Michael Leveritt

Concurrent strength and endurance training: A review

AbstractConcurrent strength and endurance training appears to inhibit strength development when compared with strength training alone. Our understanding of the nature of this inhibition and the mechanisms responsible for it is limited at present. This is due to the difficulties associated with comparing results of studies which differ markedly in a number of design factors, including the mode, frequency, duration and intensity of training, training history of participants, scheduling of training sessions and dependent variable selection. Despite these difficulties, both chronic and acute hypotheses have been proposed to explain the phenomenon of strength inhibition during concurrent training. The chronic hypothesis contends that skeletal muscle cannot adapt metabolically or morphologically to both strength and endurance training simultaneously. This is because many adaptations at the muscle level observed in response to strength training are different from those observed after endurance training. The observation that changes in muscle fibre type and size after concurrent training are different from those observed after strength training provide some support for the chronic hypothesis. The acute hypothesis contends that residual fatigue from the endurance component of concurrent training compromises the ability to develop tension during the strength element of concurrent training. It is proposed that repeated acute reductions in the quality of strength training sessions then lead to a reduction in strength development over time. Peripheral fatigue factors such as muscle damage and glycogen depletion have been implicated as possible fatigue mechanisms associated with the acute hypothesis. Further systematic research is necessary to quantify the inhibitory effects of concurrent training on strength development and to identify different training approaches that may overcome any negative effects of concurrent training.

Neural influences on sprint running: training adaptations and acute responses.

AbstractPerformance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint performance.An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest H-reflex has been reported to be lower in athletes trained for explosive events compared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sensitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indicative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint-trained athletes.Fatigue of neural origin both during and following sprint exercise has implications with respect to optimising training frequency and volume. Research suggests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage.Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance.

Long-Term Metabolic and Skeletal Muscle Adaptations to Short-Sprint Training Implications for Sprint Training and Tapering

AbstractThe adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (>10-second) or short (<10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus.Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type IIa muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca2+. Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.

Effect of recovery modality on 4-hour repeated treadmill running performance and changes in physiological variables.

The purpose of this study was to compare the effectiveness of three different recovery modalities--active (ACT), passive (PAS) and contrast temperature water immersion (CTW)--on the performance of repeated treadmill running, lactate concentration and pH. Fourteen males performed two pairs of treadmill runs to exhaustion at 120% and 90% of peak running speed (PRS) over a 4-hour period. ACT, PAS or CTW was performed for 15-min after the first pair of treadmill runs. ACT consisted of running at 40% PRS, PAS consisted of standing stationary and CTW consisted of alternating between 60-s cold (10 degrees C) and 120-s hot (42 degrees C) water immersion. Run times were converted to time to cover set distance using critical power. Type of recovery modality did not have a significant effect on change in time to cover 400 m (Mean +/- SD; ACT 2.7 +/- 3.6 s, PAS 2.9 +/- 4.2 s, CTW 4.2 +/- 6.9 s), 1000 m (ACT 2.2 +/- 4.0 s, PAS 4.8 +/- 8.6 s, CTW 2.1 +/- 7.2 s) or 5000 m (ACT 1.4 +/- 29.0 s, PAS 16.7 +/- 58.5 s, CTW 11.7 +/- 33.0 s). Post exercise blood lactate concentration was lower in ACT and CTW compared with PAS. Participants reported an increased perception of recovery in the CTW compared with ACT and PAS. Blood pH was not significantly influenced by recovery modality. Data suggest both ACT and CTW reduce lactate accumulation after high intensity running, but high intensity treadmill running performance is returned to baseline 4-hours after the initial exercise bout regardless of the recovery strategy employed.

Acute effects of high-intensity endurance exercise on subsequent resistance activity

This study investigated the effect of high-intensity endurance on subsequent isoinertial and isokinetic resistance exercise. One woman and five men (mean 6 SD: age 5 20.3 6 2.5 years; body mass 5 75.1 6 10.2 kg; height 5 177.8 6 10.3 cm) performed isoinertial and isokinetic resistance exercise under control conditions (no experimental intervention) and after an acute bout of high-intensity endurance exercise. Endurance exercise consisted of five 5-minute bouts of incremental cycle exercise at between 40 and 100% of peak cycle ergometer oxygen consumption (peak V˙ O2). Isoinertial resistance exercise consisted of three sets of squats with a load of 80% of one repetition maximum. Isokinetic resistance exercise consisted of five repetitions of leg extensions performed at five different contractile speeds (1.05, 2.09, 3.14, 4.19, and 5.24 rad•s21). Significant reductions in isokinetic torque at 0.52 rad from full extension (T30) were observed after high-intensity endurance exercise. Endurance exercise also caused significant reductions in the number of isoinertial squat lifts performed. Plasma lactate values, measured before subjects performed resistance activity, were significantly higher after high intensity endurance exercise (6.16 6 2.28 mmol•L21) when compared with the control condition (0.50 6 0.45 mmol•L21). It was concluded that an acute bout of high-intensity endurance exercise may inhibit performance in a subsequent bout of resistance activity.

Acute exercise and subsequent energy intake. A meta-analysis

The precise magnitude of the effect of acute exercise on subsequent energy intake is not well understood. Identifying how large a deficit exercise can produce in energy intake and whether this is compensated for, is important in design of long-term exercise programs for weight loss and weight maintenance. Thus, this paper sought to review and perform a meta-analysis on data from the existing literature. Twenty-nine studies, consisting of 51 trials, were identified for inclusion. Exercise duration ranged from 30 to 120min at intensities of 36-81% VO(2)max, with trials ranging from 2 to 14h, and ad libitum test meals offered 0-2h post-exercise. The outcome variables included absolute energy intake and relative energy intake. A random effects model was employed for analysis due to expected heterogeneity. Results indicated that exercise has a trivial effect on absolute energy intake (n=51; ES=0.14, 95% CI: -0.005 to 0.29) and a large effect on relative energy intake (creating an energy deficit, n=25; ES=-1.35, 95% CI: -1.64 to -1.05). Despite variability among studies, results suggest that exercise is effective for producing a short-term energy deficit and that individuals tend not to compensate for the energy expended during exercise in the immediate hours after exercise by altering food intake.

Concurrent Strength and Endurance Training: The Influence of Dependent Variable Selection

Twenty-six active university students were randomly allocated to resistance (R, n 5 9), endurance (E, n 5 8), and concurrent resistance and endurance (C, n 5 9) training con-ditions. Training was completed 3 times per week in all conditions, with endurance training preceding resistance training in the C group. Resistance training involved 4 sets of upper- and lower-body exercises with loads of 4–8 repetition maximum (RM). Each endurance training session consisted of five 5-minute bouts of incremental cycle exercise at between 40 and 100% of peak oxygen uptake (VO2peak). Parameters measured prior to and following training included strength (1RM and isometric and isokinetic [1.04, 3.12, 5.20, and 8.67 rad·s 21] strength), VO2peak and Wingate test performance (peak power output [PPO], average power, and relative power decline). Significant improvements in 1RM strength were observed in the R and C groups following training. VO2peak significantly increased in E and C but was significantly reduced in R after training. Effect size (ES) transformations on the other dependent variables suggested that performance changes in the C group were not always similar to changes in the R or E groups. These ES data suggest that statistical power and dependent variable selection are significant issues in enhancing our insights into concurrent training. It may be necessary to assess a range of performance parameters to monitor the relative effectiveness of a particular concurrent training regimen.

Caffeine, cycling performance, and exogenous CHO oxidation: a dose-response study.

PURPOSE This study investigated the effects of a low and moderate caffeine dose on exogenous CHO oxidation and endurance-exercise performance. METHODS Nine trained and familiarized male cyclists (mean +/- SD: 29.4 +/- 4.5 yr, 81.3 +/- 10.8 kg body weight [BW], 183.8 +/- 8.2 cm, V O2peak = 61.7 +/- 4.8 mL.kg.min) undertook three trials, with training and high CHO diet being controlled. One hour before exercise, subjects ingested capsules containing placebo and 1.5 or 3 mg.kg BW of caffeine using a double-blind administration protocol. Trials consisted of 120 min steady-state cycling at approximately 70% V O2peak, immediately followed by a 7-kJ.kg BW time trial (TT). During exercise, subjects were provided with fluids containing C-glucose every 20 min to determine exogenous CHO oxidation. RESULTS No significant TT performance improvements were observed during caffeine-containing trials (mean +/- SD: placebo = 30 min 25 s +/- 3 min 10 s; 1.5 mg.kg BW = 30 min 42 s +/- 3 min 41 s; and 3 mg.kg BW = 29 min 51 s +/- 3 min 38 s). Furthermore, caffeine failed to significantly alter maximal exogenous CHO oxidation (maximal oxidation rates: placebo = 0.95 +/- 0.2 g.min; 1.5 mg.kg BW = 0.92 +/- 0.2 g.min; and 3 mg.kg BW = 0.96 +/- 0.2 g.min). CONCLUSION Low and moderate doses of caffeine have failed to improve endurance performance in fed, trained subjects.

The effects of different doses of caffeine on endurance cycling time trial performance

Abstract This study investigated the effects of two different doses of caffeine on endurance cycle time trial performance in male athletes. Using a randomised, placebo-controlled, double-blind crossover study design, sixteen well-trained and familiarised male cyclists (Mean ± s: Age = 32.6 ± 8.3 years; Body mass = 78.5 ± 6.0 kg; Height = 180.9 ± 5.5 cm [Vdot]O2peak = 60.4 ± 4.1 ml · kg−1 · min−1) completed three experimental trials, following training and dietary standardisation. Participants ingested either a placebo, or 3 or 6 mg · kg−1 body mass of caffeine 90 min prior to completing a set amount of work equivalent to 75% of peak sustainable power output for 60 min. Exercise performance was significantly (P < 0.05) improved with both caffeine treatments as compared to placebo (4.2% with 3 mg · kg−1 body mass and 2.9% with 6 mg · kg−1 body mass). The difference between the two caffeine doses was not statistically significant (P = 0.24). Caffeine ingestion at either dose resulted in significantly higher heart rate values than the placebo conditions (P < 0.05), but no statistically significant treatment effects in ratings of perceived exertion (RPE) were observed (P = 0.39). A caffeine dose of 3 mg · kg−1 body mass appears to improve cycling performance in well-trained and familiarised athletes. Doubling the dose to 6 mg · kg−1 body mass does not confer any additional improvements in performance.

Nutrition in General Practice: Role and Workforce Preparation Expectations of Medical Educators

Nutrition advice from general practitioners (GPs) is held in high regard by the general public, yet the literature investigating the role of GPs in the provision of nutrition care is limited. This qualitative study aimed to explore the perceptions of general practice medical educators (GPMEs) regarding the role of GPs in general practice nutrition care, the competencies required by GPs to provide effective nutrition care and the learning and teaching strategies best suited to develop these competencies. Twenty medical educators from fourteen Australian and New Zealand universities participated in an individual semi-structured telephone interview, guided by an inquiry logic informed by the literature. Interviews were transcribed verbatim and thematically analysed. Medical educators identified that nutrition was an important but mostly superficially addressed component of health care in general practice. Numerous barriers to providing nutrition care in general practice were identified. These include a lack of time and associated financial disincentives, perceptions of inadequate skills in nutrition counselling associated with inadequate training, ambiguous attitudes and differing perceptions about the role of GPs in the provision of nutrition care. Further research is required to identify strategies to improve nutrition care and referral practices provided in the general practice setting, in order to utilise the prime position of GPs as gatekeepers of integrated care to the general public.