Changes

''Bala'' (physical fitness) of the individual has to be assessed through ''[[vyayama]] shakti'' (exercise capacity), which corresponds to the time taken for spending one’s ''ardha shakti'' (half strength). Based on the outcome of this assessment, ''pravara'' (maximum), ''avara'' (minimum) and ''madhyama'' (medium) ''bala'' have to be assessed. Based upon the results of these ''bala'' assessments, ''maha sweda'' (whole body sudation for an extended duration) and various minor/major ''sweda'' measures could be prescribed.

''Bala'' (physical fitness) of the individual has to be assessed through ''[[vyayama]] shakti'' (exercise capacity), which corresponds to the time taken for spending one’s ''ardha shakti'' (half strength). Based on the outcome of this assessment, ''pravara'' (maximum), ''avara'' (minimum) and ''madhyama'' (medium) ''bala'' have to be assessed. Based upon the results of these ''bala'' assessments, ''maha sweda'' (whole body sudation for an extended duration) and various minor/major ''sweda'' measures could be prescribed.

Exercise intolerance has a significant impact on heat intolerance. People who exhibit exercise intolerance (like in the case of mitochondrial diseases, or in persons leading a sedentary lifestyle) may have autonomic dysfunction including vascular autonomia characterized by tachycardia, dizziness, changes in heart rate and blood pressure, heat intolerance and unusual sweating pattern. Also, deficiency in energy metabolism may cause exercise intolerance and reduced stamina. It is evident that exercise intolerance leads to heat intolerance and abnormal sweating pattern, making it difficult - and hazardous- to conduct ''[[swedana]]'' in those individuals. An interesting observation is that if an individual is acclimatized to hot environment, he gradually attains exercise tolerance by an increase in plasma and thereby increase in blood volume, increased venous return, increased cardiac output, sub maximal heart rate, sustained sweat response, earlier onset of sweat and increased capacity for evaporative cooling, decreased osmolality of sweat and electrolyte conservation and decreased likelihood for fatigue<ref name="ref2">Kondo, N., et. al, (2009), Global Environmental research, Thermoregulatory adaptations in Humans and its modifying factors, 13 (1), 35 - 41.- online research</ref>

Exercise intolerance has a significant impact on heat intolerance. People who exhibit exercise intolerance (like in the case of mitochondrial diseases, or in persons leading a sedentary lifestyle) may have autonomic dysfunction including vascular autonomia characterized by tachycardia, dizziness, changes in heart rate and blood pressure, heat intolerance and unusual sweating pattern. Also, deficiency in energy metabolism may cause exercise intolerance and reduced stamina. It is evident that exercise intolerance leads to heat intolerance and abnormal sweating pattern, making it difficult - and hazardous- to conduct ''[[swedana]]'' in those individuals. An interesting observation is that if an individual is acclimatized to hot environment, he gradually attains exercise tolerance by an increase in plasma and thereby increase in blood volume, increased venous return, increased cardiac output, sub maximal heart rate, sustained sweat response, earlier onset of sweat and increased capacity for evaporative cooling, decreased osmolality of sweat and electrolyte conservation and decreased likelihood for fatigue<ref name="ref2"> Kondo, N., et. al, (2009), Global Environmental research, Thermoregulatory adaptations in Humans and its modifying factors, 13 (1), 35 - 41.</ref>

Contemporary science believes that heat has a beneficial effect (through thermotherapy, for instance) on pain relief. Effect of heat on pain is mediated by heat-sensitive channels. These channels respond to heat by increasing intracellular calcium (Ca). An increase in intracellular Ca generates action potentials that increase the stimulation of sensory nerves. These channels are a part of a family of receptors called TRPV receptors. TRPV1 and TRPV2 channels are sensitive to noxious heat, while TRPV4 channels are sensitive to normal physiological heat. These channels have certain characteristics in common, such as sensitivity to menthol, etc. Multiple binding sites allow a number of factors to activate these channels. Once activated, they can also inhibit the purin pain receptors. These receptors, termed as P2X2 and P2Y2, are mediated pain receptors located in the peripheral small nerve endings. For peripheral pain, heat can directly inhibit pain. However when pain is originating from deeper tissues, heat stimulates peripheral pain receptors that can alter what can be termed as “gating” in the spinal cord and reduce the sensation of deep pain. Another effect of heat is its ability to increase circulation. These same TRPV1 and TRPV4 receptors, along with nociceptor, increase blood flow in response to heat. The initial response to heat is mediated through the sensory nerves that release substance P and calcitonin-related peptide to increase circulation. After approximately one minute, Nitric Oxide is produced in vasculature endothelial cells and is responsible for sustained response of circulation to heat. This increase in circulation is considered to be essential in tissue protection from heat and repair of damaged tissue. Thermotherapy is of two types: dry and moist. A study was conducted to assess the effect of moist and dry heat on delayed onset of muscle soreness. Moist heat not only had similar benefits as dry heat but in some cases was more beneficial, requiring only 25% of time for application as dry heat. This study was conducted on quadriceps muscles. The study also witnessed immediate (and maximum) reduction in pain on application of moist heat, since moist heat penetrates deeper tissues faster than dry heat. Also, dry heat draws out moisture from the areas of application leaving them dehydrated, unlike moist heat.  

Contemporary science believes that heat has a beneficial effect (through thermotherapy, for instance) on pain relief. Effect of heat on pain is mediated by heat-sensitive channels. These channels respond to heat by increasing intracellular calcium (Ca). An increase in intracellular Ca generates action potentials that increase the stimulation of sensory nerves. These channels are a part of a family of receptors called TRPV receptors. TRPV1 and TRPV2 channels are sensitive to noxious heat, while TRPV4 channels are sensitive to normal physiological heat. These channels have certain characteristics in common, such as sensitivity to menthol, etc. Multiple binding sites allow a number of factors to activate these channels. Once activated, they can also inhibit the purin pain receptors. These receptors, termed as P2X2 and P2Y2, are mediated pain receptors located in the peripheral small nerve endings. For peripheral pain, heat can directly inhibit pain. However when pain is originating from deeper tissues, heat stimulates peripheral pain receptors that can alter what can be termed as “gating” in the spinal cord and reduce the sensation of deep pain. Another effect of heat is its ability to increase circulation. These same TRPV1 and TRPV4 receptors, along with nociceptor, increase blood flow in response to heat. The initial response to heat is mediated through the sensory nerves that release substance P and calcitonin-related peptide to increase circulation. After approximately one minute, Nitric Oxide is produced in vasculature endothelial cells and is responsible for sustained response of circulation to heat. This increase in circulation is considered to be essential in tissue protection from heat and repair of damaged tissue. Thermotherapy is of two types: dry and moist. A study was conducted to assess the effect of moist and dry heat on delayed onset of muscle soreness. Moist heat not only had similar benefits as dry heat but in some cases was more beneficial, requiring only 25% of time for application as dry heat. This study was conducted on quadriceps muscles. The study also witnessed immediate (and maximum) reduction in pain on application of moist heat, since moist heat penetrates deeper tissues faster than dry heat. Also, dry heat draws out moisture from the areas of application leaving them dehydrated, unlike moist heat.  

#Expanded plasma volume  

#Expanded plasma volume  

#lower core temperature at an equivalent workload, and  

#lower core temperature at an equivalent workload, and  

#Superior Na and Cl reabsorption from sweat, and an elevated sweat secretion. <ref name="ref2">Kondo, N., et. al, (2009), Global Environmental research, Thermoregulatory adaptations in Humans and its modifying factors, 13 (1), 35 - 41.</ref> [verse 13]

#Superior Na and Cl reabsorption from sweat, and an elevated sweat secretion. <ref name="ref2"/> [verse 13]

It is very essential to differentiate heat exhaustion from heatstroke. Both come under the concept of ''atiswinna'' (over sudation). But from the treatment advised for ''atiswinna'', we may infer it as heat exhaustion. Contemporary science advises fluid replacement therapy for heat exhaustion whereas rapid aggressive cooling techniques are prescribed for heat stroke. [[Charak Samhita]] advises treatment procedures that include ''greeshma ritucharya'' along with ''madhura, snigdha, seethala prayogas'' as ''ahara'' & ''vihara''. Symptoms of heat exhaustion include normal to slightly elevated core temperature (39 – 40°C), fatigue or malaise, orthostatic hypotension, tachycardia, clinical signs of dehydration, nausea, vomiting, and diarrhea (due to splanchnic and renal vasoconstriction). Similarly, Symptoms of heat stroke include elevated core temperature (usually greater than 40.5°C), vague symptom of weakness, nausea, vomiting, headache, CNS symptoms including confusion, ataxia, coma, seizures, delirium, hot, dry skin, hyperdynamic cardiovascular systems (high central venous pressure [CVP], low systemic vascular resistance [SVR], tachycardia), elevated hepatic transaminases (usually in the tens of thousands range), coagulopathy, rhabdomyolysis, and renal failure <ref name="ref1" /> [verse 14-15]

It is very essential to differentiate heat exhaustion from heatstroke. Both come under the concept of ''atiswinna'' (over sudation). But from the treatment advised for ''atiswinna'', we may infer it as heat exhaustion. Contemporary science advises fluid replacement therapy for heat exhaustion whereas rapid aggressive cooling techniques are prescribed for heat stroke. [[Charak Samhita]] advises treatment procedures that include ''greeshma ritucharya'' along with ''madhura, snigdha, seethala prayogas'' as ''ahara'' & ''vihara''. Symptoms of heat exhaustion include normal to slightly elevated core temperature (39 – 40°C), fatigue or malaise, orthostatic hypotension, tachycardia, clinical signs of dehydration, nausea, vomiting, and diarrhea (due to splanchnic and renal vasoconstriction). Similarly, Symptoms of heat stroke include elevated core temperature (usually greater than 40.5°C), vague symptom of weakness, nausea, vomiting, headache, CNS symptoms including confusion, ataxia, coma, seizures, delirium, hot, dry skin, hyperdynamic cardiovascular systems (high central venous pressure [CVP], low systemic vascular resistance [SVR], tachycardia), elevated hepatic transaminases (usually in the tens of thousands range), coagulopathy, rhabdomyolysis, and renal failure <ref name="ref1" /> [verse 14-15]