Gøran Paulsen

Neuromuscular fatigue and recovery in elite female soccer : effects of active recovery

PURPOSE To investigate the time course of recovery from neuromuscular fatigue and some biochemical changes between two female soccer matches separated by an active or passive recovery regime. METHODS Countermovement jump (CMJ), sprint performance, maximal isokinetic knee flexion and extension, creatine kinase (CK), urea, uric acid, and perceived muscle soreness were measured in 17 elite female soccer players before, immediately after, 5, 21, 45, 51, and 69 h after a first match, and immediately after a second match. Eight players performed active recovery (submaximal cycling at 60% of HRpeak and low-intensity resistance training at < 50% 1RM) 22 and 46 h after the first match. RESULTS In response to the first match, a significant decrease in sprint performance (-3.0 +/- 0.5%), CMJ (-4.4 +/- 0.8%), peak torque in knee extension (-7.1 +/- 1.9%) and flexion (-9.4 +/- 1.8%), and an increase in CK (+ 152 +/- 28%), urea (15 +/- 2), uric acid (+ 11 +/- 2%), and muscle soreness occurred. Sprint ability was first to return to baseline (5 h) followed by urea and uric acid (21 h), isokinetic knee extension (27 h) and flexion (51 h), CK, and muscle soreness (69 h), whereas CMJ was still reduced at the beginning of the second match. There were no significant differences in the recovery pattern between the active and passive recovery groups. The magnitude of the neuromuscular and biochemical changes after the second match was similar to that observed after the first match. CONCLUSION The present study reveals differences in the recovery pattern of the various neuromuscular and biochemical parameters in response to a female soccer match. The active recovery had no effects on the recovery pattern of the four neuromuscular and three biochemical parameters.

Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double-blind, randomised, controlled trial

Recent studies have indicated that antioxidant supplementation may blunt adaptations to exercise, such as mitochondrial biogenesis induced by endurance training. However, studies in humans are sparse and results are conflicting. Isolated vitamin C and E supplements are widely used, and unravelling the interference of these vitamins in cellular and physiological adaptations to exercise is of interest to those who exercise for health purposes and to athletes. Our results show that vitamin C and E supplements blunted the endurance training‐induced increase of mitochondrial proteins (COX4), which is important for improving muscular endurance. Training‐induced increases in V̇O2 max and running performance were not detectably affected by the supplementation. The present study contributes to understanding of how antioxidants may interfere with adaptations to exercise in humans, and the results indicate that high dosages of vitamins C and E should be used with caution.

Subcellular movement and expression of HSP27, αB-crystallin, and HSP70 after two bouts of eccentric exercise in humans

The aims of this study were to investigate the sarcomeric accumulation and expression of heat shock proteins (HSPs) after two bouts of maximal eccentric exercise. Twenty-four subjects performed two bouts of 70 maximal voluntary eccentric actions using the elbow flexors in one arm. The bouts were separated by 3 wk. The changes in concentric (60 degrees/s) and isometric (90 degrees) force-generating capacity were monitored for 9 days after each bout, and biopsies were taken 1 and 48 h and 4 and 7 days after bout 1 and 1 and 48 h after bout 2. The content of HSP27, alphaB-crystallin, HSP70, and desmin in the cytosolic and cytoskeleton/myofibrillar fractions of homogenized muscle samples was determined by immunoassays, and the cellular and subcellular localization of the HSPs in the myofibrillar structure was analyzed by conventional and confocal immunofluorescence microscopy and quantitative electron microscopy. The force-generating capacity was reduced by approximately 50% and did not recover completely during the 3 wk following bout 1. After bout 2, the subjects recovered within 4 days. The HSP levels increased in the cytosolic fraction after bout 1, especially HSP70 (approximately 300% 2-7 days after exercise). Increased levels of HSP27, alphaB-crystallin, and HSP70 were found in the cytoskeletal/myofibrillar fraction after both bouts, despite reduced damage after bout 2. At the ultrastructural level, HSP27 and alphaB-crystallin accumulated in Z-disks, in intermediate desmin-like structures (alphaB-crystallin), and in areas of myofibrillar disruption. In conclusion, HSP27 and alphaB-crystallin accumulated in myofibrillar structures, especially in the Z-disks and the intermediate structures (desmin). The function of the small HSPs is possibly to stabilize and protect the myofibrillar structures during and after unaccustomed eccentric exercise. The large amount of HSP27, alphaB-crystallin, and HSP70 in the cytoskeletal/myofibrillar fraction after a repeated bout of exercise suggests a protective role as part of the repeated-bout effect.

Changes in Calpain Activity, Muscle Structure, and Function after Eccentric Exercise

PURPOSE The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. METHODS Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. RESULTS In the exercised leg, peak torque was reduced by 47 +/- 5% during exercise and was still 22 +/- 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 +/- 6% of all fibers in exercised muscle and in 2 +/- 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. CONCLUSIONS Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.

Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans.

Eccentric muscle actions are associated with ultrastructural changes. The severity and types of change depend on the nature of the stimulation protocol, and on the method for assessing such changes, and can be regarded as a continuum from mild changes to pathological-like changes. Most studies describing more severe changes have been performed on animals and only a few in humans, some using electrical stimuli. Hence, a debate has emerged on whether voluntary actions are associated with the pathological-like end of the continuum. The aim of this study was to determine whether severe muscle damage, i.e., extensive ultrastructural changes, is confined to animal studies and studies on humans using electrical stimuli. Second, because there is no generally approved method to quantify the degree of muscle damage, we compared two published methods, analyzing the Z disks or sarcomeres, as well as novel analyses of pathological-like changes. A group of untrained subjects performed 70 voluntary maximal eccentric muscle actions using the elbow flexors. On the basis of large reductions in maximal force-generating capacity (on average, -62 +/- 3% immediately after exercise, and -35 +/- 6% 9 days later), five subjects were selected for further analysis. Biopsies were taken from m. biceps brachii in both the exercised and nonexercised arm. In exercised muscle, more disrupted (13 +/- 4 vs. 3 +/- 3%) and destroyed (15 +/- 6 vs. 0%) Z disks were found compared with nonexercised muscle. A significant proportion of exercised myofibers had focal (85 +/- 5 vs. 11 +/- 7%), moderate (65 +/- 7 vs. 11 +/- 6%), and extreme (38 +/- 9 vs. 0%) myofibrillar disruptions. Hypercontracted myofibrils, autophagic vacuoles, granular areas, central nuclei, and necrotic fiber segments were found to various degrees. The present study demonstrates that the more severe end of the continuum of ultrastructural changes occurs in humans after voluntary exercise when maximal eccentric muscle actions are involved.

A COX‐2 inhibitor reduces muscle soreness, but does not influence recovery and adaptation after eccentric exercise

The aim of this study was to investigate the effect of a cyclooxygenase (COX)‐2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty‐three young males and females participated in a double‐blind, placebo‐controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks. The test group participants were administered 400 mg/day of celecoxib for 9 days after bout 1. After both bouts 1 and 2, concentric and isometric force‐generating capacity was immediately reduced (∼40–50%), followed by the later appearance of muscle soreness and increased serum creatine kinase levels. Radiolabelled autologous leukocytes (detected by scintigraphy) and monocytes/macrophages (histology) accumulated in the exercised muscles, simultaneously with increased satellite cell activity. These responses were reduced and recovery was faster after bout 2 than 1, demonstrating a repeated‐bout effect. No differences between the celecoxib and placebo groups were detected, except for muscle soreness, which was attenuated by celecoxib. In summary, celecoxib, a COX‐2 inhibitor, did not detectably affect recovery of muscle function or markers of inflammation and regeneration after unaccustomed eccentric exercise, nor did the drug influence the repeated‐bout effect. However, it alleviated muscle soreness.

Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

Although antioxidant supplements are generally believed to give health benefits, recent experiments show that they may adversely affect adaptations to endurance exercise. This study is the first to investigate the effects of high dosages of vitamins C and E on the cellular and physiological adaptations to strength training in humans. Here we report that vitamin C and E supplementation interfered with exercise‐induced signalling in muscle cells after a session of strength training, by reducing the phosphorylation of p70S6 kinase and mitogen‐activated protein kinases p38 and ERK1/2. The vitamin C and E supplement did not significantly blunt muscle hypertrophy during 10 weeks of training; however, some measurements of muscle strength revealed lower increases in the supplemented group than the placebo group. Even though the cellular events are not clearly reflected in physiological and performance measurements, this study implies that redox signalling is important for inducing skeletal muscle adaptations to strength training and that vitamin C and E supplements in high dosages should be avoided by healthy, young individuals engaged in strength training.

Differences in the inflammatory plasma cytokine response following two elite female soccer games separated by a 72-h recovery

We investigated changes in a large battery of pro‐ and anti‐inflammatory cytokines in elite female soccer players following two 90‐min games separated by a 72‐h active or passive recovery. Blood samples were taken from 10 players before, within 15–20 min, 21, 45 and 69 h after the first game and within 15–20 min after the second game. The leukocyte count was analyzed, together with several plasma pro‐ and anti‐inflammatory cytokines, using a multiplex bead array system. After the first and second game, the total leukocytes and neutrophils increased significantly. Likewise, increases (P<0.05) in pro‐inflammatory cytokines [interleukin (IL)‐12, tumor necrosis factor‐α (TNF‐α), interferon‐γ (INF‐γ), IL‐17], chemokines [monocyte chemotactic protein‐1 (MCP‐1), IL‐8 and monokine induced by gamma interferon (MIG)], anti‐inflammatory cytokines (IL‐2R, IL‐4, IL‐5, IL‐7, IL‐10, IL‐13, INF‐α) and the mixed cytokine IL‐6 were observed. Leukocyte and cytokine levels were normalized within 21 h. Active recovery (low‐intensity exercises) did not affect the cytokine responses. A dampened cytokine response was observed after the second game as only IL‐12, IL‐6, MCP‐1, IL‐8 and MIG increased (P<0.05). In conclusion, a robust pro‐ and anti‐inflammatory cytokine response occurs after the first but not the second soccer game. The implications of the dampened cytokine response in female players after the second game are unknown.

Acute response and subcellular movement of HSP27, αB-crystallin and HSP70 in human skeletal muscle after blood-flow-restricted low-load resistance exercise.

Heat‐shock proteins (HSP) are important chaperones for stressed and damaged proteins. Low‐load blood‐flow‐restricted resistance exercise (BFRE) is generally believed not to induce significant muscle damage, but is hitherto unverified with intracellular markers. Consequently, the aim of this study was to investigate the HSP response after BFRE in human skeletal muscle.

Acute Effect of Whole-Body Vibration on Power, One-Repetition Maximum, and Muscle Activation in Power Lifters

Rønnestad, BR, Holden, G, Samnøy, LE, and Paulsen, G. Acute effect of whole-body vibration on power, one-repetition maximum, and muscle activation in power lifters. J Strength Cond Res 26(2): 531–539, 2012—The purpose of this study was to investigate the acute effect of whole-body vibration with a frequency of 50 Hz (WBV50Hz) on peak power in squat jump (SJ), 1 repetition maximum (1RM) in parallel squat, and electromyography (EMG) activity and compare them with no-vibration conditions in power lifters. Twelve national level male power lifters (age 24 ± 5 years, body mass 110 ± 24 kg, height 179 ± 7 cm) tested peak power in SJ and 1RM in parallel squat while they were randomly exposed to WBV50Hz or to no vibration. These tests were performed in a Smith Machine. Peak power output was higher while performed with a WBV50Hz compared with the no-WBV condition (p < 0.05). This increase in power output was accompanied by higher EMG starting values and EMG peak values of the investigated thigh muscles during WBV50Hz (p < 0.05). There was no difference between adding WBV50Hz and no-vibration conditions in 1RM parallel squat. In conclusion, the results of this study suggest that the application of WBV50Hz acutely increases peak power output during SJ in well strength trained individuals such as power lifters. This increase in power was accompanied by an increased EMG activity in the quadriceps muscles. However, in 1RM parallel squat, there was no difference between WBV50Hz and no-vibration conditions. Therefore, adding WBV50Hz has no acute additive effect on 1RM parallel squat in power lifters and, based on the present findings, may thus not be recommended in the training to improve 1RM in power lifters. However, WBV50Hz seems to have an acute additive effect on peak power output and may be used in well strength trained individuals for whom a high power output is important for performance.