The nutrition care needs of patients newly diagnosed with type 2 diabetes: informing dietetic practice.

BACKGROUND: Understanding patients' experiences and preferences for health care is important with respect to informing how to provide best-practice, patient-centred care. The present study aimed to explore the perceptions of patients who have been recently diagnosed with type 2 diabetes regarding nutrition care received from dietitians. METHODS: Ten individuals recently diagnosed with type 2 diabetes participated in three individual semi-structured qualitative telephone interviews: at baseline, then at 3 and 6 months after recruitment. Data were analysed using content analysis at each time point and meta-synthesis of findings over time. RESULTS: Participants' initial interactions with dietitians were challenging and overwhelming as a result of the instructional nature of consultations. Many participants questioned the use of dietary guidelines to inform nutrition care because this was not adapted to the individual. Some participants valued receiving education on topics such as label reading and serving sizes; however, others considered that the nutrition care was rushed and overly directive. Very few participants perceived that an ongoing relationship with a dietitian would be useful, and limited interaction was planned beyond 6 months after diagnosis. CONCLUSIONS: These findings suggest that there is considerable opportunity for dietitians to enhance the nutrition care provided to patients with type 2 diabetes. Tailoring of dietary guidelines to individuals, utilising supportive counselling styles, and focusing on open communication in consultations that facilitate ongoing, useful care for patients, may help patients with type 2 diabetes achieve and maintain healthy dietary behaviours.

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.

Long-term metabolic and skeletal muscle adaptations to short-sprint training: implications for sprint training and tapering.

The 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 Ca(2+). 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.

Adaptation to chronic eccentric exercise in humans: the influence of contraction velocity.

We compared changes in muscle fibre composition and muscle strength indices following a 10 week isokinetic resistance training programme consisting of fast (3.14 rad x s(-1)) or slow (0.52 rad x s(-1)) velocity eccentric muscle contractions. A group of 20 non-resistance trained subjects were assigned to a FAST (n = 7), SLOW (n = 6) or non-training CONTROL (n = 7) group. A unilateral training protocol targeted the elbow flexor muscle group and consisted of 24 maximal eccentric isokinetic contractions (four sets of six repetitions) performed three times a week for 10 weeks. Muscle biopsy samples were obtained from the belly of the biceps brachii. Isometric torque and concentric and eccentric torque at 0.52 and 3.14 rad x s(-1) were examined at 0, 5 and 10 weeks. After 10 weeks, the FAST group demonstrated significant [mean (SEM)] increases in eccentric [29.6 (6.4)%] and concentric torque [27.4 (7.3)%] at 3.14 rad x s(-1), isometric torque [21.3 (4.3)%] and eccentric torque [25.2 (7.2)%] at 0.52 rad x s(-1). The percentage of type I fibres in the FAST group decreased from [53.8 (6.6)% to 39.1 (4.4)%] while type IIb fibre percentage increased from [5.8 (1.9)% to 12.9 (3.3)%; P < 0.05]. In contrast, the SLOW group did not experience significant changes in muscle fibre type or muscle torque. We conclude that neuromuscular adaptations to eccentric training stimuli may be influenced by differences in the ability to cope with chronic exposure to relatively fast and slow eccentric contraction velocities. Possible mechanisms include greater cumulative damage to contractile tissues or stress induced by slow eccentric muscle contractions.

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

Performance 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.

Changes in leg strength 8 and 32 h after endurance exercise.

The aim of this study was to determine the effects of a single bout of endurance exercise on subsequent strength performance. Eight males with a long history of resistance training performed isokinetic, isometric and isotonic leg extension strength tests 8 and 32 h after 50 min of cycle ergometry at 70-110% of critical power. The participants also completed a control condition in which no cycling was performed. Plasma lactate and ammonia were measured before and immediately after each strength test. Isokinetic, isometric and isotonic leg extension torques were not significantly different 8 or 32 h after endurance exercise compared with the control condition (P > 0.05). A large (50.3%), but not statistically significant, increase in plasma ammonia was evident during the strength tests performed 8 h after endurance exercise, while a significant (P < 0.05) increase in ammonia was also seen 32 h after endurance exercise. No significant changes in plasma ammonia were evident in the control condition. Our results suggest that leg extension strength was not compromised by an earlier bout of endurance cycling. However, metabolic activity during the strength tests might have been altered by the preceding bout of endurance exercise.

Concurrent strength and endurance training. A review.

Concurrent 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.