Body mass and V'O2 at rest affect gross efficiency during moderate-intensity cycling in untrained young healthy men: correlations with V'O2MAX.

Seventeen young healthy physically active males (age 23 ±3 years; body mass (BM) 72.5 ±7.9 kg; height 178 ±4 cm, (mean ±SD)), not specifically trained in cycling, participated in this study. The subjects performed two cycling incremental tests at the pedalling rate of 60 rev x min-1. The first test, with the power output (PO) increases of 30 W every 3 min, was to determine the maximal oxygen uptake (V'O2max) and the power output (PO) at V'O2max, while the second test (series of 6 minutes bouts of increasing intensity) was to determine energy expenditure (EE (V'O2)), gross efficiency (GE (V'O2/PO)) and delta efficiency (DE(ΔV'O2/DPO)) during sub-lactate threshold (LT) PO. V'O2max was 3.79 ±0.40 L x min-1 and the PO at V'O2max was 288 ±27 W. In order to calculate GE and DE the V'O2 was expressed in W, by standard calculations. GE measured at 30 W, 60 W, 90 W and 120 W was 11.6 ±1.4%, 17.0 ±1.4%, 19.6 ±1.2% and 21.4 ±1.1%, respectively. DE was 29.8 ±1.9%. The subjects' BM (range 59-87 kg) was positively correlated with V'O2 at rest (p<0.01) and with the intercept of the linear V'O2 vs. PO relationship (p<0.01), whereas no correlation was found between BM and the slope of V'O2 vs. PO. No correlation was found between BM and DE, whereas GE was negatively correlated with BM (p<0.01). GE was also negatively correlated with V'O2max and the PO at V'O2max (p<0.01). We conclude that: V'O2 at rest affects GE during moderate-intensity cycling and GE negatively corelates with V'O2max and the PO at V'O2max in young healthy men.

Characterization of age-dependent decline in spontaneous running performance in the heart failure Tgαq*44 mice.

In this study we characterize the impact of aging on the spontaneous running performance of the Tgαq*44 mice (transgenic murine model of chronic heart failure) as compared to the wild-type FVB mice. In 166 mice we have recorded the following parameters of their physical activities in the running wheels: the total distance covered during the experiment (Dsum), the maximal distance covered in single-effort (Dmax), mean time spent on running per 24 h (Tmean), mean running speed (νmean), the maximum instantaneous speed of run (νmax) and the number of efforts (i.e. the number of running events undertaken by the mice) during 54 days, in four age groups ~4, ~10, ~12 and ≥12.5 months of age. The level of spontaneous running performance of the FVB mice remained essentially unchanged, but a strong impact of aging in the Tgαq*44 mice on their running performance was found. Namely, the Dsum, Dmax, Tmean and νmean in the Tgαq*44 mice at the age of ≥12.5 months decreased by ~50%, when compared to its level corresponding level at the age of ~4 months, with far lesser effect of aging on their Vmax. Surprisingly, the number of attempts to perform running by the Tgαq*44 mice at the age of 4 - 12 months remained essentially unchanged. This suggests that the exercise intolerance of the aging heart failure (HF) mice seems to be more dependent on deterioration of heart and muscles function linked to HF than on a possible ageing-related impairment of the 'willngness' to initiate running, generated by the central nervous system.

Effect of pedaling rates and myosin heavy chain composition in the vastus lateralis muscle on the power generating capability during incremental cycling in humans.

In this study, we have determined power output reached at maximal oxygen uptake during incremental cycling exercise (P(I, max)) performed at low and at high pedaling rates in nineteen untrained men with various myosin heavy chain composition (MyHC) in the vastus lateralis muscle. On separate days, subjects performed two incremental exercise tests until exhaustion at 60 rev min(-1) and at 120 rev min(-1). In the studied group of subjects P(I, max) reached during cycling at 60 rev min(-1) was significantly higher (p=0.0001) than that at 120 rev min(-1) (287+/-29 vs. 215+/-42 W, respectively for 60 and 120 rev min(-1)). For further comparisons, two groups of subjects (n=6, each) were selected according to MyHC composition in the vastus lateralis muscle: group H with higher MyHC II content (56.8+/-2.79 %) and group L with lower MyHC II content in this muscle (28.6+/-5.8 %). P(I, max) reached during cycling performed at 60 rev min(-1) in group H was significantly lower than in group L (p=0.03). However, during cycling at 120 rev min(-1), there was no significant difference in P(I, max) reached by both groups of subjects (p=0.38). Moreover, oxygen uptake (VO(2)), blood hydrogen ion [H(+)], plasma lactate [La(-)] and ammonia [NH(3)] concentrations determined at the four highest power outputs completed during the incremental cycling performed at 60 as well as 120 rev min(-1), in the group H were significantly higher than in group L. We have concluded that during an incremental exercise performed at low pedaling rates the subjects with lower content of MyHC II in the vastus lateralis muscle possess greater power generating capabilities than the subjects with higher content of MyHC II. Surprisingly, at high pedaling rate, power generating capabilities in the subjects with higher MyHC II content in the vastus lateralis muscle did not differ from those found in the subjects with lower content of MyHC II in this muscle, despite higher blood [H(+)], [La(-)] and [NH(3)] concentrations. This indicates that at high pedaling rates the subjects with higher percentage of MyHC II in the vastus lateralis muscle perform relatively better than the subjects with lower percentage of MyHC II in this muscle.

Non-linear relationship between oxygen uptake and power output in the Astrand nomogram-old data revisited.

For the last decade there have been considerable discussion concerning the linearity / non-linearity of the oxygen uptake (V(O2)) - power output (W) relationship with strong experimental evidence of non-linearity provided mainly by breath-by-breath measurements. In this study, we attempted to answer the question whether the V(O2) - W relationship in the Astrand nomogram, as presented in the Textbook of Work Physiology, P.-O. Astrand et al. (2003), page 281, based on the Douglas bag method, is indeed linear, as stated by the authors before, or if a change point in V(O2), described by Zoladz et al. (1998) Eur J Appl Physiol 78: 369-377, can possibly be detected in those data. The V(O2) - W data were taken from the Astrand nomogram referenced above and from the Table 9.5 on page 282 in the same reference and tested for the presence of the change point in V(O2), using our two-phase model (see the reference above). In the first phase, a linear V(O2) - W relationship was assumed, whereas in the second one (above the so-called change point) an additional increase in V(O2) above the values expected from the linear model was allowed. It was found that in the data taken from the Astrand nomogram (data for men), as well as in the data taken from the Table 9.5, statistically significant change points in V(O2) were present at the power output of 150 W. The documentation of the presence of a change point in the V(O2) - W relationship in the Astrand data provides further evidence for the existence of a non-linearity in the V(O2) - W relationship in incremental exercise tests of humans, also in V(O2) data based upon the Douglas bag method.

High content of MYHC II in vastus lateralis is accompanied by higher VO2/power output ratio during moderate intensity cycling performed both at low and at high pedalling rates.

The aim of this study was to examine the relationship between the content of various types of myosin heavy chain isoforms (MyHC) in the vastus lateralis muscle and pulmonary oxygen uptake during moderate power output incremental exercise, performed at low and at high pedalling rates. Twenty one male subjects (mean +/- SD) aged 24.1 +/- 2.8 years; body mass 72.9 +/- 7.2 kg; height 179.1 +/- 4.8 cm; BMI 22.69 +/- 1.89 kg.m(-2); VO2max 50.6 +/- 5.3 ml.kg.min(-1), participated in this study. On separate days, they performed two incremental exercise tests at 60 rev.min(-1) and at 120 rev.min(-1), until exhaustion. Gas exchange variables were measured continuously breath by breath. Blood samples were taken for measurements of plasma lactate concentration prior to the exercise test and at the end of each step of the incremental exercise. Muscle biopsies were taken from the vastus lateralis muscle, using Bergström needle, and they were analysed for the content of MyHC I and MyHC II using SDS--PAGE and two groups (n=7, each) were selected: group H with the highest content of MyHC II (60.7 % +/- 10.5 %) and group L with the lowest content of MyHC II (27.6 % +/- 6.1 %). We have found that during incremental exercise at the power output between 30-120 W, performed at 60 rev.min(-1), oxygen uptake in the group H was significantly greater than in the group L (ANCOVA, p=0.003, upward shift of the intercept in VO2/power output relationship). During cycling at the same power output but at 120 rev.min(-1), the oxygen uptake was also higher in the group H, when compared to the group L (i.e. upward shift of the intercept in VO2/power output relationship, ANCOVA, p=0.002). Moreover, the increase in pedalling rate from 60 to 120 rev.min(-1) was accompanied by a significantly higher increase of oxygen cost of cycling and by a significantly higher plasma lactate concentration in subjects from group H. We concluded that the muscle mechanical efficiency, expressed by the VO2/PO ratio, during cycling in the range of power outputs 30-120 W, performed at 60 as well as 120 rev.min(-1), is significantly lower in the individuals with the highest content of MyHC II, when compared to the individuals with the lowest content of MyHC II in the vastus lateralis.

Change point in VCO2 during incremental exercise test: a new method for assessment of human exercise tolerance.

The main purpose of this study was to present a new method to determine the level of power output (PO) at which VCO2 during incremental exercise test (IT) begins to rise non-linearly in relation to power output (PO) - the change point in VCO2 (CP-VCO2). Twenty-two healthy non-smoking men (mean +/- SD: age 22.0 +/- 0.9 years; body mass 74.5 +/- 7.5 kg; height 181 +/- 7 cm; VO2max 3.753 +/- 0.335 l min-1) performed an IT on a cycloergometer. The IT started at a PO of 30 W, followed by gradual increases of 30 W every 3 min. Antecubital venous blood samples were taken at the end of each step and analysed for plasma lactate concentration [La]pl, blood PO2, PCO2 [HCO3-]b and [H+]b. In the detection of the change-point VCO2 (CP-VCO2), a two-phase model was assumed for the 'third-minute-data' of each step of the test. In the first phase, a linear relationship between VCO2 and PO was assumed, whereas in the second, an additional increase in VCO2 was allowed, above the values expected from the linear model. The PO at which the first phase ends is called the change point in VCO2. The identification of the model consists of two steps: testing for the existence of the change point, and estimating its location. Both procedures are based on suitably normalized recursive residuals (see Zoladz et al. 1998a. Eur J Appl Physiol 78, 369-377). In the case of each of our subjects it was possible to detect the CP-VCO2 and the CP-VO2 as described in our model. The PO at the CP-VCO2 amounted to 134 +/- 42 W. The CP- VO2 was detected at 136 +/- 32 W, whereas the PO at the LT amounted to 128 +/- 30 W and corresponded to 49 +/- 11, 49 +/- 8 and 47 +/- 8.6% VO2max, respectively, for the CP-VCO2, CP-VO2 and the LT. The [La]pl at the CP-VCO2 (2.65 +/- 0.76 mmol L-1), at the CP-VO2 (2.53 +/- 0. 56 mmol L-1) and at the LT (2.25 +/- 0.49 mmol L-1) were already significantly higher (P < 0.01, Students t-test) than the value reached at rest (1.86 +/- 0.43 mmol L-1). Our study illustrates that the CP-VCO2 and the CP-VO2 occur at a very similar power output as the LT. We therefore postulate that the CP-VCO2 and the CP-VO2 be applied as an additional criterion to assess human exercise tolerance.

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance.

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (VO2) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (VO2max) 3.726 (SD 0.363) l x min(-1)], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev x min(-1). The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]pl, partial pressure of O2 and CO2 and hydrogen ion concentration [H+]b. The lactate threshold (LT) in this study was defined as the highest power output above which [La-]pl showed a sustained increase of more than 0.5 mmol x l(-1) x step(-1). The VO2 was measured breath-by-breath. In the analysis of the change point (CP) of VO2 during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: Xi = at(i) + b + epsilon(i) for i = 1,2, ..., T, and E(Xi) > at(i) + b for i = T + 1, ..., n, where X1, ..., Xn are independent and epsilon(i) approximately N(0, sigma2). In the first phase, a linear relationship between VO2 and power output was assumed, whereas in the second phase an additional increase in VO2 above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-VO2). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-VO2 as described in our model. The power output at CP-VO2 amounted to 136.8 (SD 31.3) W. It was only 11 W -- non significantly -- higher than the power output corresponding to LT. The VO2 at CP-VO2 amounted to 1.828 (SD 0.356) l x min(-1) was [48.9 (SD 7.9)% VO2max]. The [La-]pl at CP-VO2, amounting to 2.57 (SD 0.69) mmol x l(-1) was significantly elevated (P < 0.01) above the resting level [1.85 (SD 0.46) mmol x l(-1)], however the [H+]b at CP-VO2 amounting to 45.1 (SD 3.0) nmol x l(-1), was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol x l(-1). An increase of power output of 30 W above CP-VO2 was accompanied by a significant increase in [H+]b above the resting level (P = 0.03).