Blood lactate clearance after maximal exercise depends on active recovery intensity.

AIM: High-intensity exercise is time-limited by onset of fatigue, marked by accumulation of blood lactate. This is accentuated at maximal, all-out exercise that rapidly accumulates high blood lactate. The optimal active recovery intensity for clearing lactate after such maximal, all-out exercise remains unknown. Thus, we studied the intensity-dependence of lactate clearance during active recovery after maximal exercise. METHODS: We constructed a standardized maximal, all-out treadmill exercise protocol that predictably lead to voluntary exhaustion and blood lactate concentration>10 mM. Next, subjects ran series of all-out bouts that increased blood lactate concentration to 11.5±0.2 mM, followed by recovery exercises ranging 0% (passive)-100% of the lactate threshold. RESULTS: Repeated measurements showed faster lactate clearance during active versus passive recovery (P<0.01), and that active recovery at 60-100% of lactate threshold was more efficient for lactate clearance than lower intensity recovery (P<0.05). Active recovery at 80% of lactate threshold had the highest rate of and shortest time constant for lactate clearance (P<0.05), whereas the response during the other intensities was graded (100%=60%>40%>passive recovery, P<0.05). CONCLUSION: Active recovery after maximal all-out exercise clears accumulated blood lactate faster than passive recovery in an intensity-dependent manner, with maximum clearance occurring at active recovery of 80% of lactate threshold.

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 (VO(2max)) 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.

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.

Mechanisms of exercise-induced improvements in the contractile apparatus of the mammalian myocardium.

One of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction. For instance, myocardial improvements may still be observed after exercise training in post-myocardial infarction heart failure. In both health and disease, it is the changes that occur in the individual cardiomyocytes with respect to their ability to contract that by and large drive the exercise training-induced adaptation to the heart. Here, we review the evidence and the mechanisms by which exercise training induces beneficial changes in the mammalian myocardium, as obtained by means of experimental and clinical studies, and argue that these changes ultimately alter the function of the whole heart and contribute to the changes in whole-body function.

Reduced pH and contractility in failing rat cardiomyocytes.

AIM: To determine whether reduced cardiomyocyte contractility in heart failure is associated with reduced intracellular pH (pH(i)). Involvement of the Na(+)/H(+) exchanger and the H(+)/K(+) ATPase were investigated with specific blockers. METHODS: Myocardial infarction and subsequent heart failure in Sprague-Dawley rats were induced by chronic occlusion of the left coronary artery. 6 weeks post-ligation, contractility (cell shortening) and pH(i) (BCECF fluorescence) were recorded in freshly dissociated cardiomyocytes during 2-10 Hz electrical stimulation, with or without either Na(+)/H(+) exchanger or H(+)/K(+) ATPase inhibition. RESULTS: Elevated end-diastolic and reduced peak systolic pressures confirmed heart failure. Increased heart weights (20-30%; P < or = 0.01) and cardiomyocyte lengths and widths (22-25%; P < or = 0.01) confirmed substantial cardiac hypertrophy. In myocytes isolated from sham operated rats, a positive staircase response occurred with stimulation rates from 2 to 7 Hz; further increases in stimulation rate up to 10 Hz reduced contractility. In contrast, pH(i) fell progressively over the entire stimulation range. In failing myocytes, pH(i) was consistently 0.07 pH units lower and contractility 40% lower (P < or = 0.01) than sham control values; the shape of the contractility staircase remained similar to controls. At all stimulation frequencies, Na(+)/H(+) exchanger inhibition reduced pH(i) by 0.05 pH units (P < or = 0.01) and contractility by 22% (P < or = 0.05) in cardiomyocytes from the heart failure group. A significantly smaller decrease of pH(i) and reduction in contractility was observed after inhibition of Na(+)/H(+) exchanger (10 micro m HOE694) in sham myocytes. H(+)/K(+) ATPase inhibition (100 micro m SCH28080) had no effect on pH(i). CONCLUSION: Reduced pH(i) is accompanied by reduced cardiomyocyte contractility in isolated myocytes from post-MI heart failure. The data suggest compensatory Na(+)/H(+) exchanger activation in heart failure, whereas H(+)/K(+) ATPase does not appear to contribute significantly to pH(i) maintenance.

Trans-sodium crocetinate does not affect oxygen uptake in rats during treadmill running.

Trans-sodium crocetinate (TSC), the isomer of the carotenoid compound crocetin, is found markedly to increase survival in hemorrhagic shock subsequent to 50-60% blood loss, mainly via restored resting oxygen consumption (VO(2)), blood pressure and heart rate. The proposed mechanism is that TSC increases oxygen diffusivity, and thus availability, in plasma. If this were found to be a prominent feature in the oxygen transfer from blood to skeletal muscle fiber mitochondria, increased VO(2) during exercise would be expected because of reduced partial pressure of venous oxygen (increased utilization), which we aimed to elucidate in this study. Male Sprague-Dawley rats were intravenously injected with 0.3 mL kg(-1) TSC (40 microg mL(-1)) or placebo and immediately thereafter tested on a ramped treadmill test protocol. Rats were introduced to the experimental protocols beforehand. Administration of TSC had a neutral effect on submaximal and maximal VO(2) (VO(2max)) as well as running performance measured as maximal running time and maximal aerobic running velocity. Thus, in this study we cannot report any effects of TSC on steady-state submaximal VO(2) or VO(2max) at exhaustive exercise.

Strength and endurance differences between elite and junior elite ice hockey players. The importance of allometric scaling.

The aim of this study was to investigate differences in strength and endurance between elite and elite junior ice hockey players. Participants included 18 elite players and 21 junior elite male players (24.2 +/- 4.7 vs. 17.6 +/- 0.9 years of age, 84.2 +/- 8.1 vs. 72.3 +/- 6.0 kg body mass (p < 0.01), 179.9 +/- 6.1 vs. 179.0 +/- 7.0 cm). Absolute maximal oxygen uptake was significantly higher in elite than junior players (4.8 vs. 4.2 L x min(-1), p < 0.01), but relative expressions, including allometric scaling, eliminated the difference. Elite players lifted significantly more weight than juniors in 1 repetition maximum squats (200.0 +/- 28.9 vs. 140.3 +/- 19.5 kg, p < 0.01) and in bench press (100.8 +/- 12.8 vs. 75.3 +/- 12.8 kg, p < 0.01). Elite players also ran significantly faster in the 10 m sprint (1.80 +/- 0.07 vs. 1.88 +/- 0.08 s, p < 0.01), and had greater jumping height (27.2 +/- 3.2 vs. 20.5 +/- 3.0 cm, p < 0.01) and peak force (2336.4 +/- 219.9 vs. 2011.9 +/- 180.1 N, p < 0.01) when holding 50 extra kg. No differences were found for the 40 m sprint or for the rate of force development in jumping. This study revealed that the main differences between elite and junior ice hockey players at a high performance level seem to be in strength and body mass. The results therefore identify important factors for juniors to improve in the transition phase from junior to elite level.

Soccer specific testing of maximal oxygen uptake.

AIM: Endurance capacity in soccer players is important. A soccer specific test for direct measurement of maximal oxygen uptake does, however, not exist. The aim of this study was to evaluate maximal oxygen uptake in a soccer specific field test, compared to treadmill running. METHODS: Ten male soccer players (age 21.9+/-3.0 years, body mass 73.3+/-9.5 kg, height 179.9+/-4.7 cm) participated in the study, and 5 endurance trained men (age 24.9+/-1.8 years, body mass 81.5+/-3.7 kg, height 185.6+/-3.1 cm) took part in a comparison of the portable and the stationary metabolic test systems. The soccer players accomplished a treadmill test and a soccer specific field test containing dribbling, repetitive jumping, accelerations, decelerations, turning and backwards running. RESULTS: Maximal oxygen uptake was similar in field (5.0+/-0.5 L x min(-1)) and laboratory (5.1+/-0.7 L x min(-1)) tests, as were maximal heart rate, maximal breathing frequency, respiratory exchange ratio and oxygen pulse. Maximal ventilation was 5.4% higher at maximal oxygen uptake during treadmill running. CONCLUSION: These findings show that testing of maximal oxygen uptake during soccer specific testing gives similar results as during treadmill running, and therefore serves as a valid test of maximal oxygen uptake in soccer players.

Soccer specific aerobic endurance training.

BACKGROUND: In professional soccer, a significant amount of training time is used to improve players' aerobic capacity. However, it is not known whether soccer specific training fulfils the criterion of effective endurance training to improve maximal oxygen uptake, namely an exercise intensity of 90-95% of maximal heart rate in periods of three to eight minutes. OBJECTIVE: To determine whether ball dribbling and small group play are appropriate activities for interval training, and whether heart rate in soccer specific training is a valid measure of actual work intensity. METHODS: Six well trained first division soccer players took part in the study. To test whether soccer specific training was effective interval training, players ran in a specially designed dribbling track, as well as participating in small group play (five a side). Laboratory tests were carried out to establish the relation between heart rate and oxygen uptake while running on a treadmill. Corresponding measurements were made on the soccer field using a portable system for measuring oxygen uptake. RESULTS: Exercise intensity during small group play was 91.3% of maximal heart rate or 84.5% of maximal oxygen uptake. Corresponding values using a dribbling track were 93.5% and 91.7%. No higher heart rate was observed during soccer training. CONCLUSIONS: Soccer specific exercise using ball dribbling or small group play may be performed as aerobic interval training. Heart rate monitoring during soccer specific exercise is a valid indicator of actual exercise intensity.

Intensity-controlled treadmill running in rats: VO(2 max) and cardiac hypertrophy.

Physiological studies of long-term cardiovascular adaptation to exercise require training regimens that give robust conditioning effects and adequate testing procedures to quantify the outcome. We developed a valid and reproducible protocol for measuring maximal oxygen uptake (VO(2 max)), which was reached at a 25 degrees inclination with a respiratory exchange ratio > 1.05 and blood lactate > 6 mmol/l. The effect of intensity-controlled aerobic endurance training was studied in adult female and male rats that ran 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of VO(2 max) and 2 min at 50-60% of VO(2 max), with adjustment of exercise level according to VO(2 max) every week. After 7 wk, the increase in VO(2 max) plateaued at 60-70% above sedentary controls. Ventricular weights and myocyte length were up 25-30% and 6-12%, respectively. Work economy, oxygen pulse, and heart rate were sufficiently changed to indicate substantial cardiovascular adaptation. The model mimics important human responses to training and could be used in future studies on cellular, molecular, and integrative mechanisms of improved cardiovascular function.