Journal: European journal of applied physiology
To assess the validity of RR intervals and short-term heart rate variability (HRV) data obtained from the Polar V800 heart rate monitor, in comparison to an electrocardiograph (ECG).
To compare the effects of a periodic resistance training (PTR) program with those of a continuous resistance training (CTR) program on muscle size and function, 14 young men were randomly divided into a CTR group and a PTR group. Both groups performed high-intensity bench press exercise training [75 % of one repetition maximum (1-RM); 3 sets of 10 reps] for 3 days per week. The CTR group trained continuously over a 24-week period, whereas the PTR group performed three cycles of 6-week training (or retraining), with 3-week detraining periods between training cycles. After an initial 6 weeks of training, increases in cross-sectional area (CSA) of the triceps brachii and pectoralis major muscles and maximum isometric voluntary contraction of the elbow extensors and 1-RM were similar between the two groups. In the CTR group, muscle CSA and strength gradually increased during the initial 6 weeks of training. However, the rate of increase in muscle CSA and 1-RM decreased gradually after that. In the PTR group, increase in muscle CSA and strength during the first 3-week detraining/6-week retraining cycle were similar to that in the CTR group during the corresponding period. However, increase in muscle CSA and strength during the second 3-week detraining/6-week retraining cycle were significantly higher in the PTR group than in the CTR group. Thus, overall improvements in muscle CSA and strength were similar between the groups. The results indicate that 3-week detraining/6-week retraining cycles result in muscle hypertrophy similar to that occurring with continuous resistance training after 24 weeks.
Recent studies have suggested that dietary inorganic nitrate (NO(3) (-)) supplementation may improve muscle efficiency and endurance exercise tolerance but possible effects during team sport-specific intense intermittent exercise have not been examined. We hypothesized that NO(3) (-) supplementation would enhance high-intensity intermittent exercise performance. Fourteen male recreational team-sport players were assigned in a double-blind, randomized, crossover design to consume 490 mL of concentrated, nitrate-rich beetroot juice (BR) and nitrate-depleted placebo juice (PL) over ~30 h preceding the completion of a Yo-Yo intermittent recovery level 1 test (Yo-Yo IR1). Resting plasma nitrite concentration ([NO(2) (-)]) was ~400 % greater in BR compared to PL. Plasma [NO(2) (-)] declined by 20 % in PL (P < 0.05) and by 54 % in BR (P < 0.05) from pre-exercise to end-exercise. Performance in the Yo-Yo IR1 was 4.2 % greater (P < 0.05) with BR (1,704 ± 304 m) compared to PL (1,636 ± 288 m). Blood [lactate] was not different between BR and PL, but the mean blood [glucose] was lower (3.8 ± 0.8 vs. 4.2 ± 1.1 mM, P < 0.05) and the rise in plasma [K(+)] tended to be reduced in BR compared to PL (P = 0.08). These findings suggest that NO(3) (-) supplementation may promote NO production via the nitrate-nitrite-NO pathway and enhance Yo-Yo IR1 test performance, perhaps by facilitating greater muscle glucose uptake or by better maintaining muscle excitability. Dietary NO(3) (-) supplementation improves performance during intense intermittent exercise and may be a useful ergogenic aid for team sports players.
The evaluation of rate of force development during rapid contractions has recently become quite popular for characterising explosive strength of athletes, elderly individuals and patients. The main aims of this narrative review are to describe the neuromuscular determinants of rate of force development and to discuss various methodological considerations inherent to its evaluation for research and clinical purposes. Rate of force development (1) seems to be mainly determined by the capacity to produce maximal voluntary activation in the early phase of an explosive contraction (first 50-75 ms), particularly as a result of increased motor unit discharge rate; (2) can be improved by both explosive-type and heavy-resistance strength training in different subject populations, mainly through an improvement in rapid muscle activation; (3) is quite difficult to evaluate in a valid and reliable way. Therefore, we provide evidence-based practical recommendations for rational quantification of rate of force development in both laboratory and clinical settings.
Regular exercise protects against degenerative joint disorders, yet the mechanisms that underlie these benefits are poorly understood. Chronic, low-grade inflammation is widely implicated in the onset and progression of degenerative joint disease.
The aim of the present study was to test the hypothesis that consuming protein does not attenuate AMPK signalling when exercise is commenced in a glycogen-depleted state. After performing a glycogen-depleting protocol the evening before, the subsequent morning ten active men performed 45 min steady-state cycling at 50 % of peak power output (PPO) followed by an exercise capacity test (1-min intervals at 80 % PPO interspersed with 1-min periods at 40 % PPO). In a repeated measures design, subjects consumed 20 g of a casein hydrolysate solution (PRO) 45 min before exercise, 10 g during and a further 20 g immediately post-exercise, or an equivalent volume of a non-calorie taste matched placebo (PLA). Resting (PRO = 134 ± 29; PLA = 136 ± 28 mmol kg(-1)) and post-exercise muscle glycogen (PRO = 43 ± 16; PLA = 47 ± 18 mmol kg(-1)) was not different (P > 0.05) between trials nor was exercise capacity (PRO = 26 ± 9; PLA = 25 ± 10 min, P > 0.05). Phosphorylation of AMPK(Thr172) increased threefold immediately post-exercise (P < 0.05) and PGC1-mRNA increased sixfold at 3 h post-exercise (P < 0.05), though there were no differences between conditions (P > 0.05). In contrast, there was a trend (P = 0.08) for a divergent response in eEF2(Thr56) phosphorylation such that 1.5 fold increases post- and 3 h post-exercise in PLA were blunted with PRO, thus indicative of greater eEF2 activation. We conclude that athletes who deliberately incorporate training phases with reduced muscle glycogen into their training programmes may consume protein before, during and after exercise without negating signalling through the AMPK cascade.
We investigated the effects of a 3-week dietary periodization on immunity and sleep in triathletes.
This study was designed to examine whether concurrent sprint interval and strength training (CT) would result in compromised strength development when compared to strength training (ST) alone. In addition, maximal oxygen consumption (VO2max) and time to exhaustion (TTE) were measured to determine if sprint interval training (SIT) would augment aerobic performance.
The aim of this longitudinal study was to compare two recovery modes (active vs. passive) during a seven-week high-intensity interval training program (SWHITP) aimed to improve maximal oxygen uptake ([Formula: see text]), maximal aerobic velocity (MAV), time to exhaustion (t (lim)) and time spent at a high percentage of [Formula: see text], i.e., above 90 % (t90 [Formula: see text]) and 95 % (t95 [Formula: see text]) of [Formula: see text]. Twenty-four adults were randomly assigned to a control group that did not train (CG, n = 6) and two training groups: intermittent exercise (30 s exercise/30 s recovery) with active (IE(A), n = 9) or passive recovery (IE(P), n = 9). Before and after seven weeks with (IE(A) and IE(P)) or without (CG) high-intensity interval training (HIT) program, all subjects performed a maximal graded test to determine their [Formula: see text] and MAV. Subsequently only the subjects of IE(A) and IE(P) groups carried out an intermittent exercise test consisting of repeating as long as possible 30 s intensive runs at 105 % of MAV alternating with 30 s active recovery at 50 % of MAV (IE(A)) or 30 s passive recovery (IE(P)). Within IE(A) and IE(P), mean t (lim) and MAV significantly increased between the onset and the end of the SWHITP and no significant difference was found in t90 VO(2max) and t95 VO(2max). Furthermore, before and after the SWHITP, passive recovery allowed a longer t (lim) for a similar time spent at a high percentage of VO(2max). Finally, within IE(A), but not in IE(P), mean VO(2max) increased significantly between the onset and the end of the SWHITP both in absolute (p < 0.01) and relative values (p < 0.05). In conclusion, our results showed a significant increase in VO(2max) after a SWHITP with active recovery in spite of the fact that t (lim) was significantly longer (more than twice longer) with respect to passive recovery.
The purpose of this study was to estimate the percentage of the increase in whole body maximal oxygen consumption ([Formula: see text]O(2max)) that is accounted for by increased respiratory muscle oxygen uptake after altitude training. Six elite male distance runners ([Formula: see text]O(2max) = 70.6 ± 4.5 ml kg(-1) min(-1)) and one elite female distance runner ([Formula: see text]O(2max) = 64.7 ml kg(-1) min(-1)) completed a 28-day “live high-train low” training intervention (living elevation, 2,150 m). Before and after altitude training, subjects ran at three submaximal speeds, and during a separate session, performed a graded exercise test to exhaustion. A regression equation derived from published data was used to estimate respiratory muscle [Formula: see text]O(2) ([Formula: see text]O(2RM)) using our ventilation ([Formula: see text] (E)) values. [Formula: see text]O(2RM) was also estimated retrospectively from a larger group of distance runners (n = 22). [Formula: see text]O(2max) significantly (p < 0.05) increased from pre- to post-altitude (196 ± 59 ml min(-1)), while [Formula: see text] (E) at [Formula: see text]O(2max) also significantly (p < 0.05) increased (13.3 ± 5.3 l min(-1)). The estimated [Formula: see text]O(2RM) contributed 37 % of Δ[Formula: see text]O(2max). The retrospective group also saw a significant increase in [Formula: see text]O(2max) from pre- to post-altitude (201 ± 36 ml min(-1)), along with a 10.8 ± 2.1 l min(-1) increase in [Formula: see text] (E), thus requiring an estimated 27 % of Δ[Formula: see text]O(2max). Our data suggest that a substantial portion of the improvement in [Formula: see text]O(2max) with chronic altitude training goes to fuel the respiratory muscles as opposed to the musculature which directly contributes to locomotion. Consequently, the time-course of decay in ventilatory acclimatization following return to sea-level may have an impact on competitive performance.