ONLINE DRIVERS MEDIA

No, the sun does not kill you. If you control your exposure it may extend your life and improve your life-quality significantly.

Its about time to "let there be light" to illuminate the benefits of regular well-timed exposure to sunlight and its short frequency component. Only recently, researchers from the Japanese National Institute of Advanced Industrial Science and Technology (AIST) were able to show that daytime light exposure has significant beneficial effects on cognitive brain activity. Significant enough to have the subjects perform better on an oddball task and to significantly increase cortical activity related to cognitive processes (Okamoto. 2014).

But is that really all, bright light, or more specifically, the regular and well-timed exposure to bright light can do for you?
Certainly not. I mean if its ill-timed, like the evening use of light-emitting eReaders it will negatively affect your sleep, mess up your circadian rhythm and decrease your alertness on the next morning. Similar results, i.e. drowsiness and suppression of energy metabolism the following morning, have been reported by other studies, as well (Kayaba. 2014).

As a SuppVersity reader you do yet know all about those negative effects from the circadian rhythm series, anyway. Reason enough for me, to focus primarily on all the good stuff, the well-timed exposure to bright light can do for you in todays Special of the SuppVersity Short News.

• If you cant let go off your mobile at night, use blue blocker glasses as a countermeasure for alerting effects of evening light-emitting diode screen exposure - According to researchers from the Psychiatric Hospital of the University of Basel, blue blocker glasses (BB) significantly attenuate LED-induced melatonin suppression in the evening and decrease vigilant attention and subjective alertness before bedtime.
  
  Strangely, though, visually scored sleep stages and behavioral measures collected the morning after were not modified. Still, van der Lely et al. conclude: "BB glasses may be useful in adolescents as a countermeasure for alerting effects induced by light exposure through LED screens and therefore potentially impede the negative effects modern lighting imposes on circadian physiology in the evening "(van der Lely. 2014).
• UV-light protects against "brainflammation" in MS model - Scientists from the University of Wisconsin-Madison report in their latest paper that UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis.
  
  Previous studies have already shown that UV radiation (UVR) can suppress experimental autoimmune encephalomyelitis (EAE), an animal model of multiple-sclerosis (MS), independent of vitamin D production. The mechanism of this suppression did yet remain to be elucidated, until Wang et al. (2014) observed that UVR (10kJ/m²) does not just inhibit the inflammation and demyelination of the spinal cord, but will also dramatically and significantly reduce spinal cord chemokine CCL5 mRNA and protein levels.
  
  In conjunction with an increased production of intereron-gamma (IFN-?) and IL-10, which are actually used to treat all sorts of autoimmune diseases, artificial and natural UV light can thus actually "prevent the migration of inflammatory cells into the CNS" (Wang. 2014).

• Melatonin conc. after 4 days w/ dim vs. bright light and tryptophan rich vs. poor breakfast (Fukushige. 2014).

  Bright light in the AM and the consumption of a breakfast thats high in tryptophan can help you maintain a healthy circadian rhythm - In case you are asking yourself how you can grasp all the benefits that are associated with having an intact circadian rhythm, you may be intrigued to hear that researchers from the Fukuoka Womens University have been able to show that an increase in tryptophan intake at breakfast combined with daytime light exposure has beneficial effects on melatonin secretion and sleep quality. As you can see in the figure to the left it will significantly elevate the evening melatonin peak, which is critical for an optimal circadian rhythm.
  
  If you are looking to optimize your internal clock bright light (either sunlight or a 10,000 Lux daylight lamp) + tryptophan (seeds, nuts, soy, cheese, chicken, turkey, fish, oats, beans and eggs are the TOP10 sources) are the way to go. If you want an extra "kick" add some coffee to the equation. This will increase the light responsiveness of the circadian pacemaker - well, at least in mice it does (Diepen. 2014).

• Bright lights at work will keep you sane, happy and alert - If you are working in an insufficiently lit office without natural sunlight, you should be prepared to develop physiological, sleep and depressive symptoms.
  
  Assuming you have a window in your office, you will get a significantly more pronounced total and peak exposure to bright light thats going to correlate with 33% reduced levels of the stress hormone cortisol, a more natural rhythm of melatonin and a reduced risk of minor psychiatric disorders and depressive symptoms (MA) in the evening.
  
  Thats at least what the results of a recent study from the UFRGS in Porto Alegre indicates (Harb. 2014). A study the authors of which proudly say that their "study demonstrated that not only may light pollution affect human physiology but also lack of exposure to natural light is related to high levels of cortisol and lower levels of melatonin at night, and these, in turn, are related to depressive symptoms and poor quality of sleep" (Harb. 2014).

• If you want to light up the darkness, when its actually time to sleep do it with green (555nm) or red, not blue light, which suppresses melatonin (Bonmati-Carrion. 2014).

  Staying away from nightly night exposure may also help to keep your arteries clean even in the old age - Studies indicate that even after  adjustment for confounding factors, including age, gender, body mass index, current smoking status, hypertension, diabetes, dyslipidemia, sleep medication, estimated glomerular filtration rate, nocturia, bedtime, duration in bed (scotoperiod), day length (photoperiod), urinary 6-sulfatoxymelatonin excretion and daytime and nighttime physical activity, exposure to light at night is associated with carotid intima-media thickness (Obayashi. 2014).
  
  If you dont want to develop subclinical carotid atherosclerosis, when you are old, it would thus be a good idea to adhere to the basic rules of sleep hygiene: a dark room and/or blindfolds will keep your arteries clean and may thus save your life ;-)
• If you have kidney problems, get out in the sun if you want to survive - Scientists from the University of California Irvine Medical Center were able to show that dialysis patients residing in higher UV index regions have lower all-cause mortality compared to those living in moderate-high UV regions (Shapiro. 2014).
  
  More specifically, the ~60year-old subjects residing in moderate-high UV index regions had a 16% reduced risk of all-cause mortality. Those living in very-high UV index regions had a 1% higher risk reduction (17%). Interestingly, there was a similar inverse association between UV index and mortality was observed across all subgroups, but it was more pronounced among whites vs. non-whites.
• Wear those shades (or bluelight blocker glasses) before any important sport event - Why? Stupid question. If you dabble around with your smartphone "unprotected" the evening before an important sport event for only 30 minutes, this can influence exercise performance under hot conditions during the subsequent early morning (Thompson. 2014).

Sleep disturbance and adaptive immunity. Following a night of sleep loss, or during a period of sleep disturbance, nerve fibers from the sympathetic nervous system (SNS) release the neurotransmitter norepinephrine into primary and secondary lymphoid organs and stimulate the adrenal gland to release stored epinephrine into systemic circulation. Both neuromediators stimulate leukocyte adrenergic receptors (e.g., ADRB2) and activate nuclear factor (NF)-?B-mediated inflammatory programs (Irwin. 2015).

• If your grandparents have Alzheimers install a timer-based light system - This may not just increase their sleep quality, but it will also improve their behavior and mood as indicated by reduced depression scores on the Cornell Scale for Depression in Dementia and agitation scores from the Cohen-Mansfield Agitation Inventory (Figueiro. 2014).
  
  I must warn you, though: The recent field study from the Rensselaer Polytechnic Institute is promising, but the results should be replicated using a larger sample size and perhaps using longer treatment duration.
• If you have to work night shifts consider using 1-5mg melatonin 1h before you go to bed - Why? You have to counter the natural decline in melatonin production that occurs over consecutive days of night work (Dumont. 2014).
  
  In a recent study from the Sacre-Coeur Hospital of Montreal the melatonin production of the healthy volunteers decreased progressively decreased over consecutive days of simulated night work, both during nighttime and over the 24?h. Interestingly, this decrease was larger in women using oral contraceptives and independent of bright light exposure.
• Get out into the sun and cure your back pain - If your back hurts and neither you or your doctor have a clue why, try getting into the sun. A study from the UMIT in Austria shows that only three sessions in front of 5.000?lx lamp improved the depressive symptoms and reduced the pain intensity in CNBP adults with chronic nonspecific back pain (Leichtfried. 2014).

References:

• Bonmati-Carrion, Maria Angeles, et al. "Protecting the Melatonin Rhythm through Circadian Healthy Light Exposure." International Journal of Molecular Sciences 15.12 (2014): 23448-23500.
• Diepen, Hester C., et al. "Caffeine increases light responsiveness of the mouse circadian pacemaker." European Journal of Neuroscience 40.10 (2014): 3504-3511.
• Dumont, Marie, and Jean Paquet. "Progressive decrease of melatonin production over consecutive days of simulated night work." Chronobiology international 0 (2014): 1-8.
• Figueiro, Mariana G., et al. "Tailored lighting intervention improves measures of sleep, depression, and agitation in persons with Alzheimer’s disease and related dementia living in long-term care facilities." Clinical interventions in aging 9 (2014): 1527.
• Fukushige, Haruna, et al. "Effects of tryptophan-rich breakfast and light exposure during the daytime on melatonin secretion at night." breast cancer 4 (2014): 9.
• Harb, Francine, Maria Paz Hidalgo, and Betina Martau. "Lack of exposure to natural light in the workspace is associated with physiological, sleep and depressive symptoms." Chronobiology international 0 (2014): 1-8. 
• Irwin Michael, R. "Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective." Annual Review of Psychology 66 (2015): 143-172.
• Kayaba, Momoko, et al. "The effect of nocturnal blue light exposure from light-emitting diodes on wakefulness and energy metabolism the following morning." Environmental health and preventive medicine 19.5 (2014): 354-361. 
• Leichtfried, Veronika, et al. "Short?Term Effects of Bright Light Therapy in Adults with Chronic Nonspecific Back Pain: A Randomized Controlled Trial." Pain Medicine 15.12 (2014): 2003-2012.
• Obayashi, Kenji, Keigo Saeki, and Norio Kurumatani. "Light exposure at night is associated with subclinical carotid atherosclerosis in the general elderly population: The HEIJO-KYO cohort." Chronobiology international 0 (2014): 1-8.
• Okamoto, Yosuke, and Seiji Nakagawa. "Effects of daytime light exposure on cognitive brain activity as measured by the ERP P300." Physiology & behavior 138 (2015): 313-318.
• Partonen, Timo. "Obesity= physical activity+ dietary intake+ sleep stages+ light exposure." Annals of medicine 46.5 (2014): 245-246.
• Shapiro, Bryan B., et al. "The Relationship Between Ultraviolet Light Exposure and Mortality in Dialysis Patients." American journal of nephrology 40.3 (2014): 224-232. 
• Thompson, A., et al. "The Effects of Evening Bright Light Exposure on Subsequent Morning Exercise Performance." International journal of sports medicine EFirst (2014).
• van der Lely, Stéphanie, et al. "Blue blocker glasses as a countermeasure for alerting effects of evening light-emitting diode screen exposure in male teenagers." Journal of Adolescent Health (2014).
• Virginie, Gabel, et al. "Dawn simulation light impacts on different cognitive domains under sleep restriction." Behavioural Brain Research (2014).
• Wang, et al. "UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis." Arch Biochem Biophys. (2014). [Epub ahead of print]
• Zeitzer, Jamie M., et al. "Millisecond Flashes of Light Phase Delay the Human Circadian Clock during Sleep." Journal of biological rhythms (2014): 0748730414546532.

It was about time for an artificial sweetener update, wasnt it?

Alright, I have to admit I am not following the artificial sweetener scene closely enough to have heard about SUCRAM, an artificial sweetener that is composed of saccharin (a classic) and neohepseridin dihydrochalcone, the new kid on the blog, which is yet not officially approved by either the FDA or it European equivalent o be used in the processed junk, most people call "food", these days. If we put some faith into the latest study investigating the effects of this agent, which is apparently already heavily used in animal feeds in Europe it does yet "dramatically reduce enteric disease" and "enhance growth performance in early-weaned piglets." (Daly. 2014)

Whether and to which extent these beneficial effects on gut health are mediated by changes in the gut microbiome is yet still uncertain; and since "uncertain" is a word scientists dont like, Kristian Daily and his colleagues from the University of Liverpool conducted a study to find out, whether the non-negligible health benefits would be brought about by AI <> gut interactions.
To this ends, the scientists employed a DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or said artificial sweetener (SUCRAM)

Figure 1: Total and lactobacillus OTU4228 concentrations in piglets on hydrolzysate carbohydrate diet without sweeteners, with lactose or SUCRAM diets and corresponding concentration of lactic acid in the caecal contents (Daly. 2014)

As you can see in Figure 1, both, the addition of lactose and the saccharin/NHDC mix lead to dramatical increases in the caecal Lactobacillus population and could well explain the previously reported "pro gut health" effect of SUCRAM in piglets (Vente-Spreeuwenberg. 2004; Pierce. 2006)

But thats obviously not all thats news-worthy!

I did after all promise you news on products you may be using, as well - aspartame and acesulfame-k, to be precise. Now, while the former is a constant target of public (mostly broscientific) criticism, the latter has been a thorn in my side ever since I have started investigating artificial sweeteners.

Lean more about the "Gut Type Diet" - No Fad, Guaranteed!

And while previous studies only suggested that the effects of acesulfam-k on the pancreas could have pro-obesogenic consequences, a recent model experiment from the Louisiana State University appears to finally prove that acesulfam-k may actively promote the deposition of body fat in the presence of insulin resistance.

Ok, the results have been derived in a Caenorhabditis elegans, a "worm", but one that has long and actually surprisingly successfully been used as a "model for studying the basic biology of obesity" (Jones. 2009) - I know, I am not convinced either, but if the results do actually translate to humans, this would be major (bad) news for the food industry.

In view of the fact that most companies have been pulling acesulfame-k from their products over the past years, anyway, I would not discard the findings Jolene Zheng et al. present in their latest paper in Chemico-Biological Interactions as meaningless, not despite, but rather because a scientists from PepsiCo was part of the research team which observed these significant increases in intestinal fat (=visceral fat of the worm) when the critters were fed with acesulfam-k sweetened coke.
References: 

• Payne, A. N., C. Chassard, and C. Lacroix. "Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity." Obesity Reviews 13.9 (2012): 799-809.
• Pierce, K. M., et al. "The effect of lactose and inulin on intestinal morphology, selected microbial populations and volatile fatty acid concentrations in the gastro-intestinal tract of the weanling pig." ANIMAL SCIENCE-GLASGOW THEN PENICUIK- 82.3 (2006): 311.
• Jones, Kevin T., and Kaveh Ashrafi. "Caenorhabditis elegans as an emerging model for studying the basic biology of obesity." Disease models & mechanisms 2.5-6 (2009): 224-229.
• Vente-Spreeuwenberg, M. A. M., et al. "Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets." Livestock Production Science 86.1 (2004): 169-177.

Nigella sativa is available in form of seeds, oils and all sorts of ointments and for many of them there are studies suggesting that they work.

SuppVersity reader Amaan Mueen asks on Facebook: "In traditional Oriental medicine its said that blackseed is a cure for everything except death, is there any truth to that?" I probably dont give away too much, when I tell you that blackseed (also "black seed") aka "nigella sativa" is not going to cure everything, but death, but that does not mean that modern Western medicine has not been able to confirm what Oriental "doctors" have known for centuries.

In the following I am going to present an allegedly cursory overview of the existing evidence with a focus on those health benefits that could be relevant for the average and extra-ordinary SuppVersity reader.

• General anti-oxidant effects - The complete oil of N. sativa, as well as thymoquinone (the main compound of the essential oil) have been shown to significantly reduce non-enzymatic lipid peroxidation in liposomes (Houghton. 1995). Significant anti-oxidant effects have also been observed for other compounds isolated from N. sativa, uncluding thymoquinone, carvacol, t-anethole and 4-terpineol.
  
  

  Figure 1: The tymoquinone rich fraction of blackseed (TQRF-X) has dose dependent (L,M,H) effects on antioxidant enzyems in hypercholesterolemic (Ismail. 2010).

  These compounds were found in a series of other in vitro tests to have variable antioxidant, but no pro-oxidant properties.
  
  Most importantly, though, the different compounds in the oil were found to act in a synergistic manner (i.e. more than the mere summation of the actions of the individual compounds). This stresses the importance of using the whole oil (or the crude extract) of the seeds in pharmacological studies.
  
  As Ali and Blunden point out in their review of the literature, "the antioxidant property of N. sativa is multifactorial, [but] it does not seem to involve iron-complexing activity (Ali. 2003). It rather appears as if its general ability to scavenge free radicals, which may be, at least partially, the basis of many human diseases and conditions, could be at the heart of its ability to protect, for example, against CCl4 hepatotoxicity (Nagi. 1999), liver fibrosis and cirrhosis (Türkdogan. 2000), and hepatic damage induced by Schistosoma mansoni infection (Mahmoud. 2002).
• Antiinflammatory and analgesic actions -Its one thing to scavenge free radicals. Its yet a completely different thing to effectively reduce the inflammation thats often, but not always triggered by the presence of free radicals. Against that background its important to note that an aqueous extract from nigella sativa exhibits strong anti-inflammatory effects, as well (Al-Ghamdi, 2001). Using carrageenan-induced paw oedema as a model of inflammation, and the hot plate reaction time as a model of nociception, the extract was found to possess significant antiinflammatory and analgesic (=pain reducing) action.
  
  As Ali & Blunden (2003) point out, this finding lends some credence to the folk medicinal use of the plant as an antiinflammatory and analgesic substance, and also confirms previous reports on the antinociceptive (Abdel-Fattah. 2000) and antiinflammatory (Mutabagani. 1997) effects of N. sativa oil and its major component, thymoquinone, in mice.
  
  The possible mechanism by which N. sativa exerts its antiinflammatory action has been studied. Thymoquinone has been shown to be a potent inhibitor of eicosanoid generation, namely thromboxane B2 and leucotrienes B4, by inhibiting both cyclooxygenase and lipooxygenase, respectively (Houghton. 1995). Interestingly, it was found that the fixed oil of N. sativa had both antioxidant and anti-eicosanoid effects greater than thymoquinone, which is its active constituent (Houghton. 1995)

• Anti-Cancer Effect - In an in-vitro study from the late 1990s researchers from the Tobacco and Health Research Institute in Lexington were able to show that the thymoquinone (TQ) and dithymoquinone (DIM) content of nigella sativa have the astonishing ability to kill several parental and multi-drug resistant (MDR) human tumor cell lines (Worthen. 1997).
  

  Figure 2: A schematic diagram showing major molecular targets of TQ. As an anticancer agent, TQ inhibits the activity of CYP enzymes, which are involved in metabolic activation carcinogens, and induces the expression and activities of cytoprotective enzymes by activating Nrf2 signaling. TQ selectively induces tumor cell death in an ROS-dependent manner following both intrinsic and extrinsic pathways of apoptosis. TQ exerts anti-proliferative, anti-inflammatory, anti-migratory, anti-invasive and anti-metastatic effects by blocking the activation of NF-?B- and STAT3-regulated gene products (Kundu. 2014).

  In spite of the fact that there are as of yet no studies that show that humans were cured with blackseed, recent studies have shown that Thymoquinone, a component of Nigella sativa, decreases oxidative DNA damage in a rat model of mammary cancer (Sindi. 2014) and protect the brain, liver and other organs from radiation induced damage during cancer therapy (Ahlatci. 2014; Cikman. 2014). So, even if it were not for its established cytotoxic effects in various human cancer cells (e.g. Liver, Khan. 2014; Kidney, Tabasi. 2014; Prostate & Breast Cancer, Schneider-Stock. 2014; Cervix, Ichwan. 2014; etc.), it would still make sense to use black seed extracts as antioxidants during radiation and as studies indicate also chemotherapy (Pace. 2003; Almog. 2014).
• Anti-allergic effects - In a study from 2003 Kalus et al. observed significant reductions in subjective feeling of allergic symptoms in 152 patients with allergic diseases (allergic rhinitis, bronchial asthma, atopic eczema) who were treated with Nigella sativa oil, given in capsules at a dose of 40 to 80 mg/kg/day.
  
  

  Figure 3: The addition of blackseeds at a dosage of 2g/day propels the beneficial effects of subcutaneous allergen-specific immunotherapy on polymorphonuclear leukocyte (PMN) function in 24 patients sensitive to house dust mites with allergic rhinitis (I??k. 2010)

  Other studies confirm that Nigella sativa can reduce the peripheral blood eosinophil count, IgG1 and IgG2a, cytokine profiles and lung inflammation in murine model of allergic asthma (Abbas. 2004) that are equal to the corticosteriod dexamethasone and scientists from the Gaziosmanpasa University Medical Faculty say that "N. sativa display its antioxidant and regulatory effects via inflammatory cells rather than the host tissue (brain and medulla spinalis)" in a rodent model of experimental allergic encephalomyelitis (Ozugurlu. 2005). Effects that were also observed in a 2010 human study which indicates that "N. sativa seed supplementation during specific immunotherapy of allergic rhinitis may be considered a potential adjuvant therapy" (I??k. 2010 | see Figure 3).
• Anti-diabetes effects: The volatile compounds in nigella sativa oil have been shown to exert potent glucose lowering effects in healthy and diabetic animals (Al-Hader. 1993). Effects that occured in the absence of changes in insulin levels and are almost unsettlingly pronounced.
  

  Figure 4: Reduction in fasting blood glucose in the hours after the administration of 50mg/kg volatile oil extract to normal and diabetic rodents (Al-Hader. 1993).

  For those of you who are hovering around in the netherlands of glucose levels, anyway, the 14% reduction Al-Hader et al. observed in the healthy rabbits in their 1993 could in fact be enough to induce mild hypoglycemia and side effects such as ravenous appetite, feeling cold, cold sweat, being irritable and so on - an effect thats going to be particularly pronounced, because blacksee will at the same time inhibit the production of glucose in the liver that would otherwise compensate the drop in blood glucose (Al-Awadi. 1991).
  
  With comparatively lower doses of only 5ml of nigella sativa oil, Mohtashami et al. have recently demonstrated that the beneficial effects on blood glucose are not rodent specific.
  
  

  Figure 5: Blackseed consumed in 2x2.5ml servings everydy improves blood glucose management in healthy humans, too (Mohtashami. 2011)

  In their randomized clinical trial with 70 healthy subjects who received either 2.5 ml Black seed oil or a similarly looking mineral oil two times a day, the scientists observed achieved less pronounced, but still significant reductions in fasting blood glucose and the long(er)-term glucose marker HbA1c within only two months.
  
  In view of the comparatively small reductions in blood sugar (see Figure 5), its also not surprisng that the only side effect was an occasional case of transient nausea. Notable changes in liver enzyme and kidney functional adverse effects, on the other hand, were not observed..
  
  Similar results have been reported for subjects with diabetes (Najmi. 2008), intact and diabetic rats (Hawsawi. 2001; Houcher. 2007) and in several cell models, like muscle cells, where it increases AMPK and GLUT4 expression (Benhaddou-Andaloussi. 2011) or the Langerhans cells (Rchid. 2004) of the pancreas of which Fararh et al. (2002) were able to show that they can partly recover their ability to release insulin in a rodent model of diabetes, when nigella sativa is administered in conjunction with nicotinic acid.
• Cardiovascular effects - The results of a 2014 study by Mohammad et al. indicate that "[t]he use of N. sativa as an alternative therapy for hypercholesterolemia could have profound impact on the management of CVD among menopausal women especially in countries where it is readily available." In the corresponding study 1g of nigella sativa powder consumed after breakfast lead to significant improvements in lipid profiles of menopausal women (decreased total cholesterol, low density lipoprotein cholesterol and triglyceride, and increased high density lipoprotein cholesterol)within 2 months. Improvements that were lost almost completely after one month without the capped Nigella sativa supplement.
  
  Rather ambigous - at least at first sight - are the effects of nigella sativa on the physiology of the heart, while Al-Asoom et al. (2014a) were able to show that the IFG-1 boosting effects Nigella sativa exerts on exercising rats could make it a valuable tool for the treatment of heart failure with superior advantages to exercise training alone, the same effects are often mentioned as potential unwanted side effects of Nigella sativa.
  

  Figure 6: In trained rats, the Nigella sativa induced boost in IGF-1 (left) promotes the exercise induced increase in heart weight (right | Al-Asoom. 2014a)

  Whether thats actually a problem is yet questionable. In view of the nature of the cardiac hypertrophy, its rather an augmentation of the beneficial cardiac remodeling due to exercise similar to the one we call "athletes heart" than a pathological increase in the size of the heart. Whether similar effects can be observed for skeletal muscle has, at least as far as I know, yet not been tested - its yet certainly not impossible.

References

• Abbas, Ayman Talatt, et al. "Effect of dexamethasone and Nigella sativa on peripheral blood eosinophil count, IgG1 and IgG2a, cytokine profiles and lung inflammation in murine model of allergic asthma." The Egyptian journal of immunology/Egyptian Association of Immunologists 12.1 (2004): 95-102.
• Abdel-Fattah, Abdel-Fattah Mohamed, Kinzo Matsumoto, and Hiroshi Watanabe. "Antinociceptive effects of< i> Nigella sativa</i> oil and its major component, thymoquinone, in mice." European journal of pharmacology 400.1 (2000): 89-97. 
• Al-Saaidi, J. A. A., A. L. D. Al-Khuzai, and N. F. H. Al-Zobaydi. "Effect of alcoholic extract of Nigella sativa on fertility in male rats." Iraq J Verterin Sci 23 (2009): 123-8.
• Al-Asoom, L. I., et al. "Effect of Nigella sativa Supplementation to Exercise Training in a Novel Model of Physiological Cardiac Hypertrophy." Cardiovascular toxicology (2014a): 1-8. 
• Al-Asoom, Lubna Ibrahim, et al. "Comparison of Nigella sativa-and Exercise-Induced Models of Cardiac Hypertrophy: Structural and Electrophysiological Features." Cardiovascular toxicology (2014b): 1-6.
• Al-Awadi, Fatania, and U. Shamte. "The effect of a plants mixture extract on liver gluconeogenesis in streptozotocin induced diabetic rats." Diabetes research (Edinburgh, Scotland) 18.4 (1991): 163-168.
• Al-Hader, Aqel, M. Aqel, and Z. Hasan. "Hypoglycemic effects of the volatile oil of Nigella sativa seeds." Pharmaceutical Biology 31.2 (1993): 96-100.
• Ali, B. H., and Gerald Blunden. "Pharmacological and toxicological properties of Nigella sativa." Phytotherapy Research 17.4 (2003): 299-305. 
• Ahlatci, Adem, et al. "Radiation-modifying abilities of< i> Nigella sativa</i> and Thymoquinone on radiation-induced nitrosative stress in the brain tissue." Phytomedicine 21.5 (2014): 740-744. 
• Benhaddou-Andaloussi, Ali, et al. "The in vivo antidiabetic activity of Nigella sativa is mediated through activation of the AMPK pathway and increased muscle Glut4 content." Evidence-Based Complementary and Alternative Medicine 2011 (2011).
• Cikman, Oztekin, et al. "Radioprotective Effects of Nigella Sativa Oil Against Oxidative Stress in Liver Tissue of Rats Exposed to Total Head Irradiation." Journal of Investigative Surgery (2014).
• Fararh, K. M., et al. "Isulinotropic properties of< i> Nigella sativa</i> oil in Streptozotocin plus Nicotinamide diabetic hamster." Research in veterinary science 73.3 (2002): 279-282.
• Hawsawi, Zubaida A., Basil A. Ali, and Abdullah O. Bamosa. "Effect of Nigella sativa (black seed) and thymoquinone on blood glucose in albino rats." Annals of Saudi medicine 21.3-4 (2001): 242-244. 
• Houcher, Zahira, et al. "Effects of methanolic extract and commercial oil of Nigella sativa L. on blood glucose and antioxidant capacity in alloxan-induced diabetic rats." Pteridines 18.1 (2007): 8-18.
• Houghton PJ, Zarka R, de las Heras B, Hoult JRS."Fixed oil of Nigella sativa and derived thymoquinone inhibit eicosanoid generation in leukocytes and membrane lipid peroxidation". Planta Med 61 (1995): 33–36.
• Ichwan, S. J., et al. "Apoptotic Activities of Thymoquinone, an Active Ingredient of Black Seed (Nigella sativa), in Cervical Cancer Cell Lines." The Chinese journal of physiology 57.5 (2014).
• Lautenbacher LM. "Schwarzkümmelöl." Dtsch Apoth Ztg 137 (1997): 68–69.
• Khan, Fazal, et al. "Evaluation of the effect of Nigella sativa extract on human hepatocellular adenocarcinoma cell line (HepG2) in vitro." BMC Genomics 15.Suppl 2 (2014): P63.
• Kundu, Juthika, et al. "Mechanistic Perspectives on Cancer Chemoprevention/Chemotherapeutic Effects of Thymoquinone." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis (2014).
• Mahmoud, M. R., H. S. El-Abhar, and S. Saleh. "The effect of< i> Nigella sativa</i> oil against the liver damage induced by< i> Schistosoma mansoni</i> infection in mice." Journal of ethnopharmacology 79.1 (2002): 1-11. 
• Mohtashami, R., et al. "Blood Glucose Lowering Effects of Nigella Sativa L. Seeds Oil in Healthy Volunteers: a Randomized, Double-Blind, Placebo-Controlled Clinical Trial." Journal of Medicinal Plant 10.36 (2011): 90-94.
• Mutabagani, A., and S. A. M. El-Mahdy. "A study of the anti-inflammatory activity of Nigella sativa L. and thymoquinone in rats." Saudi Pharmaceutical Journal 5 (1997): 110-113.
• Nagi, Mahmoud N., et al. "Thymoquinone protects against carbon tetrachloride hetatotoxicity in mice via an antioxidant mechanism." IUBMB Life 47.1 (1999): 153-159. 
• Najmi, Ahmad, et al. "Effect of Nigella sativa oil on various clinical and biochemical parameters of insulin resistance syndrome." International journal of diabetes in developing countries 28.1 (2008): 11.
• Ozugurlu, F., et al. "The effect of Nigella sativa oil against experimental allergic encephalomyelitis via nitric oxide and other oxidative stress parameters." Cellular and molecular biology (Noisy-le-Grand, France) 51.3 (2005): 337-342.
• Pace, Andrea, et al. "Neuroprotective effect of vitamin E supplementation in patients treated with cisplatin chemotherapy." Journal of Clinical Oncology 21.5 (2003): 927-931. 
• Paarakh, Padmaa M. "Nigella sativa Linn.–A comprehensive review." Indian J Nat Prod Resour 1 (2010): 409-29.
• Rchid, Halima, et al. "Nigella sativa seed extracts enhance glucose?induced insulin release from rat?isolated Langerhans islets." Fundamental & clinical pharmacology 18.5 (2004): 525-529.
• Sindi, Abrar, and Karen Carlberg. "Thymoquinone, a component of the Middle East spicy seed Nigella sativa, decreases oxidative DNA damage in a rat model of mammary cancer (693.21)." The FASEB Journal 28.1 Supplement (2014): 693-21.
• Tabasi, Nafise, et al. "Cytotoxic and apoptogenic properties of Nigella sativa and thymoquinone, its constituent, in human renal cell carcinoma are comparable with cisplatin." Food and Agricultural Immunology ahead-of-print (2014): 1-19.
• Türkdo?an, M. K., et al. "The role of antioxidant vitamins (C and E), selenium and Nigella sativa in the prevention of liver fibrosis and cirrhosis in rabbits: new hopes." DTW. Deutsche tierarztliche Wochenschrift 108.2 (2001): 71-73.
• Worthen, David R., Omar A. Ghosheh, and P. A. Crooks. "The in vitro anti-tumor activity of some crude and purified components of blackseed, Nigella sativa L." Anticancer research 18.3A (1997): 1527-1532.

Blueberries and other foods w/ tons of polyphenols are GSH boosters (Moskaug. 2005) and make supplements obsolete.

If you have been interested in dietary supplements for some time, I am pretty sure that you will have heard about oral glutathione ob(GSH) supplements in one of the "snake oil warnings" on various websites. The "master antioxidant" as it is called is after all believed by many to be not bioavailable - at least not orally. Studies in animal models, however, have already shown that oral GSH, administered either in the diet or by gavage, has the ability to increase plasma and tissue GSH levels ( Loven. 1986; Aw. 1991; Favilli. 1997; Kariya. 2007). It would thus be more appropriate to say that the efficacy of oral glutathione in humans has not yet been tested in peer-reviewed studies.
Now, the absence of human studies should definitely ring an alarm bell in the head of every healthily skeptic supplement user, what it should not do, though is mislead you to believe that GSH supplements dont work in human beings.

Now this is where John P. Richie Jr. and his colleagues from the Penn State Cancer Institute, the Department of Microbiology and Immunology at the Penn State University College of Medicine and the Orentreich Foundation for the Advancement of Science, come into play. As the scientist state, their "objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults." (Richie. 2014)
To this end, they conducted a 6-month randomized, double-blinded,placebo-controlled trial in the course of which the subjects, 41 women and 13 men (6 dropouts not included) with a normal BMI and no known health issues, consumed either ...

• an oral GSH supplement dosed at 250mg/day,
• an oral GSH supplement dosed at 1,000mg/day, or
• an identically looking placebo.

The main study outcomes were obviously analyses of the GSH levels in (a) blood, (b) erythrocytes, (c) plasma, (d) lymphocytes and (e) exfoliated buccal mucosal cells (the effects on a battery of immune markers was tested only in a handful of subjects).

Figure 1: Effects of 6 months GSH supplementation on ratio of oxidized to reduced GSH and natural killer cell cytotoxicity in healthy men and women aged 28-72y (Richie. 2014)

As the data in Figure 1 already suggests, there was a dose-dependent increase in GSH levels. With the high dose (1,000mg/day) producing GSH increases of 30–35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells (P<0.05) and increases of 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P<0.05 - data not shown in Figure 1).

These improvements had beneficial downstream effects on the overall status of the subjects antioxidant defense system. A fact you can conclude based on the decreased ratio of oxidized (used) to reduced (fresh) glutathione in whole blood the scientists observed in their subjects after 6 months. These benefits came hand in hand with an increase in natural killer cytotoxicity (+100%), another potentially highly desirable health benefit.

References:

• Aw, Tak Yee, Grazyna Wierzbicka, and Dean P. Jones. "Oral glutathione increases tissue glutathione in vivo." Chemico-biological interactions 80.1 (1991): 89-97.
• Favilli, Fabio, et al. "Effect of orally administered glutathione on glutathione levels in some organs of rats: role of specific transporters." British journal of nutrition 78.02 (1997): 293-300.
• Kariya, Chirag, et al. "A role for CFTR in the elevation of glutathione levels in the lung by oral glutathione administration." American Journal of Physiology-Lung Cellular and Molecular Physiology 37.6 (2007): L1590.
• Loven, Dean, et al. "Effect of insulin and oral glutathione on glutathione levels and superoxide dismutase activities in organs of rats with streptozocin-induced diabetes." Diabetes 35.5 (1986): 503-507.
• Moskaug, Jan Ø., et al. "Polyphenols and glutathione synthesis regulation." The American journal of clinical nutrition 81.1 (2005): 277S-283S.
• Richie Jr, John P., et al. "Randomized controlled trial of oral glutathione supplementation on body stores of glutathione." European journal of nutrition (2014): 1-13.