768-km Multi-Stage Ultra-Trail Case Study-Muscle Damage, Biochemical Alterations and Strength Loss on Lower Limbs

A series of case studies aimed to evaluate muscular fatigue in running a 768-km ultra-trail race in 11 days. Four non-professional athletes (four males) were enrolled. Muscle damage blood biomarkers (creatine kinase (CK), lactodeshydrogenase (LDH), aspartate transaminase (AST) and alanine aminotransferase (ALT) and lower limb strength were evaluated by using Bosco jumps test; squat jump (SJ), countermovement jump (CMJ) and Abalakov jump (ABA) were assessed before (pre), after the race (post) and for two and nine days during the recovery period (rec2 and rec9), respectively. Results showed: pre-post SJ = −28%, CMJ = −36% and ABA = −21%. Values returned to basal during rec9: SJ = −1%, CMJ = −2% or even exceeded pre-values ABA = +3%. On the contrary, muscle damage blood biomarkers values increased at post; CK = +888%, LDH = +172%, AST = +167% and ALT = +159% and the values returned gradually to baseline at rec9 except for AST = +226% and ALT = +103% which remained higher. Nonparametric bivariate Spearman’s test showed strong correlations (Rs ≥ 0.8) between some jumps and muscle damage biomarkers at post (SJ-LDH Rs = 0.80, SJ-AST Rs = 0.8, ABA-LD H Rs = 0.80 and ABA-AST Rs = 0.80), at rec2 (SJ-CK Rs = 0.80 and SJ-ALT Rs = 0.80) and even during rec9 (ABA-CK). Similarly, some parameters such as accumulated elevation and training volume showed a strong correlation with LDH values after finishing the ultra-trail race. The alteration induced by completing an ultra-trail event in the muscle affects lower limb strength and may in some circumstances result in serious medical conditions including post- exertional rhabdomyolysis.

Skeletal muscle regeneration is altered in the R6/2 mouse model of Huntington's disease

Huntington's disease (HD) is caused by CAG repeat expansion in the huntingtin (HTT) gene. Skeletal muscle wasting alongside central pathology is a well-recognized phenomenon seen in patients with HD and HD mouse models. HD muscle atrophy progresses with disease and affects prognosis and quality of life. Satellite cells, progenitors of mature skeletal muscle fibers, are essential for proliferation, differentiation, and repair of muscle tissue in response to muscle injury or exercise. In this study, we aim to investigate the effect of mutant HTT on the differentiation and regeneration capacity of HD muscle by employing in vitro mononuclear skeletal muscle cell isolation and in vivo acute muscle damage model in R6/2 mice. We found that, similar to R6/2 adult mice, neonatal R6/2 mice also exhibit a significant reduction in myofiber width and morphological changes in gastrocnemius and soleus muscles compared to WT mice. Cardiotoxin (CTX)-induced acute muscle damage in R6/2 and WT mice showed that the Pax7+ satellite cell pool was dampened in R6/2 mice at 4 weeks post-injection, and R6/2 mice exhibited an altered inflammatory profile in response to acute damage. Our results suggest that, in addition to the mutant HTT degenerative effects in mature muscle fibers, expression of mutant HTT in satellite cells might alter developmental and regenerative processes to contribute to the progressive muscle mass loss in HD. Taken together, the results presented here encourage further studies evaluating the underlying mechanisms of satellite cell dysfunction in HD mouse models.

Effects of Resistance Training on Oxidative Stress Markers and Muscle Damage in Spinal Cord Injured Rats

Background: Spinal cord injury (SCI) is a condition that affects the central nervous system, is characterized by motor and sensory impairments, and impacts individuals’ lives. The objective of this study was to evaluate the effects of resistance training on oxidative stress and muscle damage in spinal cord injured rats. Methodology: Forty Wistar rats were selected and divided equally into five groups: Healthy Control (CON), Sham (SHAM) SCI Untrained group (SCI-U), SCI Trained group (SCI- T), SCI Active Trained group (SCI- AT). Animals in the trained groups were submitted to an incomplete SCI at T9. Thereafter, they performed a protocol of resistance training for four weeks. Results: Significant differences in muscle damage markers and oxidative stress in the trained groups, mainly in SCI- AT, were found. On the other hand, SCI- U group presented higher levels of oxidative stress and biomarkers of LDH and AST. Conclusion: The results highlight that resistance training promoted a decrease in oxidative stress and a significative response in muscle damage markers.

American Ginseng Attenuates Eccentric Exercise-Induced Muscle Damage via the Modulation of Lipid Peroxidation and Inflammatory Adaptation in Males

Exercise-induced muscle damage (EIMD) is characterized by a reduction in functional performance, disruption of muscle structure, production of reactive oxygen species, and inflammatory reactions. Ginseng, along with its major bioactive component ginsenosides, has been widely employed in traditional Chinese medicine. The protective potential of American ginseng (AG) for eccentric EIMD remains unclear. Twelve physically active males (age: 22.4 ± 1.7 years; height: 175.1 ± 5.7 cm; weight: 70.8 ± 8.0 kg; peak oxygen consumption [V˙O2peak] 54.1 ± 4.3 mL/kg/min) were administrated by AG extract (1.6 g/day) or placebo (P) for 28 days and subsequently challenged by downhill (DH) running (−10% gradient and 60% V˙O2peak). The levels of circulating 8-iso-prostaglandin F 2α (PGF2α), creatine kinase (CK), interleukin (IL)-1β, IL-4, IL-10, and TNF-α, and the graphic pain rating scale (GPRS) were measured before and after supplementation and DH running. The results showed that the increases in plasma CK activity induced by DH running were eliminated by AG supplementation at 48 and 72 h after DH running. The level of plasma 8-iso-PGF2α was attenuated by AG supplementation immediately (p = 0.01 and r = 0.53), 2 h (p = 0.01 and r = 0.53) and 24 h (p = 0.028 and r = 0.45) after DH running compared with that by P supplementation. Moreover, our results showed an attenuation in the plasma IL-4 levels between AG and P supplementation before (p = 0.011 and r = 0.52) and 72 h (p = 0.028 and r = 0.45) following DH running. Our findings suggest that short-term supplementation with AG alleviates eccentric EIMD by decreasing lipid peroxidation and promoting inflammatory adaptation.

Dietary Supplementation for Attenuating Exercise-Induced Muscle Damage and Delayed-Onset Muscle Soreness in Humans

Dietary supplements are widely used as a nutritional strategy to improve and maintain performance and achieve faster recovery in sports and exercise. Exercise-induced muscle damage (EIMD) is caused by mechanical stress and subsequent inflammatory responses including reactive oxygen species and cytokine production. Therefore, dietary supplements with anti-inflammatory and antioxidant properties have the potential to prevent and reduce muscle damage and symptoms characterized by loss of muscle strength and delayed-onset muscle soreness (DOMS). However, only a few supplements are considered to be effective at present. This review focuses on the effects of dietary supplements derived from phytochemicals and listed in the International Olympic Committee consensus statement on muscle damage evaluated by blood myofiber damage markers, muscle soreness, performance, and inflammatory and oxidative stress markers. In this review, the effects of dietary supplements are also discussed in terms of study design (i.e., parallel and crossover studies), exercise model, and such subject characteristics as physical fitness level. Future perspectives and considerations for the use of dietary supplements to alleviate EIMD and DOMS are also discussed.

Effect of Multiple-Nutrient Supplement on Muscle Damage, Liver, and Kidney Function After Exercising Under Heat: Based on a Pilot Study and a Randomised Controlled Trial

Objective: This study explored the effect of multiple-nutrient supplementation on muscle damage and liver and kidney function after vigorous exercise under heat.Methods: After an initial pilot trial comprising 89 male participants, 85 participants were recruited and assigned into three groups: a multiple-nutrient (M) group, a glucose (G) group, and a water (W) group. Multiple-nutrient supplements contain glucose, fructose, maltose, sodium, potassium, vitamin B1, vitamin B2, vitamin C, vitamin K, and taurine. Participants were organised to take a 3-km running test (wet-bulb globe temperature 32°C) after a short-term (7 days) supplement. Blood samples were obtained to detect biochemical parameters [glucose (GLU), aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), uric acid (UA), creatinine (Cr), creatine kinase (CK), lactate dehydrogenase (LDH), and lactic acid], inflammation factors [interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α)], and oxidative stress biomarkers [superoxide dismutase (SOD) and 8-iso-prostaglandin F (2alpha) (8-iso-PGF2α)].Results: In the pilot trial, BUN decreased significantly in the M and G groups immediately after the running test. AST, Cr, and UA were significantly reduced 24 h after the running test with single-shot multiple-nutrient supplementation. In the short-term trial, multiple nutrients further prevented the elevation of CK (p = 0.045) and LDH (p = 0.033) levels 24 h after strenuous exercise. Moreover, we found that multiple nutrients significantly reduced IL-6 (p = 0.001) and TNF-α (p = 0.015) elevation immediately after exercise. Simultaneously, SOD elevation was significantly higher in the M group immediately after exercising than in the other two groups (p = 0.033). 8-iso-PGF2α was reduced in the M group 24 h after exercise (p = 0.036).Conclusions: This study found that multiple-nutrient supplementation promoted the recovery of muscle damage and decreased liver and kidney function caused by strenuous exercise in a hot environment, probably through the inhibition of secondary damage induced by increased inflammatory reactions and oxidative stress. In this respect, the current study has important implications for the strategy of nutritional support to accelerate recovery and potentially prevent heat-related illness. This study was prospectively registered on clinicaltrials.gov on June 21, 2019 (ID: ChiCTR1900023988).

Circulating Skeletal Troponin During Weaning From Mechanical Ventilation and Their Association to Diaphragmatic Function: A Pilot Study

Background: Patients with acute respiratory failure (ARF) may need mechanical ventilation (MV), which can lead to diaphragmatic dysfunction and muscle wasting, thus making difficult the weaning from the ventilator. Currently, there are no biomarkers specific for respiratory muscle and their function can only be assessed trough ultrasound or other invasive methods. Previously, the fast and slow isoform of the skeletal troponin I (fsTnI and ssTnI, respectively) have shown to be specific markers of muscle damage in healthy volunteers. We aimed therefore at describing the trend of skeletal troponin in mixed population of ICU patients undergoing weaning from mechanical ventilation and compared the value of fsTnI and ssTnI with diaphragmatic ultrasound derived parameters.Methods: In this prospective observational study we enrolled consecutive patients recovering from acute hypoxemic respiratory failure (AHRF) within 24 h from the start of weaning. Every day an arterial blood sample was collected to measure fsTnI, ssTnI, and global markers of muscle damage, such as ALT, AST, and CPK. Moreover, thickening fraction (TF) and diaphragmatic displacement (DE) were assessed by diaphragmatic ultrasound. The trend of fsTnI and ssTnI was evaluated during the first 3 days of weaning.Results: We enrolled 62 consecutive patients in the study, with a mean age of 67 ± 13 years and 43 of them (69%) were male. We did not find significant variations in the ssTnI trend (p = 0.623), but fsTnI significantly decreased over time by 30% from Day 1 to Day 2 and by 20% from Day 2 to Day 3 (p < 0.05). There was a significant interaction effect between baseline ssTnI and DE [F(2) = 4.396, p = 0.015], with high basal levels of ssTnI being associated to a higher decrease in DE. On the contrary, the high basal levels of fsTnI at day 1 were characterized by significant higher DE at each time point.Conclusions: Skeletal muscle proteins have a distinctive pattern of variation during weaning from mechanical ventilation. At day 1, a high basal value of ssTnI were associated to a higher decrease over time of diaphragmatic function while high values of fsTnI were associated to a higher displacement at each time point.