Differences in swimming smoothness between elite and non-elite swimmers.

The aim of the study was to investigate whether jerk cost (JC) can discriminate between swimming levels. Nine elite and nine non-elite swimmers swam a 50-m front-crawl sprint wearing a 3D accelerometer on their back between the inferior angles of the scapulae. Lap times and JC were calculated from the acceleration signal and compared between groups and between swimmers within a group. The elite swimmers swam significantly faster lap times than the non-elite swimmers (p < 0.001). They did so with significantly lower levels of JC compared to the non-elite swimmers (p = 0.005). Furthermore, a stepwise multiple linear regression showed JC accounted for 32.9% of the variation in lap time of the elite swimmers. These results indicate that it is possible to discriminate elite from non-elite swimmers using JC: elite swimmers swim with lower JCs than non-elite swimmers. Additionally, swimming at higher speed is associated with more accelerations and decelerations in both elite and non-elite swimmers, which is reflected by higher JCs and lower smoothness. In sum, JC provides an index of swimming technique that is easy to use in training practice.

Heart-Rate Recovery After Warm-up in Swimming: A Useful Predictor of Training Heart-Rate Response?

For training to be optimal, daily training load has to be adapted to the momentary status of the individual athlete, which is often difficult to establish. Therefore, the current study investigated the predictive value of heart-rate recovery (HRR) during a standardized warm-up for training load. Training load was quantified by the variation in heart rate during standardized training in competitive swimmers. Eight female and 5 male Dutch national-level swimmers participated in the study. They all performed 3 sessions consisting of a 300-m warm-up test and a 10 × 100-m training protocol. Both protocols were swum in front crawl at individually standardized velocities derived from an incremental step test. Velocity was related to 75% and 85% heart-rate reserve (% HRres) for the warm-up and training, respectively. Relative HRR during the first 60 s after the warm-up (HRRw-up) and differences between the actual and intended heart rate for the warm-up and the training (ΔHRw-up and ΔHRtr) were determined. No significant relationship between HRRw-up and ΔHRtr was found (F1,37 = 2.96, P = .09, R2 = .07, SEE = 4.65). There was considerable daily variation in ΔHRtr at a given swimming velocity (73-93% HRres). ΔHRw-up and ΔHRtr were clearly related (F1,37 = 74.31, P < .001, R2 = .67, SEE = 2.78). HRR after a standardized warm-up does not predict heart rate during a directly subsequent and standardized training session. Instead, heart rate during the warm-up protocol seems a promising alternative for coaches to make daily individual-specific adjustments to training programs.

The effect of intermittent hypobaric hypoxic exposure and sea level training on submaximal economy in well-trained swimmers and runners.

To evaluate the effect of intermittent hypobaric hypoxia combined with sea level training on exercise economy, 23 well-trained athletes (13 swimmers, 10 runners) were assigned to either hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normobaric normoxia (0-500 m) in a randomized, double-blind design. Both groups rested in a hypobaric chamber 3 h/day, 5 days/wk for 4 wk. Submaximal economy was measured twice before (Pre) and after (Post) the treatment period using sport-specific protocols. Economy was estimated both from the relationship between oxygen uptake (V(.-)o2) and speed, and from the absolute V(.-)o2 at each speed using sport-specific protocols. V(.-)o2 was measured during the last 60 s of each (3-4 min) stage using Douglas bags. Ventilation (V(.-)E), heart rate (HR), and capillary lactate concentration ([La(-)]) were measured during each stage. Velocity at maximal V(.-)o2 (velocity at V(.-)o2max) was used as a functional indicator of changes in economy. The average V(.-)o2 for a given speed of the Pre values was used for Post test comparison using a two-way, repeated-measures ANOVA. Typical error of measurement of V(.-)o2 was 4.7% (95% confidence limits 3.6-7.1), 3.6% (2.8-5.4), and 4.2% (3.2-6.9) for speeds 1, 2, and 3, respectively. There was no change in economy within or between groups (ANOVA interaction P = 0.28, P = 0.23, and P = 0.93 for speeds 1, 2, and 3). No differences in submaximal HR, [La-], Ve, or velocity at V(.-)o2(max) were found between groups. It is concluded that 4 wk of intermittent hypobaric hypoxia did not improve submaximal economy in this group of well-trained athletes.

Performance of runners and swimmers after four weeks of intermittent hypobaric hypoxic exposure plus sea level training.

This double-blind, randomized, placebo-controlled trial examined the effects of 4 wk of resting exposure to intermittent hypobaric hypoxia (IHE, 3 h/day, 5 days/wk at 4,000-5,500 m) or normoxia combined with training at sea level on performance and maximal oxygen transport in athletes. Twenty-three trained swimmers and runners completed duplicate baseline time trials (100/400-m swims, or 3-km run) and measures for maximal oxygen uptake (VO(2max)), ventilation (VE(max)), and heart rate (HR(max)) and the oxygen uptake at the ventilatory threshold (VO(2) at VT) during incremental treadmill or swimming flume tests. Subjects were matched for sex, sport, performance, and training status and divided randomly between hypobaric hypoxia (Hypo, n = 11) and normobaric normoxia (Norm, n = 12) groups. All tests were repeated within the first (Post1) and third weeks (Post2) after the intervention. Time-trial performance did not improve in either group. We could not detect a significant difference between groups for a change in VO(2max), VE(max), HR(max), or VO(2) at VT after the intervention (group x test interaction P = 0.31, 0.24, 0.26, and 0.12, respectively). When runners and swimmers were considered separately, Hypo swimmers appeared to increase VO(2max) (+6.2%, interaction P = 0.07) at Post2 following a precompetition taper and increased VO(2) at VT (+8.9 and +12.1%, interaction P = 0.007 and 0.006, at Post1 and Post2). We conclude that this "dose" of IHE was not sufficient to improve performance or oxygen transport in this heterogeneous group of athletes. Whether there are potential benefits of this regimen for specific sports or training/tapering strategies may require further study.

Intermittent hypobaric hypoxia exposure does not cause sustained alterations in autonomic control of blood pressure in young athletes.

Intermittent hypoxia (IH), which refers to the discontinuous use of hypoxia to reproduce some key features of altitude acclimatization, is commonly used in athletes to improve their performance. However, variations of IH are also used as a model for sleep apnea, causing sustained sympathoexcitation and hypertension in animals and, thus, raising concerns over the safety of this model. We tested the hypothesis that chronic IH at rest alters autonomic control of arterial pressure in healthy trained individuals. Twenty-two young athletes (11 men and 11 women) were randomly assigned to hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normoxia (500 m) in a double-blind and placebo-controlled design. Both groups rested in a hypobaric chamber for 3 h/day, 5 days/wk for 4 wk. In the sitting position, resting hemodynamics, including heart rate (HR), blood pressure (BP), cardiac output (Q(c), C(2)H(2) rebreathing), stroke volume (SV = Q(c)/HR), and total peripheral resistance (TPR = mean BP/Q(c)), were measured, dynamic cardiovascular regulation was assessed by spectral and transfer function analysis of cardiovascular variability, and cardiac-vagal baroreflex function was evaluated by a Valsalva maneuver, twice before and 3 days after the last chamber exposure. We found no significant differences in HR, BP, Q(c), SV, TPR, cardiovascular variability, or cardiac-vagal baroreflex function between the groups at any time. These results suggest that exposure to intermittent hypobaric hypoxia for 4 wk does not cause sustained alterations in autonomic control of BP in young athletes. In contrast to animal studies, we found no secondary evidence for sustained physiologically significant sympathoexcitation in this model.

Effect of fatigue on stroking characteristics in an arms-only 100-m front-crawl race.

PURPOSE: Race analyses during swimming provide information on the time-dependent values of, among other variables, a swimmer's clean swimming speed (v), stroke rate (SR), and stroke length (SL). The effect of fatigue on changes in v, SR, and SL was investigated. METHODS: Lap-averaged values of v, SR, and SL while swimming 100 m all out with arms only (trial 1) were related to the decline in mechanical power output measured during an all-out 100-m swim on the MAD system (trial 2), with legs immobilized in both trials. RESULTS: Swimming a 100-m front-crawl sprint using arms only led to a significant 24% decrease in lap-averaged mechanical power output (from 200 to 153 W, P < 0.01). This reduction in power-generating capacity led to a 12.4% decrease in v when lap 1 was compared with lap 4 (from 1.69 to 1.48 m x s(-1), P < 0.01). SR declined throughout the race by 10.6% from 0.85 Hz (lap 1) to 0.76 Hz (lap 4, P < 0.05). Analysis revealed that this decrease in SR was linearly related to the decrease in v. The reduction in SR reflected the reduced propulsive force required to overcome the v-dependent, and therefore lower, drag. CONCLUSION: Decreases in swimming speed throughout a 100-m front-crawl race are the result of decreases in the power-producing capacity of the swimmer (fatigue). This fatigue-induced reduction in swimming speed will lead to a reduction in drag. The SR seems to be accommodated to this reduced power output capacity and concomitant diminished propulsion requirements.

Increased serum erythropoietin but not red cell production after 4 wk of intermittent hypobaric hypoxia (4,000-5,500 m).

This study tested the hypothesis that athletes exposed to 4 wk of intermittent hypobaric hypoxia exposure (3 h/day, 5 days/wk at 4,000-5,500 m) or double-blind placebo increase their red blood cell volume (RCV) and hemoglobin mass (Hbmass) secondary to an increase in erythropoietin (EPO). Twenty-three collegiate level athletes were measured before (Pre) and after (Post) the intervention for RCV via Evans blue (EB) dye and in duplicate for Hbmass using CO rebreathing. Hematological indexes including EPO, soluble transferrin receptor, and reticulocyte parameters were measured on 8-10 occasions spanning the intervention. The subjects were randomly divided among hypobaric hypoxia (Hypo, n = 11) and normoxic (Norm, n = 12) groups. Apart from doubling EPO concentration 3 h after hypoxia there was no increase in any of the measures for either Hypo or Norm groups. The mean change in RCV from Pre to Post for the Hypo group was 2.3% (95% confidence limits = -4.8 to 9.5%) and for the Norm group was -0.2% (-5.7 to 5.3%). The corresponding changes in Hbmass were 1.0% (-1.3 to 3.3%) for Hypo and -0.3% (-2.6 to 3.1%) for Norm. There was good agreement between blood volume (BV) from EB and CO: EB BV = 1.03 x CO BV + 142, r2 = 0.85, P < 0.0001. Overall, evidence from four independent techniques (RCV, Hbmass, reticulocyte parameters, and soluble transferrin receptor) suggests that intermittent hypobaric hypoxia exposure did not accelerate erythropoiesis despite the increase in serum EPO.