Exercise training and muscle microvascular oxygenation: functional role of nitric oxide

Exercise training induces multiple adaptations within skeletal muscle that may improve local O(2) delivery-utilization matching (i.e., Po(2)mv). We tested the hypothesis that increased nitric oxide (NO) function is intrinsic to improved muscle Po(2)mv kinetics from rest to contractions after exercise training. Healthy young Sprague-Dawley rats were assigned to sedentary (n = 18) or progressive treadmill exercise training (n = 10; 5 days/wk, 6-8 wk, final workload of 60 min/day at 35 m/min, -14% grade) groups. Po(2)mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1-Hz twitch contractions under control (Krebs-Henseleit solution), sodium nitroprusside (SNP, NO donor; 300 μM), and N(G)-nitro-l-arginine methyl ester (l-NAME, nonspecific NO synthase blockade; 1.5 mM) superfusion conditions. Exercise-trained rats had greater peak oxygen uptake (Vo(2peak)) than their sedentary counterparts (81 ± 1 vs. 72 ± 2 ml·kg(-1)·min(-1), respectively; P < 0.05). Exercise-trained rats had significantly slower Po(2)mv fall throughout contractions (τ(1); time constant for the first component) during control (sedentary: 8.1 ± 0.6; trained: 15.2 ± 2.8 s). Compared with control, SNP slowed τ(1) to a greater extent in sedentary rats (sedentary: 38.7 ± 5.6; trained: 26.8 ± 4.1 s; P > 0.05) whereas l-NAME abolished the differences in τ(1) between sedentary and trained rats (sedentary: 12.0 ± 1.7; trained: 11.2 ± 1.4 s; P < 0.05). Our results indicate that endurance exercise training leads to greater muscle microvascular oxygenation across the metabolic transient following the onset of contractions (i.e., slower Po(2)mv kinetics) partly via increased NO-mediated function, which likely constitutes an important mechanism for training-induced metabolic adaptations.     

Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes

Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose regulation and skeletal muscle metabolic capacity in patients with type 2 diabetes. Eight patients with type 2 diabetes (63 ± 8 yr, body mass index 32 ± 6 kg/m(2), Hb(A1C) 6.9 ± 0.7%) volunteered to participate in this study. Participants performed six sessions of HIT (10 × 60-s cycling bouts eliciting ～90% maximal heart rate, interspersed with 60 s rest) over 2 wk. Before training and from ～48 to 72 h after the last training bout, glucose regulation was assessed using 24-h continuous glucose monitoring under standardized dietary conditions. Markers of skeletal muscle metabolic capacity were measured in biopsy samples (vastus lateralis) before and after (72 h) training. Average 24-h blood glucose concentration was reduced after training (7.6 ± 1.0 vs. 6.6 ± 0.7 mmol/l) as was the sum of the 3-h postprandial areas under the glucose curve for breakfast, lunch, and dinner (both P < 0.05). Training increased muscle mitochondrial capacity as evidenced by higher citrate synthase maximal activity (～20%) and protein content of Complex II 70 kDa subunit (～37%), Complex III Core 2 protein (～51%), and Complex IV subunit IV (～68%, all P < 0.05). Mitofusin 2 (～71%) and GLUT4 (～369%) protein content were also higher after training (both P < 0.05). Our findings indicate that low-volume HIT can rapidly improve glucose control and induce adaptations in skeletal muscle that are linked to improved metabolic health in patients with type 2 diabetes.     

Interactive effects of body posture and exercise training on maximal oxygen uptake

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of endurance exercise training on muscle glycogen accumulation in humans.

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 +/- 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher (P < 0.05) in the trained than in the untrained state: 10.5 +/- 0.2 and 4.5 +/- 1.3 mmol. kg wet wt(-1). h(-1), respectively. Muscle glycogen concentration was higher (P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher (P < 0.05) in the trained than in the untrained state (10.7 +/- 1.2 and 4.7 +/- 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise (r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.     

Two weeks of muscle immobilization impairs functional sympatholysis but increases exercise hyperemia and the vasodilatory responsiveness to infused ATP

During exercise, contracting muscles can override sympathetic vasoconstrictor activity (functional sympatholysis). ATP and adenosine have been proposed to play a role in skeletal muscle blood flow regulation. However, little is known about the role of muscle training status on functional sympatholysis and ATP- and adenosine-induced vasodilation. Eight male subjects (22 ± 2 yr, Vo(2max): 49 ± 2 ml O(2)·min(-1)·kg(-1)) were studied before and after 5 wk of one-legged knee-extensor training (3-4 times/wk) and 2 wk of immobilization of the other leg. Leg hemodynamics were measured at rest, during exercise (24 ± 4 watts), and during arterial ATP (0.94 ± 0.03 μmol/min) and adenosine (5.61 ± 0.03 μmol/min) infusion with and without coinfusion of tyramine (11.11 μmol/min). During exercise, leg blood flow (LBF) was lower in the trained leg (2.5 ± 0.1 l/min) compared with the control leg (2.6 ± 0.2 l/min; P < 0.05), and it was higher in the immobilized leg (2.9 ± 0.2 l/min; P < 0.05). Tyramine infusion lowers LBF similarly at rest, but, when tyramine was infused during exercise, LBF was blunted in the immobilized leg (2.5 ± 0.2 l/min; P < 0.05), whereas it was unchanged in the control and trained leg. Mean arterial pressure was lower during exercise with the trained leg compared with the immobilized leg (P < 0.05), and leg vascular conductance was similar. During ATP infusion, the LBF response was higher after immobilization (3.9 ± 0.3 and 4.5 ± 0.6 l/min in the control and immobilized leg, respectively; P < 0.05), whereas it did not change after training. When tyramine was coinfused with ATP, LBF was reduced in the immobilized leg (P < 0.05) but remained similar in the control and trained leg. Training increased skeletal muscle P2Y2 receptor content (P < 0.05), whereas it did not change with immobilization. These results suggest that muscle inactivity impairs functional sympatholysis and that the magnitude of hyperemia and blood pressure response to exercise is dependent on the training status of the muscle. Immobilization also increases the vasodilatory response to infused ATP.     

Effect of range of motion on muscle strength and thickness

The purpose of this investigation was to compare partial range-of-motion vs. full range-of-motion upper-body resistance training on strength and muscle thickness (MT) in young men. Volunteers were randomly assigned to 3 groups: (a) full range of motion (FULL; n = 15), (b) partial range of motion (PART; n = 15), or (c) control (CON; n = 10). The subjects trained 2 d · wk(-1) for 10 weeks in a periodized program. Primary outcome measures included elbow flexion maximal strength measured by 1 repetition maximum (1RM) and elbow flexors MT measured by ultrasound. The results indicated that elbow flexion 1RM significantly increased (p < 0.05) for the FULL (25.7 ± 9.6%) and PART groups (16.0 ± 6.7%) but not for the CON group (1.7 ± 5.5%). Also, FULL 1RM strength was significantly greater than the PART 1RM after the training period. Average elbow flexor MT significantly increased for both training groups (9.65 ± 4.4% for FULL and 7.83 ± 4.9 for PART). These data suggest that muscle strength and MT can be improved with both FULL and PART resistance training, but FULL may lead to greater strength gains.     

The effect of players' standard and tactical strategy on game demands in men's basketball

The purpose of the present study was to examine the effects of competitive level and team tactic on game demands in men's basketball. Sixteen international-level male basketball players (INPs) and 22 national-level male basketball players (NLPs) were studied during 6 games. Time-motion analysis was performed to track game activities. Game physiological demands were assessed by monitoring heart rate (HR) and blood-lactate concentration. Results showed that INPs sprinted significantly more and performed more high-intensity shuffling than did NLPs (p < 0.05). Game-activity changes and frequency of high-intensity bouts were similar in man-to-man and zone-marking games (1,053 vs. 1,056 and 253 vs. 224, respectively, p > 0.05). Time spent in the maximal (>95% of HRmax) and high-intensity zone (85-95% of HRmax) was greater in the INPs than in the NLPs (17.8 vs. 15.2%, p < 0.01 and 59.1 vs. 54.4%, p < 0.05, respectively). No significant differences in mean HR were evident between man-to-man and zone-marking games (93.3 ± 2.1 vs. 92.8 ± 1.8% of HRmax, p > 0.05). Blood-lactate concentration was higher in the INPs than in the NLPs (6.60 ± 1.22 vs. 5.66 ± 1.19 mmol·L?1 at halftime and 5.65 ± 1.21 vs. 4.43 ± 1.43 mmol·L?1 at full time, p < 0.05). No mean or peak blood-lactate concentration differences resulted between man-to-man and zone-marking games (5.15 ± 1.32 vs. 5.83 ± 1.10 and 5.90 ± 1.25 vs. 6.30 ± 1.27 mmol·L?1, respectively, p > 0.05). These results suggest an effect of competitive level over game demands in men's basketball. No marking strategy effect was evident. Basketball coaches and fitness trainers should develop the ability to repeatedly perform high-intensity activity during the game. Repeated sprinting and high-intensity shuffling ability should be trained to successfully play man-to-man and zone defense, respectively.     

The 10-20-30 training concept improves performance and health profile in moderately trained runners

The effect of an alteration from regular endurance to interval (10-20-30) training on the health profile, muscular adaptations, maximum oxygen uptake (Vo(2max)), and performance of runners was examined. Eighteen moderately trained individuals (6 females and 12 males; Vo(2max): 52.2 ± 1.5 ml·kg(-1)·min(-1)) (means ± SE) were divided into a high-intensity training (10-20-30; 3 women and 7 men) and a control (CON; 3 women and 5 men) group. For a 7-wk intervention period the 10-20-30 replaced all training sessions with 10-20-30 training consisting of low-, moderate-, and high-speed running (<30%, <60%, and >90% of maximal intensity) for 30, 20, and 10 s, respectively, in three or four 5-min intervals interspersed by 2 min of recovery, reducing training volume by 54% (14.0 ± 0.9 vs. 30.4 ± 2.3 km/wk) while CON continued the normal training. After the intervention period Vo(2max) in 10-20-30 was 4% higher, and performance in a 1,500-m and a 5-km run improved (P < 0.05) by 21 and 48 s, respectively. In 10-20-30, systolic blood pressure was reduced (P < 0.05) by 5 ± 2 mmHg, and total and low-density lipoprotein (LDL) cholesterol was lowered (P < 0.05) by 0.5 ± 0.2 and 0.4 ± 0.1 mmol/l, respectively. No alterations were observed in CON. Muscle membrane proteins and enzyme activity did not change in either of the groups. The present study shows that interval training with short 10-s near-maximal bouts can improve performance and Vo(2max) despite a ～50% reduction in training volume. In addition, the 10-20-30 training regime lowers resting systolic blood pressure and blood cholesterol, suggesting a beneficial effect on the health profile of already trained individuals.     

Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 +/- 1 yr; peak oxygen uptake = 50 +/- 2 ml.kg(-1).min(-1)) performed 4-6 x 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by approximately 35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining (P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained approximately 20% higher compared with baseline during detraining (P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.     

Effect of different frequencies of creatine supplementation on muscle size and strength in young adults

The purpose was to determine if creatine supplementation, consumed immediately before and immediately after exercise, with different dosing frequency (i.e., 2 or 3 d wk) could enhance the gains in muscle size and strength from resistance training (RT) in young adults. A group of 38 physically active, nonresistance trained university students (21-28 years) was randomly allocated to 1 of 4 groups: CR2 (0.15 g·kg creatine during 2 d wk of RT; 3 sets of 10 repetitions; n = 11, 6 men, 5 women), CR3 (0.10 g·kg creatine during 3 d wk of RT; 2 sets of 10 repetitions; n = 11, 6 men, 5 women;), PLA2 (placebo during 2 d wk of RT; n = 8, 5 men, 3 women), and PLA3 (placebo during 3 d wk of RT; n = 8, 4 men, 4 women) for 6 weeks. Before and after training, measurements were taken for muscle thickness of the elbow and knee flexor and extensor muscle groups (ultrasound), 1-repetition maximumleg press and chest press strength, and kidney function (urinary microalbumin). Repeated-measures analysis of variance showed that strength and muscle thickness increased in all groups with training (p < 0.05). The CR2 (0.6 ± 0.9 cm or 20%; p < 0.05) and CR3 groups (0.4 ± 0.6 cm or 16.4%; p < 0.05) experienced greater change in muscle thickness of the elbow flexors compared to the PLA2 (0.05 ± 0.5 cm or 2.3%) and PLA3 groups (0.13 ± 0.7 cm or 6.3%). Men supplementing with creatine experienced a greater increase in leg press strength (77.3 ± 51.2 kg or 62%) compared to women on creatine (21.3 ± 10 kg or 34%, p < 0.05). We conclude that creatine supplementation during RT has a small beneficial effect on regional muscle thickness in young adults but that giving the creatine over 3 d wk did not differ from giving the same dose over 2 d wk.     

A method for detecting the temporal sequence of muscle activation during cycling using MRI

Surface electromyography (EMG) can assess muscle recruitment patterns during cycling, but has limited applicability to studies of deep muscle recruitment and electrically stimulated contractions. We determined whether muscle recruitment timing could be inferred from MRI-measured transverse relaxation time constant (T(2)) changes and a cycle ergometer modified to vary power as a function of pedal angle. Six subjects performed 6 min of single-leg cycling under two conditions (E0°-230° and E90°-230°), which increased the power from 0°-230° and 90-230° of the pedal cycle, respectively. The difference condition produced a virtual power output from 0-180° (V0°-180°). Recruitment was assessed by integrating EMG over the pedal cycle (IEMG) and as the (post-pre) exercise T(2) change (ΔT(2)). For E0°-230°, the mean IEMG for vastus medialis and lateralis (VM/VL; 49.3 ± 3.9 mV·s; mean ± SE) was greater (P < 0.05) than that for E90°-230° (17.9 ± 1.9 mV·s); the corresponding ΔT(2) values were 8.7 ± 1.0 and 1.4 ± 0.5 ms (P < 0.05). For E0°-230° and E90°-230°, the IEMG values for biceps femoris/long head (BF(L)) were 37.7 ± 5.4 and 27.1 ± 5.6 mV·s (P > 0.05); the corresponding ΔT(2) values were 0.9 ± 0.9 and 1.5 ± 0.9 ms (P > 0.05). MRI data indicated activation of the semitendinosus and BF/short head for E0°-230° and E90°-230°. For V0°-180°, ΔT(2) was 7.2 ± 0.9 ms for VM/VL and -0.6 ± 0.6 ms for BF(L); IEMG was 31.5 ± 3.7 mV·s for VM/VL and 10.6 ± 7.0 mV·s for BF(L). MRI and EMG data indicate VM/VL activity from 0 to 180° and selected hamstring activity from 90 to 230°. Combining ΔT(2) measurements with variable loading allows the spatial and temporal patterns of recruitment during cycling to be inferred from MRI data.     

Regional muscle blood flow capacity and exercise hyperemia in high-intensity trained rats

The purpose of this study was to determine the effects of high-intensity treadmill exercise training on 1) the regional distribution of muscle blood flow within and among muscles in rats during high-intensity treadmill exercise (phase I) and 2) on the total and regional hindlimb skeletal muscle blood flow capacities as measured in isolated perfused rat hindquarters during maximal papaverine vasodilation (phase II). Two groups of male Sprague-Dawley rats were trained 5 days/wk for 6 wk with a program consisting of 6 bouts/day of 2.5-min runs at 60 m/min up a 15% grade with 4.5-min rest periods between bouts. After training, blood flows were measured with the radiolabeled microsphere technique (phase I) in pair-weighted sedentary control and exercise-trained rats while they ran at 60 m/min (0% grade). In phase II of the study, regional vascular flow capacities were determined at three perfusion pressures (30, 40, and 50 mmHg) in isolated perfused hindquarters of control and trained rats maximally vasodilated with papaverine. The results indicate that this exercise training program produces increases in the vascular flow capacity of fast-twitch glycolytic muscle tissue of rats. However, these changes were not apparent in the magnitude or distribution of muscle blood flow in conscious rats running at 60 m/min, since blood flows within and among muscles during exercise were the same in trained and control rats.     

Skeletal muscle lactate dehydrogenase isozyme alterations in men and women marathon runners

Total lactate dehydrogenase (LD) and LD isozyme activities in gastrocnemius muscle from trained men and women runners were measured in response to the chronic stress of training for a marathon race (42.2 km). Following 9 wk of training, total LD activity in skeletal muscle from men and women runners significantly (P less than 0.02) decreased 2.26 and 2.25 U/mg protein, respectively. However, men's total LD activities were significantly (P less than 0.001) less than the women's both before and after training. Significant (P less than 0.05) increases in LD1 activities in skeletal muscle in men and women runners were also observed after training. No significant correlations were detected between percent fiber type composition in men or women vs. the changes in total LD activity, changes in LD1 activity, maximal O2 consumption or training distance averaged per week after the training period. The biochemical adaptations in skeletal muscle that occurred in the LD isozyme composition in both men and women runners make the runners skeletal muscle appear similar to heart muscle in LD1 and LD2 activities.     

Effects of high-intensity sprint training on skeletal muscle blood flow in rats.

The regional blood flow response (via radioactive microspheres) was determined for female rats after 6 wk of high-intensity sprint training (HIST) or limited cage activity as the animals exercised at work loads that would elicit maximal O2 uptake. Blood flow to the different organs of the abdominal region was greatly reduced during maximal exercise conditions, and the magnitude of the reduction appeared to be similar for both the HIST group of rats and their sedentary (SED) control counterparts. Of the 20 different hindlimb muscles examined in the present study, blood flow to the soleus, plantaris, gastrocnemius, flexor hallicus longus, vastus lateralis, rectus femoris, biceps femoris, and adductor magnus and brevis muscles was significantly greater (P less than 0.05) in the HIST rats during maximal exercise conditions than in the SED control rats. Correspondingly, blood flow to the total hindlimb during maximal exercise was also significantly greater in the HIST rats than in the SED control rats [240 +/- 18 vs. 192 +/- 15 (SE) ml.min-1.100 g-1]. These results support the contention that the increase in maximal cardiac output that is produced by HIST in the rat is primarily directed toward the working skeletal muscle and not toward the organs found in the abdominal region. We conclude from these experiments that HIST will produce significant adaptations in central cardiac function and skeletal muscle blood flow in the rat.     

Exercise training augments the dynamic heart rate response to vagal but not sympathetic stimulation in rats

We examined the transfer function of autonomic heart rate (HR) control in anesthetized sedentary and exercise-trained (16 wk, treadmill for 1 h, 5 times/wk at 15 m/min and 15-degree grade) rats for comparison to HR variability assessed in the conscious resting state. The transfer function from sympathetic stimulation to HR response was similar between groups (gain, 4.2 ± 1.5 vs. 4.5 ± 1.5 beats·min(-1)·Hz(-1); natural frequency, 0.07 ± 0.01 vs. 0.08 ± 0.01 Hz; damping coefficient, 1.96 ± 0.55 vs. 1.69 ± 0.15; and lag time, 0.7 ± 0.1 vs. 0.6 ± 0.1 s; sedentary vs. exercise trained, respectively, means ± SD). The transfer gain from vagal stimulation to HR response was 6.1 ± 3.0 in the sedentary and 9.7 ± 5.1 beats·min(-1)·Hz(-1) in the exercise-trained group (P = 0.06). The corner frequency (0.11 ± 0.05 vs. 0.17 ± 0.09 Hz) and lag time (0.1 ± 0.1 vs. 0.2 ± 0.1 s) did not differ between groups. When the sympathetic transfer gain was averaged for very-low-frequency and low-frequency bands, no significant group effect was observed. In contrast, when the vagal transfer gain was averaged for very-low-frequency, low-frequency, and high-frequency bands, exercise training produced a significant group effect (P < 0.05 by two-way, repeated-measures ANOVA). These findings suggest that, in the frequency domain, exercise training augments the dynamic HR response to vagal stimulation but not sympathetic stimulation, regardless of the frequency bands.     

Adaptations in human muscle sarcoplasmic reticulum to prolonged submaximal training.

In this study, we employed single-leg submaximal cycle training, conducted over a 10-wk period, to investigate adaptations in sarcoplasmic reticulum (SR) Ca(2+)-regulatory proteins and processes of the vastus lateralis. During the final weeks, the untrained volunteers (age 21.4 +/- 0.3 yr; means +/- SE, n = 10) were exercising 5 times/wk and for 60 min/session. Analyses were performed on tissue extracted by needle biopsy approximately 4 days after the last training session. Compared with the control leg, the trained leg displayed a 19% reduction (P < 0.05) in homogenate maximal Ca(2+)-ATPase activity (192 +/- 11 vs. 156 +/- 18 micromol. g protein(-1). min(-1)), a 4.3% increase (P < 0.05) in pCa(50), defined as the Ca(2+) concentration at half-maximal activity (6.01 +/- 0.05 vs. 6.26 +/- 0.07), and no change in the Hill coefficient (1.75 +/- 0.15 vs. 1.76 +/- 0.21). Western blot analysis using monoclonal antibodies (7E6 and A52) revealed a 13% lower (P < 0.05) sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) 1 in trained vs. control in the absence of differences in SERCA2a. Training also resulted in an 18% lower (P < 0.05) SR Ca(2+) uptake and a 26% lower (P < 0.05) Ca(2+) release. It is concluded that a downregulation in SR Ca(2+) cycling in vastus lateralis occurs with aerobic-based training, which at least in the case of Ca(2+) uptake can be explained by reduction in Ca(2+)-ATPase activity and SERCA1 protein levels.     

Sweating responses and the muscle metaboreflex under mildly hyperthermic conditions in sprinters and distance runners

To investigate the effects of different training methods on nonthermal sweating during activation of the muscle metaboreflex, we compared sweating responses during postexercise muscle occlusion in endurance runners, sprinters, and untrained men under mild hyperthermia (ambient temperature, 35°C; relative humidity, 50%). Ten endurance runners, nine sprinters, and ten untrained men (maximal oxygen uptakes: 57.5 ± 1.5, 49.3 ± 1.5, and 36.6 ± 1.6 ml·kg(-1)·min(-1), respectively; P < 0.05) performed an isometric handgrip exercise at 40% maximal voluntary contraction for 2 min, and then a pressure of 280 mmHg was applied to the forearm to occlude blood circulation for 2 min. The Δ change in mean arterial blood pressure between the resting level and the occlusion was significantly higher in sprinters than in untrained men (32.2 ± 4.4 vs. 17.3 ± 2.6 mmHg, respectively; P < 0.05); however, no difference was observed between distance runners and untrained men. The Δ mean sweating rate (averaged value of the forehead, chest, forearm, and thigh) during the occlusion was significantly higher in distance runners than in sprinters and untrained men (0.38 ± 0.07, 0.19 ± 0.03, and 0.11 ± 0.04 mg·cm(-2)·min(-1), respectively; P < 0.05) and did not differ between sprinters and untrained men. Our results suggest that the specificity of training modalities influences the sweating response during activation of the muscle metaboreflex. In addition, these results imply that a greater activation of the muscle metaboreflex does not cause a greater sweating response in sprinters.     

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.     

Effects of cross-education on the muscle after a period of unilateral limb immobilization using a shoulder sling and swathe

The purpose of this study was to apply cross-education during 4 wk of unilateral limb immobilization using a shoulder sling and swathe to investigate the effects on muscle strength, muscle size, and muscle activation. Twenty-five right-handed participants were assigned to one of three groups as follows: the Immob + Train group wore a sling and swathe and strength trained (n = 8), the Immob group wore a sling and swathe and did not strength train (n = 8), and the Control group received no treatment (n = 9). Immobilization was applied to the nondominant (left) arm. Strength training consisted of maximal isometric elbow flexion and extension of the dominant (right) arm 3 days/wk. Torque (dynamometer), muscle thickness (ultrasound), maximal voluntary activation (interpolated twitch), and electromyography (EMG) were measured. The change in right biceps and triceps brachii muscle thickness [7.0 ± 1.9 and 7.1 ± 2.2% (SE), respectively] was greater for Immob + Train than Immob (0.4 ± 1.2 and -1.9 ± 1.7%) and Control (0.8 ± 0.5 and 0.0 ± 1.1%, P < 0.05). Left biceps and triceps brachii muscle thickness for Immob + Train (2.2 ± 0.7 and 3.4 ± 2.1%, respectively) was significantly different from Immob (-2.8 ± 1.1 and -5.2 ± 2.7%, respectively, P < 0.05). Right elbow flexion strength for Immob + Train (18.9 ± 5.5%) was significantly different from Immob (-1.6 ± 4.0%, P < 0.05). Right and left elbow extension strength for Immob + Train (68.1 ± 25.9 and 32.2 ± 9.0%, respectively) was significantly different from the respective limb of Immob (1.3 ± 7.7 and -6.1 ± 7.8%) and Control (4.7 ± 4.7 and -0.2 ± 4.5%, P < 0.05). Immobilization in a sling and swathe decreased strength and muscle size but had no effect on maximal voluntary activation or EMG. The cross-education effect on the immobilized limb was greater after elbow extension training. This study suggests that strength training the nonimmobilized limb benefits the immobilized limb for muscle size and strength.     

Exercise training increases branched-chain oxoacid dehydrogenase kinase content in human skeletal muscle

The branched-chain oxoacid dehydrogenase complex (BCOAD) is rate determining for the oxidation of branched-chain amino acids (BCAAs) in skeletal muscle. Exercise training blunts the acute exercise-induced activation of BCOAD (BCOADa) in human skeletal muscle (McKenzie S, Phillips SM, Carter SL, Lowther S, Gibala MJ, Tarnopolsky MA. Am J Physiol Endocrinol Metab 278: E580-E587, 2000); however, the mechanism is unknown. We hypothesized that training would increase the muscle protein content of BCOAD kinase, the enzyme responsible for inactivation of BCOAD by phosphorylation. Twenty subjects [23 +/- 1 yr; peak oxygen uptake (.VO(2peak)) = 41 +/- 2 ml.kg(-1).min(-1)] performed 6 wk of either high-intensity interval or continuous moderate-intensity training on a cycle ergometer (n = 10/group). Before and after training, subjects performed 60 min of cycling at 65% of pretraining .VO(2peak), and needle biopsy samples (vastus lateralis) were obtained before and immediately after exercise. The effect of training was demonstrated by an increased .VO(2peak), increased citrate synthase maximal activity, and reduced muscle glycogenolysis during exercise, with no difference between groups (main effects, P < 0.05). BCOADa was lower after training (main effect, P < 0.05), and this was associated with a approximately 30% increase in BCOAD kinase protein content (main effect, P < 0.05). We conclude that the increased protein content of BCOAD kinase may be involved in the mechanism for reduced BCOADa after exercise training in human skeletal muscle. These data also highlight differences in models used to study the regulation of skeletal muscle BCAA metabolism, since exercise training was previously reported to increase BCOADa during exercise and decrease BCOAD kinase content in rats (Fujii H, Shimomura Y, Murakami T, Nakai N, Sato T, Suzuki M, Harris RA. Biochem Mol Biol Int 44: 1211-1216, 1998).