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ABSTRACTPurpose: In U.S. collegiate soccer, matches that end drawn after 90-min of regulation time (RT) proceed to two 10-min extra time (ET) periods. This study quantified the physical demands and heart rate (HR) responses of playing ET matches in women’s collegiate soccer matches and compared performances during ET to those of RT.Methods: 25 female collegiate players (age = 18-22y) played 10 ET and 11 RT matches. Total and high-intensity distances, energy expended and HR were determined using GPS, accelerometry and HR monitoring. Players were categorized a full-time (FULL) or part-time (PART) players based on the minutes played during RT.Results: For both groups, physical performance measures showed only small changes over the course of the match and were generally maintained during both ET periods. During ET, performances of FULL players were similar to PART players. Also, performances of FULL during the RT portion of ET matches were similar to those during RT of competitive non-ET matches.Conclusions: These results suggest that female collegiate players maintain physical performance through RT and during an extra 20 min of ET. The ET periodscan increase total match workload by 20–25%. This increase should be considered when addressing short- and long-term periodization strategies.

It is thought that changes in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) of skeletal muscle contribute to alterations in skeletal muscle function during congestive heart failure (CHF). It is well established that exercise training can improve muscle function. However, it is unclear whether similar adaptations will result from exercise training in a CHF patient. Therefore, the purpose of this study was to determine whether skeletal muscle during moderate CHF adapts to increased activity, utilizing the functional overload (FO) model. Significant increases in plantaris mass of the CHF-FO and sham-FO groups compared with the CHF and control (sham) groups were observed. Ca2+uptake rates were significantly elevated in the CHF group compared with all other groups. No differences were detected in Ca2+uptake rates between the CHF-FO, sham, and sham-FO groups. Increases in Ca2+uptake rates in moderate-CHF rats were not due to changes in SERCA isoform proportions; however, FO may have attenuated the CHF-induced increases through alterations in SERCA isoform expression. Therefore, changes in skeletal muscle Ca2+handling during moderate CHF may be due to alterations in regulatory mechanisms, which exercise may override, by possibly altering SERCA isoform expression.

The purpose of the present study was to investigate the effects of fatiguing muscular activity on glycogen, glycogen phosphorylase (GP), and Ca2+uptake associated with the sarcoplasmic reticulum (SR). Tetanic contractions (100 ms, 75 Hz) of the gastrocnemius and plantaris muscles, elicited once per second for 15 min, significantly reduced force to 26.5 ± 4.0% and whole muscle glycogen to 23% of rested levels. SR glycogen levels were 415.4 ± 76.6 and 20.4 ± 2.1 μg/mg SR protein in rested and fatigued samples, respectively. The optical density of GP from SDS-PAGE was reduced to 21% of control, whereas pyridoxal 5′-phosphate concentration, a quantitative indicator of GP content, was significantly reduced to 3% of control. GP activity after exercise, in the direction of glycogen breakdown, was reduced to 4% of control. Maximum SR Ca2+uptake rate was also significantly reduced to 81% of control. These data demonstrate that glycogen and GP associated with skeletal muscle SR are reduced after fatiguing activity.

Sarcoplasmic reticulum (SR) responses to repeated sprints and to physical conditioning were studied in 10 Quarter Horses. Exercise tests (four repeated sprints on a treadmill) were conducted before and after 12 wk of sprint conditioning. Muscle samples from the middle gluteal muscle were taken before and after each exercise test, and SR vesicles were isolated. Calcium uptake was determined spectrophotometrically using antipyrylazo III, and Ca2+-ATPase activity was determined using an enzyme-linked optical assay. Conditioning increased calcium uptake rate and Ca2+-ATPase activity by 14 and 38%, respectively, before exercise and by 25 and 26% after exercise. Exercise decreased calcium uptake rate and Ca2+-ATPase activity by 37 and 27%, respectively, before conditioning and by 28 and 21% after conditioning. Decreases in calcium uptake and Ca2+-ATPase activity of SR have been associated with fatigue during exercise, and this association is strengthened by the moderating effect of conditioning.

WILLIAMS, J. H S. K. POWERS, and M. K. STUART. Hemoglobin desaturation in highly trained athletes during heavy exercise. Med. Sci. Sports Exerc., Vol. 18, No. 2, pp. 168–173, 1986. It has been generally accepted that during exercise at sea level, the pulmonary system of normal, healthy individuals is capable of maintaining arterial oxygen tension at near resting levels. However, recent evidence questions whether this generalization applies to the highly trained endurance athlete who is capable of achieving very high levels of metabolic demand. Hence, the purpose of these experiments was to examine the relationship between maximal oxygen consumption (O2max) and arterial oxygen-hemoglobin saturation (SaO2) during short-term heavy exercise in trained athletes and untrained individuals. Ten trained distance runners and 7 untrained males exercised at 95 of O2maxfor 3 min. Minute-by-minute measurement of SaO2was obtained via ear oximetry. The correlation coefficients between SaO2and O2max, during exercise were r = −0.68, r = −0.74, and r = −0.72 (P< 0.05) for minutes 1 through 3, respectively. In general those individuals with the highest O2maxshowed the greatest decrease in SaO2. By comparison there was no difference (P> 0.05) in resting SaO2between the trained (96.3 ± 0.2 [SE]) and the untrained (96.3 ± 0.4) subjects. However, at minute 3 of exercise, SaO2was significantly lower (P< 0.05) in the trained subjects (87.0 ± 0.7) than in the untrained subjects (92.6 ± 0.7). These data demonstrate that arterial desaturation occurs in healthy, highly trained endurance athletes during heavy exercise and that the level of the arterial desaturation is inversely related to O2max.

Williams, Jay H. Contractile apparatus and sarcoplasmic reticulum function: effects of fatigue, recovery, and elevated Ca2+. J. Appl. Physiol.83(2): 444–450, 1997.—This investigation tested the notion that fatiguing stimulation induces intrinsic changes in the contractile apparatus and sarcoplasmic reticulum (SR) and that these changes are initiated by elevated intracellular Ca2+concentration ([Ca2+]i). Immediately after stimulation of frog semitendinosus muscle, contractile apparatus and SR function were measured. Despite a large decline in tetanic force (Po), maximal Ca2+-activated force (Fmax) of the contractile apparatus was not significantly altered. However, Ca2+sensitivity was increased. In conjunction, the rate constant of Ca2+uptake by the SR was diminished, and the caffeine sensitivity of Ca2+release was decreased. During recovery, Po, contractile apparatus, and SR function each returned to near-initial levels. Exposure of skinned fibers to 0.5 μM free Ca2+for 5 min depressed both Fmaxand Ca2+sensitivity of the contractile apparatus. In addition, caffeine sensitivity of Ca2+release was diminished. Results suggest that fatigue induces intrinsic alterations in contractile apparatus and SR function. Changes in contractile apparatus function do not appear to be mediated by increased [Ca2+]i. However, a portion of the change in SR Ca2+release seems to be due to elevated [Ca2+]i.

The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (Po) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice (n= 164) were injured in vivo with 150 eccentric contractions. Po, caffeine-, 4-chloro-m-cresol-, and K+-induced contracture forces, sarcoplasmic reticulum (SR) Ca2+release and uptake rates, and intracellular Ca2+concentration ([Ca2+]i) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in Po(∼51%) compared with caffeine-induced force (∼11–21%), we estimate that E-C coupling failure can explain 57–75% of the Podecrement from 0 to 5 days postinjury. Comparable reductions in Poand K+-induced force (51%), and minor reductions (0–6%) in the maximal SR Ca2+release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting [Ca2+]iwas elevated and peak tetanic [Ca2+]iwas reduced, whereas peak 4-chloro-m-cresol-induced [Ca2+]iwas unchanged immediately after injury. By 3 days postinjury, 4-chloro-m-cresol-induced [Ca2+]ibecame depressed, probably because of decreased SR Ca2+release and uptake rates (17–31%). These data indicate that the decrease in Poduring the first several days after injury primarily stems from a failure in the E-C coupling process.

Twenty subjects were randomly assigned to: 1) prophylactic ibuprofen (N= 5) [400 mg TID initiated 4 h before collection of baseline data and strenuous eccentric exercise bout], 2) therapeutic ibuprofen (N= 5) [400 mg TID initiated 24 h after baseline], 3) placebo (N= 5), or 4) control (N= 5). Muscle soreness perception, plasma creatine kinase, knee extensor torque, and EMG of the quadriceps were evaluated at baseline, 24, and 48 h. The prophylactic ibuprofen group had between 40 and 50 less muscle soreness perception and significantly less decline in isometric, concentric, and eccentric torque at 24 h compared with the other three groups (P< 0.05). At 48 h both prophylactic and therapeutic ibuprofen had significantly less muscle soreness perception and decline in torque than the placebo and control groups (P< 0.05). There was no difference between the amount of muscle damage between the four groups at 24 and 48 h. Vastus medialis and lateralis EMG magnitude decreased across time. Vastus lateralis EMG magnitude had significantly less decline from baseline for prophylactic ibuprofen compared with the other three treatments at 24 h, while both prophylactic and therapeutic ibuprofen had significantly less decline at 48 h. These data indicate that a prophylactic dosage of ibuprofen does not prevent CK release from muscle, but does decrease muscle soreness perception and may assist in restoring muscle function.

Prostaglandins may alter neuronal noradrenaline release or vascular responsiveness to sympathoexcitation. The purpose of this study was to determine if indomethacin, a prostaglandin synthesis inhibitor, influences the sympathetic and circulatory adjustments to a commonly utilized laboratory stressor in the clinical assessment of autonomic function, the cold pressor test. Venous plasma noradrenaline levels (n = 8), mean arterial pressure and heart rate (n = 10) were measured in healthy male subjects during immersion of the non-dominant hand in cold water (1°C) for 90 s. The subjects were given either placebo or indomethacin (100 mg) in a double-blind manner. The order of administration was counterbalanced and a 1 week period was given for systemic clearance of the drug. The absolute level of mean arterial pressure was elevated during the resting control period after indomethacin treatment (88 in placebo vs. 92 mmHg in indomethacin). Both heart rate and venous plasma noradrenaline levels were similar between trials during the resting control period. Mean arterial pressure and heart rate increased similarly during cold pressor testing in both indomethacin and placebo. Venous plasma noradrenaline levels increased during cold pressor testing 162 ± 39 vs. 200 ± 69 pg/ml in indomethacin vs. placebo (p > 0.05), respectively. In addition, perceived pain (peak level = 7 ± 1 vs. 6 ± 1 units; indomethacin vs. placebo, respectively) was not different between the trials. These results suggest that administration of indomethacin in a maximal single therapeutic dose, does not affect the sympathetic nervous system or circulatory responsiveness to cold pressor testing. It may not be necessary to discontinue indomethacin prior to autonomic function testing.

KANDARIAN, S. C. and J. H. WILLIAMS. Contractile properties of skinned fibers from hypertrophied skeletal muscle. Med. Sci. Sports Exerc., Vol. 25, No. 9, pp. 999–1004, 1993. We have previously shown deficits in specific tension (N·cm−2) in whole hypertrophied skeletal muscle (18–30). The purpose of the present study was to determine if this intrinsic deficit exists in chemically skinned, hypertrophied single fibers, and also to measure their Ca2+sensitivity. One group of rats (N= 4) had bilateral surgical ablation o the gastrocnemius and soleus muscles, and another group (N= 4) had the gastrocnemius and plantaris muscles ablated to induce hypertrophy in the plantaris and soleus muscles, respectively. Thirty days after surgery five fibers were dissected and analyzed from each of eight muscles per group, including control muscles. In hypertrophied plantaris and soleus muscles, fiber cross-sectional area (CSA) was 20 and 29 greater, respectively, than control values. Maximal Ca2+activated tension (Po, pCa 4.5) was 15 greater in hypertrophied plantaris fibers and 18 greater in hypertrophied soleus fibers compared with respective control values (P0.05). Therefore, Po expressed per fiber CSA was slightly depressed (3–8) in both plantaris and soleus fibers (P< 0.05). Regarding Ca2+sensitivity, the Ca2+concentration to elicit 50 of Po (i.e., pCa50) was significantly lower in hypertrophied soleus (58) and plantaris (29) fibers. This leftward shift in the force-pCa curve reflects greater Ca2+sensitivity in hypertrophied fibers. Since the single fiber Po/CSA was only slightly decreased, these data suggest that during tetanic stimulation of whole muscle Ca2+delivery to the contractile apparatus may be impaired. The shift in the force-pCa curve may reflect alterations in myofibrillar proteins known to affect Ca2+sensitivity, and/or changes in the kinetics of cross-bridge cycling.

This study examined the effects of fatigue on the functional aspects of the contractile apparatus and sarcoplasmic reticulum (SR). Frog semitendinosus muscles were stimulated to fatigue, and skinned fibers or a homogenate fraction was prepared from both fatigued and rested contralateral muscles. In fatigued fibers, maximal Ca2+-activated force of the contractile apparatus was unaltered, whereas maximal actomyosin-ATPase activity was depressed by 20%. The Ca2+sensitivity of force was increased, whereas that of actomyosin-ATPase was not altered. Also, the rate constant for tension redevelopment was decreased at submaximal Ca2+concentration. These latter findings suggest that fatigue slows the dissociation of force-generating myosin cross bridges. Ca2+uptake and Ca2+-ATPase activity of the SR were depressed by 46 and 21%, respectively, in the fatigued muscles. Fatigue also reduced the rates of SR Ca2+release evoked by AgNO3and 4-chloro-m-cresol by 38 and 45%, respectively. During fatigue, the contractile apparatus and SR undergo intrinsic functional alterations. These changes likely result in altered force production and energy consumption by the intact muscle.

Analysis of elbow-extension movements, executed at maximal velocity, show positive correlations of timing of agonist-antagonist EMG activity with both movement velocity and displacement. Results indirectly support the notion that the antagonist musculature provides a braking force to arrest rapid limb movements.