1.
Effect of citrulline on post-exercise rating of perceived exertion, muscle soreness, and blood lactate levels: A systematic review and meta-analysis.
Rhim, HC, Kim, SJ, Park, J, Jang, KM
Journal of sport and health science. 2020;(6):553-561
Abstract
BACKGROUND Citrulline is one of the non-essential amino acids that is thought to improve exercise performance and reduce post-exercise muscle soreness. We conducted a systematic review and meta-analysis to determine the effect of citrulline supplements on the post-exercise rating of perceived exertion (RPE), muscle soreness, and blood lactate levels. METHODS A random effects model was used to calculate the effect sizes due to the high variability in the study design and study populations of the articles included. A systematic search of PubMed, Web of Science, and ClinicalTrials.gov was performed. Eligibility for study inclusion was limited to studies that were randomized controlled trials involving healthy individuals and that investigated the acute effect of citrulline supplements on RPE, muscle soreness, and blood lactate levels. The supplementation time frame was limited to 2 h before exercise. The types and number of participants, types of exercise tests performed, supplementation protocols for L-citrulline or citrulline malate, and primary (RPE and muscle soreness) and secondary (blood lactate level) study outcomes were extracted from the identified studies. RESULTS The analysis included 13 eligible articles including a total of 206 participants. The most frequent dosage used in the studies was 8 g of citrulline malate. Citrulline supplementation significantly reduced RPE (n = 7, p = 0.03) and muscle soreness 24-h and 48-h after post-exercise (n = 7, p = 0.04; n = 6, p = 0.25, respectively). However, citrulline supplementation did not significantly reduce muscle soreness 72-h post-exercise (n = 4, p = 0.62) or lower blood lactate levels (n = 8, p = 0.17). CONCLUSION Citrulline supplements significantly reduced post-exercise RPE and muscle soreness without affecting blood lactate levels.
2.
Impact of Pre-exercise Hypohydration on Aerobic Exercise Performance, Peak Oxygen Consumption and Oxygen Consumption at Lactate Threshold: A Systematic Review with Meta-analysis.
Deshayes, TA, Jeker, D, Goulet, EDB
Sports medicine (Auckland, N.Z.). 2020;(3):581-596
Abstract
BACKGROUND Progressive exercise-induced dehydration may impair aerobic exercise performance (AEP). However, no systematic approach has yet been used to determine how pre-exercise hypohydration, which imposes physiological challenges differing from those of a well-hydrated pre-exercise state, affects AEP and related components such as peak oxygen consumption [Formula: see text] and [Formula: see text] at lactate threshold [Formula: see text]. OBJECTIVE To determine, using a systematic approach with meta-analysis, the magnitude of the effect of pre-exercise hypohydration on AEP, [Formula: see text] and [Formula: see text]. DESIGN This was a systematic review with meta-analysis of well-controlled studies. DATA SOURCES MEDLINE, SPORTDiscus and CINAHL databases and cross-referencing. INCLUSION CRITERIA FOR SELECTING STUDIES (1) well-controlled human (≥ 18 years) studies; (2) pre-exercise hypohydration induced at least 1 h prior to exercise onset; (3) pre-exercise body mass loss in the hypohydrated, experimental condition was ≥ 1% and ≥ 0.5% than the well-hydrated, control condition; (4) following the dehydrating protocol body mass change in the control condition was within - 1% to + 0.5% of the well-hydrated body mass. RESULTS A total of 15 manuscripts were included, among which 14, 6 and 6 met the inclusion criteria for AEP, [Formula: see text] and [Formula: see text], respectively, providing 21, 10 and 9 effect estimates, representing 186 subjects. Mean body mass decrease was 3.6 ± 1.0% (range 1.7-5.6%). Mean AEP test time among studies was 22.3 ± 13.5 min (range 4.5-54.4 min). Pre-exercise hypohydration impaired AEP by 2.4 ± 0.8% (95% CI 0.8-4.0%), relative to the control condition. Peak oxygen consumption and [Formula: see text], respectively, decreased by 2.4 ± 0.8% (95% CI 0.7-4.0%) and 4.4 ± 1.4% (95% CI 1.7-7.1%), relative to the control condition. Compared with starting an exercise hypohydrated, it is respectively likely, possible and likely that AEP, [Formula: see text] and [Formula: see text] benefit from a euhydrated state prior to exercise. Meta-regression analyses did not establish any significant relationship between differences in body mass loss and differences in the percent change in AEP or [Formula: see text]. However, [Formula: see text] was found to decrease by 2.6 ± 0.8 % (95% CI 0.7-4.5%) for each percent loss in body mass above a body mass loss threshold of 2.8%. CONCLUSION Pre-exercise hypohydration likely impairs AEP and likely reduces [Formula: see text] (i.e., the aerobic contribution to exercise was lower) during running and cycling exercises ≤ 1 h across different environmental conditions (i.e., from 19 to 40 °C). Moreover, pre-exercise hypohydration possibly impedes [Formula: see text] during such exercises.
3.
Blood Lactate or Lactate Clearance: Which Is Robust to Predict the Neurological Outcomes after Cardiac Arrest? A Systematic Review and Meta-Analysis.
Zhou, BC, Zhang, Z, Zhu, JJ, Liu, LJ, Liu, CF
BioMed research international. 2018;:8014213
Abstract
AIMS: Lactate and lactate clearance were supposed to be associated with cardiac arrest outcomes, but studies obtained different results. Thus, we conducted this meta-analysis to investigate the association between lactate or lactate clearance and neurological outcomes and their usefulness for prediction of neurological outcomes. METHODS We conducted a systematic search in PubMed, Web of science, EMBASE, Medline, and Google Scholar until May 1, 2018, for relevant studies. Studies reporting lactate, lactate clearance on admission, or other time points after admission associated with neurological outcomes were included in our analysis. Pooled effect date was shown as weighed mean difference (WMD) and 95% confidence interval (CI). To measure the usefulness of lactate on admission to predict neurological outcomes, we also pooled the data of diagnostic test. RESULTS 23 studies involving 6720 cardiac arrest (CA) patients were included. Results from our analysis indicated that patients with good neurological outcomes tended to have a lower lactate level on admission (WMD: -2.66 mmol/L, 95%CI: -3.39 to -1.93) and 12h, 24h, and 48h after admission (P<0.001). Furthermore, the pooled AUC for lactate level on admission to predict neurological outcomes was 0.77 (95%CI: 0.73-0.80). However, a significant association between lactate clearance and neurological outcomes was only found in 24h but not 12h lactate clearance rate. CONCLUSIONS Lactate levels on admission and all time points up to 48h were associated with neurological outcomes after CA, whereas the association between lactate clearance and neurological outcomes was not so stable. Lactate was a more robust surrogate marker than lactate clearance to predict neurological outcomes after CA.
4.
Acute metformin overdose: examining serum pH, lactate level, and metformin concentrations in survivors versus nonsurvivors: a systematic review of the literature.
Dell'Aglio, DM, Perino, LJ, Kazzi, Z, Abramson, J, Schwartz, MD, Morgan, BW
Annals of emergency medicine. 2009;(6):818-23
Abstract
STUDY OBJECTIVE Metformin is known to cause potentially fatal metabolic acidosis with an increased lactate level in both overdose and therapeutic use. No association between mortality and serum pH, lactate level, or metformin concentrations, though intuitive, has yet been described. This systematic literature review is designed to evaluate the association between mortality and serum pH, lactate level, and metformin concentrations in acute metformin overdose. METHODS We reviewed the literature by using the MEDLINE, EMBASE, CINAHL, and TOXNET databases for cases of metformin overdose with documented mortality data and values of serum pH, lactate level, and metformin concentrations. When available, patient age, patient sex, and whether patients received intravenous sodium bicarbonate therapy or hemodialysis were also analyzed. Cases meeting inclusion criteria were analyzed to determine whether a difference in distribution of nadir serum pH, peak serum lactate level, or peak serum metformin concentrations existed between overdose survivors and nonsurvivors. RESULTS We identified 10 articles that had 1 or more cases meeting our inclusion criteria. In total, there were 22 cases of metformin overdose (5/22 died) that met inclusion criteria. No intentional overdose patients died whose serum pH nadir was greater than 6.9, maximum lactate concentration less than 25 mol/L, or maximum metformin concentration less than 50 microg/mL (therapeutic range 1 to 2 microg/mL). Intentional overdose patients with a nadir serum pH less than 6.9 had 83% mortality (5/6), those with lactate concentration greater than 25 mmol/L had 83% mortality (5/6), and those with metformin concentration greater than 50 microg/mL had 38% mortality (5/12). Nadir serum pH and peak serum lactate and metformin concentration distributions in survivors and nonsurvivors revealed that survivors had a median nadir pH of 7.30, interquartile range (IQR) 7.22, 7.36; nonsurvivors, a median nadir pH of 6.71, IQR 6.71, 6.73; survivors, a median peak lactate level of 10.8 mmol/L, IQR 4.2, 12.9; nonsurvivors, a median peak lactate level of 35.0 mmol/L, IQR 33.3, 39.0; survivors, a median peak metformin level of 42 microg/mL, IQR 6.6, 67.6; and nonsurvivors, a median peak metformin level of 110 microg/mL, IQR 110, 110. CONCLUSION No cases of acute metformin overdose meeting the study's inclusion criteria were found in which patients with a nadir serum pH greater than 6.9, peak serum lactate concentrations less than 25 mmol/L, or peak serum metformin concentrations less than 50 microg/mL died. Patients with acute metformin overdose who died had much lower serum pH nadirs and much higher peak serum lactate and metformin concentrations than those who survived.