close up of woman's bicep as she lifts weight


Cramping can bring even the best trained, most nutritionally savvy triathlete to their knees. It happens on the road, on the bike or even in the water. And Delayed Onset Muscle Soreness after an intense workout can keep athletes from getting back out there or pushing as hard as they want.


The journey to better understanding muscle cramps started when friends (and fellow neurophysiologists), Dr. Rod McKinnon, a Nobel Prize-winning neuroscientist, and Dr. Bruce Bean, were deep-sea kayaking off Cape Cod when danger struck out of nowhere. Almost instantaneously in their separate kayaks, they were hit with one of the most baffling conditions an athlete can face: muscle cramping.

Rod and Bruce had checked all the boxes of nutrition, hydration and conditioning before their launch. What they learned the hard way was that the familiar preventative measures for cramps most athletes turn to (bananas, magnesium tablets, electrolyte drinks, etc.) were mostly based on wild guesses, not science. That life-threatening experience flipped the switch on their curiosity.

What they discovered is a performance unlock that goes beyond just muscle cramps.


They quickly learned cramps are not triggered by dehydration, electrolyte imbalance, or even the lack of training or conditioning.  Significant research over the years has pointed to something else altogether. It’s neurological.

In an important study with over 200 Ironman triathletes, no difference was shown in hydration levels in the athletes suffering muscle cramping from those who did not. Nor was there any evidence cramping results from a loss of electrolytes as a result of sweating. There was also no difference in level of preparation – in fact, the only correlation was that the fastest athletes were more likely to cramp.1

In truth, cramping is like a mini-seizure localized to the neurons that control the contraction of a particular muscle. In exercise-associated muscle cramping, this is almost always a muscle that has undergone prolonged repetitive use. The localization of cramping to muscles being used heavily is more evidence against the idea that it results from changes in blood levels of water or electrolytes, which would affect all muscles.

We know the firing of motor neurons is sensitive to inputs from a huge number of other neurons – the most powerful are inputs coming from the conscious brain to initiate the voluntary muscle contraction, but there are also inputs coming back into the spinal cord from nerves originating in the muscle itself, which report on the degree of contraction of the muscle. Most of the time, this positive feedback is helpful in promoting the most effective use of the muscle. But just a small perturbation might switch the system into uncontrolled oscillation.

In one experiment, a group of scientists demonstrated that muscle cramping requires feedback from the muscle to the spinal cord. When the nerve back from the muscle to the spinal cord is blocked by anesthetic, the muscle no longer cramps.2

Delayed Onset Muscle Soreness (DOMS) affects both elite and recreational athletes alike. For a time, many thought the build-up of lactic acid was the cause of next-day muscle soreness, but that misconception was disproved decades ago. While there’s still a lot unknown about DOMS, research has shown it is triggered by eccentric exercise where greater mechanical stress happens: activities like the lowering of a weight during a shoulder press or curl, the downward motion of a push up, the lowering of the body during a crunch, or running / walking downhill.

Like cramps, research supports the idea that nerves are playing a role in that feeling of delayed muscle pain from the mechanical stress.  DOMS start with microtrauma to muscles that comes with intense or new eccentric exercise. As part of the recovery process, the inflammatory response such as fluids and electrolytes begin to move to the strained muscle and begin to stimulate free nerve endings which then create the sensation of pain that we feel.

“Although the exact cellular mechanisms involved in DOMS are unknown, a model was proposed by Armstrong in 1984 and has continued to be validated and refined by researchers in more recent years. The proposed cellular mechanisms occur as follows: 1) High tension in muscle fiber results in microtrauma, 2) Structural damage of the cell membrane disrupts calcium homeostasis, causing necrosis, that peaks 48 hours post exercise, and 3) Intracellular contents, such as histamine, kinins, and potassium, and the products of the inflammatory process accumulate in the interstitium, stimulating the free nerve endings, which result in the pain associated with DOMS.”

South African Family Practice in 20153

One response to the impact of this mechanical stress is to alter the feedback systems between muscle and the muscle circuits that control them, which include sensory neurons with endings in the muscle fibers.

Prevention of muscle soreness is difficult as it is a physiological response to exercise and activity.  The most effective preventative measure would be abstaining from intense or new exercises altogether… but that is unrealistic for any athlete.  Minimizing that feeling of delayed soreness post exercise without interfering with the recovery process is the best way to help athletes keep working out until their body adjusts and adapts and DOMS subside.



There have always been stories about bicyclists using pickle brine to treat muscle cramps and marathoners using mustard mixed into warm water to relieve their cramps. It occurred to Rod and Bruce that pickle brine and mustard most likely activate TRP channels in the mouth, esophagus and stomach that can trigger a response from the nervous system that calms down the motor neurons in the spinal cord.

Many of the sensory neurons in the mouth, esophagus, and stomach project (send a signal) to the brain, and others project directly to the spinal cord. The sensory neurons that project to the brainstem are activated by the TRPV1 and TRPA1 stimulators and then in the brain, cause changes in activity of the neurons from the brain that project to the spinal cord and regulate motor neuron excitability. Through this, they reduce excitability to stop a muscle cramp and reduce delayed onset muscle soreness.

Rod and Bruce realized there are much more potent and efficacious TRPV1 and TRPA1 activators than pickle brine available in many natural products, including capsicum (TRPV1), mustard (TRPA1), wasabi (TRPA1), garlic (TRPA1), and many others so they set out to find the perfect combination.



HOTSHOT is a proprietary formulation of natural ingredients specifically designed to trigger the TRPV1 and TRPA1 activators and is the first scientifically proven formula to prevent and treat muscle cramps and muscle soreness.

HOTSHOT has been proven to work by researchers at Penn State University4 and in numerous Field Studies and an in-Home Use Test. Results from the cramping research have been presented at the American Academy of Neurology, the Conference of Experimental Biology and the Society for Neuroscience and published in Muscle & Nerve magazine and the American Medical Athletic Association Journal.


 1: Schwellnus MP, Drew N, Collins M. (2011) Increased running speed and previous cramps rather than dehydration or serum sodium changes predict exercise-associated muscle cramping: a prospective cohort study in 210 Ironman triathletes. Br J Sports Med. 45:650-656.

2: M.A.Minetto, A.Holobar, A.Botter,R.Ravenni, D.Farina,J.Physiol Mechanisms of cramp contractions: Peripheral or central generation 589:5759-5773,2011

3: PC Zondi, DC Jansevan Rensburg, CC Grant, A Jansen va Rensburg

4: Craighead DH, Shank SW, Gottschall JS, Passe DH, Murray B, Alexander LM, Kenney WL. Ingestion of transient receptor potential channel agonists attenuates exercise-induced muscle cramps. (2017) Muscle Nerve. 56:379-385.


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