ONLINE DRIVERS MEDIA

Remember: If anything fructose from beverages (including juices), yet not fructose from whole fruit is a problem. In fact eating whole fruits will decrease your blood lipids and high sensitivity C reactive protein (hs-CRP) inflammation markers.

Fructose is bad for you, right? Right. According to the latest study from the University of Newcastle, the consumption of only one drink containing containing 50 g of either fructose or glucose or sucrose dissolved in water will have detrimental effects on the #1 indicator of whole body inflammation, which is high sensitivity C-reactive protein (hs-CRP).

Much to the researchers surprise, though, the same amount of fructose had significant beneficial effects on the plasma lipid levels of the healthy male and female adults (n = 14) between the ages of 18-60 years who were recruited by advertisement and underwent study procedures at the Nutraceuticals Research Group Clinic rooms at the University of Newcastle in Australia.
Since the exclusion criteria were: diagnosed hyperlipidaemia, diabetes, gastrointestinal disorders, currently on fructose/sugar restricted diet, vegan diet or weight loss program, undergone any surgical procedure for obesity, pregnant or lactating mother, taking lipid-lowering or anti-inflammatory drugs and BMI >30kg/m², the results may well be different in "sicker" individuals, but for the guys and gals who drank the three 50g "sugar" solutions on three different occasions after an overnight fast, the "negative effects" of fructose were far from being conclusive.

Figure 1: Changes in hs-CRP, HDL and LDL in response to the ingestion of the test drinks (Jameel. 2014).

Even if you belong to the ever-increasing numbers of brainwashed fructose haters who believe that fructose and not a general overconsumption of energy was to blame for the obesity epidemic, you will have to admit that the data in Figure 1 leaves the significance of concomitant increases in hs-CRP and significant improvements in the HDL/LDL ratio, as the scientists phrase it, "to be delineated when considering health effects of feeding fructose-rich diets" (Jameel. 2014).
Well, yes, but (a) its only an acute response and (b) while increased levels of hs-CRP have been found to be associated with heart disease (Rifai. 2001; Danesh. 2004), the same can be said for a high LDL/HDL ratio (Fernandez. 2008).

Figure 2: CRP-dependent risk levels for cardiovascular disease according to the American Hear Association.

If we also take into consideration that the baseline hs-CRP level of the subjects was 1.5mg/L and thus low to mid-range for the average Westerner (depending on his or her ethnicity | Albert. 2004), an increase of 10% to a maximal value of 1.65mg/L would not bring them to critical heights of which the Farmingham study says that they start at 3mg/L for Westerners (Wilson. 2005). Thats not ana optimal level, but considering the fact that we are talking about "average Joes and Janes" who probably dont work out, eat whatever they like and give a damn about their sleep hygiene (all three factors have previously been linked to elevated hs-CRP levels) thats not astonishing and has absolutely nothing to do with the ingestion of 50g of fructose.

Furthermore, a comparison of the predictive value of different risk markers for cardiovascular disease by Folsom, et al. (2006) indicates that the hs-CRP values did not add to the prognostic value of the standard risk factors which are age, race, sex, systolic blood pressure, smoking status, diabetes and - you guessed it - total and high density lipoprotein cholesterol, which increased by almost 7% while the amount of LDL dropped by maximally 6%. Thus the LDL/HDL ratio decreased from 1.84 to 1.62. Thats a 12% decrease that would be health relevant if the subjects LDL/HDL ratio was not far away from the danger-zone (>5 | see Manninen. 1992), already. Similarly, the total cholesterol to HDL ratio dropped by -1.97 but wasnt in the danger zone before, either.
References:

• Danesh, John, et al. "C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease." New England Journal of Medicine 350.14 (2004): 1387-1397. 
• Fernandez, Maria Luz, and Densie Webb. "The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk." Journal of the American College of Nutrition 27.1 (2008): 1-5.
• Folsom, Aaron R., et al. "An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study." Archives of internal medicine 166.13 (2006): 1368-1373. 
• Hermsdorff, Helen Hermana M., et al. "Research Fruit and vegetable consumption and proinflammatory gene expression from peripheral blood mononuclear cells in young adults: a translational study." (2010).
• Jameel, Faizan, et al. "Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation." Lipids in Health and Disease 13.1 (2014): 195.
• Manninen, Vesa, et al. "Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment." Circulation 85.1 (1992): 37-45.
• Oliveira, A., F. Rodriguez-Artalejo, and C. Lopes. "The association of fruits, vegetables, antioxidant vitamins and fibre intake with high-sensitivity C-reactive protein: sex and body mass index interactions." European journal of clinical nutrition 63.11 (2009): 1345-1352. 
• Ravn-Haren, Gitte, et al. "Intake of whole apples or clear apple juice has contrasting effects on plasma lipids in healthy volunteers." European journal of nutrition 52.8 (2013): 1875-1889.
• Rifai, Nader, and Paul M. Ridker. "High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease." Clinical chemistry 47.3 (2001): 403-411.
• Wilson, Peter WF, et al. "C-reactive protein and risk of cardiovascular disease in men and women from the Framingham Heart Study." Archives of internal medicine 165.21 (2005): 2473-2478.

Remember: HIIT does not have to happen on the treadmill.

If you havent already done so, I suppose you are currently revising last years training regimen: Reviewing what worked and what didnt work; and thinking about (new) goals and the best ways to achieve them.

If you havent yet decided on what type of cardio training you want to do, todays SuppVersity article may help you make the right endurance / cardiovascular exercise choices for 2015. In that, the headline already revealed: At least 50% of your 2015 "Cardio" training should be high intensity interval training (HIIT) - and here is why.

1. HIIT is more time efficient - Unless you have lost your hob and are looking to kill the newly won time in 2015, you are probably similarly short on time as most of us. Against that background, the mere time efficiency of HIIT workouts are an argument even the most feverish advocates of  low-intensity hour-long cardio cannot deny (Gaesser. 2011; Gillen. 2013).
   

   Figure 1: In contrast to often-heard claims, HIIT is not just a "glucose burner" its also a fat burner. It does (a) increase the oxidation of fatty acids after the workout and (b) increases your muscles and other cells general ability to oxidize fat as fuel (see figure from Talanian. 2007).

   "As few as 6 sessions of HIIT over a 2-week period for a total of about 15 minutes of very intense exercise (equating to approximately 600 kJ or 143 cal) have been shown to increase skeletal muscle oxidative capacity and alter metabolic control during aerobic-based exercise (Gibala. 2008). And 7 HIIT sesssions performed over 2 weeks significantly heightened whole body and skeletal muscle capacity for fatty acid oxidation during exercise in moderately active women (Talanian. 2007). For those who have limited time to work out, this makes HIIT an intriguing option" (Schoenfeld. 2009).

   And even if your goal is not to get fitter, but rather to burn more energy, HIIT can do what steady state cardio will never achieve, i.e. burn 14.5 kcal/min (see "Tabata Workouts: Do They Work & How Energy-Demanding Are They? 14.5 Kcal/Min Sounds Nice, But You Must Earn It!" | learn more). In the end, short workouts will thus increase your 24h energy expenditure to the same extend endless steady-state workouts would do (Skelly. 2014).
   

   "HIIT may help insufficiently active individuals overcome a major barrier to maintaining a physically active lifestyle, that of a perceived lack of time. An added bonus is that from a time:benefit perspective, HIIT may prove to be a good example where less can be more" (Gaesser. 2011).

   And it does not even take a Tabata workout to time-efficiently improve your health. As a SuppVersity reader you will be aware that "4x4 Minutes of HIIT Per Week Thats All It Takes For Already Well-Conditioned Individuals to Stimulate Mitochondrial Growth ? 15% Increase in VO2Max, Peak & Mean Power" | learn more.
2. HIIT has more favorable effects on your glucose metabolism and heart health - You probably have heard that 1h on the treadmill was the ideal exercise for the obese type II diabetic, right? Well, this may in fact be true, but the reason thats ideal for an obese type II diabetic is that even walking on a treadmill is a high intensity exercise for someone who weighs 300-450lbs.
   

   Figure 2: A 2008 study in healthy, normal-weight young women proves: HIIT "cardio" training leads to significantly more pronounced improvements in all three central variables of glucose metabolism than a comparable steady-state "cardio" workout (Trapp. 2008).

   That being said, for all of you with at least a decent amount of fitness, HIIT training with its ability to burn tons of glycogen within just a few minutes should be the preferred mode of exercise. A mode of exercise which has far more potent effects on the expression of the anti-diabetic, anti-obesity and anti-metabolic syndrome proteins AMPK and SIRT-1 than any other form of exercise (Gurd. 2010) and has thus not surprisingly been shown to have superior effects on central markers of glucose metabolism in a 2008 study by Trapp et al. - and that in healthy, lean, young women (see Figure 2).
   
   A similar superiority has been observed by Weston et al. (2013) in patients with lifestyle-induced cardiometabolic disease. Their systematic review and meta-analysis in the British Journal of Sports Medicine indicates that "HIIT significantly increases CRF [cardio-respiratory fitness] by almost double that of MICT in patients with lifestyle-induced chronic diseases." (Weston. 2013).
3. HIIT exercise will help curb your cravings - While steady-state "cardio" has repeatedly been associated with increases in appetite, hunger and most importantly food intake, there is good evidence that "Intensity [is] the Key to Minimize Exercise Induced Cravings?" (learn more)
   

   Figure 3: Effects of exercise duration and intensity on energy intake; exemplary study results from Erdmann et al. (2007, left) and Larson-Meyer et al. (2012, right).

   I dont want to repeat myself on this one. Instead I will just refer you to a recent SuppVersity article on that matter and the plethora of evidence that confirms the negligible or beneficial effects of high intensity interval training on appetite, hunger and how much food you eat and thus ruin any exercise-induced reduction in your daily energy balance (Alkahtani. 2014; Martins. 2014).
   
   

   Figure 4: VAS scores for hunger (A), desire to eat (B), fullness (C), and thirst (D) during REST (black line) and EX (gray line) (n = 15). Hatched rectangles represent the treadmill run/rest; striped rectangles represent the fMRI scan (Crabtree. 2014).

   Before I go on to the #4 on the benefits list, I would yet like to highlight the following result from a recent study from the University college of London:
   

   "Exercise increases neural responses in reward-related regions of the brain in response to images of low-calorie foods and suppresses activation during the viewing of high-calorie foods" (Crabtree. 2014)

   Cant believe what you just read? Look at the figure on the right which depicts the VAS scores for hunger, desire to eat, fullness, and thirst, during REST (black line) and EX (gray line) in N=15 lean healthy men who completed two 60-min trials—exercise and a resting control trial (REST).
   
   Thus, the study clearly confirms the validity of the suggestion to stay scrap your steady-state cardio workouts and replace them with HIIT, in order to finally be able to stick to your diet plans and see the fat loss you are looking for.
4. HIIT ramps up the metabolism instead of ruining it - As long as you dont overdo it by training too often or extending your HIIT sessions to 1h, HIIT will produce a profound "after burn" thats 3x higher than in the case of classic steady-state "cardio" workouts.
   

   Figure 5: EPOC and corresponding additional energy expenditure in the high intensity 3x Wingate group (SPIE) and the 30min continuous exercise group (HIE) during the 30 min right after the workout (Townsend. 2013)

   As a standalone, this previously reported benefit is hardly worth the paper it is printed on. In conjunction with the previously mentioned benefits, however, it is an important benefit of HIIT that must not be underestimated.
5. HIIT is perfectly scalable - Unlike steady-state cardio, where you would have to endlessly increase your workout times, HIIT workouts are easily scalable. You can either...
   

   • HRV = heart rate recovery analyses are a great tool to monitor your training & recovery | learn more

     do an additional interval (volume increase),
      
   • increase the resistance on your training device or run / cycle on a more difficult track (intensity increase),
   • increase the speed at which you run, pedal or row (intensity increase), or
      
   • reduce the time of active rest between the intervals (intensity increase)
   and thus have many more options to tweak the workouts to your individuals needs. For beginners this is not that important. An obese type II diabetic has plenty of room to increase the pace and / or duration of his / her steady-state "cardio" workouts. A trained athletes, on the other hand, will soon hit a wall, when he / she begins to cycle at 90% intensity for 2h everyday.

References:

• Alkahtani, Shaea A., et al. "Acute interval exercise intensity does not affect appetite and nutrient preferences in overweight and obese males." Asia Pacific journal of clinical nutrition 23.2 (2014): 232.
• Crabtree, Daniel R., et al. "The effects of high-intensity exercise on neural responses to images of food." The American journal of clinical nutrition 99.2 (2014): 258-267.
• Erdmann, Johannes, et al. "Plasma ghrelin levels during exercise—effects of intensity and duration." Regulatory peptides 143.1 (2007): 127-135.
• Gaesser, Glenn A., and Siddhartha S. Angadi. "High-intensity interval training for health and fitness: can less be more?." Journal of Applied Physiology 111.6 (2011): 1540-1541.
• Gibala, Martin J., and Sean L. McGee. "Metabolic adaptations to short-term high-intensity interval training: a little pain for a lot of gain?." Exercise and sport sciences reviews 36.2 (2008): 58-63.
• Gillen, Jenna B., and Martin J. Gibala. "Is high-intensity interval training a time-efficient exercise strategy to improve health and fitness?." Applied Physiology, Nutrition, and Metabolism 39.3 (2013): 409-412.
• Gurd, Brendon J., et al. "High-intensity interval training increases SIRT1 activity in human skeletal muscle." Applied Physiology, Nutrition, and Metabolism 35.3 (2010): 350-357. 
• Larson-Meyer, D. Enette, et al. "Influence of running and walking on hormonal regulators of appetite in women." Journal of obesity 2012 (2012).
• Martins, Catia, et al. "Effect of Moderate-and High-Intensity Acute Exercise on Appetite in Obese Individuals." Medicine and science in sports and exercise (2014). 
• Owens, Krystyna. "The effectiveness of high intensity interval training in improving VO< sub> 2</sub> max for performance gains as compared to standard endurance training in athletes." (2013).
• Schoenfeld, Brad, and Jay Dawes. "High-intensity interval training: Applications for general fitness training." Strength & Conditioning Journal 31.6 (2009): 44-46. 
• Skelly, Lauren E., et al. "High-intensity interval exercise induces 24-h energy expenditure similar to traditional endurance exercise despite reduced time commitment." Applied Physiology, Nutrition, and Metabolism 39.999 (2014): 1-4.
• Talanian, Jason L., et al. "Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women." Journal of applied physiology 102.4 (2007): 1439-1447. 
• Townsend JR, Stout JR, Morton AB, Jajtner AR, Gonzalez AM, Wells AJ, Mangine GT, McCormack, WP Emerson NS, Robinson EH, Hoffman JR, Fragala MS Cosio-Lima L. Excess Post-Exercise Oxygen Consumption (EPOC) Following Multiple Effort Sprint And Moderate Aerobic Exercise. Kinesiology. 2013; 45(1):16-21
• Trapp, E. G., et al. "The effects of high-intensity intermittent exercise training on fat loss and fasting insulin levels of young women." International journal of obesity 32.4 (2008): 684-691. 
• Weston, Kassia S., Ulrik Wisløff, and Jeff S. Coombes. "High-intensity interval training in patients with lifestyle-induced cardiometabolic disease: a systematic review and meta-analysis." British journal of sports medicine (2013): bjsports-2013.

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.
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