More Time In Bed Boosts Basketball Performance

Looking for that extra edge on the basketball court?  Want to increase your free throw percentage and gain an extra step in quickness?  Is it a new performance enhancing drug or training technique?  No, a new study suggests it may be as easy as spending a few extra hours in bed.

Cheri Mah and colleagues from Stanford University and the University of California, San Francisco recently published their research on sleep and athletic performance in the journal Sleep.  They introduce the study by noting that extensive research documents the adverse effect of limited sleep.  However, little research examines the effect of increased sleep on performance.  Their study objective was to do just that.

Members of the Stanford University mens basketball team were recruited for the study.  The study took place over two seasons and included a baseline period of usual sleep patterns.  Then the intervention group extended their sleep pattern with a goal of a minimum of 10 hours in bed daily.

Compliance with this intervention was measured through sleep journals and actigraphy.  Actigraphy is accomplished by a wrist device that is worn and measures movement.  From this data the total sleep time can be estimated.  Sleep journal data and activity data estimated the increase in total daily sleep time to be between 100 and 150 minutes of additional sleep during the intervention period.

Athletes in the intervention groups were tested on a variety of psychometric and basketball performance skills during the baseline and intervention period.  The results of the intervention were pretty impressive.  Here is a summary of the improvement noted in the study:

• Free throw percentage increased by 11%
• Three point percentage increased by 14%
• Sprint test time decreased by 4%

Other psychometric variables were improved including a reduction in time on the Psychomotor Vigilance Task, a reduction in the Epworth Sleepiness Scale score and improvement on multiple components of the Profile of Mood States including ratings of fatigue, depression and tension.

The authors note the study has some significant limitations in research design.  Only eleven athletes received the intervention.  Subjects were not blinded as to the intervention and it is possible a some of the improvement came from an expectancy effect.  Travel schedules made it difficult to assure compliance with the 10 hours in bed intervention for every day of the study.

However, this study does suggest that many athletes may be performing in the context of ongoing sleep deprivation.  Forcing compliance with an extended sleep duration holds promise of improving performance on the basketball court.  This effect appears to occur in the context of subjective improvement in psychological function.

If I were an NCAA basketball athlete, I would send a copy of this study to my coach and training staff.  Athletes now have some research to support the importance of getting plenty of sleep to achieve peak performance.

Photo of Los Angeles Clipper Player Blake Griffin Shooting Free Throw Courtesy of Tim Yates

Mah CD, Mah KE, Kezirian EJ, & Dement WC (2011). The Effects of Sleep Extension on the Athletic Performance of Collegiate Basketball Players. Sleep, 34 (7), 943-950 PMID: 21731144

Decoding the Faces of Depression: Anhedonia and Dopamine

Diego Pizzagalli presented the March 2011 Warren Frontiers in Neuroscience Series lecture in Tulsa, Oklahoma on March 1, 2011.  Dr. Pizzagalli works at the Harvard Medical School affiliated Center for Depression, Anxiety and Stress Research & Neuroimaging Center at McLean Hospital in Boston.  He has been involved in research related to brain abnormalities in major depression as well as predictors of treatment response.  I will highlight some of the key points from his lecture and incorporate three recent research manuscripts related to this topic:

• There are over 100 symptom combinations to diagnosis major depression (5 of 9 symptoms required)
• Distinct depressive phenotypes (clinical presentations) are difficult to define--but the phenotype defined by anhedonia (pervasive lack of ability to experience pleasure) has significant research support
• Depression with anhedonia also has a biological component--the brain reward pathways involving dopamine and the striatum.
• Anhedonia has been linked to impaired dopamine function in these brain reward pathways
• Anhedonia appears more heritable than depression and may be related to abnormalities in genes controlling dopamine neurotransmission
• The dopamine reward pathway (substantia nigra-striatum-cingulate/prefrontal cortex) is vulnerable to stress (acute stress increases dopamine, chronic stress reduces it in the rat model)
• He and colleagues developed a heuristic model of the functional neuroanatomy of anhedonia: both environmental and biological factors influence risk of depression: depression includes a decrease in the brains reward response, exaggerated stress responsivity and eventually a blunted mesolimbic dopamine system (and anhedonia)
• Laboratory models and psychometric measures of anhedonia have been developed--studies suggest the ventral striatum (nucleus accumbens) is involved in hedonic coding while the dorsal striatum (caudate) is involved in positive re-inforcement
• Decreased activation of cingulate and caudate with monetary incentive delay task is seen in untreated depression
• Untreated depression (and anhedonia) also linked to decreased size of the caudate
• Early life stress (abuse) may increase depression risk through dysregulation of mesolimbic pathways including left putamen and left pallidum
• Stress even in healthy individuals impairs brains reward processing pathway
• Some genes related to anhedonia may work through stress pathways, i.e. mineralcorticoids, corticotrophin hormone (CRH)
• Future research will focus on further parsing of the heterogeneity associated with depression, developing animal models of reward tasks, using PET to better understand the role of dopamine in depression, using dopaminergic drugs (i.e. pramipexole) in stimulation models of depression and further study of the neurobiology of stress-induced anhedonia

I agree that evaluating the role of dopaminergic drugs in depression accompanied by anhedonia is worthy of basic and clinical research study.  Among typical antidepressants, only bupropion appears to have dopaminergic effects.  Other compounds such as psychostimulants also increase dopamine but carry the risk for abuse.  Several of the dopaminergic drugs used for Parkinson disease are beginning to see more use off-label for the treatment of depression.  I will look at this issue in a future Brain Post. 

Photo of Blake Griffin shooting free throw against Oklahoma City Thunder in 2011 NBA game courtesy of Tim Yates.

Pizzagalli DA, Holmes AJ, Dillon DG, Goetz EL, Birk JL, Bogdan R, Dougherty DD, Iosifescu DV, Rauch SL, & Fava M (2009). Reduced caudate and nucleus accumbens response to rewards in unmedicated individuals with major depressive disorder. The American journal of psychiatry, 166 (6), 702-10 PMID: 19411368

Wacker J, Dillon DG, & Pizzagalli DA (2009). The role of the nucleus accumbens and rostral anterior cingulate cortex in anhedonia: integration of resting EEG, fMRI, and volumetric techniques. NeuroImage, 46 (1), 327-37 PMID: 19457367

Pizzagalli DA (2011). Frontocingulate dysfunction in depression: toward biomarkers of treatment response. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 36 (1), 183-206 PMID: 20861828