We investigated the time course of RR interval variability during exercise and subsequent 50 minutes of recovery in seven well-trained male cyclists who performed an exercise with 3 successive 8 min stages at 40 %, 70 % and 90 % of their maximal oxygen uptake. The goal of the study was to check whether the decrease in the amplitude of heart rate variability during heavy exercise was accompanied by changes in the chaotic structure of the fluctuations. Heart rate variability was analysed in the temporal and frequency domain using traditional tools and using non-linear methods (Largest Lyapunov Exponent, Detrended Fluctuation Analysis, Minimum Embedding Dimension). When compared to rest, variability at the heaviest exercise intensity was significantly lower (RR: 0.94 +/- 0.22 vs. 0.34 +/- 0.01 ms; SDRR: 0.11 +/- 0.04 vs. 0.01 +/- 0.00 ms) due to a decrease in both LF (2101 +/- 1450 vs. 0.14 +/- 0.09 ms (2) . Hz (-1)) and HF spectral energy (1148 +/- 1126 vs. 7.88 +/- 9.24 ms (2) . Hz (-1)). Non-linear analyses showed that heart rate variability remained chaotic whatever the exercise intensity (the largest Lyapunov exponent was positive at 90 % of the maximal oxygen uptake), with a fractal organisation that tended towards white noise (DFA value close to 0.5) during heavy exercise. During recovery, temporal and spectral variables came back to their rest values within about 30 minutes following an exponential pattern. Non-linear analyses revealed that heartbeat dynamics were disorganised at the beginning of recovery, and involved more regulating systems than at rest, even after 50 minutes of recovery. We concluded that, during heavy exercise, heart rate variability was mainly influenced by other factors than autonomous nervous system, and suggest that mechanical or neurological couplings between the cardiac, locomotor and respiratory systems could play an important part in the observed changes.

Inflammatory abnormalities may be involved in the inadequate basal oxidant/antioxidant balance and local exercise-induced oxidative stress in chronic obstructive pulmonary disease (COPD) patients.The time course of oxidative stress and inflammation was investigated in 10 COPD patients and seven healthy subjects before and after local dynamic quadriceps endurance exercise at 40% of maximal strength. Venous samples were collected before, immediately after and up to 48 h after exercise.At rest, levels of an oxidant released by stimulated phagocytes, the superoxide anion, were significantly higher in patients, as were plasma levels of C-reactive protein, tumour necrosis factor-a and interleukin-6, inflammatory markers. An inverse relationship was found between baseline C-reactive protein levels and endurance time in patients. Six hours after exercise, superoxide anion release and levels of protein oxidation products, an index of oxidative stress, increased similarly in both groups, whereas thiobarbituric acid reactive substance levels, another index of oxidative stress, increased significantly only in patients. Plasma nonenzymatic antioxidant and inflammatory cytokine levels were unchanged by the exercise protocol.The increased baseline systemic inflammation in chronic obstructive pulmonary disease patients could be related to disturbed oxidant/antioxidant balance, and, together, these may have triggered the exercise-induced oxidative stress. The absence, however, of local exercise-induced systemic inflammation suggests that additional mechanisms explain local exercise-induced oxidative stress.

The aim of the present study was to determine the effects of 40 km of cycling on the biomechanical and cardiorespiratory responses measured during the running segment of a classic triathlon, with particular emphasis on the time course of these responses. Seven male triathletes underwent four successive laboratory trials: (1) 40 km of cycling followed by a 10-km triathlon run (TR), (2) a 10-km control run (CR) at the same speed as TR, (3) an incremental treadmill test, and (4) an incremental cycle test. The following ventilatory data were collected every minute using an automated breath-by-breath system: pulmonary ventilation VE, l x min[-1]), oxygen uptake (VO2, ml x min(-1) x kg[-1]), carbon dioxide output (ml x min[-1]), respiratory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2), respiratory exchange ratio (R) respiratory frequency (f, breaths x min[-1]), and tidal volume (ml). Heart rate (HR, beats x min[-1]) was monitored using a telemetric system. Biomechanical variables included stride length (SL) and stride frequency (SF) recorded on a video tape. The results showed that the following variables were significantly higher (analysis of variance, P < 0.05) for TR than for CR: VO2 [51.7 (3.4) vs 48.3 (3.9) ml x kg(-1) x min(-1), respectively], VE [100.4 (1.4) l x min(-1) vs 84.4 (7.0) l x min(-1)], VE/VO2 [24.2 (2.6) vs 21.5 (2.7)] VE/VCO2 [25.2 (2.6) vs 22.4 (2.6)], f[55.8 (11.6) vs 49.0 (12.4) breaths x min(-1)] and HR [175 (7) vs 168 (9) beats x min(-1)]. Moreover, the time needed to reach steady-state was shorter for HR and VO2 (1 min and 2 min, respectively) and longer for VE (7 min). In contrast, the biomechanical parameters, i.e. SL and SF, remained unchanged throughout TR versus CR. We conclude that the first minutes of the run segment after cycling in an experimental triathlon were specific in terms of VO2 and cardiorespiratory variables, and nonspecific in terms of biomechanical variables.

The aim of this study was to determine the physiological profile of young triathletes who began triathlon competition as their first sport. Twenty-nine male competitive triathletes (23 regionally and nationally ranked triathletes and 6 elite, internationally ranked triathletes) performed two tests, one on a cycle ergometer (CE VO2max) and one on a treadmill (TM VO2max). Results showed (a) no difference between CE VO2max and TM VO2max in the triathletes (69.1 +/- 7.2 vs. 70.2 +/- 6.2 mL x kg(-1) x min(-1), respectively), (b) values of CE VO2max and TM VO2max in elite triathletes (75.9 +/- 5.2 and 78.5 +/- 3.6 mL x kg(-1) x min(-1), respectively) that were comparable to those reported in elite single-sport athletes in these specialities, and (c) although the ventilatory threshold (Th(vent)) was similar in CE and TM, TM Th(vent) was consistently lower for triathletes than TM Th(vent) usually reported for runners.

The purpose of this study was to determine the effects of age in relation to anthropometric characteristics upon maximal anaerobic power of legs in sixty-nine young boys aged 11 to 19 years. Maximal anaerobic power (Wmax) was measured by the force-velocity test. Lean body mass (LBM) was determined from all four skin-fold thickness measurements, leg volume (LV) was estimated by anthropometric method, and anthropometric measurements were used to determine total muscular mass (TMM). Wmax increased significantly (F = 44.1, p less than 0.001) between 11 and 19 years and was correlated with LV (r = 0.84) and TMM (r = 0.88). It was most highly correlated with LBM (r = 0.94), which best explained the percentage of the total variance of Wmax (88%). Normalized Wmax (Wmax/LBM) also increased significantly between 11 and 19 years (F = 21.9, p less than 0.001). In conclusion, Wmax determined by the force-velocity test was closely related to anthropometric characteristics, especially LBM, during the growth period. Furthermore, even when corrected for lean body mass, maximal anaerobic power was always found to increase. This suggests that other undetermined factors, in addition to the amount of lean tissue mass, may explain the increase of Wmax during the force-velocity test.