Selected B vitamins and their possible link to the aetiology of age-related sarcopenia: relevance of UK dietary recommendations.

The possible roles of selected B vitamins in the development and progression of sarcopenia are reviewed. Age-related declines in muscle mass and function are associated with huge and increasing costs to healthcare providers. Falls and loss of mobility and independence due to declining muscle mass/function are associated with poor clinical outcomes and their prevention and management are attractive research targets. Nutritional status appears a key modifiable and affordable intervention. There is emerging evidence of sarcopenia being the result not only of diminished anabolic activity but also of declining neurological integrity in older age, which is emerging as an important aspect of the development of age-related decline in muscle mass/function. In this connection, several B vitamins can be viewed as not only cofactors in muscle synthetic processes, but also as neurotrophic agents with involvements in both bioenergetic and trophic pathways. The B vitamins thus selected are examined with respect to their relevance to multiple aspects of neuromuscular function and evidence is considered that requirements, intakes or absorption may be altered in the elderly. In addition, the evidence base for recommended intakes (UK recommended daily allowance) is examined with particular reference to original datasets and their relevance to older individuals. It is possible that inconsistencies in the literature with respect to the nutritional management of sarcopenia may, in part at least, be the result of compromised micronutrient status in some study participants. It is suggested that in order, for example, for intervention with amino acids to be successful, underlying micronutrient deficiencies must first be addressed/eliminated.

Wide-pulse electrical stimulation to an intrinsic foot muscle induces acute functional changes in forefoot-rearfoot coupling behaviour during walking.

Interventions for strengthening intrinsic foot muscles may be beneficial for rehabilitation from overuse injuries. In this study the acute effects of high-frequency, low-intensity wide-pulse electrical stimulation (WPS) over an intrinsic muscle on subsequent foot function during walking was assessed in healthy participants. WPS was delivered to the m. abductor hallucis (m.AH) of the non-dominant foot during relaxed standing. 3-dimensional forefoot (FF)--rearfoot (RF) coordination was quantified with a vector coding technique within separate periods of the stance phase to study WPS functional effects on foot motion. 4 types of coordinative strategies between the FF and RF were interpreted and compared PRE-to-POST-WPS for both the experimental and control feet. Bilateral electromyography (EMG) from m.AH was analysed during the intervention period for evidence of acute neuromuscular adaptation. The results showed that WPS significantly modulated FF-RF coordination during mid-stance, indicative of a more stable foot. Specifically, a statistically significant increase in FF eversion with concomitant RF inversion in the frontal plane and RF-dominated adduction in the transverse plane was observed. Subject-specific increases in post-stimulus m.AH EMG activation were observed but this was not reflected in an overall group effect. It is concluded that the structural integrity of the foot during walking is enhanced following an acute session of WPS and that this mechanical effect is most likely due to stimulation induced post-tetanic potentiation of synaptic transmission.

Decline in voluntary activation contributes to reduced maximal performance of fatigued human lower limb muscles.

In upper limb muscles, altered corticospinal excitability and reduction in neural drive are observed in parallel with peripheral fatigue during prolonged and/or repeated contractions. However, the fatigue-induced adaptations of central and peripheral elements and their relative contribution to lower limb muscle performance are yet to be fully explored. In the present study, corticospinal excitability and peripheral contractility of ankle flexor muscles were quantified before, during and after repeated brief unilateral maximal dorsiflexions to fatigue in eleven healthy volunteers. Transcranial magnetic stimulation of the motor cortex area related to lower limb muscles was performed, and the evoked twitch and EMG responses in tibialis anterior (TA) and soleus (SOL) were measured. The motor evoked potentials (MEPs) in fatigued TA during post-exercise maximal dorsiflexions were smaller (-20 ± 6 %, p = 0.026) and remained depressed for at least 5 min. Post-exercise MEPs in fatigued SOL and silent periods in TA and SOL were not different compared to pre-exercise. These changes were accompanied by lower voluntary torque (-8 ± 3 %, p = 0.013), estimated resting twitch (-36 ± 5 %, p = 0.003) and voluntary activation (-17 ± 9 %, p = 0.021) versus pre-exercise. During last versus first maximal contraction in the fatiguing protocol lower voluntary torque (-40 ± 4 %, p = 0.003), higher MEP amplitudes (>+49 %, p < 0.021) and longer silent periods (>+24 %, p < 0.004) were recorded in both muscles. Decreased corticospinal excitability contributes significantly to the reduced maximal performance of fatigued lower limb muscles. During prolonged intermittent maximal dorsiflexions the performance of ankle muscles declines despite enhanced corticospinal excitability presumably due to deficient descending drive and/or spinal motoneuron responsiveness to the cortical drive.