scholarly journals Monitoring Exercise-Induced Muscle Fatigue and Adaptations: Making Sense of Popular or Emerging Indices and Biomarkers

Sports ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 153 ◽  
Author(s):  
George Theofilidis ◽  
Gregory Bogdanis ◽  
Yiannis Koutedakis ◽  
Christina Karatzaferi

Regular exercise with the appropriate intensity and duration may improve an athlete’s physical capacities by targeting different performance determinants across the endurance–strength spectrum aiming to delay fatigue. The mechanisms of muscle fatigue depend on exercise intensity and duration and may range from substrate depletion to acidosis and product inhibition of adenosinetriphosphatase (ATPase) and glycolysis. Fatigue mechanisms have been studied in isolated muscles; single muscle fibers (intact or skinned) or at the level of filamentous or isolated motor proteins; with each approach contributing to our understanding of the fatigue phenomenon. In vivo methods for monitoring fatigue include the assessment of various functional indices supported by the use of biochemical markers including blood lactate levels and more recently redox markers. Blood lactate measurements; as an accompaniment of functional assessment; are extensively used for estimating the contribution of the anaerobic metabolism to energy expenditure and to help interpret an athlete’s resistance to fatigue during high intensity exercise. Monitoring of redox indices is gaining popularity in the applied sports performance setting; as oxidative stress is not only a fatigue agent which may play a role in the pathophysiology of overtraining syndrome; but also constitutes an important signaling pathway for training adaptations; thus reflecting training status. Careful planning of sampling and interpretation of blood biomarkers should be applied; especially given that their levels can fluctuate according to an athlete’s lifestyle and training histories.

2019 ◽  
Vol 55 (3) ◽  
pp. 171
Author(s):  
Yusni Yusni ◽  
Amiruddin Amiruddin

High-intensity exercise (3000-meter runner) contributes to muscle fatigue. Fatigue can be determined by measuring blood lactate levels. Blood lactate levels are a product of anaerobic metabolism. Lactate accumulation due to anaerobic physical activity can inhibit the glycolytic enzyme that affects decreased ATP production, damage of the calcium and sodium pumps in the muscles and causes fatigue. This study aimed to analyze the effect of vitamin E on the level of fatigue through the response of blood lactate levels in the runner 3000 meters. This research was a quasi-experimental research with a pretest-posttest design. Research subjects were 9 volunteer athletes (3000 meters runners) Aceh province, male, and aged 15-20 years. The treatments were vitamin E at a dose of 1x400 IU per day and administered for 14 days. Blood lactate levels were examined using the method of calorimetry. The statistical analysis was using the homogeneity test of variance (Levene's test), the normality test (Kolmogorov-Smirnov test) and paired t-test with a significant level of 5% (p-value<0.05). The results showed that blood lactate levels decreased approximately 13.93% after vitamin E supplementation. There was no significant difference (p=0.27) between blood lactate levels before and after vitamin E supplementation in athletes. In conclusion, vitamin E supplementation did not significantly lower blood lactate levels therefore vitamin E did not significantly reduce muscle fatigue in men's athletics.


2020 ◽  
Vol 319 (4) ◽  
pp. E792-E804
Author(s):  
Rasmus Liegnell ◽  
William Apró ◽  
Sebastian Danielsson ◽  
Björn Ekblom ◽  
Gerrit van Hall ◽  
...  

Lactate has been implicated as a potential signaling molecule. In myotubes, lactate incubation increases mechanistic target of rapamycin complex 1 (mTORC1)- and ERK-signaling and induces hypertrophy, indicating that lactate could be a mediator of muscle adaptations to resistance exercise. However, the potential signaling properties of lactate, at rest or with exercise, have not been explored in human tissue. In a crossover design study, 8 men and 8 women performed one-legged resistance exercise while receiving venous infusion of saline or sodium lactate. Blood was sampled repeatedly, and muscle biopsies were collected at rest and at 0, 90, and 180 min and 24 h after exercise. The primary outcomes examined were intracellular signaling, fractional protein synthesis rate (FSR), and blood/muscle levels of lactate and pH. Postexercise blood lactate concentrations were 130% higher in the Lactate trial (3.0 vs. 7.0 mmol/L, P < 0.001), whereas muscle levels were only marginally higher (27 vs. 32 mmol/kg dry wt, P = 0.003) compared with the Saline trial. Postexercise blood pH was higher in the Lactate trial (7.34 vs. 7.44, P < 0.001), with no differences in intramuscular pH. Exercise increased the phosphorylation of mTORS2448 (∼40%), S6K1T389 (∼3-fold), and p44T202/T204 (∼80%) during recovery, without any differences between trials. FSR over the 24-h recovery period did not differ between the Saline (0.067%/h) and Lactate (0.062%/h) trials. This study does not support the hypothesis that blood lactate levels can modulate anabolic signaling in contracted human muscle. Further in vivo research investigating the impact of exercised versus rested muscle and the role of intramuscular lactate is needed to elucidate its potential signaling properties.


1994 ◽  
Vol 76 (2) ◽  
pp. 846-852 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Antonio Sarmento ◽  
Guilherme Fregonezi ◽  
Maria Lira ◽  
Layana Marques ◽  
Francesca Pennati ◽  
...  

AbstractMuscle fatigue is a complex phenomenon enclosing various mechanisms. Despite technological advances, these mechanisms are still not fully understood in vivo. Here, simultaneous measurements of pressure, volume, and ribcage inspiratory muscle activity were performed non-invasively during fatigue (inspiratory threshold valve set at 70% of maximal inspiratory pressure) and recovery to verify if inspiratory ribcage muscle fatigue (1) leads to slowing of contraction and relaxation properties of ribcage muscles and (2) alters median frequency and high-to-low frequency ratio (H/L). During the fatigue protocol, sternocleidomastoid showed the fastest decrease in median frequency and slowest decrease in H/L. Fatigue was also characterized by a reduction in the relative power of the high-frequency and increase of the low-frequency. During recovery, changes in mechanical power were due to changes in shortening velocity with long-lasting reduction in pressure generation, and slowing of relaxation [i.e., tau (τ), half-relaxation time (½RT), and maximum relaxation rate (MRR)] was observed with no significant changes in contractile properties. Recovery of median frequency was faster than H/L, and relaxation rates correlated with shortening velocity and mechanical power of inspiratory ribcage muscles; however, with different time courses. Time constant of the inspiratory ribcage muscles during fatigue and recovery is not uniform (i.e., different inspiratory muscles may have different underlying mechanisms of fatigue), and MRR, ½RT, and τ are not only useful predictors of inspiratory ribcage muscle recovery but may also share common underlying mechanisms with shortening velocity.


2021 ◽  
Author(s):  
Megumi Hoshiai ◽  
Kaori Ochiai ◽  
Yuma Tamura ◽  
Tomoki Tsurumi ◽  
Masato Terashima ◽  
...  

AbstractNeuromuscular electrical stimulation has been used to treat cardiovascular diseases and other types of muscular dysfunction. A novel whole-body neuromuscular electrical stimulation (WB-NMES) wearable device may be beneficial when combined with voluntary exercises. This study aimed to investigate the safety and effects of the WB-NMES on hemodynamics, arrhythmia, and sublingual microcirculation. The study included 19 healthy Japanese volunteers, aged 22–33 years, who were not using any medication. Electrocardiogram (ECG), echocardiography, and blood sampling were conducted before a 20-min WB-NMES session and at 0 and 10 min after termination of WB-NMES. Their tolerable maximum intensity was recorded using numeric rating scale. Arrhythmia was not detected during neuromuscular electrical stimulation or during 10 min of recovery. Blood pressure, heart rate, left ventricular ejection fraction, and diastolic function remained unchanged; however, mild mitral regurgitation was transiently observed during WB-NMES in a single male participant. A decrease in blood glucose and an increase in blood lactate levels were observed, but no changes in blood fluidity, sublingual microcirculation, blood levels of noradrenaline, or oxidative stress were shown. WB-NMES is safe and effective for decreasing blood glucose and increasing blood lactate levels without changing the blood fluidity or microcirculation in healthy people.


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