Blood lactate clearance during active recovery after an intense running bout depends on the intensity of the active recovery

High-intensity exercise training contributes to the production and accumulation of blood lactate, which is cleared by active recovery. However, there is no commonly agreed intensity or mode for clearing accumulated blood lactate. We studied clearance of accumulated blood lactate during recovery at various exercise intensities at or below the lactate threshold after high-intensity interval runs that prompted lactate accumulation. Ten males repeated 5-min running bouts at 90% of maximal oxygen uptake ([Vdot]O2max), which increased blood lactate concentration from 1.0 ± 0.1 to 3.9 ± 0.3 mmol · l-1. This was followed by recovery exercises ranging from 0 to 100% of lactate threshold. Repeated blood lactate measurements showed faster clearance of lactate during active versus passive recovery, and that the decrease in lactate was more rapid during higher (60-100% of lactate threshold) than lower (0-40% of lactate threshold) (P < 0.05) intensities. The more detailed curve and rate analyses showed that active recovery at 80-100% of lactate threshold had shorter time constants for 67% lactate clearance and higher peak clearance rates than 40% of lactate threshold or passive recovery (P < 0.05). Finally, examination of self-regulated intensities showed enhanced lactate clearance during higher versus lower intensities, further validating the intensity dependence of clearance of accumulated blood lactate. Therefore, active recovery after strenuous exercise clears accumulated blood lactate faster than passive recovery in an intensity-dependent manner. Maximum clearance occurred at active recovery close to the lactate threshold

Interval training normalizes cCardiomyocyte function, diastolic Ca²⁺ control, and SR Ca²⁺ release synchronicity in a mouse model of diabetic cardiomyopathy

In the present study we explored the mechanisms behind excitation-contraction (EC)-coupling defects in cardiomyocytes from mice with type-2 diabetes (db/db), and determined whether 13-weeks of aerobic interval training could restore cardiomyocyte Ca2+ cycling and EC-coupling. Reduced contractility in cardiomyocytes isolated from sedentary db/db was associated with increased diastolic sarcoplasmic reticulum (SR)-Ca2+ leak, reduced synchrony of Ca2+ release, reduced transverse (T)-tubule density, and lower peak systolic and diastolic Ca2+ and caffeine-induced Ca2+ release. Additionally, the rate of SR Ca2+ ATPase (SERCA2a)-mediated Ca2+ uptake during diastole was reduced, whereas a faster recovery from caffeine-induced Ca2+ release indicated increased Na+/Ca2+- exchanger (NCX) activity. The increased SR-Ca2+ leak was attributed to increased Ca2+-calmodulindependent protein kinase (CaMKIIδ) phosphorylation, supported by the normalization of SR-Ca2+ leak upon inhibition of CaMKIIδ (AIP). Exercise training restored contractile function associated with restored SR Ca2+ release synchronicity, T-tubule density, twitch Ca2+ amplitude, SERCA2a and NCX activities, and SR-Ca2+ leak. The latter was associated with reduced phosphorylation of cytosolic CaMKIIδ. Despite normal contractile function and Ca2+ handling after the training period, phospholamban was hyperphosphorylated at Serine-16. Protein kinase A (PKA) inhibition (H-89) in cardiomyocytes from the exercised db/db group abolished the differences in SR-Ca2+ load when compared with the sedentary db/db mice. EC-coupling changes were observed without changes in serum insulin or glucose levels, suggesting that the exercise training-induced effects are not via normalization of the diabetic condition. These data demonstrate that aerobic interval training almost completely restored the contractile function of the diabetic cardiomyocyte to levels close to sedentary wild type (WT)

Experimental evidence may inform the debate

No abstract availabl

Animal models in the study of exercise-induced cardiac hypertrophy

Exercise training-induced cardiac hypertrophy occurs following a program of aerobic endurance exercise training and it is considered as a physiologically beneficial adaptation. To investigate the underlying biology of physiological hypertrophy, we rely on robust experimental models of exercise training in laboratory animals that mimic the training response in humans. A number of experimental strategies have been established, such as treadmill and voluntary wheel running and swim training models that all associate with cardiac growth. These approaches have been applied to numerous animal models with various backgrounds. However, important differences exist between these experimental approaches, which may affect the interpretation of the results. Here, we review the various approaches that have been used to experimentally study exercise training-induced cardiac hypertrophy; including the advantages and disadvantages of the various models

Strength and endurance in elite football players

We aimed to improve the physical capacity of a top-level elite football team during its pre-season by implementing a maximal strength and high-intensity endurance training program. 21 first league elite football players (20-31 yrs, height 171-194 cm, mass 58.8-88.1 kg) having recently participated in the UEFA Champions' League, took part in the study. Aerobic interval-training at 90-95% of maximal heart rate and half-squats strength training with maximum loads in 4 repetitions ×4 sets were performed concurrently twice a week for 8 weeks. The players were not familiar with maximal strength training as part of their regular program. Maximal oxygen uptake (VO2max) increased 8.6% (1.7-16.6) (p<0.001), from 60.5 (51.7-67.1) to 65.7 (58.0-74.5) mL · kg−1 · min−1 whereas half-squat one repetition maximum increased 51.7% (13.3-135.3) (p<0.001), from 116 (85-150) to 176 (160-210) kg. The 10-m sprint time also improved by 0.06 s (0.02-0.16) (p<0.001); while counter movement jump improved 3.0 cm (0.1-6.2) (p<0.001), following the training program. The concurrent strength and endurance training program together with regular football training resulted in considerable improvement of the players' physical capacity and so may be successfully introduced to elite football players

Exercise-induced changes in calcium handling in left ventricular cardiomyocytes

Regular exercise training results in beneficial adaptation of the heart by improving its contractile capacity. This has important consequences for both healthy individuals and those with depressed myocardial function, e.g. heart failure. Studies combining experimental animal models of exercise training and heart failure with biophysical and biochemical characterization of heart function have extended our understanding of how exercise training improves cardiac contractile function at the cellular level. Exercise training improves the strength of contraction and increases the rates of shortening and relengthening of cardiomyocytes. Myocardial force production and power output in heart cells studied under loaded conditions is also increased. These changes are associated with faster rise and decay of the intracellular calcium transient and improved myofilament sensitivity to calcium. Translated to global cardiac function, these cellular changes explain exercise training-induced improvements in left ventricular systolic and diastolic function. In particular, exercise training is able to restore depressed contractility and calcium cycling associated with heart failure, to a value comparable to healthy individuals

Myocardial sarcoplasmic reticulurn Ca2+ ATPase function is increased by aerobic interval training

Objective Reduced activity of the sarcoplasmic reticulum Ca2+ ATPase-2a (SERCA-2a) contributes to myocardial dysfunction. Exercise training improves myocardial Ca2+-handling, but SERCA-2a function is uncertain. We assessed SERCA-2a activity after exercise training. Methods SERCA-2a function was assessed by sarcoplasmic reticulum Ca2+ uptake in cardiornyocytes with other Ca2+ uptake mechanisms blocked, in mice after aerobic interval training versus sedentary controls. Results We established protocols to assess SERCA-2a function, and show that aerobic interval training increases the maximal rate of Ca2+ uptake by 30%. This is at least partly explained by reduced phospholamban-to-SERCA-2a ratio. Conclusion Aerobic interval training improves myocardial SERCA-2a performance, explaining at least partly why myocardial Ca2+-handling improves after exercise training

Unilateral arm strength training improves contralateral peak force and rate of force development

Neural adaptation following maximal strength training improves the ability to rapidly develop force. Unilateral strength training also leads to contralateral strength improvement, due to cross-over effects. However, adaptations in the rate of force development and peak force in the contralateral untrained arm after one-arm training have not been determined. Therefore, we aimed to detect contralateral effects of unilateral maximal strength training on rate of force development and peak force. Ten adult females enrolled in a 2-month strength training program focusing of maximal mobilization of force against near-maximal load in one arm, by attempting to move the given load as fast as possible. The other arm remained untrained. The training program did not induce any observable hypertrophy of any arms, as measured by anthropometry. Nevertheless, rate of force development improved in the trained arm during contractions against both submaximal and maximal loads by 40-60%. The untrained arm also improved rate of force development by the same magnitude. Peak force only improved during a maximal isometric contraction by 37% in the trained arm and 35% in the untrained arm. One repetition maximum improved by 79% in the trained arm and 9% in the untrained arm. Therefore, one-arm maximal strength training focusing on maximal mobilization of force increased rapid force development and one repetition maximal strength in the contralateral untrained arm. This suggests an increased central drive that also crosses over to the contralateral side

One-arm maximal strength training improves work economy and endurance capacity but not skeletal muscle blood flow

Maximal strength training with a focus on maximal mobilization of force in the concentric phase improves endurance performance that employs a large muscle mass. However, this has not been studied during work with a small muscle mass, which does not challenge convective oxygen supply. We therefore randomized 23 adult females with no arm-training history to either one-arm maximal strength training or a control group. The training group performed five sets of five repetitions of dynamic arm curls against a near-maximal load, 3 days a week for 8 weeks. This training increased maximal strength by 75% and improved rate of force development during both strength and endurance exercise, suggesting that each arm curl became more efficient. This coincided with a 17-18% reduction in oxygen cost at standardized submaximal workloads (work economy), and a 21% higher peak oxygen uptake and 30% higher peak load during maximal arm endurance exercise. Blood flow assessed by Doppler ultrasound in the axillary artery supplying the working biceps brachii and brachialis muscles could not explain the training-induced adaptations. These data suggest that maximal strength training improved work economy and endurance performance in the skeletal muscle, and that these effects are independent of convective oxygen supply