Human movement science

Abstract

An early afternoon in late March, I am of looking out over the spring-like Karolinska Institutet campus in Stockholm and thinking about some of the discoveries originating from the neighbouring buildings. The house closest to my window was once the prestigious Anatomy–Histology department. Today, this department does not exist, but the Petrén Lecture hall remains to commemorate the legendary anatomist Ture Petrén. I still have a vivid memory of Ture Petrén as a rather strict lecturer and examiner during my anatomy course in the fall of 1966. Petrén's close collaborator in the Anatomy department Sven Carlsöö worked on the biomechanics of the musculoskeletal system and wrote his thesis in 1952 on the ‘Nervous coordination and mechanical function of the mandibular elevators’ at the Royal Gymnastic Central Institute (GCI) in Stockholm. This Institute had been founded in 1813 by Pehr Henrik Ling, the father of medical gymnastics. Carlsöö was a pioneer in the area of human movement sciences and was active at a time where this research field underwent strong development owing to the entrance of computers. Carlsöö's book ‘How man moves’ (Carlsöö 1972) is a classical publication in this area and furthermore contains analyses of different sport-specific movements. In his January 2012 Editorial, the Acta Physiologica Chief Editor wrote about another person, who made an important contribution to human movement science, Emil Du Bois-Reymond (Persson 2012). Du Bois-Reymond, the father of experimental electrophysiology, made observations and performed method developments that paved the way for Electromyography. Interestingly, Du Bois-Reymond once had his laboratory in the same building at the Charité in Berlin, where the Acta Physiologica Chief Editor Pontus Persson and Editorial secretary Carola Neubert now reside. Today, research on human movement science, or kinesiology, integrates knowledge from many different scientific areas such as neurophysiology, neurology, muscle physiology and biomechanics, with an overall aim to obtain increased insight into human motor behaviour. By tradition, this is a main area in Acta Physiologica. Although the importance of the motor cortex has been recognized for almost one and a half centuries (Fritsch & Hitzig 1870), it has become clear that there are different levels of motor cortical involvement in specific tasks. The homunculus is the well-known motor map with the body's musculature draped over the motor cortex that implies that each small area in the motor cortex corresponds to a particular movement (Penfield & Rasmussen 1952). The homunculus was based on results from motor evoked potential research that involved direct observations by stimulating the human brain with weak electrical shocks in conscious patients who were undergoing surgery (Penfield & Boldrey 1937). Although much of these early data are still valid, it is now known that even for the precise movements of the hand, the cortical input arises from a much wider region of the cortex. In addition, cortical areas interact in different ways with each other and with spinal interneurones and motor neurones to produce specific movements. This is discussed in a recent review in Acta Physiologica (Petersen et al. 2010), which also describes several sources of nonlinearity between the cortical and the motoneuronal output. Such sources may include varying efficacy of the corticomotoneuronal synapse (Hultborn et al. 1996), but also the actual motoneuronal firing rate, which determines the responsiveness of the motor neurone pool (Matthews 1999). The motoneuronal output may also be changed with ageing and it was recently shown that the maximal neural drive to elbow flexors and extensors is impaired in older adults. This occurs most notably in the elbow flexors with negative consequences for upper limb motor control (Dalton et al. 2010). The decreased ability of the muscle fibres to produce force with fatigue is accompanied by a fatigue-induced decline in the firing rate of motor neurones. This is partly caused by a reduction in the discharge rate of stimulatory 1a afferent fibres from muscle spindles (Vallbo 1974, Macefield et al. 1991), but also by increased activity in inhibitory groups III and IV small diameter muscle afferents (sensitive to mechanical, thermal and chemical stimuli) (Martin et al. 2006). The latter may be dependent on muscle type and mainly seems to exist in extensor muscles. Changes in motoneuronal firing may give rise to compensatory adaptations in the cortical drive to motor neurones, including a changed excitability of inhibitory circuits controlling corticospinal output (Seifert & Petersen 2010). In a recent Acta Physiologica article, evidence was presented that Writer's cramp, a focal dystonia of the hand owing to repetitive, stereotyped writing movements, most likely involves an abnormal facilitation of these cortical inhibitory mechanisms (Boyadjian et al. 2011). Fatigue-associated changes in skeletal muscle tissue itself include disturbances of the excitation–contraction (E-C) coupling (Allen et al. 2008) and of the potassium (K+) displacement across the muscle cell surface or T-tubular membranes (Edman & Lou 1992). In addition, a marked slowing of relaxation may be an important factor that limits the ability of muscle to produce work during fatiguing cyclic contractions, like running or walking (McDaniel et al. 2010). Muscle fatigue after a prolonged session of aerobic-based exercise or after unaccustomed physical exercise with a large eccentric component resulting in muscle damage involves force depression particularly at low frequencies of stimulation. This force depression may persist over several days and has been termed low-frequency fatigue (LFF) (Kamandulis et al. 2010). With LFF, there are disturbances in E-C coupling and specifically in Ca2+ release from the sarcoplasmic reticulum (Green et al. 2011). Why fatigue is not observed at high frequencies of stimulation may be explained by the exponential nature of the relationship between muscle force and intracellular-free Ca2+ concentration, where, at high force levels (and stimulation frequencies), Ca2+ reductions have a negligible effect (Allen et al. 2008). Interestingly, impaired E-C coupling owing to decreased Ca2+ release from the sarcoplasmic reticulum has also been implicated in the decline in muscle quality (reduction in force production per unit muscle tissue) with ageing (Russ et al. 2011). The increased muscle quality with resistance training, on the other hand, has been speculated to result from either increased myofilament packing density or a preferential hypertrophy of fast twitch muscle fibres that have a higher specific tension (Erskine et al. 2010). During intense exercise, the extracellular K+ concentration increases progressively with increasing exercise intensity to reach values in excess of 10 mm. This may reduce the intracellular K+ concentration from 165 mm to values below 130 mm (Sjøgaard et al. 1985). The observed K+ changes can cause muscle fatigue by inhibiting E-C coupling (Edman & Lou 1992). Several different K+ channels contribute to this K+ imbalance as recently reviewed in this journal (Kristensen & Juel 2010). It is proposed that especially the Na+,K+-ATPase α2 dimers, the KCa1.1 and Kir2.1 channels are important in the K+ regulation during muscle fatigue. Because of the importance of the Na+, K+-ATPase for the energy demanding maintenance of Na+ and K+ gradients across cell membranes, it is not surprising that different exercise training regimens result in increased Na+, K+-ATPase protein expression in skeletal muscle. In recent studies, it was furthermore shown that, both at the protein and mRNA level, Na+, K+-ATPase increases with just one session of exercise (Nordsborg et al. 2010, Green et al. 2011). There is a higher relative content of K+-transporting proteins in oxidative than in glycolytic muscle fibres, which may explain the increased tolerance to high extracellular K+ concentrations detected in more oxidative muscles (Kristensen & Juel 2010). The question why muscle fibres have such a large variability in contractile properties was considered in a recent review (Canepari et al. 2010). It is concluded that this variability mainly depends on the different expression of myosin isoforms, although the variability in twitch profile to a large extent is determined by different properties of the sarcoplasmic reticulum (Schiaffino 2010). Nevertheless, it has also been shown that profound adaptability is possible with respect to velocity and power with no change in myosin isoform content, for example, with ageing and disuse (Larsson et al. 1996, 1997). A review summarizing the evolution of the notion of muscle fibre types as well as current work to identify regulatory factors involved in fibre type diversification has been presented in Acta Physiologica (Schiaffino 2010). This short summary illustrates the many different perspectives of kinesiological research published in Acta Physiologica, which can provide important insight into human motor behaviour. I am confident that this will continue to constitute a main area in Acta Physiologica.

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