Plantar Flexor Muscle Fatigue Research Articles

Effects of α-lactalbumin on strength, fatigue and psychological parameters: a randomised double-blind cross-over study.

The neurotransmitter serotonin has a strong effect on behaviour and motor control. Regarding motor control, serotonin contributes to the development of fatigue and is also involved in the ability of motor neurones to operate across a large range of forces (gain control). The consumption of tryptophan-rich supplements (such as α-lactalbumin) is of interest because this amino acid is the only precursor for brain serotonin synthesis. Therefore, the purpose of this study was to determine the effects of α-lactalbumin supplementation on neuromuscular performance. Using a randomised double-blind cross-over design, 16 healthy participants performed plantar flexor and handgrip maximal voluntary contractions, a 30-s submaximal handgrip contraction, and a plantar flexor fatigue protocol before and 90min after consuming either 40g of α-lactalbumin, an isonitrogenous beverage (Zein) or an isocaloric beverage (corn-starch). Sleepiness, mood, and cognition were assessed to evaluate any psychological effects. α-Lactalbumin decreased force steadiness by 25% during the sustained submaximal handgrip contraction (p < 0.01) and induced greater fatigue (15% reduction in total torque-time integral, p = 0.01) during the fatigue protocol. These effects were not observed for the other control beverages. No effects were found for maximal or explosive strength, or psychological measurements. 40g of α-lactalbumin increased handgrip force variability and reduced performance during fatiguing muscle contractions but did not influence brief maximal contractions or psychological parameters in healthy individuals. These findings support the hypothesis that the consumption of α-lactalbumin can increase motor neurone input-output gain and exacerbate central fatigue during sustained maximal exercise.

EFFECT OF FOOTBALL ON REHABILITATION OF ANKLE INJURY PATIENTS

ABSTRACT Introduction: Brief introduction: Ankle tendon and ligament sports injuries are common in football players. Objective: To continue to improve special strength training related to the characteristics of football after rehabilitation of injured ankle tendons and ligaments. Methods: Two master football sportsmen were rehabilitated by multi-point equal-length, short-arc and long-arc equal-speed training combined with balance ability exercises. Results: There were two long muscle L be maintain muscle tone plantar flexors force four times of 96 n/m, n/m 121, 140 n/m, 145 n/m than back flexors force of 63 n/m, 52 n/m, 60 n/m, 74 n/m tall. Plantar flexor fatigue was 57%, 30%, 29%, 12%, 28%, 18%, 20%, 21%. Conclusions: With the passing of time, the relative peak moment value of the right ankle plantar flexor muscle group of the two patients kept rising, the dorsiflexor muscle was basically flat, and the work fatigue index decreased step by step, indicating that the right ankle muscle strength level was significantly improved, the anti-fatigue ability was improved, and the rehabilitation treatment had a good effect. Level of evidence II; Therapeutic studies - investigation of treatment results.

The Influence of Kinesio Tape and an Ankle Brace on the Lower Extremity Joint Motion in Fatigued, Unstable Ankles during a Lateral Drop Landing.

Background: An unstable ankle along with plantar flexor muscle fatigue may exacerbate landing performance. External support may be an option to control the ankle motion and protect joints from injuries. Research goal: To investigate the immediate changes in the joint motion of a lower extremity under ankle plantar flexors fatigue conditions in athletes with unstable ankles using different external supports. Methods: A total of 44 participants were allocated to a control (Cn) group, an ankle brace (AB) group, and a kinesio tape (KT) group, and were asked to perform a lateral drop landing before and after a fatigue protocol. The outcome measures were fatigue-induced changes in the maximal joint angle and changes in the angle ranges of the hip, knee, and ankle. Results: Smaller changes in the maximal hip abduction were found in the AB group (p = 0.025), and the KT group exhibited smaller changes in the maximal ankle dorsiflexion (p = 0.009). The AB group landed with a smaller change in the range of hip flexion and knee flexion (p = 0.008 and 0.006). The Cn group had greater fatigue-induced changes in the COM range than AB and KT group (p = 0.002 and 0.028). Significance: Despite the beneficial effect in the postural control in the frontal plane, the use of AB might constrain the distal joint motion which might lead to an extended knee landing posture resulting in secondary injuries to the knee joint. Therefore, the use of AB in conjunction with an additional training of landing strategy might be recommended from the injury prevention perspective.

The Effects of Lower Extremity Muscle Fatigue on Dynamic Balance in Volleyball Players

Objectives: Lower extremity muscles are critical for maintaining dynamic balance and athletic performance. Fatigue of these muscles may affect dynamic balance. It is unclear whether fatigue in a particular muscle group can affect dynamic balance more than that in other groups. This study was conducted to evaluate and compare the effects of fatigue in 5 muscle groups on dynamic balance in volleyball players. Methods: Fifteen healthy male volleyball players separately performed the Star Excursion Balance Test before and immediately after the occurrence of fatigue of ankle Plantar Flexor (PF), knee extensor, knee flexor, hip abductor, and hip adductor muscles. Composite reach distance and distance in anterior, posteromedial, and posterolateral directions were recorded, accordingly. Results: Repeated-measures Analysis of Variance (ANOVA) data indicated that fatigue of all muscle groups significantly decreased the mean score of composite (P&lt;0.001). Anterior, posteromedial, and posterolateral distance scores decreased following muscle fatigue of knee extensors and ankle PFs (P&lt;0.05). Discussion: This study suggested that regarding composite reach score, fatigue of ankle, knee, and hip muscles similarly decreased dynamic balance. However, evaluating three main directions revealed that knee extensors and ankle PFs muscles fatigue presented more prominent effects on the explored volleyball players’ balance, compared to the other muscles.

Statin Treatment Attenuates Muscular and Cardiorespiratory Adaptations to Treadmill Training in Mice

Individuals with hypercholesterolemia are at increased risk for developing heart disease and are often prescribed statins, the most effective cholesterol‐lowering drugs, as well as exercise. A highly reported side effect of statins is muscle pain and dysfunction that may be exacerbated with exercise. However, we previously reported that muscle force and cardiorespiratory fitness were not negatively impacted by statin treatment during treadmill training in mice with genetically high cholesterol, ApoE−/−. Both exercise and statins have been associated with reduced inflammatory cytokines such as interleukin‐6 (IL‐6). To date, no studies have investigated if statin treatment in C57 mice (wild type control for ApoE−/−) impacts muscular and cardiorespiratory adaptations to treadmill training. We hypothesized that statin treatment would negatively impact muscular and cardiorespiratory adaptations to treadmill training, and such impairments would be associated with higher inflammatory cytokine levels. Adult mice were divided into 4 groups (n= 8–10/group) and completed 14d of treadmill training (60 min/day) or remained sedentary while receiving daily placebo or atorvastatin. Cardiorespiratory adaptations were assessed by pre‐ and post‐maximal treadmill tests. Plantarflexor muscle force and fatigue (% of max force after 10 contractions) were measured in vivo. Muscle IL‐6 and vascular endothelial factor (VEGF) protein levels were quantified with ELISA. Data were analyzed with 2‐way ANOVAs and post‐hoc tests. Atorvastatin was associated with decreased maximal isometric force relative to body mass in treadmill groups only with no difference in sedentary groups (1.6±0.06 vs. 1.1±0.05 and 1.6±0.07 vs. 1.5±0.08 g/g body mass, respectively, p&lt;0.05). Muscle fatigability was similar among all conditions. Cardiorespiratory fitness increased in both treadmill groups; however, increases were greater in placebo than statin mice with 13:30±2:00 and 7:55±0:42 min increases in test time, respectively (p&lt;0.05). Maximal test time was unchanged in sedentary groups. Muscle IL‐6 levels were unchanged with treadmill training; however, statin treatment was associated with decreased muscle IL‐6 compared to placebo in both sedentary and treadmill groups (p&lt;0.05). Statin treatment decreased IL‐6 66 and 82% compared to placebo, in sedentary and treadmill groups, respectively (p&lt;0.05). Treadmill training was associated with increases in muscle VEGF in placebo group only (p&lt;0.05). These findings suggest statin treatment impairs muscle strength when combined with treadmill training and attenuates increases in maximal test time with training. It is unclear whether the treadmill test performance was due to muscular and/or cardiorespiratory limitations; however, reductions in muscle strength suggest a muscular component. The finding that statin treatment prevented training associated increases in muscle VEGF suggest a potential vascular component. These findings are in contrast to results in ApoE−/− mice in which statin treatment did not impair muscular or cardiorespiratory adaptations to treadmill training. Further research is needed to determine genetic and/or cellular mechanisms whereby statin treatment impacts skeletal muscle.

Effects of 21\xa0days of bed rest and whey protein supplementation on plantar flexor muscle fatigue resistance during repeated shortening contractions

PurposeSpace flight and bed rest (BR) lead to a rapid decline in exercise capacity. Whey protein plus potassium bicarbonate diet-supplementation (NUTR) could attenuate this effect by improving oxidative metabolism. We evaluated the impact of 21-day BR and NUTR on fatigue resistance of plantar flexor muscles (PF) during repeated shortening contractions, and whether any change was related to altered energy metabolism and muscle oxygenation.MethodsTen healthy men received a standardized isocaloric diet with (n = 5) or without (n = 5) NUTR. Eight bouts of 24 concentric plantar flexions (30 s each bout) with 20 s rest between bouts were employed. PF muscle size was assessed by means of peripheral quantitative computed tomography. PF muscle volume was assessed with magnetic resonance imaging. PF muscle force, contraction velocity, power and surface electromyogram signals were recorded during each contraction, as well as energy metabolism (31P nuclear magnetic resonance spectroscopy) and oxygenation (near-infrared spectroscopy). Cardiopulmonary parameters were measured during an incremental cycle exercise test.ResultsBR caused 10–15% loss of PF volume that was partly recovered 3 days after re-ambulation, as a consequence of fluid redistribution. Unexpectedly, PF fatigue resistance was not affected by BR or NUTR. BR induced a shift in muscle metabolism toward glycolysis and some signs of impaired muscle oxygen extraction. NUTR did not attenuate the BR-induced-shift in energy metabolism.ConclusionsTwenty-one days’ BR did not impair PF fatigue resistance, but the shift to glycolytic metabolism and indications of impaired oxygen extraction may be early signs of developing reduced muscle fatigue resistance.

The role of SIRT1 in skeletal muscle function and repair of older mice.

BackgroundSirtuin 1 (SIRT1) is a NAD+ sensitive deacetylase that has been linked to longevity and has been suggested to confer beneficial effects that counter aging‐associated deterioration. Muscle repair is dependent upon satellite cell function, which is reported to be reduced with aging; however, it is not known if this is linked to an aging‐suppression of SIRT1. This study tested the hypothesis that Sirtuin 1 (SIRT1) overexpression would increase the extent of muscle repair and muscle function in older mice.MethodsWe examined satellite cell dependent repair in tibialis anterior, gastrocnemius, and soleus muscles of 13 young wild‐type mice (20–30 weeks) and 49 older (80+ weeks) mice that were controls (n = 13), overexpressed SIRT1 in skeletal muscle (n = 14), and had a skeletal muscle SIRT1 knockout (n = 12) or a satellite cell SIRT1 knockout (n = 10). Acute muscle injury was induced by injection of cardiotoxin (CTX), and phosphate‐buffered saline was used as a vector control. Plantarflexor muscle force and fatigue were evaluated before or 21 days after CTX injection. Satellite cell proliferation and mitochondrial function were also evaluated in undamaged muscles.ResultsMaximal muscle force was significantly lower in control muscles of older satellite cell knockout SIRT1 mice compared to young adult wild‐type (YWT) mice (P < 0.001). Mean contraction force at 40 Hz stimulation was significantly greater after recovery from CTX injury in older mice that overexpressed muscle SIRT1 than age‐matched SIRT1 knockout mice (P < 0.05). SIRT1 muscle knockout models (P < 0.05) had greater levels of p53 (P < 0.05 MKO, P < 0.001 OE) in CTX‐damaged tissues as compared to YWT CTX mice. SIRT1 overexpression with co‐expression of p53 was associated with increased fatigue resistance and increased force potentiation during repeated contractions as compared to wild‐type or SIRT1 knockout models (P < 0.001). Muscle structure and mitochondrial function were not different between the groups, but proliferation of satellite cells was significantly greater in older mice with SIRT1 muscle knockout (P < 0.05), but not older SIRT1 satellite cell knockout models, in vitro, although this effect was attenuated in vivo after 21 days of recovery.ConclusionsThe data suggest skeletal muscle structure, function, and recovery after CTX‐induced injury are not significantly influenced by gain or loss of SIRT1 abundance alone in skeletal muscle; however, muscle function is impaired by ablation of SIRT1 in satellite cells. SIRT1 appears to interact with p53 to improve muscle fatigue resistance after repair from muscle injury.

Older and young adults adopt different postural strategies during quiet bipedal stance after ankle plantarflexor fatigue

BackgroundThe individual effects of fatigue and age on postural control have been extensively studied. However, there is a lack of knowledge about the combined effects of fatigue and age on postural control and posture. Research questionThe purpose of this study was to investigate the influence of age and muscle fatigue on bipedal stance postural control and posture. MethodsTwenty-three participants, fourteen young adults and nine older adults performed 30-s bipedal postural trials before and after fatigue. The fatigue protocol consisted in repeating heel raises until exhaustion. Back, hip, knee and ankle joint angles and centre of pressure (COP) displacements were recorded with a 3D motion capture system and a force plate. ResultsFatigue induced similar increases in sway area and COP velocity for both populations. This was associated with a forward displacement of the COP position for both populations but with different postural adaptations. Similar increased flexions (+1.7 to 1.8°) for all joint angles (ankle, knee, hip and back) joints were observed after fatigue for older adults, whereas young adults mainly showed increased flexion for the ankle joint (+3.1°) and decreased flexion at the hip (−1.2°). SignificanceIt can be argued that older adults act on all joints because they are too weak to sufficiently modify any joint individually, contrary to young adults. These posture adaptations may be strategies to cope with fatigue by limiting the reliance on fatigued plantarflexors, increasing ankle stiffness, increasing the sensitivity of muscle spindles, increasing the number of degrees of freedom of the task.

Effects of Plantar Flexor Muscles Fatigue on Postural Control during Quiet Stance and External Perturbation in Healthy Subjects

The maintenance of postural control is a key component in dynamic physical activity, especially during muscle fatigue and against external forces. Despite many studies in this field, there is no consensus regarding the effects of plantar flexor muscles fatigue on postural control during different postural tasks. To evaluate the effects of plantar flexor muscles fatigue on postural control during quiet stance and external perturbation in healthy subjects. Twenty four healthy individuals (20-35 years) participated this interventional study. The foot center of pressure data was measured using a single force platform, and then the postural control parameters, including the center of pressure displacement and velocity in the anterior-posterior and medial-lateral direction and also path length calculated under two conditions; quiet and perturbed stance, before and after plantar flexor muscles fatigue. The statistical analysis demonstrated that mean displacement and velocity of the center of pressure in the anterior-posterior direction and also path length increased after the fatigue protocol in the perturbed condition. However, fatigue had no significant effects on postural control parameters in the quiet standing condition. These results indicated that the effects of muscle fatigue on postural control depend on the difficulty of the task and the relevance of proprioceptive information. The postural control system appears to use distinct control strategies in different situations such as quiet and perturbed stance conditions, and these strategies may be differentially altered by fatigue. In conclusion, due to the potential risk of loss of balance, it is important to take the role of plantar flexor muscle fatigue into account during more difficult postural tasks.

Localized ankle plantarflexor and dorsiflexor fatigue following volitional exhaustion using the Bruce protocol

Localized ankle plantarflexor and dorsiflexor fatigue following volitional exhaustion using the Bruce protocol

Effects of AICAR Treatment on Muscular, Cardiorespiratory, and Hsp25 Adaptations to Treadmill versus Running Wheel Exercise Training in Mice

AMPK agonists, such as AICAR, are used in the treatment of diabetes since they mimic several effects of exercise such as a more oxidative phenotype and increased insulin sensitivity. Exercise training can increase muscle levels of heat shock protein 25 (Hsp25), which is associated with improvements in muscle function and insulin‐stimulated glucose uptake. In contrast decreased Hsp25 in skeletal muscle is associated with insulin resistance in rats. Evidence in animals and humans suggests the combination of exercise and AMPK‐activating drugs may decrease exercise‐training adaptations. These experiments compared the effects of AICAR on cardiorespiratory, muscular, and Hsp25 adaptations to forced (treadmill, TM) or voluntary (running wheel, RW) training. It was hypothesized that AICAR + TM or RW would attenuate increases in exercise capacity, muscle force, and Hsp25 expression compared to training alone. Adult, male C57 mice were divided into 6 groups (n = 8–10/group): 1‐Placebo, 2‐AICAR, 3‐Placebo + TM, 4‐Aicar + TM, 5‐Placebo + RW, 6‐Aicar + RW. Groups received daily placebo or AICAR with or without TM or RW over 7 days. Plantarflexor muscle force and fatigue (% of max force after 10 contractions) were measured in vivo and exercise capacity was assessed with pre‐ and post‐ treadmill tests. Muscle Hsp25 protein levels were quantified with western blot. AICAR significantly reduced average daily RW distance vs. placebo, 1099±133 and 1923±103 m/day, respectively. AICAR + TM did not affect training‐associated increases in exercise capacity compared to Placebo + TM (Δ time pre to post: 903 ± 164 vs. 1,188 ± 99 sec. for AICAR and Placebo, respectively, p&lt;0.05); however, AICAR + RW attenuated the increases in exercise capacity compared to Placebo + RW (Δ time pre to post: 710 ± 134 vs. 921 ± 87 sec. for AICAR and Placebo, respectively, p&lt;0.05). Muscle force was increased with AICAR in TM or sedentary groups compared to placebo while AICAR + RW was associated with reduced muscle force compared to Placebo + RW (Placebo: 1.2 ± 0.07 vs. 1.3 ± 0.07 vs. 1.4 ± 0.08 and AICAR: 1.4 ± 0.08 vs. 1.5 ± 0.12 vs. 1.1± 0.11 g/g body mass, for sedentary, TM, and RW, respectively, p&lt;0.05). Fatigability was greater with AICAR in sedentary mice; however, AICAR + TM decreased fatigability compared to AICAR alone (p&lt;0.05). TM or RW increased Hsp25 levels in both placebo and AICAR groups compared to sedentary placebo (Placebo: 0.09 ± 0.01 vs. 0.15 ± 0.01 vs. 0.15 ± 0.02 and AICAR 0.15 ± 0.02 vs. 0.17 ±0.02 vs. 0.19 ± 0.03 AU, for sedentary, TM, and RW, respectively, p&lt;0.05) and AICAR increased Hsp25 in the sedentary group compared to placebo (0.15 ± 0.02 vs. 0.09 ± 0.01 AU, p&lt;0.05). These findings suggest AICAR does not impair cardiorespiratory or muscular adaptations to forced exercise while AICAR reduced RW distance and training associated adaptations to voluntary exercise. AICAR in combination with forced or voluntary exercise did not impair Hsp25 increases and AICAR alone mimics exercise induced Hsp up‐regulation in sedentary muscle and may be one mechanism whereby AICAR and/or exercise improve outcomes with diabetes.Support or Funding InformationAPS UGSRF to KGThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Voluntary wheel running increases satellite cell abundance and improves recovery from disuse in gastrocnemius muscles from mice.

Reloading of atrophied muscles after hindlimb suspension unloading (HSU) can induce injury and prolong recovery. Low-impact exercise, such as voluntary wheel running, has been identified as a nondamaging rehabilitation therapy in rodents, but its effects on muscle function, morphology, and satellite cell activity after HSU are unclear. This study tested the hypothesis that low-impact wheel running would increase satellite cell proliferation and improve recovery of muscle structure and function after HSU in mice. Young adult male and female C57BL/6 mice ( n = 6/group) were randomly placed into five groups. These included HSU without recovery (HSU), normal ambulatory recovery for 14 days after HSU (HSU+NoWR), and voluntary wheel running recovery for 14 days after HSU (HSU+WR). Two control groups were used: nonsuspended mouse cage controls (Control) and voluntary wheel running controls (ControlWR). Satellite cell activation was evaluated by providing mice 5-bromo-2'-deoxyuridine (BrdU) in their drinking water. As expected, HSU significantly reduced in vivo maximal force, decreased in vivo fatigability, and decreased type I and IIa myosin heavy chain (MHC) abundance in plantarflexor muscles. HSU+WR mice significantly improved plantarflexor fatigue resistance, increased type I and IIa MHC abundance, increased fiber cross-sectional area, and increased the percentage of type I and IIA muscle fibers in the gastrocnemius muscle. HSU+WR mice also had a significantly greater percentage of BrdU-positive and Pax 7-positive nuclei inside muscle fibers and a greater MyoD-to-Pax 7 protein ratio compared with HSU+NoWR mice. The mechanotransduction protein Yes-associated protein (YAP) was elevated with reloading after HSU, but HSU+WR mice had lower levels of the inactive phosphorylated YAPserine127, which may have contributed to increased satellite cell activation with reloading after HSU. These results indicate that voluntary wheel running increased YAP signaling and satellite cell activity after HSU and this was associated with improved recovery. NEW & NOTEWORTHY Although satellite cell involvement in muscle remodeling has been challenged, the data in this study suggest that voluntary wheel running increased satellite cell activity and suppressed Yes-associated protein (YAP) protein relative to no wheel running and this was associated with improved muscle recovery of force, fatigue resistance, expression of type I myosin heavy chain, and greater fiber cross-sectional area after disuse.

Influence of foot strike pattern and local fatigue of plantar flexors and dorsiflexors on plantar pressure during running

Influence of foot strike pattern and local fatigue of plantar flexors and dorsiflexors on plantar pressure during running

The Effect of Plantar Flexor Fatigue and Cognitive Recall Task on Standing Balance

Introduction: Previous studies have shown that fatigue of the plantar flexor muscles and mental tasks each can lead to impaired balance. The purpose of this study is to analyze the effects of a combined increase in cognitive load and plantar flexor fatigue can have on standing balance.&#x0D; Methods: Fifteen (7 males, 8 females) healthy individuals participated in one testing session. Prior to testing, participants were screened for existing balance and plantar flexor health issues via a medical history questionnaire. Participants performed a total of twelve standing balance trials, each 30 seconds in duration. These trials consisted of three control, three recall, three fatigue, and three fatigue recall trials. For each trial, participants closed their eyes and stood with their feet together on a force plate. Recall ability was evaluated based on the participant’s ability to accurately complete the reverse digit recall section of the SCAT-3. Plantar flexor fatigue was achieved by performing five repetitions of standing calf raises. Each repetition consisted of a five second eccentric contraction, a five second concentric contraction, and a five second isometric contraction. The means of the 90% radius of the center of pressure was compared to the standing baseline across all conditions.&#x0D; Results:Similar significant differences were found across 90% radius and center of pressure in both medial-lateral and anterior-posterior directions. Across all three variables, the recall condition was not significantly different (p&gt;0.05) than control standing. Both fatigue and fatigue recall conditions were significantly different (p&lt;0.05)&#x0D; Conclusion: Collectively, the data indicates that fatigue, rather than recall, had a greater effect on all measured variables of balance. This suggests that balance is a primarily muscle driven task, and not a mental task.

PERIPHERAL FATIGUE DOES NOT INFLUENCE THE ONSET OF FATIGUE IN OLDER ADULTS

AbstractMuscular fatigue is the decline in ability of a muscle group to produce force following a contraction. Although older adults are less susceptible to fatigue, they have decreased muscle mass, strength, and contractile ability. Peripheral fatigue is attributed to metabolic buildup, while central fatigue is linked to down-regulation of motor unit firing. Decreased oxygen in the tissue and brain is linked to peripheral and central fatigue, respectively. The purpose of this study was to evaluate the onset of fatigue in older adults and assess alterations in oxygenation within the soleus muscle and prefrontal cortex following a plantar-flexor fatigue protocol. Eleven participants (56.3 ± 7.6 years, 169.5 ± 6.5 cm, 75.3 ± 6.7 kg) were assessed before and after a fatigue protocol consisting of repeated maximal concentric contractions completed until <50% of isometric one-repetition maximum was reached. Peripheral fatigue was assessed via resting twitch (RT) and central fatigue was assessed via electromyography (rEMG) and percent of voluntary muscle activation (ITT). Soleus muscle oxygenation (StO) was recorded with an oximeter and central oxygenation (HbO) of the prefrontal cortex was measured via functional near infrared spectroscopy (fNIRS). Significant decreases were found for ITT (p<0.01), rEMG (p=0.03), StO (p<0.01), and prefrontal cortex oxygenation (p=0.04). The results indicated that central fatigue was the primary contributor to the observed fatigue. Fewer type II muscle fibers in older adults would cause less metabolic buildup and less peripheral fatigue. A decrease in oxygenation in either the prefrontal cortex or muscular tissue may be related to the faster onset of fatigue in populations with disease.

Ankle and knee biomechanics during normal walking following ankle plantarflexor fatigue

The purpose of this study was to investigate the immediate effects of unilateral ankle plantarflexor fatigue on bilateral knee and ankle biomechanics during gait. Lower leg kinematics, kinetics, and muscle activation were assessed before and after an ankle plantarflexor fatiguing protocol in 31 healthy individuals. Fatigue (defined as >10% reduction in maximal isometric ankle plantarflexor torque production and a downward shift in the median power frequency of both heads of the gastrocnemius muscle of the fatigued limb) was achieved in 18 individuals, and only their data were used for analysis purposes. Compared to pre-fatigue walking trials, medial gastrocnemius activity was significantly reduced in the study (fatigued) limb. Other main changes following fatigue included significantly more knee flexion during loading, and an associated larger external knee flexion moment in the study limb. At the ankle joint, participants exhibited significantly less peak plantarflexion (occurring at toe-off) with fatigue. No significant differences were observed in the contralateral (non-fatigued) limb. Findings from this study indicate that fatigue of the ankle plantarflexor muscle does not produce widespread changes in gait biomechanics, suggesting that small to moderate changes in maximal ankle plantarflexor force production capacity (either an increase or decrease) will not have a substantial impact on normal lower limb functioning during gait.

AICAR Treatment Does Not Prevent Increases in Exercise Capacity or Muscle Heat Shock Protein 25 with Treadmill Training in Mice

Exercise and 5‐aminoimidazole‐4‐carboxamide‐1‐β‐D‐ribofuranoside (AICAR) are agonists of AMP‐activated protein kinase (AMPK) and are used in type II diabetes treatment. Treatment effectiveness may be due to AMPK activation and up‐regulation of heat shock proteins (Hsps) in skeletal muscle, including Hsp25 and αB‐crystallin. Decreased Hsp25 expression in skeletal muscle is associated with insulin resistance in rats and data in both animals and humans suggests that increased Hsp expression in skeletal muscle may contribute to the prevention and treatment of insulin resistance. However, some evidence in both animals and humans suggests the combination of exercise and AMPK‐activating drugs such as AICAR may decrease exercise‐training adaptations. These experiments tested the hypothesis that AICAR + treadmill training (TM) would attenuate increases in exercise capacity, muscle force, and Hsp expression compared to training alone. Adult, male C57 mice were divided into 4 groups (n = 8–10/group): 1‐Placebo, 2‐AICAR, 3‐Placebo + TM, and 4‐Aicar + TM. Groups received daily placebo or AICAR with or without TM over 7 days. Plantarflexor muscle force and fatigue (% of max force after 10 contractions) were measured in vivo and exercise capacity was assessed with pre‐ and post‐treadmill tests. Muscle Hsp25 and αB‐crystallin protein levels were quantified with western blot. Data was statistically analyzed with 2‐way ANOVAs and post‐hoc tests. AICAR + TM did not affect training‐associated increases in exercise capacity compared to Placebo + TM (D time pre to post: 903 ± 164 vs. 1,188 ± 99 sec. for AICAR and TM, respectively, p&lt;0.05). Muscle force was unchanged with AICAR in either TM or sedentary groups compared to placebo (Placebo: 1.2 ± 0.07 vs. 1.3± 0.07 and AICAR: 1.4 ± 0.08 vs. 1.5 ± 0.12 g/g body mass, for sedentary and TM, respectively, p&lt;0.05). Fatigability was greater with AICAR in sedentary mice; however, AICAR + TM decreased fatigability compared to AICAR alone (p&lt;0.05). TM increased Hsp25 levels independent of treatment (Placebo: 0.09 ± 0.01 vs. 0.15 ± 0.01 and AICAR 0.15 ± 0.02 vs. 0.17 ±0.02 AU, for sedentary and TM, respectively, p&lt;0.05) and AICAR increased Hsp25 in the sedentary group compared to placebo (0.15 ± 0.02 vs. 0.09 ± 0.01 AU, p&lt;0.05). AICAR prevented the TM‐associated increase in αB‐crystallin compared to placebo (Placebo: 0.11 ± 0.02 vs. 0.17 ± 0.01 and AICAR: 0.10 ± 0.01 vs. 0.01 ± 0.02 AU, for sedentary and TM, respectively, p&lt;0.05). These findings suggest AICAR does not impair training‐associated increases in exercise capacity or Hsp25 muscle protein or negatively impact muscle force production. Taken together, these treatments could positively impact type II diabetics who often have reduced exercise capacity and skeletal muscle Hsp25 levels.Support or Funding InformationSupported by APS UGSRF.

Plantar flexor muscle weakness and fatigue in spastic cerebral palsy patients

BackgroundPatients with cerebral palsy develop an important muscle weakness which might affect the aetiology and extent of exercise-induced neuromuscular fatigue. AimThis study evaluated the aetiology and extent of plantar flexor neuromuscular fatigue in patients with cerebral palsy. MethodsTen patients with cerebral palsy and 10 age- and sex-matched healthy individuals (∼20 years old, 6 females) performed four 30-s maximal isometric plantar flexions interspaced by a resting period of 2–3s to elicit a resting twitch. Maximal voluntary contraction force, voluntary activation level and peak twitch were quantified before and immediately after the fatiguing task. ResultsBefore fatigue, patients with cerebral palsy were weaker than healthy individuals (341±134N vs. 858±151N, p<0.05) and presented lower voluntary activation (73±19% vs. 90±9%, p<0.05) and peak twitch (100±28N vs. 199±33N, p<0.05). Maximal voluntary contraction force was not significantly reduced in patients with cerebral palsy following the fatiguing task (−10±23%, p>0.05), whereas it decreased by 30±12% (p<0.05) in healthy individuals. ConclusionsPlantar flexor muscles of patients with cerebral palsy were weaker than their healthy peers but showed greater fatigue resistance. What this paper addsCerebral palsy is a widely defined pathology that is known to result in muscle weakness. The extent and origin of muscle weakness were the topic of several previous investigations; however some discrepant results were reported in the literature regarding how it might affect the development of exercise-induced neuromuscular fatigue. Importantly, most of the studies interested in the assessment of fatigue in patients with cerebral palsy did so with general questionnaires and reported increased levels of fatigue. Yet, exercise-induced neuromuscular fatigue was quantified in just a few studies and it was found that young patients with cerebral palsy might be more fatigue resistant that their peers. Thus, it appears that (i) conflicting results exist regarding objectively-evaluated fatigue in patients with cerebral palsy and (ii) the mechanisms underlying this muscle fatigue − in comparison to those of healthy peers − remain poorly understood. The present study adds important knowledge to the field as it shows that when young adults with cerebral palsy perform sustained maximal isometric plantar flexions, they appear less fatigable than healthy peers. This difference can be ascribed to a better preservation of the neural drive to the muscle. We suggest that the inability to drive their muscles maximally accounts for the lower extent of exercise-induced neuromuscular fatigue in patients with cerebral palsy.

Whey protein with potassium bicarbonate supplement attenuates the reduction in muscle oxidative capacity during 19 days of bed rest.

The effectiveness of whey protein plus potassium bicarbonate-enriched diet (WP+KHCO3) in mitigating disuse-induced changes in muscle fiber oxidative capacity and capillarization was investigated in a 21-day crossover design bed rest study. Ten healthy men (31 ± 6 yr) once received WP+KHCO3 and once received a standardized isocaloric diet. Muscle biopsies were taken 2 days before and during the 19th day of bed rest (BR) from the soleus (SOL) and vastus lateralis (VL) muscle. Whole-body aerobic power (V̇o2 max), muscle fatigue, and isometric strength of knee extensor and plantar flexor muscles were monitored. Muscle fiber types and capillaries were identified by immunohistochemistry. Fiber oxidative capacity was determined as the optical density (OD) at 660 nm of succinate dehydrogenase (SDH)-stained sections. The product of fiber cross-sectional area and SDH-OD (integrated SDH) indicated the maximal oxygen consumption of that fiber. The maximal oxygen consumption supported by a capillary was calculated as the integrated SDH in its supply area. BR reduced isometric strength of knee extensor muscles (P < 0.05), and the fiber oxidative capacity (P < 0.001) and V̇o2 max (P = 0.042), but had no significant impact on muscle capillarization or fatigue resistance of thigh muscles. The maximal oxygen consumption supported by a capillary was reduced by 24% in SOL and 16% in VL (P < 0.001). WP+KHCO3 attenuated the disuse-induced reduction in fiber oxidative capacity in both muscles (P < 0.01). In conclusion, following 19 days of bed rest, the decrement in fiber oxidative capacity is proportionally larger than the loss of capillaries. WP+KHCO3 appears to attenuate disuse-induced reductions in fiber oxidative capacity.

Influence of a 12.8-km military load carriage activity on lower limb gait mechanics and muscle activity

The high stress fracture occurrence in military populations has been associated with frequent load carriage activities. This study aimed to assess the influence of load carriage and of completing a load carriage training activity on gait characteristics. Thirty-two Royal Marine recruits completed a 12.8-km load carriage activity as part of their military training. Data were collected during walking in military boots, pre and post-activity, with and without the additional load (35.5 kg). Ground contact time, lower limb sagittal plane kinematics and kinetics, and electromyographic variables were obtained for each condition. When carrying load, there was increased ground contact time, increased joint flexion and joint moments, and increased plantar flexor and knee extensor muscle activity. Post-activity, there were no changes to kinematic variables, knee extensor moments were reduced, and there was evidence of plantar flexor muscle fatigue. The observed gait changes may be associated with stress fracture development.Practitioner Summary: This study identified gait changes due to load carriage and after a military load carriage training activity. Such activities are associated with lower limb stress fractures. A pre–post study design was used. Gait mechanics changed to a greater extent when carrying load, than after completion of the activity when assessed without load.