Preben K. Pedersen

The Yo-yo Intermittent Recovery Test: Physiological Response, Reliability, and Validity

PURPOSE To examine the physiological response and reproducibility of the Yo-Yo intermittent recovery test and its application to elite soccer. METHODS Heart rate was measured, and metabolites were determined in blood and muscle biopsies obtained before, during, and after the Yo-Yo test in 17 males. Physiological measurements were also performed during a Yo-Yo retest and an exhaustive incremental treadmill test (ITT). Additionally, 37 male elite soccer players performed two to four seasonal tests, and the results were related to physical performance in matches. RESULTS The test-retest CV for the Yo-Yo test was 4.9%. Peak heart rate was similar in ITT and Yo-Yo test (189 +/- 2 vs 187 +/- 2 bpm), whereas peak blood lactate was higher (P < 0.05) in the Yo-Yo test. During the Yo-Yo test, muscle lactate increased eightfold (P < 0.05) and muscle creatine phosphate (CP) and glycogen decreased (P < 0.05) by 51% and 23%, respectively. No significant differences were observed in muscle CP, lactate, pH, or glycogen between 90 and 100% of exhaustion time. During the precompetition period, elite soccer players improved (P < 0.05) Yo-Yo test performance and maximum oxygen uptake ([OV0312]O(2max)) by 25 +/- 6 and 7 +/- 1%, respectively. High-intensity running covered by the players during games was correlated to Yo-Yo test performance (r = 0.71, P < 0.05) but not to [OV0312]O(2max) and ITT performance. CONCLUSION The test had a high reproducibility and sensitivity, allowing for detailed analysis of the physical capacity of athletes in intermittent sports. Specifically, the Yo-Yo intermittent recovery test was a valid measure of fitness performance in soccer. During the test, the aerobic loading approached maximal values, and the anaerobic energy system was highly taxed. Additionally, the study suggests that fatigue during intense intermittent short-term exercise was unrelated to muscle CP, lactate, pH, and glycogen.

Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency

The purpose of this study was to investigate the hypothesis that cycling efficiency in vivo is related to mitochondrial efficiency measured in vitro and to investigate the effect of training status on these parameters. Nine endurance trained and nine untrained male subjects (, respectively) completed an incremental submaximal efficiency test for determination of cycling efficiency (gross efficiency, work efficiency (WE) and delta efficiency). Muscle biopsies were taken from m. vastus lateralis and analysed for mitochondrial respiration, mitochondrial efficiency (MEff; i.e. P/O ratio), UCP3 protein content and fibre type composition (% MHC I). MEff was determined in isolated mitochondria during maximal (state 3) and submaximal (constant rate of ADP infusion) rates of respiration with pyruvate. The rates of mitochondrial respiration and oxidative phosphorylation per muscle mass were about 40% higher in trained subjects but were not different when expressed per unit citrate synthase (CS) activity (a marker of mitochondrial density). Training status had no influence on WE (trained 28.0 ± 0.5, untrained 27.7 ± 0.8%, N.S.). Muscle UCP3 was 52% higher in untrained subjects, when expressed per muscle mass (P < 0.05 versus trained). WE was inversely correlated to UCP3 (r=−0.57, P < 0.05) and positively correlated to percentage MHC I (r= 0.58, P < 0.05). MEff was lower (P < 0.05) at submaximal respiration rates (2.39 ± 0.01 at 50%) than at state 3 (2.48 ± 0.01) but was neither influenced by training status nor correlated to cycling efficiency. In conclusion cycling efficiency was not influenced by training status and not correlated to MEff, but was related to type I fibres and inversely related to UCP3. The inverse correlation between WE and UCP3 indicates that extrinsic factors may influence UCP3 activity and thus MEff in vivo.

Improved running economy following intensified training correlates with reduced ventilatory demands.

PURPOSE To compare the effects of three types of intensive run training on running economy (RE) during exhaustive running and to establish possible relationships with changes in ventilatory function and/or muscle fiber type distribution. METHODS Thirty-six male recreational runners were divided into three groups and assigned to either exhaustive distance training (DT), long-interval training (LIT), or short-interval training (SIT) three times 20-30 minxwk(-1) for 6 wk. VO(2 max) and RE were measured during treadmill running before and after training. Muscle fiber type distribution of the vastus lateralis muscle was established from biopsy material. RESULTS VO(2max) (Lxmin(-1) increased by 5.9% (P < 0.0001), 6.0% (P < 0.0001), and 3.6% (P < 0.01) in DT, LIT, and SIT, respectively, and running speed at VO(2max) by 9% (P < 0.0001), 10% (P < 0.0001), and 4% (P < 0.05), respectively. Time-to-exhaustion at 87% of pretraining VO(2max) (mean 3.83) mxs(-1) increased by 94% in DT (P < 0.0001), 67% in LIT (P < 0.0001). Running economy improved by 3.1% in DT (P < 0.05), 3.0% in LIT (P < 0.01), and 0.9% SIT (NS): pulmonary ventilation (VE) was on average 11 Lxmin(-1) lower following training (P < 0.0001). The individual decrements in VE correlated with improvements in RE (r = 0.77; P < 0.0001) and may account for 25-70% of the decrease in aerobic demand. Muscle fiber composition, and respiratory exchange ratio, stride length, and stride frequency during running were unaltered with training. CONCLUSIONS Recreational runners can improve RE and aerobic run performance by exchanging parts of their conventional aerobic distance training with intensive distance or long-interval running, whereas short-interval running is less efficient. The improvement in RE may relate to reduced ventilatory demands. Muscle fiber type distribution was unaltered with training and showed no associations with RE.

Prior heavy exercise eliminates slow component and reduces efficiency during submaximal exercise in humans

We investigated the hypothesis that the pulmonary oxygen uptake slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak for 10 min before (CON) and after (AC) PHE. was measured continuously (breath‐by‐breath) and muscle biopsies were obtained prior to and after 3 and 10 min of exercise. Muscle lactate concentration was stable between 3 and 10 min of exercise but was 2‐ to 3‐fold higher during AC (P < 0.05 versus CON). Acetylcarnitine (ACn) concentration was 6‐fold higher prior to AC and remained higher during exercise. Phosphocreatine (PCr) concentration was similar prior to exercise but the decrease was 2‐fold greater during AC than during CON. The time constant for the initial kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in between 3 and 10 min of exercise during CON (+7.9 ± 0.2%) was not correlated with muscle or blood lactate levels. PHE eliminated the slow increase in and reduced gross exercise efficiency during AC. It is concluded that the slow component cannot be explained by a progressive acidosis because both muscle and blood lactate levels remained stable during CON. We suggest that both the slow component during CON and the reduced gross efficiency during AC are related to impaired contractility of the working fibres and the necessity to recruit additional motor units. Despite a pronounced stockpiling of ACn during AC, initial kinetics were not affected by PHE and PCr concentration decreased to a lower plateau. The discrepancy with previous studies, where initial oxidative ATP generation appears to be limited by acetyl group availability, might relate to remaining fatiguing effects of PHE.

Muscle fiber type distribution and nonlinear Vo2-power output relationship in cycling

PURPOSE We examined whether reported deviations from linearity of the oxygen uptake (.VO(2))-to-power output (W) relationship during intense cycling exercise correlated with the percentage Type II fibers in the exercising muscle. METHODS Twelve trained young men with known fiber type distribution in the vastus lateralis muscle performed step-increment exercise (40 W.3 min(-1)) to exhaustion. RESULTS .VO(2) increased linearly with W up to about 50% .VO(2max) with a regression equation of .VO(2) (mL.min-1) = 661 + 9.73 W and a correlation coefficient (r) of 1.000. Subsequent .VO(2) values were all greater than corresponding linear estimates (P < 0.001 or 0.0001). Peak exercise excess .VO(2) (measured minus estimated .VO(2) assuming linearity) averaged (SD) 434 (192) mL O(2).min-1 or 10.3 (4.7) % .VO(2max). A comprehensive curvilinearity index defined as the sum of measured minus estimated .VO(2) at the four highest completed exercise trials averaged 973 (460) mL O(2).min-1 or 21.5 (9.4) % .VO(2max). Correlations between percentage Type II fibers and either of the two expressions of curvilinearity were nonsignificant. Delta [H+] (arterialized capillary blood) from basal level to peak exercise correlated with the submaximal curvilinearity index (r = 0.59-0.64; P < 0.05) but not with peak excess .VO(2). There was a trend toward a correlation between delta La and curvilinearity index in % .VO(2max)(r = 0.52; P < 0.10) but not with any of the other curvilinearity expressions. The relative ventilatory activity expressed as .V(E)-to-.VO(2) ratio tended to correlate with peak excess .VO(2) (P < 0.10) but not with curvilinearity index. Signals from motion sensors indicate that coactivation of upper-body musculature coincided with deviation from linearity in the .VO(2)-W relationship. CONCLUSION VO2 during step-increment cycling increases linearly with power output up to about 50% .VO(2max)and then curvilinearly. The degree of curvilinearity is not related to muscle fiber type distribution in the vastus lateralis, and only marginally and insignificantly related (P < 0.10) to the relative degree of hyperventilation or to lactate response. Acidosis, on the other hand, correlated significantly with curvilinearity index. The inclusion of isometrically working, upper-body muscular groups during high-intensity cycling may also contribute to the overshoot in oxygen cost.

Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3 and KHCO3 ingestion. It was hypothesized that skeletal muscle is involved in the correction of the ensuing plasma disturbance by exchanging ions, gasses, and fluids between cells and extracellular fluids. Five male subjects, with catheters in a brachial artery and antecubital vein, ingested 3.57 mmol/kg body mass NaHCO3 or KHCO3. While seated, blood samples were taken 30 min before ingestion of the solution, at 10-min intervals during the 60-min ingestion period, and periodically for 210 min after ingestion was complete. Blood was analyzed for gases, hematocrit, plasma ions, and total protein. With NaHCO3, arterial plasma Na+ concentration ([Na+]) increased from 143 ± 1 to 147 ± 1 (SE) meq/l, H+ concentration ([H+]) decreased by 6 ± 1 neq/l, and [Formula: see text] increased by 5 ± 1 mmHg. There was no detectable net Na+ uptake by tissues. An increased plasma strong ion difference ([SID]) accounted fully for the decrease in plasma [H+]. With KHCO3, K+ concentration increased from 4.25 ± 0.10 to 7.17 ± 0.13 meq/l, plasma volume decreased by 15.5 ± 2.3%, [H+] decreased by 4 ± 1 neq/l, and there was no change in[Formula: see text]. The decrease in [H+] in the KHCO3 trial primarily arose in response to the increased [SID]. Net K+ uptake by tissues accounted for 37 ± 5% of the ingested K+. In conclusion, ingestion of NaHCO3and KHCO3 produced markedly different fluid and ionic disturbances and associated regulatory responses by skeletal muscle. Accordingly, the physicochemical origins of the acid-base disturbances also differed between treatments. The tissues did not play a role in regulating plasma [Na+] after ingestion of NaHCO3. In contrast, the net influx of K+ to tissues played an important role in removing K+ from the extracellular compartment after ingestion of KHCO3.

Increased steady-state VO2 and larger O2 deficit with CO2 inhalation during exercise

Aim:  To examine whether inhalation of CO2‐enriched gas would increase steady‐state during exercise and enlarge O2 deficit.

ENHANCED SARCOPLASMIC RETICULUM Ca2+ RELEASE FOLLOWING INTERMITTENT SPRINT-TRAINING

To evaluate the effect of intermittent sprint training on sarcoplasmic reticulum (SR) function, nine young men performed a 5 wk high-intensity intermittent bicycle training, and six served as controls. SR function was evaluated from resting vastus lateralis muscle biopsies, before and after the training period. Intermittent sprint performance (ten 8-s all-out periods alternating with 32-s recovery) was enhanced 12% (P < 0.01) after training. The 5-wk sprint training induced a significantly higher (P < 0.05) peak rate of AgNO(3)-stimulated Ca(2+) release from 709 (range 560-877; before) to 774 (596-977) arbitrary units Ca(2+). g protein(-1). min(-1) (after). The relative SR density of functional ryanodine receptors (RyR) remained unchanged after training; there was, however, a 48% (P < 0.05) increase in total number of RyR. No significant differences in Ca(2+) uptake rate and Ca(2+)-ATPase capacity were observed following the training, despite that the relative density of Ca(2+)-ATPase isoforms SERCA1 and SERCA2 had increased 41% and 55%, respectively (P < 0.05). These data suggest that high-intensity training induces an enhanced peak SR Ca(2+) release, due to an enhanced total volume of SR, whereas SR Ca(2+) sequestration function is not altered.