Physical activity, heart rate variability-based stress and recovery, and subjective stress during a 9-month study period.

The aim of this study was to investigate the association between physical activity (PA) and objective heart rate variability (HRV)-based stress and recovery with subjective stress in a longitudinal setting. Working-age participants (n = 221; 185 women, 36 men) were overweight (body mass index, 25.3-40.1 kg/m2 ) and psychologically distressed (≥3/12 points on the General Health Questionnaire). Objective stress and recovery were based on HRV recordings over 1-3 work days. Subjective stress was assessed with the Perceived Stress Scale and PA level with a questionnaire. Data were collected at three time points: baseline, 10 weeks post intervention, and at the 36-week follow-up. We adopted a latent growth model to investigate the initial level and change in PA, objective stress and recovery, and subjective stress at the three measurement time points. The results showed that initial levels of PA (P < 0.001) and objective stress (P = 0.001) and recovery (P < 0.01) were associated with the change in subjective stress. The results persisted after adjustment for intervention group. The present results suggest that high PA and objectively assessed low stress and good recovery have positive effects on changes in subjective stress in the long-term.

High-intensity endurance training increases nocturnal heart rate variability in sedentary participants.

The effects of endurance training on endurance performance characteristics and cardiac autonomic modulation during night sleep were investigated during two 4-week training periods. After the first 4-week training period (3 x 40 min per week, at 75% of HRR) the subjects were divided into HIGH group (n = 7), who performed three high-intensity endurance training sessions per week; and CONTROL group (n = 8) who did not change their training. An incremental treadmill test was performed before and after the two 4-week training periods. Furthermore, nocturnal RR-intervals were recorded after each training day. In the second 4-week training period HIGH group increased their VO2max (P = 0.005) more than CONTROL group. At the same time, nocturnal HR decreased (P = 0.039) and high-frequency power (HFP) increased (P = 0.003) in HIGH group while no changes were observed in CONTROL group. Furthermore, a correlation was observed between the changes in nocturnal HFP and changes in VO2max during the second 4-week training period (r = 0.90, P < 0.001). The present study showed that the increased HFP is related to improved VO2max in sedentary subjects suggesting that nocturnal HFP can provide a useful method in monitoring individual responses to endurance training.

Neuromuscular and cardiovascular adaptations during concurrent strength and endurance training in untrained men.

This study examined the effects of concurrent strength and endurance training on neuromuscular and endurance characteristics compared to strength or endurance training alone. Previously untrained men were divided into strength (S: n=16), endurance (E: n=11) or concurrent strength and endurance (SE: n=11) training groups. S and E trained 2 times and SE 2 + 2 times a week for strength and endurance during the 21-week period. Maximal unilateral isometric and bilateral concentric forces of leg muscles increased similarly in S and SE by 20-28% (p<0.01) and improvements in isometric forces were accompanied by increases (p<0.05) of maximal muscle activation. Rate of force development of isometric action (p<0.05) improved only in S. The increase in muscle cross-sectional area of the quadriceps femoris in SE (11%, p<0.001) were greater than in S (6%, p<0.001) or in E (2%, p<0.05). SE and E increased maximal cycling power (SE: 17% and E: 11%, p<0.001) and VO(2MAX) (SE: 17%, p<0.001 and E: 5%, ns.). These results suggest that the present moderate volume 21-week concurrent SE training in previously untrained men optimizes the magnitude of muscle hypertrophy, maximal strength and endurance development, but interferes explosive strength development, compared with strength or endurance training alone.

Effects of moderate and heavy endurance exercise on nocturnal HRV.

This study examined the effects of endurance exercise on nocturnal autonomic modulation. Nocturnal R-R intervals were collected after a rest day, after a moderate endurance exercise and after a marathon run in ten healthy, physically active men. Heart rate variability (HRV) was analyzed as a continuous four-hour period starting 30 min after going to bed for sleep. In relation to average nocturnal heart rate after rest day, increases to 109+/-6% and 130+/-11% of baseline were found after moderate endurance exercise and marathon, respectively. Standard deviation of R-R intervals decreased to 90+/-9% and 64+/-10%, root-mean-square of differences between adjacent R-R intervals to 87+/-10% and 55+/-16%, and high frequency power to 77+/-19% and 34+/-19% of baseline after moderate endurance exercise and marathon, respectively. Also nocturnal low frequency power decreased to 56+/-26% of baseline after the marathon. Changes in nocturnal heart rate and HRV suggest prolonged dose-response effects on autonomic modulation after exercises, which may give useful information on the extent of exercise-induced nocturnal autonomic modulation and disturbance to the homeostasis.

Endurance performance and nocturnal HRV indices.

The effects of endurance training on endurance performance characteristics and cardiac autonomic modulation during night sleep were investigated. Twenty-four sedentary subjects trained over four weeks two hours per week at an average running intensity of 76+/-4% of their heart rate reserve. The R to R ECG-intervals were recorded and heart rate variability indices including high frequency power (HFP) were calculated for the nights following the training days every week. The subjects were divided into responders and non-responders according to the improvements in the maximal velocity of the incremental treadmill test (v(max)). The responders improved their v(max) by 10.9+/-46 % (p < 0.001) while no changes were observed in the non-responders (1.6+/-3.0%), although there were no differences in any training load variables between the groups. In the responders nocturnal HFP was significantly higher during the fourth training week compared to the first training week (p=0.036). Furthermore, a significant correlation was observed between the change in v(max) and the change in nocturnal HFP (r=0.482, p=0.042). It was concluded that after similar training, an increase in cardiac vagal modulation was related to improved v(max) in the sedentary subjects.

Fatigue during a 5-km running time trial.

This study investigated fatigue-induced changes in neuromuscular and stride characteristics during and immediately after the 5-km running time trial. Eighteen well-trained male distance runners performed a maximal 20-m sprint test and maximal voluntary contraction (MVC) in a leg press machine before and immediately after the 5-km running time trial. In all the tests the EMG of five lower limb muscles was measured. The results of the present study showed that muscle fatigue measured in maximal exercises like 20-m sprint and MVC are not related to the fatigue induced changes during the 5-km time trial. The fatigue in the 20-m sprint test was related to the maximal 20-m pretest velocity (r=0.58, p<0.05), but the velocity loss during the 5-km time trial was inversely related to 5-km performance (r= - 0.60, p<0.05) and training volume (r= - 0.58, p<0.05). It was concluded that the fatigue in 5-km running measured pre- and postexercise at maximal effort is more related to sprint performance rather than endurance performance, but the fatigue measured during the 5-km running is related to endurance performance and factors affecting pacing strategy.

Post-exercise heart rate variability of endurance athletes after different high-intensity exercise interventions.

Methodological problems have limited the number of studies on heart rate variability (HRV) dynamics immediately after exercise. We used the short-time Fourier transform method to study immediate (5 min) and slow (30 min) recovery of HRV after different high-intensity exercise interventions. Eight male athletes performed two interval interventions at 85% and 93% (IV(85) and IV(93)) and two continuous interventions at 80% and 85% (CO(80) and CO(85)) of the velocity at VO2max (vVO2max). We found no increase in high frequency power (HFP), but low frequency (LFP) and total power (TP) increased (P<0.05) during the first 5 min of the recovery after each intervention. During the 30-min recovery, HFP, LFP and TP (1) increased slowly toward resting values, but HFP remained lower (P<0.01) than at rest, (2) were lower (P<0.05) after IV(93) and CO(85) when compared with IV(85) and CO(80), respectively and (3) were lower (P<0.01) after CO(85) when compared with IV(85). HRV recovery was detected during the immediate recovery after interventions. Increased exercise intensity resulted in lower HRV both in interval and in continuous interventions. In addition, when interval and continuous interventions were performed at a similar workload, HRV was lower after continuous intervention.

Cardiac autonomic responses to standing up and cognitive task in overtrained athletes.

This study compared the autonomic responses to an active orthostatic test and Stroop Color Word Test (Stroop) as well as cognitive performance in Stroop in twelve severely overtrained (OA, 6 men and 6 women) and twelve control athletes (CA, 6 men and 6 women). RR-intervals were recorded during the orthostatic test, the Stroop, and a relaxation period succeeding the Stroop. Low frequency power during standing in the orthostatic test was lower in OA than in CA (1322 +/- 955 ms2 vs. 2262 +/- 1029 ms2, p = 0.030, respectively). During Stroop, OA had higher relative total power (50 +/- 47 % vs. 19 +/- 14 % of the individual total power during supine rest after awakening, p = 0.028, respectively) and high frequency power (38.5 +/- 9.4 % vs. 13.5 +/- 2.3 % of the individual high frequency power during supine rest after awakening, p = 0.035, respectively) than CA. In the Stroop, OA made more mistakes than CA (9.7 +/- 6.5 % vs. 5.4 +/- 3.0 %, p = 0.045). The increase in absolute total power from the Stroop to relaxation correlated negatively with the amount of mistakes in the Stroop (r = - 0.588, p = 0.003). Thus, cardiac autonomic modulation during orthostatic task and responses to cognitive task and to relaxation, as well as the cognitive performance were attenuated in severe overtraining.

Concurrent endurance and explosive type strength training improves neuromuscular and anaerobic characteristics in young distance runners.

To study effects of concurrent explosive strength and endurance training on aerobic and anaerobic performance and neuromuscular characteristics, 13 experimental (E) and 12 control (C) young (16 - 18 years) distance runners trained for eight weeks with the same total training volume but 19% of the endurance training in E was replaced by explosive training. Maximal speed of maximal anaerobic running test and 30-m speed improved in E by 3.0 +/- 2.0% (p < 0.01) and by 1.1 +/- 1.3% (p < 0.05), respectively. Maximal speed of aerobic running test, maximal oxygen uptake and running economy remained unchanged in both groups. Concentric and isometric leg extension forces increased in E but not in C. E also improved (p < 0.05) force-time characteristics accompanied by increased (p < 0.05) rapid neural activation of the muscles. The thickness of quadriceps femoris increased in E by 3.9 +/- 4.7% (p < 0.01) and in C by 1.9 +/- 2.0% (p < 0.05). The concurrent explosive strength and endurance training improved anaerobic and selective neuromuscular performance characteristics in young distance runners without decreases in aerobic capacity, although almost 20% of the total training volume was replaced by explosive strength training for eight weeks. The neuromuscular improvements could be explained primarily by neural adaptations.

The profile and distribution of myosin heavy chain isoforms in middle-aged sedentary persons.

AIM: Human lifestyle has drastically changed during the past century as the share of physical work in daily life has decreased. The purpose of the present study was to examine the distribution of myosin heavy chain (MHC) isoforms in middle-aged sedentary persons, to compare the proportion of MHC isoforms of middle-aged and young sedentary persons and to demonstrate the effect of physical activity of MHC isoforms in middle-aged sedentary persons. METHODS: Eighty-nine middle-aged sedentary and 13 young sedentary persons volunteered for the study. Thirty middle-aged sedentary subjects participated in strength-conditional exercise program during 9 months. Vertical jumping height and maximal anaerobic work capacity were measured. Muscle samples were taken from vastus lateralis muscle. MHC isoform composition was determined by SDS-PAGE. RESULTS: Variation of MHC I and MHC IIa isoforms in middle-age sedentary persons demonstrated normal distribution. Significant differences of MHC isoform proportions between middle-aged and young sedentary participants were not observed. The proportion of MHC IIx decreased significantly after the exercise period that significantly improved the maximal anaerobic power and jumping height of participants. CONCLUSIONS: Normal distribution illustrated the proportion of MHC I and MHC IIa isoforms in 89 middle-aged sedentary persons while significant differences of MHC isoforms proportion between young and middle-aged sedentary persons were not observed. Even small increase of physical activity improved physical performance and decrease the MHC IIx proportion of middle-aged sedentary persons. Physically active lifestyle in middle age, when age-related changes have not started yet, may delay age-related changes in skeletal muscle.

Role of skeletal muscle-fibre type in regulation of glucose metabolism in middle-aged subjects with impaired glucose tolerance during a long-term exercise and dietary intervention.

AIM: The aim of this study was to investigate the role of skeletal muscle fibre type in the regulation of glucose metabolism in middle-aged obese subjects with impaired glucose tolerance (IGT) during a 2-year exercise and dietary intervention. METHODS: Muscle biopsies (musculus vastus lateralis) were taken from 22 subjects belonging to the intervention group of the Finnish Diabetes Prevention Study [1]. According to their myosin heavy chain (MHC) profile at the baseline, the subjects were divided into two groups: IGT(slow) (n=10) with a high proportion of MHC I isoforms and IGT(fast) (n=12) with a high proportion of MHC II isoforms in the vastus lateralis muscle. The intervention consisted of dietary counselling, strength and power training and/or aerobic exercise. The amount of exercise was the same in both groups; the exercise frequency was 5.1+/-2.7 h/week in the IGT(slow) and 5.1+/-2.8 h/week in the IGT(fast) group. RESULTS: Fasting glucose (p<0.05), 2-h glucose (p<0.05), fasting insulin (p<0.05), haemoglobin A1c (HbA(1c)) (p<0.01) and insulin resistance (p<0.05) [homeostasis model assessment for insulin resistance (HOMA-IR)] decreased in the IGT(fast) group, whereas only the 2-h glucose and HbA(1c) concentrations decreased in the IGT(slow) group. The amount of the glycogen synthase kinase-3-alphabeta (GSK-3-alphabeta) decreased in the IGT(fast) group (p<0.05). Exercise training increased the lactate dehydrogenase (LDH) (p<0.01), LDH-1 (p<0.05) and citrate synthase (CS) (p<0.05) activities in the vastus lateralis muscle in the IGT(slow) group, but only the CS activity (p<0.05) in the IGT(fast) group. CONCLUSIONS: The glucose metabolism improved both in the IGT(slow) and IGT(fast) group during the 2-year exercise and dietary intervention. The change was more prominent in the IGT(fast) group than in the IGT(slow) group, associated with the decrease of the GSK-alphabeta protein expression in skeletal muscle. The exercise training improved both glycolytic and oxidative capacity in the vastus lateralis muscle. The glycolytic capacity improved in the IGT(slow) group and the oxidative capacity in both groups.

Leucine supplementation does not enhance acute strength or running performance but affects serum amino acid concentration.

This study described the effect of leucine supplementation on serum amino acid concentration during two different exercise sessions in competitive male power athletes. The subjects performed a strength exercise session (SES; n = 16; 26 +/- 4 years) or a maximal anaerobic running exercise session (MARE; n = 12; 27 +/- 5 years) until exhaustion twice at a 7-day interval. The randomized subjects consumed drinks containing leucine (100 mg x kg/body weight before and during SES or 200 mg x kg/body weight before MARE) or placebo. Blood specimens taken 10 min before (B) and after (A) the sessions were analyzed for serum amino acids. In SES the concentration of leucine was distinctly higher in the leucine supplemented group than in the placebo group in both B (p < 0.001) and A (p < 0.001) samples. The leucine concentration decreased in placebo but not in the leucine supplemented group following the exercise session. Isoleucine (p = 0.017) and valine (p = 0.006) concentration decreased more in the leucine supplemented group than in placebo in A samples. In MARE the concentration of leucine was higher in the leucine supplemented group than in placebo in both B (p < 0.001) and A (p < 0.001) samples and increased (p < 0.001) in the supplemented group following the session. Isoleucine (p = 0.020) and valine (p = 0.006) concentration decreased in the supplemented group in A samples. There were no differences in a counter movement jump after SES or in the running performance in MARE between the leucine supplemented group and placebo. These findings indicate that consuming leucine before or before and during exercise sessions results in changes in blood amino acid concentration. However, the supplementation does not affect an acute physical performance.

Neuromuscular adaptations during concurrent strength and endurance training versus strength training.

The purpose of this study was to investigate effects of concurrent strength and endurance training (SE) (2 plus 2 days a week) versus strength training only (S) (2 days a week) in men [SE: n=11; 38 (5) years, S: n=16; 37 (5) years] over a training period of 21 weeks. The resistance training program addressed both maximal and explosive strength components. EMG, maximal isometric force, 1 RM strength, and rate of force development (RFD) of the leg extensors, muscle cross-sectional area (CSA) of the quadriceps femoris (QF) throughout the lengths of 4/15-12/15 (L(f)) of the femur, muscle fibre proportion and areas of types I, IIa, and IIb of the vastus lateralis (VL), and maximal oxygen uptake (VO(2max)) were evaluated. No changes occurred in strength during the 1-week control period, while after the 21-week training period increases of 21% (p<0.001) and 22% (p<0.001), and of 22% (p<0.001) and 21% (p<0.001) took place in the 1RM load and maximal isometric force in S and SE, respectively. Increases of 26% (p<0.05) and 29% (p<0.001) occurred in the maximum iEMG of the VL in S and SE, respectively. The CSA of the QF increased throughout the length of the QF (from 4/15 to 12/15 L(f)) both in S (p<0.05-0.001) and SE (p<0.01-0.001). The mean fibre areas of types I, IIa and IIb increased after the training both in S (p<0.05 and 0.01) and SE (p<0.05 and p<0.01). S showed an increase in RFD (p<0.01), while no change occurred in SE. The average iEMG of the VL during the first 500 ms of the rapid isometric action increased (p<0.05-0.001) only in S. VO(2max) increased by 18.5% (p<0.001) in SE. The present data do not support the concept of the universal nature of the interference effect in strength development and muscle hypertrophy when strength training is performed concurrently with endurance training, and the training volume is diluted by a longer period of time with a low frequency of training. However, the present results suggest that even the low-frequency concurrent strength and endurance training leads to interference in explosive strength development mediated in part by the limitations of rapid voluntary neural activation of the trained muscles.

Effect of hyperoxia on metabolic responses and recovery in intermittent exercise.

The aim of the present study was to investigate whether the breathing of hyperoxic gas affects hemoglobin oxygen saturation (S(a)O(2)) and blood acidosis during intense intermittent exercise and recovery in sprint runners. The hypothesis was that the breathing of hyperoxic gas prevents S(a)O(2) from decreasing, delays blood acidosis during the exercise and improves the rate of heart rate recovery after the exercise. Nine sprinters ran three sets of 300 m at different velocities on a treadmill in normoxia (NOX) and in two hyperoxic conditions (ERHOX and RHOX; F(I)O(2) 0.40) in a randomized order. In ERHOX the inspired air was hyperoxic during the entire exercise and recovery and in RHOX the hyperoxic air was only inhaled during recovery periods. Blood pH and S(a)O(2) were measured from fingertip blood samples taken after each set of runs. The mean heart rate for the final 15 s of the last run in each set (HR(work)), the mean heart rate for the final 15 s of the first minute of recovery (HR(rec)) and the difference of HR(work) and HR(rec) (HR(dec)) were determined. In NOX, S(a)O(2) decreased from 95.0 +/- 2.0% to 88.7 +/- 2.0% (p < 0.001) but S(a)O(2) did not change in ERHOX (from 95.4 +/- 1.3% to 95.9 +/- 1.8%). A significant correlation was observed between the S(a)O(2) decrease in NOX and the effect of hyperoxia on blood pH in ERHOX (r = 0.63) and on HRdec in both ERHOX (r = 0.74) and RHOX (r = 0.69). We concluded that hemoglobin oxygen de-saturation occurred during intensive intermittent exercise in normoxia but hyperoxic gas during the exercise prevents S(a)O(2) from decreasing. Furthermore, the present results suggested that the beneficial effects of hyperoxia on heart rate recovery and blood acidosis during intensive intermittent exercise were related to hemoglobin de-saturation in normoxia.

Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia.

An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed the existence of a 'governor' in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle. In contrast, if the function of the heart or some other oxygen-sensitive organ is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxia compared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia.

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia.

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F(I)O2) has no effect on maximal cardiac output (Qcmax), although maximal oxygen uptake (VO2max) and exercise performance do vary along with F(I)O2. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (FI(O)2 = 0.150), normoxia (F(I)O2 = 0.209) and hyperoxia (F(I)O2=0.320). As expected, VO2max decreased in hypoxia [mean (SD) 3.58 (0.45)l.min(-1), P<0.05] and increased in hyperoxia [5.17 (0.34) l.min(-1), P<0.05] in comparison with normoxia [4.55 (0.32)l.min(-1)]. Similarly, maximal power (Wmax) decreased in hypoxia [334 (41) W, P< 0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, Qcmax was 25.99 (3.37) l.min(-1) in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l.min(-1) in normoxia and 30.13 (2.06)l.min(-1) in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in VO2max in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced Qcmax, (2) reduced Qcmax in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced Qcmax and VO2max in acute hypoxia may be the result rather than the cause of the reduced Wmax and skeletal muscle recruitment, thus supporting the existence of a central governor.

Heart rate during aerobics classes in women with different previous experience of aerobics.

This study measured heart rate during floor and step aerobic classes at three intensity levels. A group of 20 female occasional exercisers [mean age 33 (SD 8) years, mean body mass index 21 (SD 2) kg.m-2 volunteered to participate in six aerobic classes (three floor classes, three step classes) and in a laboratory test as members of one of two groups according to their prestudy regular participation in aerobics classes. Subjects in group A had participated four or more times a week and those of group B less than twice a week. The characteristics of the groups were as follows: group A, n = 10, mean maximal oxygen uptake (VO2max) 38.7 (SD 3.6) ml.kg-1.min-1, mean maximal heart rate (HRmax) 183 (SD 8) beats.min-1; group B, n = 10, VO2max 36.1 (SD 3.6) ml.kg-1.min-1, HRmax 178 (SD 7) beats.min-1. Each class consisted of a warm-up, a 20 min period of structured aerobic exercise (cardiophase) and a cool-down. The cardiophase was planned and guided as light, (rate of perceived exertion, RPE 11-12), moderate (RPE 13-14) or heavy (RPE 15-17) by an experienced instructor. The mean heart rates during the light classes were 72 (step) and 74 (floor) %HRmax in group A and 75 (step) and 79 (floor) %HRmax in group B; during the moderate classes, 84 (step) and 80 (floor) %HRmax in group A and 82 (step) and 83 (floor) %HRmax in group B, and during the heavy classes 89 (step and floor) %HRmax in group A and 88 (step) and 92 (floor) %HRmax in group B. Differences in heart rate and %HRmax were not statistically significant between the groups. However, differences in heart rate and %HRmax between the intensities (light vs moderate, moderate vs heavy and light vs heavy) were significant within both groups (all, P < 0.01). Based on the results, we conclude that intensity management during the aerobics classes was generally successful regardless of the participants' prior participation in aerobics. However, some individuals who were older and/or had less prior participation tended to exceed the targeted heart rate.

Muscle power factors and VO2max as determinants of horizontal and uphill running performance.

This study was carried out to investigate the importance of maximal oxygen uptake (VO2max) and so-called muscle power factors relating to neuromuscular and anaerobic characteristics as determinants of peak horizontal and uphill treadmill running velocity (Vmax). Muscle power factors were measured as peak velocity (VMART) and blood lactate concentration (BlaMART) in a maximal anaerobic running test and as maximal 30-m run velocity (V30m). Seven middle-distance runners, eight triathletes and eight cross-country skiers performed an incremental VO2max-test at horizontal (subscript max0) and 7 degrees uphill (subscript max7) and the MART at 3 degrees uphill on a treadmill and V30m-test on a track. The MART consisted of n x 20-s runs with a 100-s recovery between the runs and the velocity was increased by 0.41 m x s(-1) for each consecutive run until exhaustion. At 0 degrees Vmax was significantly higher but VO2max, ventilation and Bla were significantly lower than at 7 degrees inclination. Vmax0 correlated with VMART (r=0.85, P<0.001), Blamax0 (r=0.49, P<0.05) and V30m (r=0.78, P<0.001) but not with VO2max0. Vmax7 correlated with VO2max7 (r=0.78, P<0.001), VMART (r=0.61, P<0.01) and V30m (r=0.53, P<0.05). VMART correlated with BlaMART (r=0.71, P<0.01) and V30m (r=0.96, P<0.001) but not with VO2max0 or VO2max7. Middle-distance runners had a significantly (P<0.001) higher Vmax0, VMART BlaMART and V30m than triathletes and cross-country skiers, but no significant differences were found between the three groups in VO2max0, VO2max7 or Vmax7. We conclude that so-called muscle power factors, e.g. VMART, V30m and BlaMART, contribute to peak treadmill running performance and especially to horizontal running performance and that VO2max contributes more to uphill than horizontal running performance.

Acclimatization to altitude and normoxic training improve 400-m running performance at sea level.

To investigate the benefits of 'living high and training low' on anaerobic performance at sea level, eight 400-m runners lived for 10 days in normobaric hypoxia in an altitude house (oxygen content = 15.8%) and trained outdoors in ambient normoxia at sea level. A maximal anaerobic running test and 400-m race were performed before and within 1 week of living in the altitude house to determine the maximum speed and the speeds at different submaximal blood lactate concentrations (3, 5, 7, 10 and 13 mmol x l(-1)) and 400-m race time. At the same time, ten 400-m runners lived and trained at sea level and were subjected to identical test procedures. Multivariate analysis of variance indicated that the altitude house group but not the sea-level group improved their 400-m race time during the experimental period (P < 0.05). The speeds at blood lactate concentrations of 5-13 mmol x l(-1) tended to increase in the altitude house group but the response was significant only at 5 and 7 mmol x l(-1) (P < 0.05). Furthermore, resting blood pH was increased in six of the eight altitude house athletes from 0.003 to 0.067 pH unit (P < 0.05). The results of this study demonstrate improved 400-m performance after 10 days of living in normobaric hypoxia and training at sea level. Furthermore, the present study provides evidence that changes in the acid-base balance and lactate metabolism might be responsible for the improvement in sprint performance.