucleotide diaphorase: NADH-D) to whole body maximal oxygen consumption (VO2 max) was also investigated, while muscle fiber types, classified according to alkaline APTase stains, were studied and related to muscle oxidative capacity (succinate dehydrogenase: SDH), VO2 max and "in vivo" torque-velocity properties. Muscle biopsies were taken from the vastus lateralis of each subject and maximal knee extensor torques were recorded at 30 degrees from full extension at four selected velocities. While results confirm earlier reports on skeletal muscle properties and performance it was concluded that end point histochemistry could be reliably quantified and that an "oxidative" stain such as NADH-D correlates extremely well with VO2 max (r = 0.86, p less than 0.001) whereas correlations between % slow twitch fibres (Alkaline ATPase stain) and VO2 max were lower (r = 0.44, p less than 0.05). Additionally, as knee extension velocity increased from 0-1.7 rad x s-1 angle specific extensor torque production did not decline as observed in vitro and pentathletes displayed significantly larger torques at all velocities when compared to the other athletes. These data confirm that while myofibrillar ATPase staining correlates with force-velocity properties of muscle, VO2 max is better correlated with quantified oxidative staining.     

Effects of exercise order on upper-body muscle activation and exercise performance

With the purpose of manipulating training stimuli, several techniques have been employed to resistance training. Two of the most popular techniques are the pre-exhaustion (PRE) and priority system (PS). PRE involves exercising the same muscle or muscle group to the point of muscular failure using a single-joint exercise immediately before a multi-joint exercise (e.g., peck-deck followed by chest press). On the other hand, it is often recommended that the complex exercises should be performed first in a training session (i.e., chest press before peck-deck), a technique known as PS. The purpose of the present study was to compare upper-body muscle activation, total repetitions (TR), and total work (TW) during PRE and PS. Thirteen men (age 25.08 +/- 2.58 years) with recreational weight-training experience performed 1 set of PRE and 1 set of PS in a balanced crossover design. The exercises were performed at the load obtained in a 10 repetition maximum (10RM) test. Therefore, chest press and peck-deck were performed with the same load during PRE and PS. Electromyography (EMG) was recorded from the triceps brachii (TB), anterior deltoids, and pectoralis major during both exercises. According to the results, TW and TR were not significantly different (p > 0.05) between PRE and PS. Likewise, during the peck-deck exercise, no significant (p > 0.05) EMG change was observed between PRE and PS order. However, TB activity was significantly (p < 0.05) higher when chest press was performed after the peck-deck exercise (PRE). Our findings suggest that performing pre-exhaustion exercise is no more effective in increasing the activation of the prefatigued muscles during the multi-joint exercise. Also, independent of the exercise order (PRE vs. PS), TW is similar when performing exercises for the same muscle group. In summary, if the coach wants to maximize the athlete performance in 1 specific resistance exercise, this exercise should be placed at the beginning of the training session.     

Skeletal muscle glucose transport in obese Zucker rats after exercise training

Exercise training has been found to reduce the muscle insulin resistance of the obese Zucker rat (fa/fa). The purpose of the present study was to determine whether this reduction in muscle insulin resistance was associated with an improvement in the glucose transport process and if it was fiber-type specific. Rats were randomly assigned to a sedentary or training group. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 days/wk, for 6-8 wk. The rate of muscle glucose transport was assessed in the absence of insulin and in the presence of a physiological (0.15 mU/ml), a submaximal (1.50 mU/ml), and a maximal (15.0 mU/ml) insulin concentration by determining the rate of 3-O-methyl-D-glucose (3-OMG) accumulation during hindlimb perfusion. The average 3-OMG transport rate of the red gastrocnemii (fast-twitch oxidative-glycolytic fibers) was significantly higher in the trained compared with the sedentary obese rats in the absence of insulin and in the presence of the three insulin concentrations. Significant improvements in 3-OMG transport were also observed in the plantarii (mixed fibers) of trained obese rats in the presence of 0, 0.15, and 15.0 mU/ml insulin. Training appeared to have little effect on the insulin-stimulated 3-OMG transport of the soleus (slow-twitch oxidative fibers) or white gastrocnemius (fast-twitch glycolytic fibers). The results suggest that the improvement in the muscle insulin resistance of the obese Zucker rat after moderate endurance training was associated with an improvement in the glucose transport process but that it was fiber-type specific.