During low-intensity exercise stages of the lactate threshold test, blood lactate concentrations gradually diminish due to the predominant utilization of total fat oxidation. However, it is unclear why blood glucose is also reduced in well-trained athletes who also exhibit decreased lactate concentrations. This review focuses on decreased glucose and lactate concentrations at low-exercise intensity performed in well-trained athletes. During low-intensity exercise, the accrued resting lactate may predominantly be transported via blood from the muscle cell to the liver/kidney. Accordingly, there is increased hepatic blood flow with relatively more hepatic glucose output than skeletal muscle glucose output. Hepatic lactate uptake and lactate output of skeletal muscle during recovery time remained similar which may support a predominant Cori cycle (re-synthesis). However, this pathway may be insufficient to produce the necessary glucose level because of the low concentration of lactate and the large energy source from fat. Furthermore, fatty acid oxidation activates key enzymes and hormonal responses of gluconeogenesis while glycolysis-related enzymes such as pyruvate dehydrogenase are allosterically inhibited. Decreased blood lactate and glucose in low-intensity exercise stages may be an indicator of recovery ability in well-trained athletes. Athletes of intermittent sports may need this recovery ability to successfully perform during competition.

In combat sports such as taekwondo (TKD), athletes rapidly reduce body weight to achieve a desired weight category. Competition takes place 16–24 h after weigh-in and thus, the recovery time is an important factor for competition performance. The purpose of this study was to investigate the impact of rapid weight reduction (RWR) on athletic performance and associated hemorheological properties considering relevant recovery time. Five male TKD athletes reduced body weight by 5% within 3½ days. A simulated competition day (SCD) was carried out after a 16 h recovery period. Parameters were measured before RWR, at weigh-in and before and after three TKD simulation matches (SMs) at SCD. Same set-up was conducted but without RWR as control. Basal blood parameters, red blood cells (RBC) deformability and aggregation, serum glucose and fibrinogen were determined. During SMs, heart rate (HR_peak, HR_mean), oxygen uptake (VO_2peak, VO_2mean), peak lactate (Peak La^-), difference of lactate (ΔLa) and energy systems (anaerobic-alactic, -lactic and aerobic) were analyzed. Basal blood parameters remained unaltered during the interventions. RBC deformability was reduced and aggregation was increased after RWR but values returned to baseline after recovery and were not affected by the SMs. Glucose level was not affected by the interventions. Kick frequency in SMs was higher after RWR which might be responsible for higher HR_peak, VO_2peak, VO_2mean, Peak La^-, ΔLa^- and aerobic demand. The 16 h recovery is sufficient to regenerate measured physiological and hemorheological parameters. TKD-specific performance was not negatively affected during SMs after RWR.

Purpose: This study aimed at comparing previous calculating formulas of maximal lactate accumulation rate (^ν_La.max) and a modified formula of pure ^ν_La.max (P^ν_La.max) during a 15-s all-out sprint cycling test (ASCT) to analyze their relationships.Methods: Thirty male national-level track cyclists participated in this study (n = 30) and performed a 15-s ASCT. The anaerobic power output (W_peak and W_mean), oxygen uptake, and blood lactate concentrations (La⁻) were measured. These parameters were used for different calculations of ^ν_La.max and three energy contributions (phosphagen, W_PCr; glycolytic, W_Gly; and oxidative, W_Oxi). The P^ν_La.max calculation considered delta La⁻, time until W_peak (t_PCr−peak), and the time contributed by the oxidative system (t_Oxi). Other ^ν_La.max levels without t_Oxi were calculated using decreasing time by 3.5% from W_peak (t_{PCr −3.5%}) and t_PCr−peak.Results: The absolute and relative W_PCr were higher than W_Gly and W_Oxi (p < 0.0001, respectively), and the absolute and relative W_Gly were significantly higher than W_Oxi (p < 0.0001, respectively); ^ν_La.max (t_{PCr −3.5%}) was significantly higher than P^ν_La.max and ^ν_La.max (t_PCr−peak), while ^ν_La.max (t_PCr−peak) was lower than P^ν_La.max (p < 0.0001, respectively). P^ν_La.max and ^ν_La.max (t_PCr−peak) were highly correlated (r = 0.99; R² = 0.98). This correlation was higher than the relationship between P^ν_La.max and ^ν_La.max (t_{PCr −3.5%}) (r = 0.87; R² = 0.77). ^ν_La.max (t_PCr−peak), P^ν_La.max, and ^ν_La.max (t_{PCr −3.5%}) were found to correlate with absolute W_mean and W_Gly.Conclusion: P^ν_La.max as a modified calculation of ^ν_La.max provides more detailed insights into the inter-individual differences in energy and glycolytic metabolism than ^ν_La.max (t_PCr−peak) and ^ν_La.max (t_{PCr −3.5%}). Because W_Oxi and W_PCr can differ remarkably between athletes, implementing their values in P^ν_La.max can establish more optimized individual profiling for elite track cyclists.

[Purpose] Skeletal muscle regulates health and performance by maintaining or increasing strength and muscle mass. Although the molecular mechanisms in response to resistance exercise (RE) significantly target the activation of protein synthesis, a plethora of other mechanisms and structures must be involved in orchestrating the communication, repair, and restoration of homeostasis after RE stimulation. In practice, RE can be modulated by variations in intensity, continuity and volume, which affect molecular responses and skeletal muscle adaptation. Knowledge of these aspects is important with respect to planning of training programs and assessing the impact of RE training on skeletal muscle.[Methods] In this narrative review, we introduce general aspects of skeletal muscle substructures that adapt in response to RE. We further highlighted the molecular mechanisms that control human skeletal muscle anabolism, degradation, repair and memory in response to acute and repeated RE and linked these aspects to major training variables.[Results] Although RE is a key stimulus for the activation of skeletal muscle anabolism, it also induces myofibrillar damage. Nevertheless, to increase muscle mass accompanied by a corresponding adaptation of the essential substructures of the sarcomeric environment, RE must be continuously repeated. This requires the permanent engagement of molecular mechanisms that re-establish skeletal muscle integrity after each RE–induced muscle damage.[Conclusion] Various molecular regulators coordinately control the adaptation of skeletal muscle after acute and repeated RE and expand their actions far beyond muscle growth. Variations of key resistance training variables likely affect these mechanisms without affecting muscle growth.

This study aimed to evaluate the effects of warm-up intensity on energetic contribution and performance during a 100-m sprint. Ten young male sprinters performed 100-m sprints following both a high-intensity warm-up (HIW) and a low-intensity warm-up (LIW). Both the HIW and LIW were included in common baseline warm-ups and interventional warm-ups (eight 60-m runs, HIW; 60 to 95%, LIW; 40% alone). Blood lactate concentration [La⁻], time trial, and oxygen uptake (VO₂) were measured. The different energy system contribution was calculated by using physiological variables. [La⁻¹]_Max following HIW was significantly higher than in LIW (11.86 ± 2.52 vs. 9.24 ± 1.61 mmol·L⁻¹; p < 0.01, respectively). The 100-m sprint time trial was not significantly different between HIW and LIW (11.83 ± 0.57 vs. 12.10 ± 0.63 s; p > 0.05, respectively). The relative (%) phosphagen system contribution was higher in the HIW compared to the LIW (70 vs. 61%; p < 0.01, respectively). These results indicate that an HIW increases phosphagen and glycolytic system contributions as compared to an LIW for the 100-m sprint. Furthermore, an HIW prior to short-term intense exercise has no effect on a 100-m sprint time trial; however, it tends to improve times (decreased 100-m time trial; −0.27 s in HIW vs. LIW).

The diagnostics of anaerobic glycolytic metabolism which play a subordinate role in elite rowing and parameters such as maximum lactate accumulation rate (^ν_La.max) have thus far not been associated with ergometer rowing performance. The aim of the study was to quantify the glycolytic energy metabolism (W_Gly) during a 2000 m ergometer rowing time trial (RTT) and ^ν_La.max during a 10 s maximum ergometer rowing sprint test (RST) and to unravel associations between those variables and RTT performance. Combined post-exercise lactate measurements and oxygen uptake after RST and RTT were used to determine ^ν_La.max and glycolytic energy contribution (W_Gly) in seven male and three female German U 23 national rowers (N = 10, 19.8 ± 0.9 years, 183.2 ± 7.0 cm height, 79.9 ± 13.3 kg body mass, 16.4 ± 5.1 % body fat). W_Gly during RTT ranged from 7 to 15.5% and ^ν_La.max between 0.25 and 0.66 mmol∙L⁻¹∙s⁻¹. ^ν_La.max correlated with W_Gly (p < 0.05, r = 0.74) and the mechanical power output (W) for the first 300 m (300_first) during RTT (p < 0.05, r = 0.67). ^ν_La.max further correlated with ∆300_first−last (W) for the first and last 300 m (300_last) during RTT (p < 0.01, r = 0.87) and also within the subgroup of male rowers. ^ν_La.max displays a wide spectrum of individual differences in rowers. Due to this and its correlation to specific phases of RTT, it contributes to an individual energetic performance profile in rowing. Future studies must undermine the role of ^ν_La.max for exercise performance and whether it serves as a marker that can be specifically targeted for a training-induced increase or decrease.