I’d like to talk about something that’s become very personal to me: stroke. Recently, someone very close to me suffered a stroke, for which they are currently receiving very intensive treatment in the hope of making a recovery. The family, as you can imagine, has been terribly distressed by what has happened and we all hope for the best outcome. It’s a stark reminder of how fragile our health can be and how crucial it is to take proactive steps to protect it. This experience has driven me to write this article to increase our understanding of stroke, promote better awareness, and to encourage everyone to not take their health for granted.
What Is a Stroke?
A stroke occurs when blood flow to the brain is interrupted, either due to a blockage (ischemic stroke) or a rupture of a blood vessel (hemorrhagic stroke). In Australia, approximately 50,000 people experience a stroke each year, with around 472,000 Australians living with the effects of stroke, making it one of the leading causes of death and disability in the country (Stroke Foundation, 2021). The consequences can range from mild impairments to severe disability, depending on the area of the brain affected.
How to Prevent a Stroke
Prevention is always better than cure, right? Here are some key steps to lower your risk:
Maintain a Healthy Diet: A diet rich in fruits, vegetables, whole grains, and lean proteins can reduce stroke risk by controlling blood pressure and cholesterol levels. The DASH (Dietary Approaches to Stop Hypertension) diet has been shown to significantly lower blood pressure (Mozaffarian et al., 2011).
Regular Exercise: Engaging in at least 150 minutes of moderate aerobic activity weekly can decrease stroke risk by approximately 30-40% (Aune et al., 2016). Exercise helps maintain a healthy weight and reduces blood pressure.
Control Blood Pressure: High blood pressure is the leading risk factor for stroke. Studies suggest that lowering blood pressure by as little as 5 mmHg can reduce the risk of stroke by 34% (Wang et al., 2014).
Quit Smoking: Smoking increases the risk of stroke by 2 to 4 times. Quitting can significantly lower this risk over time (Roth et al., 2018).
Limit Alcohol Consumption: Moderate alcohol consumption is defined as up to one drink per day for women and two for men. Excessive drinking increases stroke risk, with studies showing that heavy drinkers have a higher incidence of hemorrhagic stroke (Bagnardi et al., 2001).
Manage Chronic Conditions: Conditions like diabetes and high cholesterol can elevate stroke risk. Effective management of these conditions is crucial for prevention (Gorelick et al., 2011).
If a Stroke Happens: Recovery Is Possible
Now, let’s talk about what happens if a stroke occurs. Recovery can be challenging, but it’s absolutely achievable. This is where strength training comes into play, particularly the concept of neuroplasticity—the brain’s ability to reorganize itself by forming new neural connections (Kleim & Jones, 2008).
After a stroke, rehabilitation often focuses on restoring lost functions, and strength training can be a key component. When you engage in strength training for the unaffected limb, there can be surprising benefits for the affected side, often referred to as cross-education.
Unilateral Strength Training and Cross-Education
What does this mean? Let’s say a stroke affects your right arm. If you focus on strength training your left arm, research shows that you may actually gain strength in your right arm as well, even though it isn’t directly being trained. A meta-analysis found that unilateral strength training can result in a strength increase of up to as high as 29% in the contralateral limb (Green & Gabriel, 2018). This occurs because the brain activates mirror neural pathways that can enhance strength in the affected side by stimulating the unaffected side.
Enhancing Physical Function and Quality of Life
Strength training doesn’t just aid in muscle recovery; it also improves overall physical function. For stroke survivors, regaining strength can lead to better mobility, increased independence, and improved quality of life. A study published in the Journal of NeuroEngineering and Rehabilitation found that strength training improved not only muscle strength but also functional abilities in stroke survivors (Lohse et al., 2014).
Moreover, engaging in strength training can boost mental well-being. Exercise releases endorphins, natural mood enhancers. For those recovering from a stroke, this can be invaluable for combating frustration or depression that often accompanies recovery.
Evidence-Based Interventions for Recovery
While strength training is a crucial part of rehabilitation, it’s not the only strategy that can enhance recovery. A multi-faceted approach incorporating various interventions has shown promising results.
Dietary Interventions: Nutrition plays a significant role in recovery. Diets rich in omega-3 fatty acids (found in fish, flaxseed, and walnuts) have been associated with improved outcomes post-stroke (Gao et al., 2019). Additionally, antioxidants found in fruits and vegetables help combat oxidative stress in the brain, potentially aiding recovery.
Exercise Beyond Strength Training: In addition to strength training, aerobic exercise has been shown to improve cardiovascular fitness, functional independence, and overall well-being in stroke survivors (Billinger et al., 2014). Activities like walking, cycling, and swimming can enhance cardiovascular health and aid in weight management, further reducing stroke risk.
Cognitive Rehabilitation: Cognitive impairments are common after a stroke, and engaging in activities that stimulate the brain can be beneficial. Playing games like chess, puzzles, or memory games can enhance cognitive function and may facilitate neuroplasticity (Tao et al., 2020). Studies show that cognitive training can lead to improvements in attention, memory, and executive functions.
Mindfulness and Stress Reduction: Stress can negatively impact recovery. Techniques such as mindfulness meditation and yoga can promote relaxation and improve psychological well-being. Research suggests that mindfulness-based interventions can reduce anxiety and depression in stroke survivors, contributing to a more positive recovery experience (Chung et al., 2019).
Supplementation: Certain supplements have shown promise in stroke recovery. For instance, B vitamins (particularly B6, B12, and folic acid) play a role in homocysteine metabolism, and elevated levels of homocysteine are linked to an increased risk of stroke. Supplementing with these vitamins may help improve outcomes, especially in individuals with deficiencies (Schnyder et al., 2019).
Community Engagement: Social support is vital for recovery. Participating in community activities, support groups, or engaging with family and friends can enhance emotional well-being. A study found that strong social ties are associated with better recovery outcomes in stroke survivors (Holt-Lunstad et al., 2010).
Exercise Physiology: Working with an Exercise Physiologist can help stroke survivors regain the physical capacity and skills needed for daily living. They can develop personalized plans that incorporate various interventions to improve strength, balance, fitness, motor skills, cognitive function, and independence.
Speech Therapy: If language or communication skills are affected, speech therapy is crucial. Therapists can employ various strategies to help patients regain their speech abilities and improve their quality of life.
A Comprehensive Approach to Recovery
Taking a holistic approach to stroke recovery is essential. Combining strength training with dietary changes, cognitive activities, mindfulness practices, and therapy can maximize recovery outcomes. Each element plays a crucial role in rebuilding strength, coordination, cognitive function, and emotional well-being.
Before starting any exercise or dietary program post-stroke, consulting with a healthcare provider or rehabilitation specialist is crucial. They can help tailor a program that’s safe and effective for your specific situation.
The Road Ahead
Recovering from a stroke is undoubtedly a journey, but with the right strategies—like preventative measures, strength training, neuroplasticity, and a multi-faceted approach to recovery—you can make significant strides. Whether you’re looking to prevent a stroke or navigate recovery, understanding the power of your body and brain can be a game-changer.
Remember, you’re not alone on this journey. Whether you’re supporting a loved one or navigating recovery yourself, there are resources and support communities there to help. Let’s embrace the science of strength training, nutrition, cognitive engagement, and overall wellness as powerful tools for a healthier, stronger future!
So, how about making sure you allocate some time to move today? Take a walk, get on your bike, do some light strength training, or even dance around to your favourite music, it all counts.
Take care of your health!
References
Aune, D., et al. (2016). “Physical Activity and the Risk of Stroke: A Meta-Analysis of Cohort Studies.” Stroke, 47(4), 1027-1035.
Bagnardi, V., et al. (2001). “Alcohol Consumption and the Risk of Stroke: A Meta-Analysis.” Stroke, 32(11), 2558-2564.
Billinger, S. A., et al. (2014). “Physical Activity and Exercise Recommendations for Stroke Survivors: A Statement for Healthcare Professionals from the American Heart Association/American Stroke Association.” Stroke, 45(8), 2535-2550.
CDC. (2021). “Stroke Facts.” Centers for Disease Control and Prevention. Retrieved from CDC.gov.
Chung, M. L., et al. (2019). “Mindfulness-Based Interventions for Patients with Cardiovascular Disease: A Systematic Review and Meta-Analysis.” Journal of Cardiovascular Nursing, 34(5), 447-458.
Gao, X., et al. (2019). “Omega-3 Fatty Acids and the Risk of Stroke: A Meta-Analysis.” Nutrients, 11(9), 2160.
Gorelick, P. B., et al. (2011). “Diagnosis and Management of Stroke Risk Factors.” Stroke, 42(8), 2363-2369.
Green, L. A., & Gabriel, D. A. (2018). The effect of unilateral training on contralateral limb strength in young, older, and patient populations: a meta-analysis of cross education. Physical Therapy Reviews, 23(4-5), 238-249.
Holt-Lunstad, J., et al. (2010). “Social Relationships and Mortality Risk: A Meta-analytic Review.” PLoS Medicine, 7(7), e1000316.
Kleim, J. A., & Jones, T. A. (2008). “Principles of Experience-Dependent Neural Plasticity: Implications for Rehabilitation After Brain Damage.” Journal of Speech, Language, and Hearing Research, 51(1), S225-S239.
Lohse, K., et al. (2014). “A Systematic Review of the Effect of Strength Training on Functional Recovery After Stroke.” Journal of NeuroEngineering and Rehabilitation, 11(1), 42.
Mozaffarian, D., et al. (2011). “Global Cardiovascular Disease and Diabetes: Current Status and Future Directions.” Journal of the American College of Cardiology, 58(14), 1404-1410.
Roth, G. A., et al. (2018). “Global and Regional Patterns in Cardiovascular Mortality from 1990 to 2013.” Global Heart, 13(3), 203-214.
Schnyder, G., et al. (2019). “The Role of B Vitamins in Stroke: A Review.” European Journal of Neurology, 26(4), 569-577.
Tao, J., et al. (2020). “Cognitive Training Improves Cognitive Function in Stroke Survivors: A Systematic Review and Meta-Analysis.” Archives of Physical Medicine and Rehabilitation, 101(5), 949-958.
Wang, Y., et al. (2014). “Systolic Blood Pressure Reduction and Risk of Stroke: A Meta-Analysis.” Journal of the American College of Cardiology, 63(10), 1090-1098.
The use of creatine (Cr) can be traced back to the early 1990s when several elite sprint athletes reported performance-enhancing benefits following gold medal winning performances at the 1992 Barcelona Olympic Games (Anderson, 1993). This sparked the birth of a new era with creatine gaining widespread popularity as a legitimate ergogenic aid (Bird, 2003). Creatine is a nitrogenous organic acid abundant in metabolically active muscle, heart and brain tissue. It is synthesised endogenously in the liver and kidneys from the amino acids arginine, glycine and methionine, and absorbed from the diet primarily from red and white meat (Chilibeck et al., 2017; Phillips, 2015). Most creatine is stored intramuscularly as phosphocreatine (PCr) (Candow et al., 2014). PCr functions principally as a temporal energy buffer by donating a high-energy phosphate to ADP through the enzymatic reaction of creatine kinase, which re-synthesises and replenishes ATP stores and thus helps maintain skeletal muscle energy availability during very short, intense anaerobic exercise (Kreider et al.,, 2017; Candow et al., 2014; Candow & Chillibeck, 2010). PCr also acts as a spatial energy buffer shuttling intracellular energy between mitochondria and sites of cellular ATP utilization (Kreider et al., 2017; Gualano et al., 2016).
Older people embrace powerlifting in Castlemaine (Australia) to avoid aged care home (courtesy ABC news)
Creatine supplementation increases the Cr/PCr reservoir by 20-40% (Kreider et al., 2017) and it is posited that this enhances PCr-mediated ATP resynthesis during and after high-intensity exercise bouts (Deane et al., 2017; Close et al., 2016), thereby allowing greater amounts of work to be accomplished (Phillips, 2015). This is particularly relevant for resistance training (RT) given that a dose-response relationship has been shown to exist between training volume and gains in skeletal muscle mass (Schoenfeld et al., 2017a; Schoenfeld et al., 2017b), and muscle strength (Figueiredo et al., 2017; Ralston et al., 2017). Other possible mechanisms to account for creatine ergogenicity are reduced exercise-induced muscle damage, reduced oxidative stress, increased GLUT4 in muscle fibre membranes, increased cell swelling that activates protein synthesis within muscle fibres, and decreased reliance on anaerobic glycolysis/reduced lactate production (Chilibeck et al., 2017; Kreider et al., 2017; Devries and Phillips, 2014). Although the exact mechanisms of action are still to be determined (Phillips, 2015), creatine supplemented RT has been extensively researched, especially in younger populations (Buford et al., 2007; Kreider et al., 2017). Consuming 5 grams of creatine (or 0.3 grams per kilogram body weight) four times daily for 5-7 days is generally viewed as the most effective way to increase muscle creatine stores and can be adequately maintained by consuming 3-5 grams/day following this loading phase (Kreider et al., 2017).
Muscle total creatine stores (figure courtesy of Kreider et al. 2017, J Int Soc Sports Nutr.)
Is creatine effective in older adults?
Three meta-analyses of randomised, placebo-controlled trials (Chilibeck et al., 2017; Candow et al., 2014; Devries and Phillips, 2014) have been published on the effects of creatine supplementation during RT on lean tissue mass and muscle strength in middle-aged and older adults (45-80 years old). No meta-analysis has yet assessed the effectiveness of creatine on RT outcomes in adults specifically 60 years or older. Most recently, Chilibeck et al. (2017, pg219) found significantly greater increases in lean tissue mass (1.4 kg; SMD=1.35), upper (i.e. chest press; SMD=0.37) and lower (i.e. leg press; SMD=0.25) body muscle strength when middle-aged to older adults (50-80 years old) were supplemented with creatine during RT. However, whilst the results of this study are often promoted as evidence that creatine has ergogenic value for this cohort, the standardised mean differences reported for muscle strength were trivial based on the effect sizes proposed by Rhea (2004) to delineate what is, and what is not meaningful following RT. If we apply more traditional effect sizes (Sullivan and Feinn, 2012), these strength improvements still remain small. One of the longest trials to investigate the impact of creatine supplementation and RT in middle-aged and older male adults (49-69 years old) found no additional benefits on measures of bone, muscle or strength after 12 months (Candow et al., 2020). Moreover, Beaudart et al., (2018) concluded that the research findings were equivocal for creatine after conducting a systematic review into the effects of various nutrients on muscle mass, muscle strength and physical performance in older adults (≥60 years old).
Taken from Rhea (2004)
At the time of writing only a handful of studies have assessed the monotherapy supplementation of creatine in older adults (≥60 years) undergoing RT (Smolarek et al., 2020; Gualano et al., 2014; Deacon et al., 2008; Pinto et al 2016; Aguiar et al., 2013; Alves et al., 2013; Brose et al 2003; Chrusch et al., 2001; Bermon et al., 1998). Of those that measured changes in lean tissue mass, participants supplemented with creatine consistently achieved greater benefits compared to placebo (Gualano et al., 2014; Pinto et al 2016; Aguiar et al., 2013; Brose et al 2003; Chrusch et al., 2001). In contrast, the effects of creatine on muscle strength were less consistent with the vast majority of studies showing no additional benefit versus placebo for core RT lower limb exercises i.e. leg press (Deacon et al., 2008; Pinto et al., 2016; Alves et al., 2013; Brose et al 2003; Bermon et al., 1998). Three of the four studies that explored the impact of creatine on physical function found no evidence of performance enhancement compared to placebo for a number of standard tests (Aguiar et al., 2013; Brose et al 2003; Gualano et al. 2014; Deacon et al., 2008); these included the 30-second chair stand test, 30 metre walk time, time to climb 14 stairs, the timed-up-and-go test, and the shuttle walk distance test. No RCTs have yet tested whether creatine supplementation in older adults (≥60 years) positively impacts balance or quality of life. Encouragingly though, Neves et al., (2011) demonstrated improved quality of life and physical function in postmenopausal women (mean age=58 years old) with knee osteoarthritis that took creatine during RT. The only study to have assessed the effect of creatine on dynamic balance found that improvement of balance performance was actually inhibited in older middle-aged adults (Johannsmeyer et al., 2016); those that were randomly allocated to the placebo group during drop-set RT experienced significantly greater improvement in dynamic balance (30.8%) compared to the creatine group (19.4%), with a reduction in balance errors detected for the placebo group only. In sum, creatine supplementation in older adults during RT appears to support increased lean tissue mass, but this has not necessarily translated into appreciable gains in muscle strength, physical function and/or improved balance versus placebo.
Is creatine well tolerated and safe?
Creatine when used in healthy, older adults appears to be well tolerated and safe. There have been no reports or evidence of any adverse effects that are serious in nature (Chilibeck et al., 2017; Goudarzian et al., 2017; Pinto et al., 2016; Gualano et al., 2014; Alves et al., 2013; Brose et al 2003; Chrusch et al., 2001; Bermon et al., 1998) and self-reported issues associated with the use of creatine have been uncommon (Pinto et al 2016; Gualano et al., 2014; Alves et al., 2013; Brose et al., 2003). No adverse events related to, nor changes in either kidney or liver function have been reported from RCTs (Gualano et al., 2014; Tarnopolsky et al., 2007; Brose et al., 2003) and other studies that included both middle-aged and older adults are devoid of any such side-effects (Johannsmeyer et al., 2016; Chilibeck et al., 2015; Lobo et al., 2015; Cornelissen et al., 2010; Eijnde et al., 2003). Some studies have reported that gastrointestinal (GI) distress and muscle cramping and/or muscle strain may be more common in those receiving creatine (Chilibeck et al., 2015; Chrusch et al., 2001). In healthy, older men (mean age=70 years old) loose stools were reported by Chrusch et al., (2001) as a side-effect during the 1-week loading phase and increased muscle cramping/strain occurred between weeks 3 and 5. Middle-aged to older postmenopausal women (mean age=57 years old) taking creatine experienced a higher number of these adverse events when GI complaints and muscle cramping were grouped for assessment (Chilibeck et al., 2015). None of these side-effects led to study discontinuation and appear to be transient in nature with no impairment of exercise training response noted.
What questions do we need further clarification on?
Many questions remain unresolved. Despite the evidence supporting increased lean tissue mass following creatine supplementation, it seems too early to claim definitively that such a strategy substantially and consistently improves muscle strength or physical function in all older adults undergoing RT. Training adaptations, in theory, should be augmented by creatine. It is well acknowledged that ageing causes skeletal muscle atrophy with disproportionately greater reduction in cross-sectional area (CSA) of PCr-rich type-II muscle fibres (Nilwik et al., 2013; Kushmerick et al., 1992), and this results in much lower levels of intramuscular creatine in the quadriceps vastus lateralis (thigh) muscle of older versus younger adults (Chilibeck et al., 2017). Lifestyle changes with ageing – particularly reduced dietary meat intakes, decreased physical activity levels (Chilibeck et al., 2017) and increased sedentary time (Diaz et al., 2017; Dunlop et al., 2015) – may further impact muscle PCr levels and modify any potential benefits of creatine supplementation. Further research is therefore required to establish whether the magnitude and heterogeneity of RT adaptations is modulated by significant inter-individual differences in creatine uptake kinetics, given that training responsiveness is correlated to the change in intramuscular creatine stores. Research by Syrotuik and Bell (2004) provide support for this possibility where it was demonstrated that young, healthy men had 3 different levels of response to a 5-day creatine load as measured by post-supplementation intramuscular creatine levels. Responders to creatine loading possessed a biological profile of the lowest initial muscle Cr/PCr levels, greatest percentage of type-II muscle fibres, largest muscle fibre CSA and lean tissue mass, plus were the only subjects to achieve improvement in 1RM leg press when compared to quasi- and non-responders. It is plausible that this may partially account for the lack of consistency in the research as such inter-individual variation could significantly water down any generalised group benefits. These responder profiles outlined above also raise another potential limitation in those older adults that are most in need of an ergogenic effect (i.e. those with sarcopenia and muscle weakness), as they may be the least likely, by extension, to reap the meaningful benefits of creatine supplementation. Furthermore, it is well accepted that intramuscular post-supplementation creatine levels (at day 28) are comparable for “slow” (3 grams/day for 1 month) and “rapid” load (4×5 grams/day for 5-7 days and 3-5 grams/day thereafter) protocols (Hultman et al., 1996). Thus, it would be prudent to compare whether the slow load approach is better tolerated than the rapid load approach (i.e. reduction of GI-related side-effects and muscle cramping/pulls) based on the evidence where some older adults appear to be more sensitive to large initiation doses of creatine.
Taken from Syrotuik & Bell (2004)
Final comments
It is worth mentioning that besides any possible beneficial effect of creatine on lean tissue mass, skeletal muscle strength or function, there are several other therapeutic reasons that may potentially justify such use in older adults. An increasing amount of data from both human and rodent experiments support multiple other benefits for creatine, including lowering cholesterol and triglyceride levels, reducing liver fat accumulation, decreasing homocysteine levels, having antioxidant properties, improving glycaemic control, slowing tumor growth in some types of cancers, mitigating bone loss, positively affecting cognitive function and in some cases, serving as an antidepressant (Kreider et al., 2017). Consequently, the position stand on the safety and efficacy of creatine supplementation in exercise, sport, and medicine published by the International Society of Sports Nutrition concluded that (2017:11):
Available short and long-term studies in healthy and diseased populations, from infants to the elderly, at dosages ranging from 0.3 to 0.8 g/kg/day for up to 5 years have consistently shown that creatine supplementation poses no adverse health risks and may provide a number of health and performance benefits.
References
Aguiar AF, Januário RS, Junior RP, Gerage AM, Pina FL, Do Nascimento MA, Padovani CR, Cyrino ES. Long-term creatine supplementation improves muscular performance during resistance training in older women. European journal of applied physiology. 2013 Apr 1;113(4):987-96.
Alves CR, Merege Filho CA, Benatti FB, Brucki S, Pereira RM, de Sá Pinto AL, Lima FR, Roschel H, Gualano B. Creatine supplementation associated or not with strength training upon emotional and cognitive measures in older women: a randomized double-blind study. PLoS One. 2013 Oct 3;8(10):e76301.
Anderson O. (1993) Creatine propels British athletes to Olympic gold medals: Is creatine the one true ergogenic aid? Running Research News 9, 1-5
Beaudart C, Rabenda V, Simmons M, Geerinck A, Araujo DC, Reginster JY, Amuthavalli TJ, Bruyère O. Effects of Protein, Essential Amino Acids, B-Hydroxy B-Methylbutyrate, Creatine, Dehydroepiandrosterone and Fatty Acid Supplementation on Muscle Mass, Muscle Strength and Physical Performance in Older People Aged 60 Years and Over. A Systematic Review on the Literature. The journal of nutrition, health & aging. 2018;22(1):117.
Bermon S, Venembre P, Sachet C, Valour S, Dolisi C. Effects of creatine monohydrate ingestion in sedentary and weight-trained older adults. Acta Physiologica Scandinavica. 1998 Oct 1;164:147-56.
Bird SP. Creatine Supplementation and Exercise Performance: A Brief Review. Journal of Sports Science & Medicine. 2003;2(4):123-132.
Brose A, Parise G, Tarnopolsky MA. Creatine supplementation enhances isometric strength and body composition improvements following strength exercise training in older adults. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. 2003 Jan 1;58(1):B11-9.
Buford TW, Kreider RB, Stout JR, Greenwood M, Campbell B, Spano M, Ziegenfuss T, Lopez H, Landis J, Antonio J. International Society of Sports Nutrition position stand: creatine supplementation and exercise. Journal of the International Society of Sports Nutrition. 2007 Aug 30;4(1):6.
Candow et al. Effect of 12 months of creatine supplementation and whole-body resistance training on measures of bone, muscle and strength in older males. Nutr Health. 2020, Nov 24 (online ahead of print)
Candow DG, Chilibeck PD. Potential of creatine supplementation for improving aging bone health. The journal of nutrition, health & aging. 2010 Feb 1;14(2):149-53.
Candow DG, Zello GA, Ling B, Farthing JP, Chilibeck PD, McLeod K, Harris J, Johnson S. Comparison of creatine supplementation before versus after supervised resistance training in healthy older adults. Research in Sports Medicine. 2014 Jan 2;22(1):61-74.
Chilibeck PD, Candow DG, Landeryou T, Kaviani M, Paus-Jenssen L. Effects of creatine and resistance training on bone health in postmenopausal women. Medicine & Science in Sports & Exercise. 2015 Aug 1;47(8):1587-95.
Chilibeck PD, Kaviani M, Candow D, Zello, G. Effect of creatine supplementation during resistance training on lean tissue mass and muscular strength in older adults: a meta-analysis. Open Access Journal of Sports Medicine 2017 Nov 2; 8: 213-226.
Chrusch MJ, Chilibeck PD, Chad KE, Davison KS, Burke DG. Creatine supplementation combined with resistance training in older men. Medicine & Science in Sports & Exercise. 2001 Dec 1;33(12):2111-7.
Close GL, Hamilton DL, Philp A, Burke LM, Morton JP. New strategies in sport nutrition to increase exercise performance. Free Radical Biology and Medicine. 2016 Sep 30;98:144-58.
Cornelissen VA, Defoor JG, Stevens A, Schepers D, Hespel P, Decramer M, Mortelmans L, Dobbels F, Vanhaecke J, Fagard RH, Vanhees L. Effect of creatine supplementation as a potential adjuvant therapy to exercise training in cardiac patients: a randomized controlled trial. Clinical rehabilitation. 2010 Nov;24(11):988-99.
Deane CS, Wilkinson DJ, Phillips BE, Smith K, Etheridge T, Atherton PJ. “Nutraceuticals” in relation to human skeletal muscle and exercise. American Journal of Physiology-Endocrinology and Metabolism. 2017 Apr 1;312(4):E282-99.
Devries MC, Phillips SM. Creatine supplementation during resistance training in older adults-a meta-analysis. Med Sci Sports Exerc. 2014;46(6):1194–203
Diaz KM, Howard VJ, Hutto B, Colabianchi N, Vena JE, Safford MM, Blair SN, Hooker SP. Patterns of sedentary behavior and mortality in US Middle-aged and older adults: a national cohort study. Annals of internal medicine. 2017 Oct 3;167(7):465-75.
Dunlop DD, Song J, Arnston EK, Semanik PA, Lee J, Chang RW, Hootman JM. Sedentary time in US older adults associated with disability in activities of daily living independent of physical activity. Journal of physical activity & health. 2015 Jan;12(1):93.
Eijnde BO, Van Leemputte M, Goris M, Labarque V, Taes Y, Verbessem P, Vanhees L, Ramaekers M, Eynde BV, Van Schuylenbergh R, Dom R. Effects of creatine supplementation and exercise training on fitness in men 55–75 yr old. Journal of Applied Physiology. 2003 Aug 1;95(2):818-28.
Figueiredo VC, de Salles BF, Trajano GS. Volume for Muscle Hypertrophy and Health Outcomes: The Most Effective Variable in Resistance Training. Sports Medicine. 2017 Oct 11:1-7.
Goudarzian M, Rahimi M, Karimi N, Samadi A, Ajudani R, Sahaf R, Ghavi S. Mobility, Balance, and Muscle Strength Adaptations to Short-Term Whole Body Vibration Training Plus Oral Creatine Supplementation in Elderly Women. Asian Journal of Sports Medicine. 2017 Mar 1;8(1).
Gualano B, Macedo AR, Alves CR, Roschel H, Benatti FB, Takayama L, de Sá Pinto AL, Lima FR, Pereira RM. Creatine supplementation and resistance training in vulnerable older women: a randomized double-blind placebo-controlled clinical trial. Experimental gerontology. 2014 May 31;53:7-15.
Gualano B, Rawson ES, Candow DG, Chilibeck PD. Creatine supplementation in the aging population: effects on skeletal muscle, bone and brain. Amino acids. 2016 Aug 1;48(8):1793-805.
Hultman E, Soderlund K, Timmons JA, Cederblad G, Greenhaff PL. Muscle creatine loading in men. Journal of applied physiology. 1996 Jul 1;81(1):232-7
Johannsmeyer S, Candow DG, Brahms CM, Michel D, Zello GA. Effect of creatine supplementation and drop-set resistance training in untrained aging adults. Experimental gerontology. 2016 Oct 31;83:112-9.
Kreider RB, Kalman DS, Antonio J, Ziegenfuss TN, Wildman R, Collins R, Candow DG, Kleiner SM, Almada AL, Lopez HL. International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. Journal of the International Society of Sports Nutrition. 2017 Jun 13;14(1):18.
Kuriansky J, Gurland B. The performance test of activities of daily living. The International Journal of Aging & Human Development.1976; 7:343-352.
Kushmerick MJ, Moerland TS, Wiseman RW. Mammalian skeletal muscle fibers distinguished by contents of phosphocreatine, ATP, and Pi. Proceedings of the National Academy of Sciences. 1992 Aug 15;89(16):7521-5
Lobo DM, Tritto AC, da Silva LR, de Oliveira PB, Benatti FB, Roschel H, Nieß B, Gualano B, Pereira RM. Effects of long-term low-dose dietary creatine supplementation in older women. Experimental gerontology. 2015 Oct 31;70:97-104.
Neves Jr M, Gualano B, Roschel H, Fuller R, Benatti FB, Pinto AL, Lima FR, Pereira RM, Lancha Jr AH, Bonfa E. Beneficial effect of creatine supplementation in knee osteoarthritis. Medicine and science in sports and exercise. 2011 Aug;43(8):1538-43.
Nilwik R, Snijders T, Leenders M, Groen BB, van Kranenburg J, Verdijk LB, van Loon LJ. The decline in skeletal muscle mass with aging is mainly attributed to a reduction in type II muscle fiber size. Experimental gerontology. 2013 May 31;48(5):492-8.
Phillips SM. Nutritional supplements in support of resistance exercise to counter age-related sarcopenia. Advances in Nutrition: An International Review Journal. 2015 Jul 1;6(4):452-60.
Pinto CL, Botelho PB, Carneiro JA, Mota JF. Impact of creatine supplementation in combination with resistance training on lean mass in the elderly. Journal of cachexia, sarcopenia and muscle. 2016 Sep 1;7(4):413-21.
Ralston GW, Kilgore L, Wyatt FB, Baker JS. The Effect of Weekly Set Volume on Strength Gain: A Meta-Analysis. Sports Medicine. 2017 Jul 28:1-7.
Rhea MR. Determining the magnitude of treatment effects in strength training research through the use of the effect size. Journal of strength and conditioning research. 2004 Nov 1;18:918-20.
Schoenfeld BJ, Ogborn D, Krieger JW. Dose-response relationship between weekly resistance training volume and increases in muscle mass: A systematic review and meta-analysis. Journal of sports sciences. 2017a Jun 3;35(11):1073-82.
Schoenfeld BJ, Ogborn D, Krieger JW. The dose–response relationship between resistance training volume and muscle hypertrophy: are there really still any doubts?. Journal of sports sciences. 2017b Oct 18;35(20):1985-7.
Sullivan, Gail M., and Richard Feinn. “Using effect size—or why the P value is not enough.” Journal of graduate medical education 4, no. 3 2012: 279-282.
Syrotuik DG, Bell GJ. Acute creatine monohydrate supplementation: A descriptive physiological profile of responders vs. nonresponders. The Journal of Strength & Conditioning Research. 2004 Aug 1;18(3):610-7.
Tarnopolsky M, Zimmer A, Paikin J, et al., Creatine monohydrate and conjugated linoleic acid improve strength and body composition following resistance exercise in older adults. PLoS One. 2007;2(10):e991.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to improve muscular strength, physical function (how you move around during the day) and quality of life or programs to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
Several years ago researchers and authors Malhotra, Noakes & Phinney published an article in the British Journal of Sports Medicine titled:
“It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet” (see here)
This created quite a storm in several fields of scientific research including many fitness and nutrition blogs. It was lambasted by some though as inaccurate and misleading – just Google the title of the article and you’ll understand what I mean. Essentially, their article claimed that regular physical activity does not promote weight loss and that excessive consumption of carbohydrates, in particular, sugar, is the primary cause of the obesity epidemic. Whilst excessive sugar consumption has played an important role in exacerbating the obesity crisis, it would be naive and short-sighted to suggest that this is the be-all and end-all in explaining society’s current predicament.
“Why you shouldn’t exercise to lose weight, explained with 60+ studies” (see here)
This article posits that exercise is unhelpful for weight loss and makes very similar claims to the Malhotra et al. paper. Of course, the real question is, are these claims valid? Could it really be true that weight loss is not facilitated by increasing daily energy expenditure and exercise? I think the answer to these questions are not black or white. My main concern with the articles mentioned above is that they are rather myopic, polarising and do not provide a fair and balanced assessment of the current evidence.
Instead, the evidence published to date demonstrates that ‘our’ increasing waistlines are closely related – but not confined to – the interaction of the following 3 factors. Firstly, the sum total of all physical movement performed whilst awake has substantially decreased over the last 50 years. Secondly, activities of a sedentary nature have dramatically increased. What are you doing right now? Thirdly, total energy intake over the last 50 years has continued to increase over and above total daily energy expenditure requirements. If movement levels are low and energy intake high – irrespective of where the excess is derived from – body weight, body fat and BMI will naturally increase. But does increasing physical activity levels via a formalised exercise program and/or non-exercise based physical activities (e.g. leisure time movement, domestic chores/activities) facilitate weight loss by increasing total daily energy expenditure? The answer to this is yes and no.
Today I want to focus on the evidence that was accessible following a brief Google Scholar search that supports exercise as well as other non-exercise increases in daily physical movement as being promoters of weight loss. For anybody not familiar with Google Scholar (https://scholar.google.com.au), it is a search engine by Google that searches for only published, peer-reviewed journal-based research and consequently provides information that is evidence-based rather than ‘opinion-based’ which is largely what would be accessed via Google, Yahoo or any other search engine. So, what did I find?
One of the more interesting pieces of research that directly contradicts the article by Malhotra and co. is that written by Church et al. (2011). They concluded that over the last 50 years in the U.S., daily occupation-related energy expenditure was estimated to have decreased by more than 100 calories per day, and this reduction in energy expenditure could account for a significant portion of the increase in mean U.S. body weights for women and men. What this would suggest is that rather than increased obesity rates being caused exclusively by too many carbs or too much sugar, as argued by the “you can’t outrun a bad diet” article, the current problem has been driven by large reductions in energy expenditure due to changes to occupation-related physical movement. In other words, we have transitioned from jobs that are active and require a lot of physical movement to jobs now that have most of us sitting on our backsides for hours on end.
Doing this all day can’t be helpful
Previous reports based on estimated caloric consumption from food production and food disappearance (food waste) estimates have concluded that increased caloric consumption could account for most, if not all, of the weight gained at a population level in the U.S. Nonetheless, a recently validated differential equation model was used to identify a conservative lower bound for the amount of food waste in the U.S. (Hall et al. 2009). This analysis determined that prior estimates of national food waste were grossly underestimated; indicating that the national average caloric intake was much lower than previously estimated. As such, these results and those of Church imply that increased caloric intake or for that matter, increased sugar consumption, cannot solely account for the observed trends in national weight gain in the US.
The following is a summary of some of the research that has been published investigating whether obesity is related to physical inactivity and what effect increased physical activity has on obesity risk and management.
1. Banks et al. (2010) reported that: “Obesity increases with increasing screen-time, independent of purposeful physical activity.”
2. Goodpaster et al. (2010) found that: “Among patients with severe obesity, a lifestyle intervention involving diet combined with initial or delayed initiation of physical activity resulted in clinically significant weight loss and favourable changes in cardiometabolic risk factors.” In the group where physical activity was delayed, the addition of such physical activity promoted greater reductions in waist circumference and hepatic fat content.
3. Banks et al. (2011)showed that: “Domestic activities and sedentary behaviours are important in relation to obesity in Thailand, independent of exercise-related physical activity. In this setting, programs to prevent and treat obesity through increasing general physical activity need to consider overall energy expenditure and address a wide range of low-intensity high-volume activities in order to be effective.”
4. Villareal et al. (2011) demonstrated that: “…in obese older adults a combination of weight loss and exercise provides greater improvement in physical function than either intervention alone.”
5. McGuire & Ross (2012) reported that: “…light physical activity, incidental physical activity and sedentary behaviour were not associated with abdominal obesity amongst inactive men and women whereas moderate-to-vigourous physical activity predicted lower visceral adipose tissue.”
6. The study by Fan et al. (2013) was: “…to test if moderate-to-vigorous physical activity (MVPA) in less than the recommended ≥10-minute bouts related to weight outcomes.” Both higher-intensity short bouts and long bouts of physical activity related to lower BMI and risk of overweight/obesity whereas neither lower-intensity short bouts nor long bouts related to BMI or risk of overweight/obesity. They concluded that: “The current ≥10-minute MVPA bouts guideline was based on health benefits other than weight outcomes. Our findings showed that for weight gain prevention, accumulated higher-intensity PA bouts of <10 minutes are highly beneficial, supporting the public health promotion message that ‘every minute counts’.”
7. Cleland et al. (2014) found that: “High sitting and low activity increased obesity odds among adults. Irrespective of sitting, men with low step counts had increased odds of obesity. The findings highlight the importance of engaging in physical activity and limiting sitting.”
8. Jakicic et al. (2014) concluded that moderate-to-vigorous physical activity (MVPA > 10) of 200-300 min per week, coupled with increased amounts of low-intensity physical activity (LPA), are associated with improved long-term weight loss. Interventions should promote engagement in these amounts and types of physical activity.
9. Murabito et al. (2015) discovered that moderate-to-vigorous physical activity (MVPA) as measured by accelerometry was associated with less visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) and better fat quality as assessed by multi-detector computed tomography. With increasing MVPA, there was a concomitant decrease in VAT. Higher levels of MVPA were associated with higher SAT fat quality, even after adjustment for SAT volume. They concluded that:
“MVPA was associated with less VAT and SAT and better fat quality.”
10. Mekary et al (2015) reported that: “….over 12 years long-term weight training is associated with less waist circumference increase, whilst moderate-to-vigorous aerobic activity was associated with less body weight gain in healthy men.”
11. Hume et al. (2016) concluded that: “….counter to the energy surfeit model of obesity, results suggest that increasing energy expenditure may be more effective for reducing body fat than caloric restriction, which is currently the treatment of choice for obesity.”
12. Myers et al. (2016)suggests that there exists clear associations among objective measures of physical activity, sedentary behaviour, energy expenditure, adiposity and appetite control. They produced data that indicates strong links between physical inactivity and obesity with this relationship likely to be bidirectional.
13. Wu et al. (2017) tested 12-weeks of low- and high-intensity exercise training in Mexican-American and Korean premenopausal overweight/obese women. Results showed that such exercise reduced body mass index, body fat percentage, fat mass and visceral adipose tissue with concurrent increases in lean mass.
14. Quist et al. (2018) examined the effects of 6-months of active commuting and leisure-time exercise on fat loss in women and men who were overweight or obese. Clinically meaningful fat loss of over 4 kilograms was elicited. Vigorous intensity exercise was shown to be more effective in reducing body fat versus moderate intensity exercise.
15. Stoner et al. (2019) concluded that the findings of their meta-regression “lend support to the use of exercise prescription for promoting weight loss and improving health outcomes in adolescents with overweight/obesity.”
16. Zhang et al. (2020) found that 12-weeks of intense exercise (without concurrent nutritional intervention, i.e. ‘put on a diet’) significantly improved cardiometabolic parameters (i.e. fasting blood glucose) and decreased weight, total percent body fat, whole-body fat mass, android, gynoid, and trunk fat mass, abdominal subcutaneous fat and abdominal visceral fat. Reductions of over 15 cm² of abdominal visceral fat were achieved in just 3 months!
17. Berge et al. (2021) produced clinically significant weight loss in people with severe obesity despite the study having no specific focus on body weight reduction. The group that performed moderate‐intensity continuous training combined with high‐intensity interval training lost an average of 5 kilograms in 24-weeks.
Staying strong as we age is critical to health
What does this research tell us?
Quite a lot I would say. Of particular note is that this only represents a very small sample of the evidence that directly counters the claim that widespread societal levels of physical inactivity have little to do with burgeoning obesity rates. What is more, it crystallizes just how contentious Malhotra, Noakes & Phinney’s editorial was. Exclusively assigning blame for the obesity epidemic to the excessive intake of sugar is not supported, I believe, by the current evidence. The dramatic reductions in the sum total of all physical activity accumulated during the day appears to account for a substantial amount of the increased weight seen in recent decades.
Firstly, there is a substantial amount of research which demonstrates that sedentary behaviours, sitting time and low physical activity levels manifestly increase one’s risk of becoming overweight or obese. Secondly, moderate-to-vigourous physical activity compared to light physical activity has been shown to be associated with less visceral and subcutaneous adipose tissue, impacts positive effects on fat quality, is related to lower BMI, lowers risk of overweight/obesity, prevents weight gain following weight loss, promotes greater reductions in waist circumference and produces favourable changes in cardio-metabolic risk factors.
So to conclude, my Google Scholar search unveiled that there is a large body of evidence that demonstrates that there may be no myth to bust regarding obesity and physical inactivity or foundation to suggesting that physical activity plays no role toward promoting weight loss. Others have been critical of this line of thinking too, in particular Dr Steven Blair, so I would suggest that if you wanted to read further on this here would be a good place to start.
My next article will explore the evidence that exercise does not assist weight loss in all exercisers due to various compensatory mechanisms (see here). Until then, stay active, keep moving and don’t forget to include some resistance exercise in your week.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to improve health, physical function and quality of life or to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
In a recent meta-analysis (see here), vitamin D was found to provide an additive benefit for older adults partaking in resistance training (RT). In other words, when compared to older adults taking a placebo, significantly greater gains in muscle strength were achieved in those supplemented with vitamin D. However, upon closer analysis several issues become obvious that are difficult to reconcile. The following discusses some of these issues inherent in the findings of this paper (see below).
The group 1 analysis of 3 trials finds vit D supplementation augments muscle strength of the lower limbs, SMD=0.98; see fig 2 below. (Please click on any image to open and make larger for viewing).
…but what is with the scale used for the x-axis; it seems all wrong…..all the green squares sit nicely on zero……. and where is my forest plot with 95% CI bars and my black triangle to show overall SMD?
As a crude comparison & to put this in context, Chilibeck et al (2017) found SMD=0.25 for the effect of creatine supplementation on lower body strength during RT in older adults. Perhaps the most effective supplement available? Could vit D really be that much better?
The authors acknowledge serious inconsistency with substantial heterogeneity (see table 5) for this outcome measure and even suggest that maybe: “….these studies were unsuitable for comparison”, but conclude nonetheless that there is: “tentative support for the additive effects of RT and vit D supplementation for the improvement of muscle strength in older adults”, including those replete in Vit D.
The Uusi-Rasi et al (2015) trial was weighted heavily (75%) and rightly so being the most well designed, largest & longest RCT to date. In fact SMD of this trial in the group 1 analysis = 1.16. This is very impressive and clinically relevant if accurate and valid. Uusi-Rasi et al (2015) in contrast states: “Irrespective of vit D, exercise increased muscle strength. The predicted mean increase in lower limb extension strength was almost 15% in both exercised groups and differed significantly from the placebo without exercise group.”
“Another unexpected finding was that exercisers treated with vit D supplementation showed consistently smaller benefits than exercisers receiving placebo……our results indicate that vit D may not improve neuromuscular function, at least when vit D intake is sufficient.” The largest and longest RCT to date found no additional – and perhaps even attenuated – benefit of vit D supplementation in replete resistance-training older adults, which is at complete odds to the meta-analysis.
The Agergaard et al (2015) trial showed no additional benefit of vit D on muscle strength in older adults (vit D replete). Sample size for older adults was very small also and weighted acccordingly in the meta.
….and Bunout et al (2006) found that combined calcium/vit D supplementation was no more effective than calcium-only supplementation in older adults undergoing RT but – and this is a critical point of difference to the other 2 studies.
– all participants were arguably vit D insufficient; to be included participants had to be 16 ng/ml (40 nmol/L) or less for serum 25(OH)D. An important point that was missed by the authors of the meta-analysis (see further below).
These 3 studies included in the group 1 analysis of muscle strength of the lower limbs were identified as “all participants took part in RT and the intervention arm was supplemented with vit D (describing the additive effect of vit D supplementation when combined with RT)”
However, Bunout et al (2006) did not include a RT group that received a ‘true’ placebo. Both exercising groups in this trial received supplementation of some sort.
….one group was supplemented with vit D & calcium (intervention), the other exercising group were supplemented with calcium-only (control). “……vit D was given along with calcium in this trial, since a low calcium intake can limit the effects of the vitamin.
To isolate the effect of the vitamin, controls for supplementation received calcium also.” However results showed there were no statistically significant differences between these groups in baseline to final percentage change for right and left quadriceps strength, and right and left hand grip strength. In fact, the RT plus calcium-only group achieved better mean numerical responses in strength (non-significant) when compared to the RT plus vit D/calcium group (see table 2)……..so is it somewhat unusual that such a large SMD was found in the meta favouring the group that received vit D?
The authors state in the meta discussion that: “Interestingly, although the studies included within group 1 did not specify serum 25(OH)D levels as inclusion/exclusion critieria, baseline and postintervention serum 25(OH)D were within the ‘sufficient’ range (>30 nmol/L).”
Now there are 2 issues with this statement. Firstly, it is false that all studies included in group 1 did not specify serum 25(OH)D levels as inclusion/exclusion criteria. Bunout et al (2006) in fact did just that and specified a cut-off point for inclusion.
Subjects were screened and included only if their serum 25(OH)D levels were 16 ng/ml (40 nmol/L) or less. Secondly, mean baseline serum 25(OH)D of the vit D supplemented group in Bunout et al (2006) was 12.4 ng/ml (30 nmol/L) and many experts would propose that serum 25(OH)D of around 30 nmol/L in older adults is insufficient. It is also worth noting that Vit D status for participants of each of the 3 studies varied considerable and could possibly confound the meta.
After reviewing the 3 trials very carefully (used in the group 1 analysis of Antonia and Greig 2017), the finding that vit D supplementation significantly augments muscular strength of older adults doing RT, including those replete for vit D (SMD=0.98), is perplexing.
It is plausible and there is some evidence that vit D supplementation may augment strength of exercising older adults that have insuffient or deficient levels of vit D [serum 25(OH)D <50 nmol/L & <25 nmol/L] but such data is as yet not forthcoming in older adults performing RT
After reviewing Antoniak & Greig (2017) in which vit D supplementation significantly enhances strength in older adults doing RT, I cannot but view the findings as an artefact possibly generated by the unresolvable and substantial heterogeneity that was detected in the analysis.
The conclusion of tentative support for the ergogenity of vit D in older RT adults, irrespective of serum 25(OH)D status, is therefore premature and unsubstantiated.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to improve muscular strength, physical function (how you move around during the day) and quality of life or programs to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
