Prosthetic gait of unilateral lower-limb amputees with current and novel prostheses: A pilot study.

BACKGROUND: Novel lower-limb prostheses aim to improve the quality of locomotion of individuals with an amputation. This study evaluates the biomechanics of a novel bionic foot during walking. METHODS: Able-bodied individuals (n = 7) and individuals with a transfemoral (n = 6) or transtibial amputation (n = 6) were included. Able-bodied individuals conducted one experimental trial, whereas individuals with transtibial and transfemoral amputations conducted a familiarization (with current prosthesis) and two experimental trials using a passive and bionic prosthesis. Each trial consisted of 3 bouts of 2 min of treadmill walking at different speeds. Biomechanical data were gathered using a force platform and motion capture system and analysed using Statistical Parametric Mapping and (non)-parametric tests. FINDINGS: Conventional prosthetic feet alter gait patterns and induce locomotion difficulties. While walking at a normal speed with the passive prosthesis, transtibial amputees display reduced maximum heel forces, increased ankle and trunk angular velocities at midstance, and increased knee angle during stance and swing phases on their effected side (P ≤ 0.026). Improved lower-limb kinematics was demonstrated during slow and normal speed walking with the bionic prosthesis; however, dynamic trunk stability was negatively impacted during this condition. The bionic prosthesis did not benefit transfemoral amputees at any walking speed. INTERPRETATION: Transtibial amputees can better approximate typical movement patterns at slow and normal walking speeds using the novel bionic prosthesis; however the same benefit was not observed in transfemoral amputees.

Electro-physiological changes in the brain induced by caffeine or glucose nasal spray.

OBJECTIVE: A direct link between the mouth cavity and the brain for glucose (GLUC) and caffeine (CAF) has been established. The aim of this study is to determine whether a direct link for both substrates also exist between the nasal cavity and the brain. METHODS: Ten healthy male subjects (age 22 ± 1 years) performed three experimental trials, separated by at least 2 days. Each trial included a 20-s nasal spray (NAS) period in which solutions placebo (PLAC), GLUC, or CAF were provided in a double-blind, randomized order. During each trial, four cognitive Stroop tasks were performed: two familiarization trials and one pre- and one post-NAS trial. Reaction times and accuracy for different stimuli (neutral, NEUTR; congruent, CON; incongruent INCON) were determined. Electroencephalography was continuously measured throughout the trials. During the Stroop tasks pre- and post-NAS, the P300 was assessed and during NAS, source localization was performed using standardized low-resolution brain electromagnetic tomography (sLORETA). RESULTS AND DISCUSSION: NAS activated the anterior cingulate cortex (ACC). CAF-NAS also increased θ and ß activity in frontal cortices. Furthermore, GLUC-NAS increased the ß activity within the insula. GLUC-NAS also increased the P300 amplitude with INCON (P = 0.046) and reduced P300 amplitude at F3-F4 and P300 latency at CP1-CP2-Cz with NEUTR (P = 0.001 and P = 0.016, respectively). The existence of nasal bitter and sweet taste receptors possibly induce these brain responses. CONCLUSION: Greater cognitive efficiency was observed with GLUC-NAS. CAF-NAS activated cingulate, insular, and sensorymotor cortices, whereas GLUC-NAS activated sensory, cingulate, and insular cortices. However, no effect on the Stroop task was found.

BDNF, IGF-I, Glucose and Insulin during Continuous and Interval Exercise in Type 1 Diabetes.

Type 1 diabetes (T1D) can have a significant impact on brain function, mostly ascribed to episodes of hypoglycemia and chronic hyperglycemia. Exercise has positive effects on acute and chronic glycemic control in T1D, and has beneficial effects on cognitive function by increasing neurotrophins such as BDNF and IGF-I in non-diabetic humans. The present study examines the effects of different types of exercise intensities on neurotrophins in T1D. 10 participants with type 1 diabetes were evaluated in 3 sessions: high-intensity exercise (10×[60 s 90%Wmax, 60 s 50 W]), continuous exercise (22 min, 70% VO2 max) and a control session. Blood glucose, serum free insulin, serum BDNF and IGF-I were assessed pre/post all the trials and after recovery. Blood glucose significantly decreased after both exercise intensities and BDNF levels increased, with a dose-response effect for exercise intensity on BDNF. IGF-I changed over time, but without a difference between the different exercise protocols. Both exercise intensities change neurotrophins in T1D, but also exhibit a dose response effect for BDNF. The intensity-dependent findings may aid in designing exercise prescriptions for maintaining or improving neurological health in T1D, but both types of exercise can be implemented.

Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimise performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimise performance is to heat acclimatise. Heat acclimatisation should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimise dehydration during exercise. Following the development of commercial cooling systems (eg, cooling-vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organisers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimising the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events, for hydration and body cooling opportunities, when competitions are held in the heat.

Consensus recommendations on training and competing in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

Neurophysiological effects of exercise in the heat.

Fatigue during prolonged exercise is a multifactorial phenomenon. The complex interplay between factors originating from both the periphery and the brain will determine the onset of fatigue. In recent years, electrophysiological and imaging tools have been fine-tuned, allowing for an improved understanding of what happens in the brain. In the first part of the review, we present literature that studied the changes in electrocortical activity during and after exercise in normal and high ambient temperature. In general, exercise in a thermo-neutral environment or at light to moderate intensity increases the activity in the ß frequency range, while exercising at high intensity or in the heat reduces ß activity. In the second part, we review literature that manipulated brain neurotransmission, through either pharmacological or nutritional means, during exercise in the heat. The dominant outcomes were that manipulations changing brain dopamine concentration have the potential to delay fatigue, while the manipulation of serotonin had no effect and noradrenaline reuptake inhibition was detrimental for performance in the heat. Research on the effects of neurotransmitter manipulations on brain activity during or after exercise is scarce. The combination of brain imaging techniques with electrophysiological measures presents one of the major future challenges in exercise physiology/neurophysiology.

Effects of caffeine and maltodextrin mouth rinsing on P300, brain imaging, and cognitive performance.

Caffeine (CAF) and maltodextrin (MALT) mouth rinses (MR) improve exercise performance. The current experiment aims to determine the effect of CAF and MALT MR on cognitive performance and brain activity. Ten healthy male subjects (age 27 ± 3 yr) completed three experimental trials. Each trial included four Stroop tasks: two familiarization tasks, and one task before and one task after an MR period. The reaction time (in milliseconds) and accuracy (percent) of simple, congruent, and incongruent stimuli were assessed. Electroencephalography was applied throughout the experiment to record brain activity. The amplitudes and latencies of the P300 were determined during the Stroop tasks before and after the MR period. Subjects received MR with CAF (0.3 g/25 ml), MALT (1.6 g/25 ml), or placebo (PLAC) in a randomized, double-blind, crossover design. During MR, the brain imaging technique standardized low-resolution brain electromagnetic tomography was applied. Magnitude-based inferences showed that CAF MR is likely trivial (63.5%) and likely beneficial (36.4%) compared with PLAC MR, and compared with MALT MR likely beneficial to reaction time on incongruent stimuli (61.6%). Additionally, both the orbitofrontal and dorsolateral prefrontal cortex were activated only during CAF MR, potentially explaining the likely beneficial effect on reaction times. MALT MR increased brain activity only within the orbitofrontal cortex. However, this brain activation did not alter the reaction time. Furthermore, no significant differences in the accuracy of stimuli responses were observed between conditions. In conclusion, only CAF MR exerted a likely beneficial effect on reaction time due to the subsequent activation of both the orbitofrontal and dorsolateral prefrontal cortexes.

A dopamine/noradrenaline reuptake inhibitor improves performance in the heat, but only at the maximum therapeutic dose.

A maximal dose of bupropion has enabled subjects to maintain a higher power output than reported during the placebo session in the heat. Because this drug is taken in different doses it is important to know if there is a dose-response relationship with regard to exercise at high ambient temperature. Ten well-trained male cyclists ingested placebo (pla; 200 mg) or bupropion (50%, 75%, 100% of maximal dose: bup50: 150 mg; bup75: 225 mg; bup100: 300 mg) the evening before and morning of the experimental trial. Trials were conducted in 30 °C (humidity 48%). Subjects cycled for 60 min at 55% W (max) , immediately followed by a time trial to measure performance. Bup100 improved performance (pla: 33'42" ± 2'06"; bup100: 32'06" ± 1'54"; P = 0.035). Bupropion increased core temperature at the end of exercise, while heart rate was higher only in the bup100 trial (P < 0.05). No changes in rating of perceived exertion (RPE) or thermal sensation were found. Lower doses of bupropion were not ergogenic, indicating there was no dose-response effect. Interestingly, despite an increase in core temperature and improved performance in the maximal dose, there was no change in RPE and thermal sensation, suggesting an altered motivation or drive to continue exercise.

Intense exercise increases circulating endocannabinoid and BDNF levels in humans--possible implications for reward and depression.

The endocannabinoid system is known to have positive effects on depression partly through its actions on neurotrophins, such as Brain-Derived Neurotrophic Factor (BDNF). As BDNF is also considered the major candidate molecule for exercise-induced brain plasticity, we hypothesized that the endocannabinoid system represents a crucial signaling system mediating the beneficial antidepressant effects of exercise. Here we investigated, in 11 healthy trained male cyclists, the effects of an intense exercise (60 min at 55% followed by 30 min at 75% W(max)) on plasma levels of endocannabinoids (anandamide, AEA and 2-arachidonoylglycerol, 2-AG) and their possible link with serum BDNF. AEA levels increased during exercise and the 15 min recovery (P<0.001), whereas 2-AG concentrations remained stable. BDNF levels increased significantly during exercise and then decreased during the 15 min of recovery (P<0.01). Noteworthy, AEA and BDNF concentrations were positively correlated at the end of exercise and after the 15 min recovery (r>0.66, P<0.05), suggesting that AEA increment during exercise might be one of the factors involved in exercise-induced increase in peripheral BDNF levels and that AEA high levels during recovery might delay the return of BDNF to basal levels. AEA production during exercise might be triggered by cortisol since we found positive correlations between these two compounds and because corticosteroids are known to stimulate endocannabinoid biosynthesis. These findings provide evidence in humans that acute exercise represents a physiological stressor able to increase peripheral levels of AEA and that BDNF might be a mechanism by which AEA influences the neuroplastic and antidepressant effects of exercise.

Central fatigue and neurotransmitters, can thermoregulation be manipulated?

Fatigue is a complex phenomenon that can be evoked by peripheral and central factors. Although it is obvious that fatigue has peripheral causes such as glycogen depletion and cardiovascular strain, recent literature also focuses on the central origin of fatigue. It is clear that different brain neurotransmitters--such as serotonin, dopamine and noradrenaline--are implicated in the occurrence of fatigue, but manipulation of these neurotransmitters produced no conclusive results on performance in normal ambient temperature. Exercise in the heat not only adds an extra challenge to the cardiorespiratory system, but also to the brain. This provides a useful tool to investigate the association between exercise-induced hyperthermia and central fatigue. This review focuses on the effects of pharmacological manipulations on performance and thermoregulation in different ambient temperatures. Dopaminergic reuptake inhibition appears to counteract hyperthermia-induced fatigue in 30 °C, while noradrenergic neurotransmission shows negative effects on performance in both normal and high temperature, and serotonergic manipulations did not lead to significant changes in performance. It is, however, unlikely that one neurotransmitter system is responsible for the delay or onset of fatigue. Further research is required to determine the exact mechanisms of fatigue in different environmental conditions.

Diagnosing overtraining in athletes using the two-bout exercise protocol.

OBJECTIVE: In this work, whether a two-bout exercise protocol can be used to make an objective, immediately available distinction between non-functional over reaching (NFO) and overtraining syndrome (OTS) was studied. DESIGN: Underperforming athletes who were diagnosed with the suspicion of NFO or OTS were included in the study. Recovery of the athletes was monitored by a sports physician to retrospectively distinguish NFO from OTS. SETTING: Sports medicine laboratory PARTICIPANTS: The protocol was started and completed by 10 underperforming athletes. NFO was retrospectively diagnosed in five athletes, and OTS was diagnosed in five athletes. INTERVENTIONS: A two-bout maximal exercise protocol was used to measure physical performance and stressinduced hormonal reactions. MAIN OUTCOME MEASUREMENTS: Exercise duration, heart rate and blood lactate concentration were measured at the end of both exercise tests. Venous concentrations cortisol, adrenocorticotrophic hormone (ACTH), prolactin and growth hormone were measured both before and after both exercise tests. RESULTS: Maximal blood lactate concentration was lower in OTS compared with NFO, while resting concentrations of cortisol, ACTH and prolactin concentrations were higher. However, sensitivity of these measures was low. The ACTH and prolactin reactions to the second exercise bout were much higher in NFO athletes compared with OTS and showed the highest sensitivity for making the distinction. CONCLUSIONS: NFO might be distinguished from OTS based on ACTH and prolactin reactions to a two-bout exercise protocol. This protocol could be a useful tool for diagnosing NFO and OTS; however, more data should be collected before this test can be used as the gold standard.