The purpose of this study was to quantify the response of the forearm musculature to combinations of wrist and forearm posture and grip force. Ten healthy individuals performed five relative handgrip efforts (5%, 50%, 70% and 100% of maximum, and 50 N) for combinations of three wrist postures (flexed, neutral and extended) and three forearm postures (pronated, neutral and supinated). ‘Baseline’ extensor muscle activity (associated with holding the dynamometer without exerting grip force) was greatest with the forearm pronated and the wrist extended, while flexor activity was largest in supination when the wrist was flexed. Extensor activity was generally larger than that of flexors during low to mid-range target force levels, and was always greater when the forearm was pronated. Flexor activation only exceeded the extensor activation at the 70% and 100% target force levels in some postures. A flexed wrist reduced maximum grip force by 40-50%, but EMG amplitude remained elevated. Women produced 60-65% of the grip strength of men, and required 5-10% more of both relative force and extensor activation to produce a 50 N grip. However, this appeared to be due to strength rather than gender. Forearm rotation affected grip force generation only when the wrist was flexed, with force decreasing from supination to pronation (p<0.005). The levels of extensor activation observed, especially during baseline and low level grip exertions, suggest a possible contributing mechanism to the development of lateral forearm muscle pain in the workplace.

Computer mouse use has become an integral part of office work in the past decade. Intensive mouse use has been associated with increased risk of upper extremity musculoskeletal disorders, including carpal tunnel syndrome. Sustained, elevated fluid pressure in the carpal tunnel may play a role in the pathophysiology of carpal tunnel syndrome. Carpal tunnel pressure was measured in 14 healthy individuals while they performed tasks using three different computer mice. Participants performed a multidirectional dragging (‘drag and drop’) task starting with the hand resting (static posture) on the mouse. With one mouse, an additional pointing (‘point-and-click’) task was performed. All mice were associated with similar wrist extension postures (p= 0.41) and carpal tunnel pressures (p= 0.48). Pressures were significantly greater during dragging and pointing tasks than when resting the hand (static posture) on the mouse (p= 0.003). The mean pressures during the dragging tasks were 28.8- 33.1 mmHg, ∼ 12 mmHg greater than the static postures. Pressures during the dragging task were higher than the pointing task (33.1 versus 28.0 mmHg), although the difference was borderline non-significant (p= 0.06). In many participants the carpal tunnel pressures measured during mouse use were greater than pressures known to alter nerve function and structure, indicating that jobs with long periods of intensive mouse use may be at an increased risk of median mononeuropathy. A recommendation is made to minimize wrist extension, minimize prolonged dragging tasks and frequently perform other tasks with the mousing hand.

Key points: Performing resistance exercise with heavier loads is often proposed to be necessary for the recruitment of larger motor units and activation of type II muscle fibres, leading to type II fibre hypertrophy. Indirect measures [surface electromyography (EMG)] have been used to support this thesis, although we propose that lighter loads lifted to task failure (i.e. volitional fatigue) result in the similar activation of type II fibres. In the present study, participants performed resistance exercise to task failure with heavier and lighter loads with both a normal and longer repetition duration (i.e. time under tension). Type I and type II muscle fibre glycogen depletion was determined by neither load, nor repetition duration during resistance exercise performed to task failure. Surface EMG amplitude was not related to muscle fibre glycogen depletion or anabolic signalling; however, muscle fibre glycogen depletion and anabolic signalling were related. Performing resistance exercise to task failure, regardless of load lifted or repetition duration, necessitates the activation of type II muscle fibres. Heavier loads (>60% of maximal strength) are considered to be necessary during resistance exercise (RE) to activate and stimulate hypertrophy of type II fibres. Support for this proposition comes from observation of higher surface electromyography (EMG) amplitudes during RE when lifting heavier vs. lighter loads. We aimed to determine the effect of RE, to task failure, with heavier vs. lighter loads and shorter or longer repetition durations on: EMG‐derived variables, muscle fibre activation, and anabolic signalling. Ten recreationally‐trained young men performed four unilateral RE conditions randomly on two occasions (two conditions, one per leg per visit). Muscle biopsies were taken from the vastus lateralis before and one hour after RE. Broadly, total time under load, number of repetitions, exercise volume, EMG amplitude (at the beginning and end of each set) and total EMG activity were significantly different between conditions (P < 0.05); however, neither glycogen depletion (in both type I and type II fibres), nor phosphorylation of relevant signalling proteins showed any difference between conditions. We conclude that muscle fibre activation and subsequent anabolic signalling are independent of load, repetition duration and surface EMG amplitude when RE is performed to task failure. The results of the present study provide evidence indicating that type I and type II fibres are activated when heavier and lighter loads are lifted to task failure. We propose that our results explain why RE training with higher or lower loads, when loads are lifted to task failure, leads to equivalent muscle hypertrophy and occurs in both type I and type II fibres.