title: Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?

authors: Rattray, Ben

subjects: Science & Technology

abstract: • Central fatigue is accepted as a contributor to overall athletic performance, yet little research directly investigates post-exercise recovery strategies targeting the brain
• Current post-exercise recovery strategies likely impact on the brain through a range of mechanisms, but improvements to these strategies is needed 
• Research is required to optimize post-exercise recovery with a focus on the brain 
Post-exercise recovery has largely focused on peripheral mechanisms of fatigue, but there is growing acceptance that fatigue is also contributed to through central mechanisms which demands that attention should be paid to optimizing recovery of the brain. In this narrative review we assemble evidence for the role that many currently utilized recovery strategies may have on the brain, as well as potential mechanisms for their action. The review provides discussion of how common nutritional strategies as well as physical modalities and methods to reduce mental fatigue are likely to interact with the brain, and offer an opportunity for subsequent improved performance. We aim to highlight the fact that many recovery strategies have been designed with the periphery in mind, and that refinement of current methods are likely to provide improvements in minimizing brain fatigue. Whilst we offer a number of recommendations, it is evident that there are many opportunities for improving the research, and practical guidelines in this area.

text: Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance? • Central fatigue is accepted as a contributor to overall athletic performance, yet little research directly investigates post-exercise recovery strategies targeting the brain
• Current post-exercise recovery strategies likely impact on the brain through a range of mechanisms, but improvements to these strategies is needed 
• Research is required to optimize post-exercise recovery with a focus on the brain 
Post-exercise recovery has largely focused on peripheral mechanisms of fatigue, but there is growing acceptance that fatigue is also contributed to through central mechanisms which demands that attention should be paid to optimizing recovery of the brain. In this narrative review we assemble evidence for the role that many currently utilized recovery strategies may have on the brain, as well as potential mechanisms for their action. The review provides discussion of how common nutritional strategies as well as physical modalities and methods to reduce mental fatigue are likely to interact with the brain, and offer an opportunity for subsequent improved performance. We aim to highlight the fact that many recovery strategies have been designed with the periphery in mind, and that refinement of current methods are likely to provide improvements in minimizing brain fatigue. Whilst we offer a number of recommendations, it is evident that there are many opportunities for improving the research, and practical guidelines in this area.

year: 2015-03-17

title: The characterisation and role of mighty during myogenesis

authors: Davies, Todd John

subjects: myogenesis

abstract: Myogenesis, or skeletal muscle formation, begins during embryogenesis and involves the proliferation of myoblasts followed by their exit from the cell-cycle to differentiate and form myotubes. This formation of skeletal muscle is a complex process involving many genes and various signalling pathways. Mighty is a novel myogenic gene discovered at AgResearch by the Functional Muscle Genomics (FMG) group in a genetic screen performed on the muscle of myostatin null and wild-type mice. It was found that heavily muscled mice, lacking myostatin, had increased expression of the mighty gene. This gene was found to be conserved, with cognates found in mammals, amphibians, teleosts, and arthropods. Mighty was found to be expressed in a variety of tissues, but only skeletal muscle showed increased mighty mRNA expression in myostatin null mice, indicating the specific regulation of mighty by myostatin in skeletal muscle (Marshall, 2005).

The aim of this study was to characterise the mighty protein and examine its role in myogenesis to elucidate mighty's function. To undertake this study, antibodies specific for the full-length mighty protein and antibodies specific for a peptide region of mighty were characterised. Results using these antibodies, showed endogenous mighty, from myoblasts, to be a low-abundant, nuclear protein which shows a mobility of ~52 kDa in SDS gels, different to that of recombinant mighty protein. The mobility difference of endogenous mighty compared to recombinant mighty appears to be due to phosphorylation and may involve other post-translational modifications. In agreement, the determined isoelectric point (~5.7) of endogenous mighty also appears to be the result of phosphorylation. Interestingly, 52 kDa mighty was not detected in muscle extracts, but a ~30 kDa protein was specifically detected, indicating multiple forms, and subsequent roles, for mighty protein. Mass spectrometry (MS) was also performed for further characterisation of the mighty protein and possible post-translational modifications. Although hits were achieved with both recombinant mighty proteins, endogenous mighty MS analysis was not accomplished due to its low-abundance.

The function of the mighty protein in myoblasts was investigated during proliferation and differentiation. The results indicate that proliferating myoblasts have low levels of mighty in G0 and increased levels in G1/S during the cell cycle. This differential expression of mighty may involve cell cycle exit at the G1/S phase. Differentiation results showed mighty to be upregulated before MyoD during differentiation, placing mighty very early in the differentiation hierarchy. This agrees with previous results by Marshall (2005) which showed mighty to upregulate MyoD through IGF-II expression. Enhanced differentiation was also seen in double muscle bovine myoblasts concomitantly with increased mighty expression.

In conclusion, mighty appears to be a post-translationally modified protein that plays an early role in myogenic differentiation. This role in differentiation appears to be upstream of MyoD through the upregulation of IGF-II and may be linked to cell cycle exit in the G1 phase of the cell cycle.

text: The characterisation and role of mighty during myogenesis Myogenesis, or skeletal muscle formation, begins during embryogenesis and involves the proliferation of myoblasts followed by their exit from the cell-cycle to differentiate and form myotubes. This formation of skeletal muscle is a complex process involving many genes and various signalling pathways. Mighty is a novel myogenic gene discovered at AgResearch by the Functional Muscle Genomics (FMG) group in a genetic screen performed on the muscle of myostatin null and wild-type mice. It was found that heavily muscled mice, lacking myostatin, had increased expression of the mighty gene. This gene was found to be conserved, with cognates found in mammals, amphibians, teleosts, and arthropods. Mighty was found to be expressed in a variety of tissues, but only skeletal muscle showed increased mighty mRNA expression in myostatin null mice, indicating the specific regulation of mighty by myostatin in skeletal muscle (Marshall, 2005).

The aim of this study was to characterise the mighty protein and examine its role in myogenesis to elucidate mighty's function. To undertake this study, antibodies specific for the full-length mighty protein and antibodies specific for a peptide region of mighty were characterised. Results using these antibodies, showed endogenous mighty, from myoblasts, to be a low-abundant, nuclear protein which shows a mobility of ~52 kDa in SDS gels, different to that of recombinant mighty protein. The mobility difference of endogenous mighty compared to recombinant mighty appears to be due to phosphorylation and may involve other post-translational modifications. In agreement, the determined isoelectric point (~5.7) of endogenous mighty also appears to be the result of phosphorylation. Interestingly, 52 kDa mighty was not detected in muscle extracts, but a ~30 kDa protein was specifically detected, indicating multiple forms, and subsequent roles, for mighty protein. Mass spectrometry (MS) was also performed for further characterisation of the mighty protein and possible post-translational modifications. Although hits were achieved with both recombinant mighty proteins, endogenous mighty MS analysis was not accomplished due to its low-abundance.

The function of the mighty protein in myoblasts was investigated during proliferation and differentiation. The results indicate that proliferating myoblasts have low levels of mighty in G0 and increased levels in G1/S during the cell cycle. This differential expression of mighty may involve cell cycle exit at the G1/S phase. Differentiation results showed mighty to be upregulated before MyoD during differentiation, placing mighty very early in the differentiation hierarchy. This agrees with previous results by Marshall (2005) which showed mighty to upregulate MyoD through IGF-II expression. Enhanced differentiation was also seen in double muscle bovine myoblasts concomitantly with increased mighty expression.

In conclusion, mighty appears to be a post-translationally modified protein that plays an early role in myogenic differentiation. This role in differentiation appears to be upstream of MyoD through the upregulation of IGF-II and may be linked to cell cycle exit in the G1 phase of the cell cycle.

year: 2006

title: Street health: Practitioner service provision for Māori homeless people in Auckland

authors: Nikora, Linda Waimarie

abstract: Homelessness is more than a transient crisis. While access to housing might solve the needs of some, research has shown that the needs of homeless people are much more complex and more a symptom of systematic structural inequalities than an unanticipated emergency (Hopper, 1998). As in other countries, the homeless population in New Zealand is made up of a diverse population of men, women and intersex groups of various ages, sexualities and ethnic backgrounds. Māori are over-represented among this population due to ongoing processes of colonisation and socioeconomic exclusion (Groot et al., 2011). When compared with domiciled citizens, homeless people are more likely to experience a raft of illnesses and unmet health needs, violence, a sense of insecurity, exclusion and fear, and are more likely to commit sui- cide (Hodgetts et al., 2007). Homeless people often experience diverse ill- nesses including asthma, heart disease, diabetes, hepatitis, renal disease, dermatological conditions, malnutrition, oral disease, depression, schizo- phrenia, substance misuse and broken bones (Ellison-Loschmann & Pearce, 2006; Joly et al., 2011; Moore et al., 2007).

text: Street health: Practitioner service provision for Māori homeless people in Auckland Homelessness is more than a transient crisis. While access to housing might solve the needs of some, research has shown that the needs of homeless people are much more complex and more a symptom of systematic structural inequalities than an unanticipated emergency (Hopper, 1998). As in other countries, the homeless population in New Zealand is made up of a diverse population of men, women and intersex groups of various ages, sexualities and ethnic backgrounds. Māori are over-represented among this population due to ongoing processes of colonisation and socioeconomic exclusion (Groot et al., 2011). When compared with domiciled citizens, homeless people are more likely to experience a raft of illnesses and unmet health needs, violence, a sense of insecurity, exclusion and fear, and are more likely to commit sui- cide (Hodgetts et al., 2007). Homeless people often experience diverse ill- nesses including asthma, heart disease, diabetes, hepatitis, renal disease, dermatological conditions, malnutrition, oral disease, depression, schizo- phrenia, substance misuse and broken bones (Ellison-Loschmann & Pearce, 2006; Joly et al., 2011; Moore et al., 2007).

year: 2016