Can exhaled volatile organic compounds differentiate high and low responders to resistance exercise?
- Bell, Leo, Wallen, Matthew, Talpey, Scott, Myers, M., O'Brien, B. J.
- Authors: Bell, Leo , Wallen, Matthew , Talpey, Scott , Myers, M. , O'Brien, B. J.
- Date: 2022
- Type: Text , Journal article
- Relation: Medical Hypotheses Vol. 162, no. (2022), p.
- Full Text:
- Reviewed:
- Description: Participation in resistance training improves muscle strength and size, as well as reduced risk of chronic disease and frailty. However, the exercise response to resistance training is highly variable. In part this may be attributed to individual physiological differences. Identification of biomarkers that can distinguish between high and low responders to exercise are therefore of interest. Exhaled volatile organic compounds may provide a non-invasive method of monitoring the physiological response to resistance training. However, the relationship between exhaled organic compounds and the acute response to resistance exercise is not fully understood. Therefore, this research will investigate exhaled volatile organic compounds in acute response to resistance exercise with an aim to discover a common group of compounds that can predict high and low responders to standardised resistance training. © 2022 Elsevier Ltd
Can exhaled volatile organic compounds differentiate high and low responders to resistance exercise?
- Authors: Bell, Leo , Wallen, Matthew , Talpey, Scott , Myers, M. , O'Brien, B. J.
- Date: 2022
- Type: Text , Journal article
- Relation: Medical Hypotheses Vol. 162, no. (2022), p.
- Full Text:
- Reviewed:
- Description: Participation in resistance training improves muscle strength and size, as well as reduced risk of chronic disease and frailty. However, the exercise response to resistance training is highly variable. In part this may be attributed to individual physiological differences. Identification of biomarkers that can distinguish between high and low responders to exercise are therefore of interest. Exhaled volatile organic compounds may provide a non-invasive method of monitoring the physiological response to resistance training. However, the relationship between exhaled organic compounds and the acute response to resistance exercise is not fully understood. Therefore, this research will investigate exhaled volatile organic compounds in acute response to resistance exercise with an aim to discover a common group of compounds that can predict high and low responders to standardised resistance training. © 2022 Elsevier Ltd
Can systemic myokine response to an acute exercise bout predict high and low responders to resistance training?
- Bell, Leo, Wallen, M., Talpey, Scott, O'Brien, B.
- Authors: Bell, Leo , Wallen, M. , Talpey, Scott , O'Brien, B.
- Date: 2022
- Type: Text , Journal article
- Relation: Medical Hypotheses Vol. 160, no. (2022), p.
- Full Text:
- Reviewed:
- Description: Resistance training is performed to increase muscle strength and mass. Associated benefits relate to improvements in physical performance as well as reduced risk of mortality. However, the exercise response to resistance training is largely variable. This may be attributed to individual physiological phenotype and flawed methods of standardised training. Recent efforts have been made to identify biomarkers which delineate between high and low responders to resistance training. Myokines associated with exercise-induced muscle secretome are biomarkers that potentially differentiate between individuals that experience large or small increases in muscle mass. However, the repeatability of these biomarkers in response to standardised resistance training is understudied. Therefore, this research seeks to address the inter and intra-reliability of myokines associated with resistance exercise, and if they confidently predict high and low responders to individually standardised resistance training. Development of a screening tool which reliably identifies individual trainability can have potential implications for personalised exercise physiology. © 2022
- Authors: Bell, Leo , Wallen, M. , Talpey, Scott , O'Brien, B.
- Date: 2022
- Type: Text , Journal article
- Relation: Medical Hypotheses Vol. 160, no. (2022), p.
- Full Text:
- Reviewed:
- Description: Resistance training is performed to increase muscle strength and mass. Associated benefits relate to improvements in physical performance as well as reduced risk of mortality. However, the exercise response to resistance training is largely variable. This may be attributed to individual physiological phenotype and flawed methods of standardised training. Recent efforts have been made to identify biomarkers which delineate between high and low responders to resistance training. Myokines associated with exercise-induced muscle secretome are biomarkers that potentially differentiate between individuals that experience large or small increases in muscle mass. However, the repeatability of these biomarkers in response to standardised resistance training is understudied. Therefore, this research seeks to address the inter and intra-reliability of myokines associated with resistance exercise, and if they confidently predict high and low responders to individually standardised resistance training. Development of a screening tool which reliably identifies individual trainability can have potential implications for personalised exercise physiology. © 2022
Development of muscle mass : How much is optimum for performance?
- Young, Warren, Talpey, Scott, Bartlett, Rogan, Lewis, Mitchell, Mundy, Stephanie, Smyth, Andrew, Welsh, Tim
- Authors: Young, Warren , Talpey, Scott , Bartlett, Rogan , Lewis, Mitchell , Mundy, Stephanie , Smyth, Andrew , Welsh, Tim
- Date: 2019
- Type: Text , Journal article
- Relation: Strength and Conditioning Journal Vol. 41, no. 3 (2019), p. 47-50
- Full Text:
- Reviewed:
- Description: Training for muscle hypertrophy can be expected to induce some increase in total body mass, and this can have positive or negative consequences for athletic performance. Positive effects may be increased strength, increased resistance to being pushed aside, and greater momentum when running, whereas possible negative effects may be reduced capacity to accelerate, decelerate, change direction, and jump. These possible effects of gaining muscle and total body mass suggest that strength and conditioning coaches should give thoughtful consideration to the amount of hypertrophy training prescribed throughout an athletes's development and should be determined by the specific needs of the athlete.
- Description: TRAINING FOR MUSCLE HYPERTROPHY CAN BE EXPECTED TO INDUCE SOME INCREASE IN TOTAL BODY MASS, AND THIS CAN HAVE POSITIVE OR NEGATIVE CONSEQUENCES FOR ATHLETIC PERFORMANCE. POSITIVE EFFECTS MAY BE INCREASED STRENGTH, INCREASED RESISTANCE TO BEING PUSHED ASIDE, AND GREATER MOMENTUM WHEN RUNNING, WHEREAS POSSIBLE NEGATIVE EFFECTS MAY BE REDUCED CAPACITY TO ACCELERATE, DECELERATE, CHANGE DIRECTION, AND JUMP. THESE POSSIBLE EFFECTS OF GAINING MUSCLE AND TOTAL BODY MASS SUGGEST THAT STRENGTH AND CONDITIONING COACHES SHOULD GIVE THOUGHTFUL CONSIDERATION TO THE AMOUNT OF HYPERTROPHY TRAINING PRESCRIBED THROUGHOUT AN ATHLETE'S DEVELOPMENT AND SHOULD BE DETERMINED BY THE SPECIFIC NEEDS OF THE ATHLETE.
- Authors: Young, Warren , Talpey, Scott , Bartlett, Rogan , Lewis, Mitchell , Mundy, Stephanie , Smyth, Andrew , Welsh, Tim
- Date: 2019
- Type: Text , Journal article
- Relation: Strength and Conditioning Journal Vol. 41, no. 3 (2019), p. 47-50
- Full Text:
- Reviewed:
- Description: Training for muscle hypertrophy can be expected to induce some increase in total body mass, and this can have positive or negative consequences for athletic performance. Positive effects may be increased strength, increased resistance to being pushed aside, and greater momentum when running, whereas possible negative effects may be reduced capacity to accelerate, decelerate, change direction, and jump. These possible effects of gaining muscle and total body mass suggest that strength and conditioning coaches should give thoughtful consideration to the amount of hypertrophy training prescribed throughout an athletes's development and should be determined by the specific needs of the athlete.
- Description: TRAINING FOR MUSCLE HYPERTROPHY CAN BE EXPECTED TO INDUCE SOME INCREASE IN TOTAL BODY MASS, AND THIS CAN HAVE POSITIVE OR NEGATIVE CONSEQUENCES FOR ATHLETIC PERFORMANCE. POSITIVE EFFECTS MAY BE INCREASED STRENGTH, INCREASED RESISTANCE TO BEING PUSHED ASIDE, AND GREATER MOMENTUM WHEN RUNNING, WHEREAS POSSIBLE NEGATIVE EFFECTS MAY BE REDUCED CAPACITY TO ACCELERATE, DECELERATE, CHANGE DIRECTION, AND JUMP. THESE POSSIBLE EFFECTS OF GAINING MUSCLE AND TOTAL BODY MASS SUGGEST THAT STRENGTH AND CONDITIONING COACHES SHOULD GIVE THOUGHTFUL CONSIDERATION TO THE AMOUNT OF HYPERTROPHY TRAINING PRESCRIBED THROUGHOUT AN ATHLETE'S DEVELOPMENT AND SHOULD BE DETERMINED BY THE SPECIFIC NEEDS OF THE ATHLETE.
Cardiomyocyte functional etiology in heart failure with preserved ejection fraction is distinctive - A new preclinical model
- Curl, Claire, Danes, Vennetia, Bell, James, Raaijmakers, Antonia, Ip, Wendy, Chandramouli, Chanchal, Harding, Tristan, Porrello, Enzo, Erickson, Jeffrey, Charchar, Fadi, Kompa, Andrew, Edgley, Amanda, Crossman, David, Soeller, Christian, Mellor, Kimberley, Kalman, Jonathan, Harrap, Stephen, Delbridge, Lea
- Authors: Curl, Claire , Danes, Vennetia , Bell, James , Raaijmakers, Antonia , Ip, Wendy , Chandramouli, Chanchal , Harding, Tristan , Porrello, Enzo , Erickson, Jeffrey , Charchar, Fadi , Kompa, Andrew , Edgley, Amanda , Crossman, David , Soeller, Christian , Mellor, Kimberley , Kalman, Jonathan , Harrap, Stephen , Delbridge, Lea
- Date: 2018
- Type: Text , Journal article
- Relation: Journal of the American Heart Association Vol. 7, no. 11 (2018), p. 1-32
- Full Text:
- Reviewed:
- Description: Background--Among the growing numbers of patients with heart failure, up to one half have heart failure with preserved ejection fraction (HFpEF). The lack of effective treatments for HFpEF is a substantial and escalating unmet clinical need-and the lack of HFpEF-specific animal models represents a major preclinical barrier in advancing understanding of HFpEF. As established treatments for heart failure with reduced ejection fraction (HFrEF) have proven ineffective for HFpEF, the contention that the intrinsic cardiomyocyte phenotype is distinct in these 2 conditions requires consideration. Our goal was to validate and characterize a new rodent model of HFpEF, undertaking longitudinal investigations to delineate the associated cardiac and cardiomyocyte pathophysiology. Methods and Results--The selectively inbred Hypertrophic Heart Rat (HHR) strain exhibits adult cardiac enlargement (without hypertension) and premature death (40% mortality at 50 weeks) compared to its control strain, the normal heart rat. Hypertrophy was characterized in vivo by maintained systolic parameters (ejection fraction at 85%-90% control) with marked diastolic dysfunction (increased E/E'). Surprisingly, HHR cardiomyocytes were hypercontractile, exhibiting high Ca
- Authors: Curl, Claire , Danes, Vennetia , Bell, James , Raaijmakers, Antonia , Ip, Wendy , Chandramouli, Chanchal , Harding, Tristan , Porrello, Enzo , Erickson, Jeffrey , Charchar, Fadi , Kompa, Andrew , Edgley, Amanda , Crossman, David , Soeller, Christian , Mellor, Kimberley , Kalman, Jonathan , Harrap, Stephen , Delbridge, Lea
- Date: 2018
- Type: Text , Journal article
- Relation: Journal of the American Heart Association Vol. 7, no. 11 (2018), p. 1-32
- Full Text:
- Reviewed:
- Description: Background--Among the growing numbers of patients with heart failure, up to one half have heart failure with preserved ejection fraction (HFpEF). The lack of effective treatments for HFpEF is a substantial and escalating unmet clinical need-and the lack of HFpEF-specific animal models represents a major preclinical barrier in advancing understanding of HFpEF. As established treatments for heart failure with reduced ejection fraction (HFrEF) have proven ineffective for HFpEF, the contention that the intrinsic cardiomyocyte phenotype is distinct in these 2 conditions requires consideration. Our goal was to validate and characterize a new rodent model of HFpEF, undertaking longitudinal investigations to delineate the associated cardiac and cardiomyocyte pathophysiology. Methods and Results--The selectively inbred Hypertrophic Heart Rat (HHR) strain exhibits adult cardiac enlargement (without hypertension) and premature death (40% mortality at 50 weeks) compared to its control strain, the normal heart rat. Hypertrophy was characterized in vivo by maintained systolic parameters (ejection fraction at 85%-90% control) with marked diastolic dysfunction (increased E/E'). Surprisingly, HHR cardiomyocytes were hypercontractile, exhibiting high Ca
Experimental and human evidence for Lipocalin-2 (Neutrophil Gelatinase-Associated Lipocalin NGAL ) in the development of cardiac hypertrophy and heart failure
- Marques, Francine, Prestes, Priscilla, Byars, Sean, Ritchie, Scott, Wurtz, Peter, Patel, Sheila, Booth, Scott, Rana, Indrajeetsinh, Minoda, Yosuke, Berzins, Stuart, Curl, Claire, Bell, James, Wai, Bryan, Srivastava, Piyush, Kangas, Antti, Soininen, Pasi, Ruohonen, Saku, Kahonen, Mika, Lehtimaki, Terho, Raitoharju, Emma, Havulinna, Aki, Perola, Markus, Raitakari, Olli, Salomaa, Veikko, Ala-Korpela, Mika, Kettunen, Johannes, McGlynn, Maree, Kelly, Jason, Wlodek, Mary, Lewandowski, Paul, Delbridge, Lea, Burrell, Louise, Inouye, Michael, Harrap, Stephen, Charchar, Fadi
- Authors: Marques, Francine , Prestes, Priscilla , Byars, Sean , Ritchie, Scott , Wurtz, Peter , Patel, Sheila , Booth, Scott , Rana, Indrajeetsinh , Minoda, Yosuke , Berzins, Stuart , Curl, Claire , Bell, James , Wai, Bryan , Srivastava, Piyush , Kangas, Antti , Soininen, Pasi , Ruohonen, Saku , Kahonen, Mika , Lehtimaki, Terho , Raitoharju, Emma , Havulinna, Aki , Perola, Markus , Raitakari, Olli , Salomaa, Veikko , Ala-Korpela, Mika , Kettunen, Johannes , McGlynn, Maree , Kelly, Jason , Wlodek, Mary , Lewandowski, Paul , Delbridge, Lea , Burrell, Louise , Inouye, Michael , Harrap, Stephen , Charchar, Fadi
- Date: 2017
- Type: Text , Journal article
- Relation: Journal of the American Heart Association Vol. 6, no. 6 (2017), p. 1-58
- Relation: http://purl.org/au-research/grants/nhmrc/1034371
- Full Text:
- Reviewed:
- Description: Background-Cardiac hypertrophy increases the risk of developing heart failure and cardiovascular death. The neutrophil inflammatory protein, lipocalin-2 (LCN2/NGAL), is elevated in certain forms of cardiac hypertrophy and acute heart failure. However, a specific role for LCN2 in predisposition and etiology of hypertrophy and the relevant genetic determinants are unclear. Here, we defined the role of LCN2 in concentric cardiac hypertrophy in terms of pathophysiology, inflammatory expression networks, and genomic determinants. Methods and Results-We used 3 experimental models: a polygenic model of cardiac hypertrophy and heart failure, a model of intrauterine growth restriction and Lcn2-knockout mouse; cultured cardiomyocytes; and 2 human cohorts: 114 type 2 diabetes mellitus patients and 2064 healthy subjects of the YFS (Young Finns Study). In hypertrophic heart rats, cardiac and circulating Lcn2 was significantly overexpressed before, during, and after development of cardiac hypertrophy and heart failure. Lcn2 expression was increased in hypertrophic hearts in a model of intrauterine growth restriction, whereas Lcn2-knockout mice had smaller hearts. In cultured cardiomyocytes, Lcn2 activated molecular hypertrophic pathways and increased cell size, but reduced proliferation and cell numbers. Increased LCN2 was associated with cardiac hypertrophy and diastolic dysfunction in diabetes mellitus. In the YFS, LCN2 expression was associated with body mass index and cardiac mass and with levels of inflammatory markers. The single-nucleotide polymorphism, rs13297295, located near LCN2 defined a significant cis-eQTL for LCN2 expression. Conclusions-Direct effects of LCN2 on cardiomyocyte size and number and the consistent associations in experimental and human analyses reveal a central role for LCN2 in the ontogeny of cardiac hypertrophy and heart failure.
- Authors: Marques, Francine , Prestes, Priscilla , Byars, Sean , Ritchie, Scott , Wurtz, Peter , Patel, Sheila , Booth, Scott , Rana, Indrajeetsinh , Minoda, Yosuke , Berzins, Stuart , Curl, Claire , Bell, James , Wai, Bryan , Srivastava, Piyush , Kangas, Antti , Soininen, Pasi , Ruohonen, Saku , Kahonen, Mika , Lehtimaki, Terho , Raitoharju, Emma , Havulinna, Aki , Perola, Markus , Raitakari, Olli , Salomaa, Veikko , Ala-Korpela, Mika , Kettunen, Johannes , McGlynn, Maree , Kelly, Jason , Wlodek, Mary , Lewandowski, Paul , Delbridge, Lea , Burrell, Louise , Inouye, Michael , Harrap, Stephen , Charchar, Fadi
- Date: 2017
- Type: Text , Journal article
- Relation: Journal of the American Heart Association Vol. 6, no. 6 (2017), p. 1-58
- Relation: http://purl.org/au-research/grants/nhmrc/1034371
- Full Text:
- Reviewed:
- Description: Background-Cardiac hypertrophy increases the risk of developing heart failure and cardiovascular death. The neutrophil inflammatory protein, lipocalin-2 (LCN2/NGAL), is elevated in certain forms of cardiac hypertrophy and acute heart failure. However, a specific role for LCN2 in predisposition and etiology of hypertrophy and the relevant genetic determinants are unclear. Here, we defined the role of LCN2 in concentric cardiac hypertrophy in terms of pathophysiology, inflammatory expression networks, and genomic determinants. Methods and Results-We used 3 experimental models: a polygenic model of cardiac hypertrophy and heart failure, a model of intrauterine growth restriction and Lcn2-knockout mouse; cultured cardiomyocytes; and 2 human cohorts: 114 type 2 diabetes mellitus patients and 2064 healthy subjects of the YFS (Young Finns Study). In hypertrophic heart rats, cardiac and circulating Lcn2 was significantly overexpressed before, during, and after development of cardiac hypertrophy and heart failure. Lcn2 expression was increased in hypertrophic hearts in a model of intrauterine growth restriction, whereas Lcn2-knockout mice had smaller hearts. In cultured cardiomyocytes, Lcn2 activated molecular hypertrophic pathways and increased cell size, but reduced proliferation and cell numbers. Increased LCN2 was associated with cardiac hypertrophy and diastolic dysfunction in diabetes mellitus. In the YFS, LCN2 expression was associated with body mass index and cardiac mass and with levels of inflammatory markers. The single-nucleotide polymorphism, rs13297295, located near LCN2 defined a significant cis-eQTL for LCN2 expression. Conclusions-Direct effects of LCN2 on cardiomyocyte size and number and the consistent associations in experimental and human analyses reveal a central role for LCN2 in the ontogeny of cardiac hypertrophy and heart failure.
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